Williams Gynecology, 3E [TRUE PDF] [3rd Edition] 0071849092, 9780071849098, 9780071849081

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Williams

GYNECOLOGY

NOTICE Medicine is an ever-changing science. As new research and clinical experience broaden our knowledge, changes in treatment and drug therapy are required. The authors and the publisher of this work have checked with sources believed to be reliable in their efforts to provide information that is complete and generally in accord with the standards accepted at the time of publication. However, in view of the possibility of human error or changes in medical sciences, neither the authors nor the publisher nor any other party who has been involved in the preparation or publication of this work warrants that the information contained herein is in every respect accurate or complete, and they disclaim all responsibility for any errors or omissions or for the results obtained from use of the information contained in this work. Readers are encouraged to confirm the information contained herein with other sources. For example and in particular, readers are advised to check the product information sheet included in the package of each drug they plan to administer to be certain that the information contained in this work is accurate and that changes have not been made in the recommended dose or in the contraindications for administration. This recommendation is of particular importance in connection with new or infrequently used drugs.

Williams

GYNECOLOGY THIRD EDITION Barbara L. Hoffman, MD John O. Schorge, MD Karen D. Bradshaw, MD Lisa M. Halvorson, MD Joseph I. Schaffer, MD Marlene M. Corton, MD

New York╇╇Chicago╇╇San Francisco╇╇Lisbon╇╇London╇╇Madrid╇╇Mexico City╇╇ Milan╇╇New Delhi╇╇San Juan╇╇Seoul╇╇Singapore╇╇Sydney╇╇Toronto

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DEDICATION This edition of Williams Gynecology is dedicated to David L. Hemsell, MD, who served as Director of the Division of Gynecology at the University of Texas Southwestern Medical Center and Parkland Memorial Hospital for more than 20 years. During this tenure, his national awards have included a Meritorious Achievement award from the Infectious Diseases Society of America and an Outstanding Service award from the American College of Obstetricians and Gynecologists. Early in his training, Dr. Hemsell joined the Air Force and served our country as a Flight Medical Officer. In these years, he pursued specialty training in reproductive endocrinology with Dr. Paul MacDonald. He joined our faculty as the Division Director of Gynecology in 1977. In addition to his Director role, Dr. Hemsell was the Chief of Gynecology at Parkland Memorial Hospital and Medical Director of the Parkland Obstetrics and Gynecology Emergency Room. In these roles, Dr. Hemsell created an environment in which evidence-based medicine was the standard for care. Accordingly, patients, residents, and junior faculty all benefitted from this scientific health care approach. He also served as Director of the Faculty Sexual Assault Examination and Testimony Program. In that role, he coordinated the examinations of many thousands of sexual assault victims and the collection of legal evidence. As a result of his efforts, Dallas County has a system regarded as among the best in medical and legal care for these victims. During his academic career, Dr. Hemsell added foundational knowledge regarding the etiology, pathogenesis, and treatment of female pelvic infections, especially those following gynecologic surgeries. With this expertise, he served as journal reviewer for multiple journals. He has added to academic knowledge through his nearly 50 book chapters and 100 peer-reviewed articles on multiple gynecologic topics. For us in the Department of Obstetrics and Gynecology, Dr. Hemsell plays an important role of mentor and colleague. His experience and clinical expertise are invaluable and provide a valuable sounding board for challenging gynecology cases. On so many levels, we have benefitted greatly from his academic and clinical contributions.

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CONTENTS Editors. . . . . . . . . . . . . . . . . .å°“ . . . . . . . . . . . . . . . . . .å°“ . . . . . . . . . . . . . . . . . .å°“ . . . . . . . . . . . . . . . . . .å°“ . . . . . . . . . . . . . . . . . .å°“ xiii Contributors. . . . . . . . . . . . . . . . . .å°“ . . . . . . . . . . . . . . . . . .å°“ . . . . . . . . . . . . . . . . . .å°“ . . . . . . . . . . . . . . . . . .å°“ . . . . . . . . . . . . . xv Artists. . . . . . . . . . . . . . . . . .å°“ . . . . . . . . . . . . . . . . . .å°“ . . . . . . . . . . . . . . . . . .å°“ . . . . . . . . . . . . . . . . . .å°“ . . . . . . . . . . . . . . . . . .å°“ xix Preface. . . . . . . . . . . . . . . . . .å°“ . . . . . . . . . . . . . . . . . .å°“ . . . . . . . . . . . . . . . . . .å°“ . . . . . . . . . . . . . . . . . .å°“ . . . . . . . . . . . . . . . . . xxi Acknowledgments. . . . . . . . . . . . . . . . . .å°“ . . . . . . . . . . . . . . . . . .å°“ . . . . . . . . . . . . . . . . . .å°“ . . . . . . . . . . . . . . . . . .å°“ . . . . . xxiii

SECTION 1 BENIGN GENERAL GYNECOLOGY ╇ 1. Well Woman Care . . . . . . . . . . . . . . . . . .尓 . . . . .

2

╇ 8. Abnormal Uterine Bleeding. . . . . . . . . . . . . . 180

╇ 2. Techniques Used for Imaging in Gynecology . . . . . . . . . . . . . . . . . .尓 . . . . . . . . . 22

╇ 9. Pelvic Mass . . . . . . . . . . . . . . . . . .尓 . . . . . . . . . . . . 202

╇ 3. Gynecologic Infection. . . . . . . . . . . . . . . . . .尓 . 50

11. Pelvic Pain. . . . . . . . . . . . . . . . . .å°“ . . . . . . . . . . . . . 249

╇ 4. Benign Disorders of the Lower Genital Tract . . . . . . . . . . . . . . . . . .尓 . . 86 ╇ 5. Contraception and Sterilization. . . . . . . . . 105 ╇ 6. First-Trimester Abortion . . . . . . . . . . . . . . . . 137 ╇ 7. Ectopic Pregnancy. . . . . . . . . . . . . . . . . .尓 . . . . 161

10. Endometriosis . . . . . . . . . . . . . . . . . .å°“ . . . . . . . . . 230 12. Breast Disease. . . . . . . . . . . . . . . . . .å°“ . . . . . . . . . 275 13. Psychosocial Issues and Female Sexuality . . . . . . . . . . . . . . . . . .å°“ . . . . . . 297 14. Pediatric Gynecology. . . . . . . . . . . . . . . . . .å°“ . . 318

vii

viii

Contents

SECTION 2 REPRODUCTIVE ENDOCRINOLOGY, INFERTILITY, AND THE MENOPAUSE 15. Reproductive Endocrinology . . . . . . . . . . . . 334

19. Evaluation of the Infertile Couple. . . . . . . . 427

16. Amenorrhea . . . . . . . . . . . . . . . . . .å°“ . . . . . . . . . . 369

20. Treatment of the Infertile Couple. . . . . . . . 449

17. Polycystic Ovarian Syndrome and Hyperandrogenism . . . . . . . . . . . . . . . . . 386

21. Menopausal Transition. . . . . . . . . . . . . . . . . .å°“ 471

18. Anatomic Disorders . . . . . . . . . . . . . . . . . .å°“ . . . 404

22. The Mature Woman. . . . . . . . . . . . . . . . . .å°“ . . . 492

SECTION 3 FEMALE PELVIC MEDICINE AND RECONSTRUCTIVE SURGERY 23. Urinary Incontinence. . . . . . . . . . . . . . . . . .å°“ . . 514 24. Pelvic Organ Prolapse. . . . . . . . . . . . . . . . . .å°“ . 538

25. Anal Incontinence and Functional Anorectal Disorders . . . . . . . . . . . . . . . . . .å°“ . . . 561 26. Genitourinary Fistula and Urethral Diverticulum . . . . . . . . . . . . . . . . . .å°“ . 577

SECTION 4 GYNECOLOGIC ONCOLOGY 27. Principles of Chemotherapy. . . . . . . . . . . . . 592

33. Endometrial Cancer . . . . . . . . . . . . . . . . . .å°“ . . . 702

28. Principles of Radiation Therapy. . . . . . . . . . 610

34. Uterine Sarcoma . . . . . . . . . . . . . . . . . .å°“ . . . . . . 722

29. Preinvasive Lesions of the Lower Genital Tract . . . . . . . . . . . . . . . . . .å°“ . . . 624

35. Epithelial Ovarian Cancer. . . . . . . . . . . . . . . . 735

30. Cervical Cancer. . . . . . . . . . . . . . . . . .å°“ . . . . . . . . 657

36. Ovarian Germ Cell and Sex Cord-Stromal Tumors . . . . . . . . . . . . . . . 760

31. Vulvar Cancer . . . . . . . . . . . . . . . . . .å°“ . . . . . . . . . 679

37. Gestational Trophoblastic Disease. . . . . . . 779

32. Vaginal Cancer. . . . . . . . . . . . . . . . . .å°“ . . . . . . . . 694

Contents

SECTION 5 ASPECTS OF GYNECOLOGIC SURGERY 38. Anatomy. . . . . . . . . . . . . . . . . .å°“ . . . . . . . . . . . . . . 796 39. Preoperative Considerations. . . . . . . . . . . . . 825 40. Intraoperative Considerations . . . . . . . . . . . 841

41. Minimally Invasive Surgery Fundamentals. . . . . . . . . . . . . . . . . .å°“ . . . . . . . . . 874 42. Postoperative Considerations. . . . . . . . . . . . 908

SECTION 6 ATLAS OF GYNECOLOGIC SURGERY 43. Surgeries for Benign Gynecologic Disorders. . . . . . . . . . . . . . . 926

43-19. Bartholin Gland Duct Marsupialization . . . . . . . . . . . . . . . . . .å°“ . . . 973

43-1. Midline Vertical Incision . . . . . . . . . . . . . . 926

43-20. Bartholin Gland Duct Cystectomy. . . . . 975

43-2. Pfannenstiel Incision . . . . . . . . . . . . . . . . . 929

43-21. Vulvar Abscess Incision and Drainage . . . . . . . . . . . . . . . . . .å°“ . . . . . . 977

43-3. Cherney Incision . . . . . . . . . . . . . . . . . .å°“ . . . 931 43-4. Maylard Incision. . . . . . . . . . . . . . . . . .å°“ . . . . 932 43-5. Ovarian Cystectomy. . . . . . . . . . . . . . . . . .å°“ 933 43-6. Salpingo-oophorectomy . . . . . . . . . . . . . 935 43-7. Interval Partial Salpingectomy . . . . . . . . 937 43-8. Salpingectomy and Salpingostomy . . . . 939 43-9. Cornuostomy and Cornual Wedge Resection . . . . . . . . . . . . . . . . . .å°“ . . . . . . . . . . 941 43-10. Abdominal Myomectomy . . . . . . . . . . . . 945 43-11. Vaginal Myomectomy for Prolapsed Leiomyoma. . . . . . . . . . . . . . . . 948 43-12. Abdominal Hysterectomy. . . . . . . . . . . . . 950 43-13. Vaginal Hysterectomy . . . . . . . . . . . . . . . . 957

43-22. Vestibulectomy . . . . . . . . . . . . . . . . . .å°“ . . . . 979 43-23. Labia Minora Reduction . . . . . . . . . . . . . . 981 43-24. Vaginal Septum Excision . . . . . . . . . . . . . 983 43-25. McIndoe Procedure . . . . . . . . . . . . . . . . . .å°“ 985 43-26. Treatment of Preinvasive Ectocervical Lesions . . . . . . . . . . . . . . . . . .å°“ 988 43-27. Cervical Conization. . . . . . . . . . . . . . . . . .å°“ . 992 43-28. Treatment of Vulvar Intraepithelial Neoplasia. . . . . . . . . . . . . . 995 44. Minimally Invasive Surgery. . . . . . . . . 1003 44-1. Diagnostic Laparoscopy. . . . . . . . . . . . 1003 44-2. Laparoscopic Sterilization . . . . . . . . . . . 1006

43-14. Trachelectomy . . . . . . . . . . . . . . . . . .å°“ . . . . . 962

44-3. Laparoscopic Salpingectomy . . . . . . . 1011

43-15. Sharp Dilatation and Curettage. . . . . . . . . . . . . . . . . .å°“ . . . . . . 964

44-4. Laparoscopic Salpingostomy . . . . . . . 1013 44-5. Laparoscopic Ovarian Cystectomy . . . . 1015

43-16. Suction Dilatation and Curettage . . . . . . . . . . . . . . . . . .å°“ . . . . . 966

44-6. Laparoscopic Salpingo-oophorectomy . . . . . . . . . . . 1019

43-17. Hymenectomy . . . . . . . . . . . . . . . . . .å°“ . . . . . 969

44-7. Ovarian Drilling . . . . . . . . . . . . . . . . . .å°“ . . . 1021

43-18. Bartholin Gland Duct Incision and Drainage. . . . . . . . . . . . . . . . . .å°“ . . . . . . . 971

44-8. Laparoscopic Myomectomy . . . . . . . . 1022 44-9. Laparoscopic Hysterectomy . . . . . . . . 1026

ix

x

Contents

44-10. Laparoscopic Supracervical Hysterectomy. . . . . . . . . . . . . . . . . .å°“ . . . . 1030

45-19. Vaginal Uterosacral Ligament Suspension. . . . . . . . . . . . . . . 1107

44-11. Total Laparoscopic Hysterectomy. . . . . . . . . . . . . . . . . .å°“ . . . . 1033

45-20. Abdominal Uterosacral Ligament Suspension. . . . . . . . . . . . . . . . . .å°“ . . . . . . . 1110

44-12. Diagnostic Hysteroscopy. . . . . . . . . . . 1037

45-21. Sacrospinous Ligament Fixation. . . . . . . . . . . . . . . . . .å°“ . . . . . . . . . . . 1112

44-13. Hysteroscopic Polypectomy . . . . . . . . 1038 44-14. Hysteroscopic Myomectomy . . . . . . . 1040 44-15. Endometrial Ablation Procedures. . . 1043 44-16. Transcervical Sterilization . . . . . . . . . . 1046 44-17. Hysteroscopic Septoplasty . . . . . . . . . 1048 44-18. Proximal Fallopian Tube Cannulation. . . . . . . . . . . . . . . . . .å°“ . . . . . . . 1050 44-19. Lysis of Intrauterine Adhesions . . . . . 1052 45.

Surgeries for Pelvic Floor Disorders . . . . . . . . . . . . . . . . . 1057

45-1. Diagnostic and Operative Cystoscopy and Urethroscopy . . . . . . 1057 45-2. Burch Colposuspension . . . . . . . . . . . . 1061

45-22. McCall Culdoplasty. . . . . . . . . . . . . . . . . .å°“ 1116 45-23. Abdominal Culdoplasty Procedures . . . . . . . . . . . . . . . . . .å°“ . . . . . . . 1118 45-24. Colpocleisis. . . . . . . . . . . . . . . . . .å°“ . . . . . . . 1120 45-25. Anal Sphincteroplasty . . . . . . . . . . . . . . 1125 45-26. Rectovaginal Fistula Repair . . . . . . . . . 1128 46.

Surgeries for Gynecologic Malignancies . . . . . . . . . . . . . . . . . .å°“ . 1134

46-1. Radical Abdominal Hysterectomy (Type III). . . . . . . . . . . . . . . . . .å°“ . . . . . . . . . . . . . . 1134 46-2. Modified Radical Abdominal Hysterectomy (Type II) . . . . . . . . . . . . . . 1140

45-3. Tension-free Vaginal Tape. . . . . . . . . . 1063

46-3. Minimally Invasive Radical Hysterectomy. . . . . . . . . . . . . . . . . .å°“ . . . . . 1142

45-4. Transobturator Tape Sling. . . . . . . . . . 1066

46-4. Total Pelvic Exenteration. . . . . . . . . . . . 1149

45-5. Pubovaginal Sling. . . . . . . . . . . . . . . . . .å°“ 1068

46-5. Anterior Pelvic Exenteration. . . . . . . . . 1155

45-6. Urethral Bulking Injections. . . . . . . . . . . 1070

46-6. Posterior Pelvic Exenteration. . . . . . . . 1156

45-7. Urethrolysis . . . . . . . . . . . . . . . . . .å°“ . . . . . . . 1072

46-7. Incontinent Urinary Conduit . . . . . . . . 1157

45-8. Midurethral Sling Release . . . . . . . . . . . 1074

46-8. Continent Urinary Conduit. . . . . . . . . . 1161

45-9. Urethral Diverticulum Repair . . . . . . . . 1075

46-9. Vaginal Reconstruction . . . . . . . . . . . . . 1165

45-10. Vesicovaginal Fistula Repair . . . . . . . . 1078

46-10. Pelvic Lymphadenectomy. . . . . . . . . . . 1169

45-11. Martius Bulbocavernosus Fat Pad Flap . . . . . . . . . . . . . . . . . .å°“ . . . . . . 1083

46-11. Paraaortic Lymphadenectomy . . . . . . 1172

45-12. Sacral Neuromodulation . . . . . . . . . . . 1085

46-12. Minimally Invasive Staging for Gynecologic Malignancies . . . . . . . . . . 1176

45-13. Anterior Colporrhaphy . . . . . . . . . . . . . 1088

46-13. En Bloc Pelvic Resection . . . . . . . . . . . . 1182

45-14. Abdominal Paravaginal Defect Repair . . . . . . . . . . . . . . . . . .å°“ . . . . . 1091

46-14. Omentectomy. . . . . . . . . . . . . . . . . .å°“ . . . . 1186

45-15. Posterior Colporrhaphy. . . . . . . . . . . . . 1093 45-16. Perineorrhaphy . . . . . . . . . . . . . . . . . .å°“ . . 1096 45-17. Abdominal Sacrocolpopexy . . . . . . . . 1098 45-18. Minimally Invasive Sacrocolpopexy. . . . . . . . . . . . . . . . . .å°“ . . 1103

46-15. Splenectomy . . . . . . . . . . . . . . . . . .å°“ . . . . . 1188 46-16. Diaphragmatic Surgery . . . . . . . . . . . . . 1190 46-17. Colostomy. . . . . . . . . . . . . . . . . .å°“ . . . . . . . . 1192 46-18. Large Bowel Resection. . . . . . . . . . . . . . 1195 46-19. Ileostomy. . . . . . . . . . . . . . . . . .å°“ . . . . . . . . . 1197

Contents

46-20. Small Bowel Resection . . . . . . . . . . . . . . 1198

46-25. Radical Partial Vulvectomy . . . . . . . . . . 1210

46-21. Low Anterior Resection. . . . . . . . . . . . . . 1200

46-26. Radical Complete Vulvectomy. . . . . . . 1213

46-22. Intestinal Bypass. . . . . . . . . . . . . . . . . .å°“ . . 1204

46-27. Inguinofemoral Lymphadenectomy. . . . . . . . . . . . . . . . . 1216

46-23. Appendectomy. . . . . . . . . . . . . . . . . .å°“ . . . 1206 46-24. Skinning Vulvectomy . . . . . . . . . . . . . . . 1208

46-28. Reconstructive Grafts and Flaps . . . . . 1219

Index. . . . . . . . . . . . . . . . . .å°“ . . . . . . . . . . . . . . . . . .å°“ . . . . . . . . . . . . . . . . . .å°“ . . . . . . . . . . . . . . . . . .å°“ . . . . . . . . . . . . . . . . . .å°“ 1225

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EDITORS Barbara L. Hoffman, MD

Lisa M. Halvorson, MD

Associate Professor, Department of Obstetrics and Gynecology University of Texas Southwestern Medical Center at Dallas

Bethesda, Maryland

John O. Schorge, MD, FACOG, FACS

Holder, Frank C. Erwin, Jr. Professorship in Obstetrics and Gynecology Director, Division of Gynecology Director, Division of Female Pelvic Medicine and Reconstructive Surgery Professor, Department of Obstetrics and Gynecology University of Texas Southwestern Medical Center at Dallas Chief of Gynecology, Parkland Memorial Hospital, Dallas

Chief of Gynecology and Gynecologic Oncology Associate Professor, Department of Obstetrics and Gynecology Massachusetts General Hospital–Harvard Medical School

Karen D. Bradshaw, MD Holder, Helen J. and Robert S. Strauss and Diana K. and Richard C. Strauss Chair in Women’s Health Director, Lowe Foundation Center for Women’s Preventative Health Care Professor, Department of Obstetrics and Gynecology Professor, Department of Surgery University of Texas Southwestern Medical Center at Dallas

Joseph I. Schaffer, MD

Marlene M. Corton, MD, MSCS Director, Anatomical Education and Research Professor, Department of Obstetrics and Gynecology University of Texas Southwestern Medical Center at Dallas

Atlas Art Director Lewis E. Calver, MS, CMI, FAMI Associate Professor, Department of Obstetrics and Gynecology University of Texas Southwestern Medical Center at Dallas

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CONTRIBUTORS April A. Bailey, MD

David M. Euhus, MD

Assistant Professor, Department of Radiology Assistant Professor, Department of Obstetrics and Gynecology University of Texas Southwestern Medical Center at Dallas Chapter 2: Techniques Used for Imaging in Gynecology Co-Director of Radiologic Images for Williams Gynecology

Professor, Department of Surgery Johns Hopkins Hospital/University Chapter 12: Breast Disease

Sunil Balgobin, MD Assistant Professor, Department of Obstetrics and Gynecology University of Texas Southwestern Medical Center at Dallas Chapter 40: Intraoperative Considerations

Karen D. Bradshaw, MD Holder, Helen J. and Robert S. Strauss and Diana K. and Richard C. Strauss Chair in Women’s Health Director, Lowe Foundation Center for Women’s Preventative Health Care Professor, Department of Obstetrics and Gynecology Professor, Department of Surgery University of Texas Southwestern Medical Center at Dallas Chapter 13: Psychosocial Issues and Female Sexuality Chapter 18: Anatomic Disorders Chapter 21: Menopausal Transition Chapter 22: The Mature Woman

Anna R. Brandon, PhD, MCS, ABPP

Rajiv B. Gala, MD, FACOG Vice-Chair, Department of Obstetrics and Gynecology Residency Program Director, Department of Obstetrics and Gynecology Ochsner Clinic Foundation Associate Professor of Obstetrics and Gynecology University of Queensland Ochsner Clinical School Chapter 7: Ectopic Pregnancy Chapter 39: Preoperative Considerations Chapter 42: Postoperative Considerations

William F. Griffith, MD Medical Director, OB/GYN Emergency Services Director, Vulvology Clinic Co-Director, Dysplasia Services Parkland Health and Hospital System, Dallas, Texas Associate Professor, Department of Obstetrics and Gynecology University of Texas Southwestern Medical Center at Dallas Chapter 4: Benign Disorders of the Lower Genital Tract Chapter 29: Preinvasive Lesions of the Lower Genital Tract

Women’s Mood Disorders Center Department of Psychiatry University of North Carolina at Chapel Hill School of Medicine Department of Psychiatry University of Texas Southwestern Medical Center at Dallas Chapter 13: Psychosocial Issues and Female Sexuality

Lisa M. Halvorson, MD

Matthew J. Carlson, MD

Cherine A. Hamid, MD

Assistant Professor, Department of Obstetrics and Gynecology University of Texas Southwestern Medical Center at Dallas Chapter 34: Uterine Sarcoma

Medical Director—Gynecology Parkland Health and Hospital Systems, Dallas, Texas Associate Professor, Department of Obstetrics and Gynecology University of Texas Southwestern Medical Center at Dallas Chapter 40: Intraoperative Considerations

Kelley S. Carrick, MD Professor, Department of Pathology University of Texas Southwestern Medical Center at Dallas Director of Surgical Pathology Images for Williams Gynecology

Bethesda, Maryland Chapter 6: First-Trimester Abortion Chapter 15: Reproductive Endocrinology Chapter 16: Amenorrhea Chapter 19: Evaluation of the Infertile Couple

Barbara L. Hoffman, MD

Director, Anatomical Education and Research Professor, Department of Obstetrics and Gynecology University of Texas Southwestern Medical Center at Dallas Chapter 25: Anal Incontinence and Functional Anorectal Disorders Chapter 38: Anatomy Chapter 43: Surgeries for Benign Gynecologic Disorders Chapter 45: Surgeries for Pelvic Floor Disorders

Associate Professor, Department of Obstetrics and Gynecology University of Texas Southwestern Medical Center at Dallas Chapter 1: Well Woman Care Chapter 8: Abnormal Uterine Bleeding Chapter 9: Pelvic Mass Chapter 10: Endometriosis Chapter 11: Pelvic Pain Chapter 40: Intraoperative Considerations Chapter 43: Surgeries for Benign Gynecologic Disorders Chapter 45: Surgeries for Pelvic Floor Disorders

Kevin J. Doody, MD

Siobhan M. Kehoe, MD

Marlene M. Corton, MD, MSCS

Director, Center for Assisted Reproduction, Bedford, TX Clinical Professor, Department of Obstetrics and Gynecology University of Texas Southwestern Medical Center at Dallas Chapter 20: Treatment of the Infertile Couple

Assistant Professor, Department of Obstetrics and Gynecology University of Texas Southwestern Medical Center at Dallas Chapter 33: Endometrial Cancer

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Contributors Kimberly A. Kho, MD, MPH, MSCS, FACOG

David E. Rogers, MD, MBA

Assistant Professor, Department of Obstetrics and Gynecology Director of Gynecology, Southwestern Center for Minimally Invasive Surgery University of Texas Southwestern Medical Center at Dallas Chapter 41: Minimally Invasive Surgery Fundamentals Chapter 44: Minimally Invasive Surgery

Associate Professor, Department of Obstetrics and Gynecology University of Texas Southwestern Medical Center at Dallas Chapter 11: Pelvic Pain

Jayanthi S. Lea, MD Patricia Duniven Fletcher Distinguished Professor in Gynecologic Oncology Director, Gynecologic Oncology Fellowship Program Associate Professor, Department of Obstetrics and Gynecology University of Texas Southwestern Medical Center at Dallas Chapter 31: Vulvar Cancer Chapter 46: Surgeries for Gynecologic Malignancies

Eddie H. McCord, MD Associate Professor, Department of Obstetrics and Gynecology University of Texas Southwestern Medical Center at Dallas Chapter 3: Gynecologic Infection

David Scott Miller, MD, FACOG, FACS Holder, Dallas Foundation Chair in Gynecologic Oncology Medical Director of Gynecology Oncology Parkland Health and Hospital System, Dallas, Texas Director, Gynecologic Oncology Fellowship Program Director of Gynecologic Oncology Professor, Department of Obstetrics and Gynecology University of Texas Southwestern Medical Center at Dallas Chapter 33: Endometrial Cancer Chapter 34: Uterine Sarcoma

Elysia Moschos, MD Professor, Department of Obstetrics and Gynecology University of Texas Southwestern Medical Center at Dallas Administrative Director of Gynecologic Ultrasound Parkland Health and Hospital System Chapter 2: Techniques Used for Imaging in Gynecology Co-Director of Radiologic Images for Williams Gynecology

David M. Owens, MD Assistant Professor, Department of Obstetrics and Gynecology University of Texas Southwestern Medical Center at Dallas Chapter 11: Pelvic Pain

Mary Jane Pearson, MD Director, Third-year & Fourth-Year Medical Student Programs Professor, Department of Obstetrics and Gynecology University of Texas Southwestern Medical Center at Dallas Chapter 1: Well Woman Care

David D. Rahn, MD Associate Professor, Department of Obstetrics and Gynecology University of Texas Southwestern Medical Center at Dallas Chapter 3: Gynecologic Infection Chapter 23: Urinary Incontinence

Debra L. Richardson, MD, FACOG Assistant Professor, Department of Obstetrics and Gynecology University of Texas Southwestern Medical Center at Dallas Chapter 30: Cervical Cancer Chapter 32: Vaginal Cancer

Anthony H. Russell Associate Professor Department of Radiation Oncology Massachusetts General Hospital—Harvard Medical School Chapter 28: Principles of Radiation Therapy

Andrea L. Russo, MD Assistant Professor Department of Radiation Oncology Massachusetts General Hospital—Harvard Medical School Chapter 28: Principles of Radiation Therapy

John O. Schorge, MD, FACOG, FACS Chief of Gynecology and Gynecologic Oncology Associate Professor, Department of Obstetrics and Gynecology Massachusetts General Hospital—Harvard Medical School Chapter 27: Principles of Chemotherapy Chapter 33: Endometrial Cancer Chapter 34: Uterine Sarcoma Chapter 35: Epithelial Ovarian Cancer Chapter 36: Ovarian Germ Cell and Sex Cord-Stromal Tumors Chapter 37: Gestational Trophoblastic Disease Chapter 46: Surgeries for Gynecologic Malignancies

Joseph I. Schaffer, MD Holder, Frank C. Erwin, Jr. Professorship in Obstetrics and Gynecology Chief of Gynecology Parkland Health and Hospital System, Dallas, Texas Director, Division of Gynecology Director, Division of Female Pelvic Medicine and Reconstructive Surgery Professor, Department of Obstetrics and Gynecology University of Texas Southwestern Medical Center at Dallas Chapter 24: Pelvic Organ Prolapse Chapter 45: Surgeries for Pelvic Floor Disorders

Geetha Shivakumar, MD, MS Mental Health Trauma Services, Dallas VA Medical Center Assistant Professor, Department of Psychiatry University of Texas Southwestern Medical Center at Dallas Chapter 13: Psychosocial Issues and Female Sexuality

Gretchen S. Stuart, MD, MPHTM Director, Family Planning Program Director, Fellowship in Family Planning Assistant Professor, Department of Obstetrics and Gynecology University of North Carolina at Chapel Hill Chapter 5: Contraception and Sterilization

Mayra J. Thompson, MD, FACOG Professor, Department of Obstetrics and Gynecology University of Texas Southwestern Medical Center at Dallas Chapter 41: Minimally Invasive Surgery Fundamentals Chapter 44: Minimally Invasive Surgery

Contributors Clifford Y. Wai, MD

Ellen E. Wilson, MD

Director, Fellowship Program in Female Pelvic Medicine and Reconstructive Surgery Associate Professor, Department of Obstetrics and Gynecology University of Texas Southwestern Medical Center at Dallas Chapter 23: Urinary Incontinence Chapter 26: Genitourinary Fistula and Urethral Diverticulum

Director of Pediatric and Adolescent Gynecology Program Children’s Medical Center, Dallas, Texas Associate Professor, Department of Obstetrics and Gynecology University of Texas Southwestern Medical Center at Dallas Chapter 14: Pediatric Gynecology Chapter 17: Polycystic Ovarian Syndrome and Hyperandrogenism

Claudia L. Werner, MD Medical Director of Dysplasia Services Co-Director Vulvology Clinic Parkland Health and Hospital System, Dallas, Texas Professor, Department of Obstetrics and Gynecology University of Texas Southwestern Medical Center at Dallas Chapter 4: Benign Disorders of the Lower Genital Tract Chapter 29: Preinvasive Lesions of the Lower Genital Tract

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ARTISTS Atlas Art Director Lewis E. Calver, MS, CMI, FAMI Associate Professor, Department of Obstetrics and Gynecology University of Texas Southwestern Medical Center at Dallas

Contributing Atlas Artists Katherine Brown

Lindsay Oksenberg

Graduate, Biomedical Communications Graduate Program University of Texas Southwestern Medical Center at Dallas

Graduate, Biomedical Communications Graduate Program University of Texas Southwestern Medical Center at Dallas

SangEun Cha

Jordan Pietz

Graduate, Biomedical Communications Graduate Program University of Texas Southwestern Medical Center at Dallas

Graduate, Biomedical Communications Graduate Program University of Texas Southwestern Medical Center at Dallas

T. J. Fels

Marie Sena

Graduate, Biomedical Communications Graduate Program University of Texas Southwestern Medical Center at Dallas

Graduate, Biomedical Communications Graduate Program University of Texas Southwestern Medical Center at Dallas

Erin Frederikson

Maya Shoemaker

Graduate, Biomedical Communications Graduate Program University of Texas Southwestern Medical Center at Dallas

Alexandra Gordon Graduate, Biomedical Communications Graduate Program University of Texas Southwestern Medical Center at Dallas

Kimberly Hoggatt Krumwiede, MA, CMI Associate Professor, Health Care Sciences—Education and Research University of Texas Southwestern Medical Center at Dallas

Richard P. Howdy, Jr. Former Instructor, Biomedical Communications Graduate Program University of Texas Southwestern Medical Center at Dallas

Belinda Klein Graduate, Biomedical Communications Graduate Program University of Texas Southwestern Medical Center at Dallas

Graduate, Biomedical Communications Graduate Program University of Texas Southwestern Medical Center at Dallas

Jennie Swensen Graduate, Biomedical Communications Graduate Program University of Texas Southwestern Medical Center at Dallas

Amanda Tomasikiewicz Graduate, Biomedical Communications Graduate Program University of Texas Southwestern Medical Center at Dallas

Kimberly VanExel Graduate, Biomedical Communications Graduate Program University of Texas Southwestern Medical Center at Dallas

Kristin Yang Graduate, Biomedical Communications Graduate Program University of Texas Southwestern Medical Center at Dallas

Anne Matuskowitz Graduate, Biomedical Communications Graduate Program University of Texas Southwestern Medical Center at Dallas

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PREFACE The first edition of Williams Obstetrics was published over a century ago. Since then, the editors of this seminal text have presented a comprehensive and evidenced-based discussion of obstetrics. Patterned after our patriarch, Williams Gynecology provides a thorough presentation of gynecology’s depth and breadth. In Section 1, general gynecology topics are covered. Sections 2 provides chapters covering reproductive endocrinology and infertility. The developing field of female pelvic medicine and reconstructive surgery is presented in Section 3. In Section 4, gynecologic oncology is discussed. Traditionally, gynecologic information has been offered within the format of either a didactic text or a surgical atlas. However, because the day-to-day activities of a gynecologist blends these two, so too did we. The initial four sections of

our book describe the evaluation and medical treatment of gynecologic problems. The remaining two sections focus on the surgical patient. Section 5 offers detailed anatomy and a discussion of perioperative considerations. Our final section presents an illustrated atlas for the surgical correction of conditions described in Sections 1 through 4. To interconnect this content, readers will find page references within one chapter that will direct them to complementary content in another. Although discussions of disease evaluation and treatment are evidence based, our text strives to assist the practicing gynecologist and resident. Accordingly, chapters are extensively complemented by illustrations, photographs, diagnostic algorithms, and treatment tables.

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ACKNOWLEDGMENTS During the creation and production of our textbook, we were lucky to have the assistance and support of countless talented professionals both within and outside our department. First, a task of this size could not be completed without the unwavering support provided by our Department Chairman, Dr. Steven Bloom, and Vice-Chairman, Dr. Barry Schwarz. Their financial and academic endorsement of our efforts has been essential. Without their academic vision, this undertaking could not have flourished. In constructing a compilation of this breadth, the expertise of physicians from several departments was needed to add vital, contemporaneous information. We were fortunate to have Dr. April Bailey, with joint appointments in the Department of Radiology and Department of Obstetrics and Gynecology, add her insight and knowledge as a specialist in radiology. Her many stunning images contribute to the academic richness of this edition. From the Department of Pathology, Dr. Kelley Carrick also shared generously from her cadre of outstanding images. She translated her extensive knowledge of gynecologic pathology into concepts relevant for the general gynecologist. From the Department of Surgery at Johns Hopkins University, Dr. David Euhus lent his considerable knowledge of breast disease to contribute both classic and state-of-the-art information to his truly comprehensive chapter, founded on his broad research and clinical expertise. From the Department of Psychiatry here at the University of Texas Southwestern Medical Center at Dallas and from the University of North Carolina at Chapel Hill School of Medicine, we were lucky to have Drs. Geetha Shivakumar and Anna Brandon provide an extensive discussion of psychosocial issues. They expertly distilled a broad topic into a logically organized, practical, and complete presentation. In addition, Dr. Gretchen Stuart, formerly of our department and now a faculty member at the Department of Obstetrics and Gynecology of the University of North Carolina at Chapel Hill, lent her considerable talents in summarizing contraceptive methods and sterilization techniques. Many warm thanks are extended to Dr. Rajiv Gala, also formerly of our department and now of the Ochsner Clinic. Rajiv masterfully organized and summarized chapters on ectopic pregnancy and perioperative practice. His extensive review of the literature and evidence-based writing shines through these chapters. In this edition, new contributors include Drs. Anthony Russell and Andrea Russo from the Department of Radiation Oncology at Massachusetts General Hospital— Harvard Medical School. In their chapter on radiation therapy, they adeptly provided clear explanations of this therapy’s fundamentals and offered extensive suggestions for clinical management of patient complications that may be encountered. Within our own department, the list is too long and the words are too few to convey our heartfelt thanks to all of our

department members for their generous contributions. From our Gynecology Division, many thanks are extended to Drs. Elysia Moschos and April Bailey, who sculpted a clear and detailed summary of traditional and new gynecologic imaging tools. In this edition, these two authors updated radiologic images as needed to present ultimate examples of normal anatomy and gynecologic pathology. We were also lucky to have experts in the field of preinvasive lesions of the lower genital tract, Drs. Claudia Werner and William Griffith. They crafted an information-packed discussion of this topic. In addition, Dr. Griffith has been a steadfast advocate of our project and has added extensive photographic content to many of our chapters. Drs. David Rahn and Eddie McCord teamed to update the chapter on gynecologic infection. Their extensive patient-care experience and rigorous literature review added greatly to the academic and clinical value of this chapter. We were also fortunate to have the expert writing talents of Drs. Mayra Thompson and Kimberly Kho, who provided a compelling and comprehensive discussion of minimally invasive surgery. Our textbook benefitted greatly from the clinical savvy and teaching-centric information that David Rogers and David Owens provided to their chapter. Also, Dr. Rogers has been a long-time supporter of our textbook. We are indebted to him for many of the classic surgical photographs in this edition. Intraoperative fundamentals were thoroughly and logically presented by Drs. Cherine Hamid and Sunil Balgobin. Their strengths in clinical practice and resident teaching are evident in their well-organized and essential chapter. Once again, blending experience and academic fundamentals, Dr. Mary Jane Pearson offered a comprehensive but concise primer on well care for the gynecologic patient. Our Reproductive Endocrinology and Infertility Division provided other talented physicians and writers. Dr. Kevin Doody lent his considerable clinical and academic prowess in the treatment of infertility. He penned a chapter that clearly describes the state of the art in this field. Dr. Doody was also a kind benefactor with his spectacular clinical photographs on the topic and contributed these generously to numerous chapters. In addition, Dr. Ellen Wilson brought her wealth of clinical experience to chapters on pediatric gynecology and androgen excess. Drawing from her academic and clinical expertise, she crafted chapters that presented practical, prescriptive, and comprehensive discussions of these topics. Dr. Marlene Corton is a skilled urogynecologist and has written extensively on pelvic anatomy. We were thrilled to have her create stunning chapters on anatomy and anal incontinence. Also from the Urogynecology and Female Pelvic Reconstruction Division, Drs. Clifford Wai and David Rahn added expanded content to their chapter on urinary incontinence. Dr. Wai also masterfully updated his chapter on xxiii

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Acknowledgments vesicovaginal fistula and urethral diverticulum. Special thanks are extended to Dr. Ann Word and her contributions to our chapter on pelvic organ prolapse. Her expertise in extracellular matrix remodeling of the female reproductive tract added fundamental content to the discussion of prolapse physiology. Dr. David Miller generously contributed his talents without hesitation, and we are indebted to him for his altruism toward our project. In addition, the Division of Gynecologic Oncology offered a deep bench of talented writers. The topic of vulvar cancer was thoroughly covered by Dr. Jayanthi Lea. Dr. Lea also assisted with updating our atlas and added essential steps for minimally invasive approaches. Her strengths in clinical practice and resident teaching are evident in her well-organized and evidence-based chapters. We also benefitted from Dr. Debra Richardson’s comprehensive presentation and clinical discussions of cervical and vaginal cancer in her two chapters. She has been a true advocate of both the text and study guide. Dr. Siobhan Kehoe described with clarity and clinical relevance the care and treatment of women with endometrial cancer. We were appreciative of Dr. Matthew Carlson, who teamed with David Miller to present the varied pathology and treatment of uterine sarcoma. With this edition, several of our valued authors have turned their efforts to other promising pursuits. We are grateful to Drs. F. Gary Cunningham, Bruce Carr, David Hemsell, Larry Word, and Phuc Nguyen for their prior contributions to Williams Gynecology. All with well-known and well-established careers, they generously contributed their academic skills without hesitation. We are indebted to them for their altruism toward our project. Of these academicians, Dr. F. Gary Cunningham provided the academic vision that led to the creation of this text. Dr. Cunningham has been the senior author for seven editions of Williams Obstetrics, spanning over 25 years. As such, we benefited greatly from his writing genius, his meticulous organization, and his tenacity to task. His dedication to evidencebased medicine established the foundation on which our textbook was built. We feel privileged to have learned the craft of clear, concise academic summary from a consummate master. New beautiful and detailed artwork in our atlas this edition was drawn by Mr. Lewis Calver, here at the University of Texas Southwestern Medical Center at Dallas. Again for this edition, he paired his academic talents with Dr. Marlene Corton to create updated hysterectomy and urogynecologic images. Both of these anatomists committed countless hours in the cadaver laboratory and in the library to create academically new presentations. These renderings were crafted and tailored with the gynecologic surgeon in mind to depict important techniques and anatomy for these surgeries. Dr. Jayanthi Lea joined this gifted duo to add complementary and informative illustrations to her description of minimally invasive cancer surgeries. We also acknowledge the efforts of our atlas artists from the first two editions: Marie Sena, Erin Frederikson, Jordan Pietz, Maya Shoemaker, SangEun Cha, Alexandra Gordon, Jennie Swensen, Amanda Tomasikiewicz, and Kristin Yang. Additionally, alumni from the Biomedical Communications Program at the University of Texas Southwestern Medical

Center provided seminal pieces. These alumni include Katherine Brown, Thomas “T. J.” Fels, Belinda Klein, Anne Matuskowitz, Lindsay Oksenberg, Kimberly VanExel, and faculty member Richard P. Howdy, Jr. Also, Ms. Kimberly Hoggatt Krumwiede graciously provided several image series to help clarify the steps and missteps of reproductive tract development. Within our text, images add powerful descriptive content to our words. Accordingly, many, many thanks are extended to those who donated surgical and clinical photographs. Of our contributors, many beautiful photographs within our book were taken by Mr. David Gresham, Chief Medical Photographer at the University of Texas Southwestern Medical Center. Dave’s eye for detail, shading, and composition allowed even simple objects to shine and be illustrated to their full potential. He has been an advocate and valued consultant. Our pathology images were presented at their best thanks to Mr. Mark Smith, a graphics designer here at the University of Texas Southwestern Medical Center. His expertise with micrographs improved the clarity and visual aesthetic of many our microscopic images. The providers in the Obstetrics and Gynecology Emergency Services (OGES) at Parkland Hospital were huge allies in our acquisition of images to illustrate normal and abnormal gynecologic findings. The skilled women’s health care nurse practitioners have been true supporters of our efforts, and we sincerely thank them. We are truly indebted to our administrative staff. For this project, we were lucky to have Ms. Sandra Davis serve as our primary administrative assistant. We are greatly appreciative of her tremendous efforts, professionalism, and efficiency. Ms. Ellen Watkins was a valuable assistant in obtaining needed journal articles. She truly helped to keep our project evidencebased. None of our image and text production would have been possible without the brilliant information technology team in our department. Knowledgeable and responsive, Mr. Charles Richards and Mr. Thomas Ames have supported our project since the first edition. We could not do our job without their expertise. Williams Gynecology was sculpted into its final form by the talented and dedicated group at McGraw-Hill Education. Once again, Ms. Alyssa Fried has brought her considerable intelligence, energetic work ethic, and creativity to our project. Her attention to detail and organizational talents have kept our project on track with efficiency and style. Our words fall well short in expressing our gratitude to her. Ms. Samantha Williams served as assistant to Ms. Fried, and we extend warm thanks for her tremendous support. Her efficiency, professionalism, hard work, accuracy, and positive attitude made coordination of this project a dream. Mr. Andrew Moyer joined our project during its final sculpting. He has taken our project under his care and has adeptly shepherded it to completion with a calm and efficient style. We happily look forward to many future collaborative editions together. Without the thoughtful, creative efforts of many, our textbook would be a barren wasteland of words. Integral to this process are Armen Ovsepyan, at McGraw-Hill Education, and Alan Barnett of Alan Barnett Design. Mr. Richard Ruzycka served as production supervisor for this edition of our textbook. He adeptly kept our project on track through an array of potential hurdles. Special

Acknowledgments thanks are extended to Mr. Joseph Varghese and Dr. Shetoli Zhimomi at Thomson Digital. They and their artistic team assisted us in revising many of our text images. Their attention to detail and accurate renderings added important academic support to our words. Our text took its final shape under the watchful care of our compositors at Aptara, Inc. Specifically, we thank Ms. Indu Jawwad for her talents in skillfully and expediently coordinating and overseeing composition. Her dedicated attention to detail and organization were vital to completion of our project. Her pleasant professionalism was appreciated daily. Also at Aptara, Mr. Shashi Lal Das served a crucial task of quality control and assisted in creating beautiful chapter layouts to highlight our content aesthetically and informatively. Special thanks go to Ms. Kristin Landon. As copyeditor for now several editions of both Williams Obstetrics and Williams Gynecology, Kristin has added precision and clarity to our efforts. Her pleasant and patient professionalism has made our text better.

We offer a sincere “thank you” to our residents in training. Their curiosity keeps us energized to find new and effective ways to convey age-old as well as cutting-edge concepts. Their logical questions lead us to holes in our text, and thereby, always help us to improve our work. Moreover, many of the photographs in this textbook were gathered with the help of our many residents. In addition, the contributors to this text owe a significant debt to the women who have allowed us to participate in their care. The images and clinical expertise presented in this text would not have been possible without their collaborative spirit to help us move medical knowledge forward. Last, we offer an enthusiastic and heartfelt “thank you” to our families and friends. Without their patience, generosity, and encouragement, this task would have been impossible. For them, too many hours with “the book” left them with new responsibilities. And importantly, time away from home left precious family memories and laughs unrealized. We sincerely thank you for your love and support.

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SECTION 1

BENIGN GENERAL GYNECOLOGY

2

CHAPTER 1

Well Woman Care MEDICAL HISTORY. .

. . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

PHYSICAL EXAMINATION. . IMMUNIZATION. .

. . . . . . . . . . . . . . . . . . . . . . . .

2

. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

7

CANCER SCREENING.

. . . . . . . . . . . . . . . . . . . . . . . . . . . . .

LIFESTYLE CHANGES. . OBESITY. .

7

. . . . . . . . . . . . . . . . . . . . . . . . . . .

10

. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

12

CARDIOVASCULAR DISEASE.

. . . . . . . . . . . . . . . . . . . . .

13

. . . . . . . . . . . . . . . . . . . . . . .

14

. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

14

CHRONIC HYPERTENSION. STROKE.

2

DYSLIPIDEMIA.

. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

DIABETES MELLITUS.

. . . . . . . . . . . . . . . . . . . . . . . . . . . .

METABOLIC SYNDROME. .

17

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17

. . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

17

PRECONCEPTIONAL COUNSELING. . REFERENCES. .

16

. . . . . . . . . . . . . . . . . . . . . . . .

GERIATRIC SCREENING. . MENTAL HEALTH. .

15

. . . . . . . . . . . . . . .

18

. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

20

Serving as both specialist and primary care provider, a gynecologist has an opportunity to diagnose and treat a wide variety of diseases. Once problems are identified, clinicians, in consultation with the patient, determine how best to manage chronic medical issues based on their experience, practice patterns, and professional interests. Although some conditions may require referral, gynecologists play an essential role in patient screening, in emphasizing ideal health behaviors, and in facilitating appropriate consultation for care beyond their scope of practice. Various organizations provide preventive care recommendations and update these regularly. Commonly accessed guidelines are those from the American College of Obstetricians and Gynecologists (ACOG), Centers for Disease Control and Prevention (CDC), U.S. Preventive Services Task Force (USPSTF), and American Cancer Society.

MEDICAL HISTORY During a comprehensive well-woman visit, patients are first queried regarding new or ongoing illness. To assist with

evaluation, complete medical, social, and surgical histories are obtained and include obstetric and gynecologic events. Gynecologic topics usually cover current and prior contraceptives; results from prior sexually transmitted disease (STD) testing, cervical cancer screening, or other gynecologic tests; sexual history, described in Chapter 3 (p. 60); and menstrual history, outlined in Chapter 8 (p. 182). Obstetric questions chronicle circumstances around deliveries, losses, or complications. Current medication lists include both prescription and over-the-counter drugs and herbal agents. Also, prior surgeries, their indications, and complications are sought. A social history covers smoking and drug or alcohol abuse. Screening for intimate partner violence or depression can be completed, as outlined on page 18 and more fully in Chapter 13 (p. 298). Discussion might also assess the patient’s support system and any cultural or spiritual beliefs that might affect her general health care. A family history helps identify women at risk for familial or multifactorial disease such as diabetes or heart disease. In families with prominent breast, ovarian, or colon cancer, genetic evaluation may be indicated, and criteria are outlined in Chapters 33 (p. 707) and 35 (p. 736). Moreover, a significant family clustering of thromboembolic events may warrant testing, as describe in Chapter 39 (p. 836), especially prior to surgery or hormone initiation. Last, a review of systems, whether performed by the clinician or office staff, may add clarity to new patient problems. For adults, following historical inventory, a complete physical examination is completed. Many women present to their gynecologist with complaints specific to the breast or pelvis. Accordingly, these are often areas of increased focus, and their evaluation is described next.

PHYSICAL EXAMINATION ■⌀ Breast Examination Clinical Evidence Self breast examination (SBE) is an examination performed by the patient herself to detect abnormalities. However, studies have shown that SBE increases diagnostic testing rates for ultimately benign breast disease and is ineffective in lowering breast cancer mortality rates (Kösters, 2008; Thomas, 2002). Accordingly, several organizations have removed SBE from their recommended screening practices (National Cancer Institute, 2015; Smith, 2015; U.S. Preventive Services Task Force, 2009). That said, the American College of Obstetricians and Gynecologists (2014b) and the American Cancer Society (2014) recommend breast self-awareness as another method of patient self-screening.

Well Woman Care

CHAPTER 1

Self-awareness focuses on breast appearance and architecture and may include SBE. Women are encouraged to report any perceived breast changes for further evaluation. In contrast, clinical breast examination (CBE) is completed by a clinical health-care professional and may identify a small portion of breast malignancies not detected with mammography. Additionally, CBE may identify cancer in young women, who are not typical candidates for mammography (McDonald, 2004). One method includes visual inspection combined with axillary and breast palpation, which is outlined in the following section. The American College of Obstetricians and Gynecologists (2014b) recommends that women receive a CBE every 1 to 3 years between ages 20 and 39. At age 40, CBE is completed annually. That said, the USPSTF (2009) and the American Cancer Society report insufficient evidence to recommend routine CBE (Oeffinger, 2015).

Breast Examination Initially during CBE, the breasts are viewed as a woman sits on the table’s edge with hands placed at her hips and with pectoralis muscles flexed (Fig. 1-1). Alone, this position enhances asymmetry. Additional arm positions, such as placing arms above the head, do not add vital information. Breast skin is inspected for breast erythema; retraction; scaling, especially over the nipple; and edema, which is termed peau d’orange change. The breast and axilla are also observed for contour symmetry. Following inspection, axillary, supraclavicular, and infraclavicular lymph nodes are palpated most easily with a woman seated and her arm supported by the examiner (Fig. 1-2). The axilla is bounded by the pectoralis major muscle ventrally and

FIGURE 1-1╇ During visual breast inspection, hands are pressed against the waist to flex the pectoralis muscles. With the patient leaning slightly forward, breasts are visually inspected for breast contour asymmetry or skin dimpling.

3

FIGURE 1-2╇ One method of axillary lymph node palpation. Finger tips extend to the axillary apex and compress tissue against the chest wall in the rolling fashion shown in Figure 1-4. The patient’s arm is supported by the examiner.

the latissimus dorsi muscle dorsally. Lymph nodes are detected as the examiner’s hand glides from high to low in the axilla and momentarily compresses nodes against the lateral chest wall. In a thin patient, one or more normal, mobile lymph nodes less than 1 cm in diameter may commonly be appreciated. The first lymph node to become involved with breast cancer metastasis (the sentinel node) is nearly always located just behind the midportion of the pectoralis major muscle belly. After inspection, breast palpation is completed with a woman supine and with one hand above her head to stretch breast tissue across the chest wall (Fig. 1-3). Examination includes breast tissue bounded by the clavicle, sternal border, inframammary crease, and midaxillary line. Breast palpation within this pentagonal area is approached in a linear fashion. Technique uses the finger pads in a continuous rolling, gliding circular motion (Fig. 1-4). At each palpation point, tissues is assessed both superficially and deeply (Fig. 1-5). During CBE, intentional attempts at nipple discharge expression are not required unless a spontaneous discharge has been described by the patient. If abnormal breast findings are noted, they are described by their location in the right or left breast, clock position, distance from the areola, and size. Evaluation and treatment of breast and nipple diseases are described more fully in Chapter  12 (p. 275). During examination, patients are educated that new axillary or breast masses, noncyclic breast pain, spontaneous nipple discharge, new nipple inversion, and breast skin changes such as dimpling, scaling, ulceration, edema, or erythema should prompt evaluation. This constitutes breast selfawareness. Patients who desire to perform SBE are counseled on its benefits, limitations, and potential harms and instructed to complete SBE the week after menses.

4

Benign General Gynecology

Speculum Examination

SECTION 1

Both metal and plastic specula are available for this examination, each in various sizes to accommodate vaginal length and laxity. The plastic speculum may be equipped with a small light that provides illumination, whereas metal specula require an external light source. Preference between these two types is provider dependent. The vagina and cervix are typically viewed after placement of either a Graves or Pederson speculum (Fig. 1-6). Prior to insertion, a speculum may be warmed with running water or by warming lights built into some examination tables. Additionally, lubricaFIGURE 1-3╇ Recommended patient positioning and direction of palpation during clinical tion may add comfort to insertion. Griffith breast examination. and colleagues (2005) found that gel lubricants did not increase unsatisfactory Pap smear cytology rates or decrease Chlamydia trachomatis detec■⌀ Pelvic Examination tion rates compared with water lubrication. If gel lubrication This examination is typically performed with a patient supine, is used, a dime-sized aliquot is applied sparingly to the outer legs in dorsal lithotomy position, and feet resting in stirrups. surface of the speculum blades. The head of the bed is elevated 30 degrees to relax abdominal wall muscles for bimanual examination. A woman is assured that she may stop or pause the examination at any time. Moreover, Superficial each part of the evaluation is announced or described before its performance.

Inguinal Lymph Nodes and Perineal Inspection Pelvic cancers and infections may drain to the inguinal lymph nodes, and these are palpated during examination. Following this, a methodical inspection of the perineum extends from the mons ventrally, to the genitocrural folds laterally, and to the anus. Notably, infections and neoplasms that involve the vulva can also involve perianal skin. Some clinicians additionally palpate for Bartholin and paraurethral gland pathology. However, in most cases, patient symptoms and asymmetry in these areas will dictate the need for this specific evaluation.

Intermediate depth

Deep

FIGURE 1-4╇ Recommended palpation technique. The finger pads and a circular rolling motion are used to palpate the entire breast.

FIGURE 1-5╇ Palpation through several depths at each point along the linear path.

Well Woman Care

Bimanual Examination A

B

C

FIGURE 1-6╇ Vaginal specula. A. Pediatric Pederson speculum. This may be selected for child, adolescent, or virginal adult examination. B. Graves speculum. This may be selected for examination of parous women with relaxed and collapsing vaginal walls. C. Pederson speculum. This may be selected for sexually active women with adequate vaginal wall tone. (Used with permission from US Surgitech, Inc.)

Immediately before insertion, the labia minora are gently separated, and the urethra is identified. Because of urethral sensitivity, the speculum is inserted well below the meatus. Alternatively, prior to speculum placement, an index finger may be placed in the vagina, and pressure placed posteriorly against the bulbospongiosus muscle. A woman is then encouraged to relax this posterior wall to improve comfort with speculum insertion. This practice may prove especially helpful for women undergoing their first examination and for those with infrequent coitus, dyspareunia, or heightened anxiety. With speculum insertion, the vagina commonly contracts, and a woman may note pressure or discomfort. A pause at this point typically is followed by vaginal muscle relaxation. As the speculum bill is completely inserted, it is angled approximately 30 degrees downward to reach the cervix. Commonly, the

A

Most often, the bimanual examination is performed after the speculum evaluation. Some clinicians prefer to complete the bimanual portion first to better identify cervical location prior to speculum insertion. Either process is appropriate. Uterine and adnexal size, mobility, and tenderness can be assessed during bimanual examination. For women with prior hysterectomy and adnexectomy, bimanual examination is still valuable and can be used to exclude other pelvic pathology. During this examination, a gloved index and middle finger are inserted together into the vagina until the cervix is reached. For cases of latex allergy, nonlatex gloves are available. To ease insertion, a water-based lubricant can be initially applied to these gloved fingers. Once the cervix is reached, uterine orientation can be quickly assessed by sweeping the index finger inward along the ventral surface of the cervix. In those with an anteverted position, the uterine isthmus is noted to sweep upward, whereas in those with a retroverted position, a soft bladder is palpated. However, in those with a retroverted uterus, if a finger is swept along the cervix’s dorsal aspect, the isthmus is felt to sweep downward. With a retroverted uterus, this same finger is continued posteriorly to the fundus and then side-to-side to assess uterine size and tenderness. To determine the size of an anteverted uterus, fingers are placed beneath the cervix, and upward pressure tilts the fundus toward the anterior abdominal wall. A clinician’s opposite

B

FIGURE 1-7╇ Uterine positions. A. Uterine position may be anteverted, midplane, or retroverted. B. As shown here, the uterine fundus can be flexed forward, and this is termed anteflexion. Similarly, the fundus may be flexed backward to create a retroverted uterus.

CHAPTER 1

uterus is anteverted, and the ectocervix lies against the posterior vaginal wall (Fig. 1-7). As the speculum is opened, the ectocervix can be identified. Vaginal walls and cervix are inspected for masses, ulceration, or unusual discharge. As outlined in Chapter 29 (p. 632), cervical cancer screening is often completed, and additional swabs for culture or microscopic evaluation can also be collected. Screening for Neisseria gonorrhoeae and Chlamydia trachomatis and other STDs is listed in Table 1-1.

5

6

Benign General Gynecology TABLE 1-1. Sexually Transmitted Disease Screening Guidelines for Nonpregnant, Sexually Active Asymptomatic Women

SECTION 1

Infectious Agent

Screening Recommendations

Risk Factors

Chlamydia trachomatis + Neisseria gonorrhoeae

All 6 mm) to evaluate skin lesions of concern and refer appropriately.

■⌀ Lifestyle Changes Smoking Cigarette smoking is the single most preventable cause of death in the United States and has been linked with certain cancers, cardiovascular disease, chronic lung diseases, and stroke. Moreover, specific to women’s health, smoking is linked to diminished fertility, pregnancy complications, and postoperative complications. These are discussed in greater detail in their respective chapters. Despite these known negative health outcomes, in 2003, only 64 percent of smokers who had routine examinations in the United States were advised by a physician to quit smoking (Torrijos, 2006). Guidelines from the U.S. Department of Health and Human Services encourage a brief behavioral patient intervention model found on page 12. Patients can also be referred to the National Cancer Institute’s smoking cessation website: www.smokefree.gov. This site provides free, evidence-based information and professional assistance to help the immediate and long-term needs of those trying to quit. Unless contraindicated, pharmacologic treatments to aid smoking cessation can be offered to all interested women and

Well Woman Care

11

TABLE 1-4. Drugs Used for Smoking Cessation Brand Name

Nicotine Replacement Patchd Habitrol Nicoderm CQ

Initial Dosing

Maintenance

If >10 CPD: a 21-mg patch is reapplied daily wk 1–6 If 200 U/ mL) or an OVA1 score ≥5.0 and postmenopausal women with any CA125 level elevation or an OVA1 score ≥4.4 are at higher risk. Ideally, for patients with suspicious adnexal masses, surgery is performed in a hospital with a pathologist able to reliably interpret an intraoperative frozen section. At minimum, samples for peritoneal cytology are obtained when the abdomen is entered. The mass is then removed intact through an incision that permits thorough staging and resection of possible metastatic sites (American College of Obstetricians and Gynecologists, 2011). If malignancy is diagnosed, then surgical staging is completed. However, in a study of more than 10,000 women with ovarian cancer, almost half of those with early-stage disease did not undergo the recommended surgical procedures (Goff, 2006). Surgeons should be prepared to appropriately stage and potentially debulk ovarian cancer or have a gynecologic oncologist immediately available. This type of careful planning has been shown to achieve the best possible surgical result and improve survival rates (Earle, 2006; Engelen, 2006; Mercado, 2010). Moreover, since broader resources are usually available, patients cared for at high-volume hospitals also tend to have better outcomes (Bristow, 2010). For women with malignancy identified only postoperatively or intraoperatively and without adequate staging, management will vary. Women with suspected early-stage disease may be restaged laparoscopically. Those with advanced disease may undergo a second laparotomy to obtain optimal tumor debulking (Grabowski, 2012). However, if extensive disease is found at the initial surgery, then chemotherapy may be selected first and followed later by laparotomy to obtain optimal interval cytoreduction. At some point during postoperative surveillance, many women with early-stage disease, depending on the diagnosis, will return to their referring physician. Monitoring for relapse is often coordinated between the gynecologic oncologist and generalist in obstetrics and gynecology, especially if no chemotherapy is required following surgery.

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B

FIGURE 35-6╇ Computed tomographic scans in a woman with ovarian cancer. A. Axial CT scan at the level of the liver and spleen reveals metastatic lesions in the spleen and liver (curved arrows) and a bulky lesion at the splenorenal ligament (arrow). B. More caudal axial CT reveals ascites (curved arrows) and marked omental caking (arrows). (Used with permission from Dr. Diane Twickler.)

Grossly, there are no distinguishing features among the types of epithelial ovarian cancer. In general, each has solid and cystic areas of varying sizes (Fig. 35-7).

Serous Tumors More than 50 percent of all epithelial ovarian cancers have serous histology. Microscopically, in well-differentiated tumors, cells may resemble fallopian tube epithelium, whereas in poorly differentiated tumors, anaplastic cells with severe nuclear atypia predominate (Fig. 35-8). During frozen section analysis, psammoma bodies are essentially pathognomonic of an ovarian-type serous carcinoma. Often, these tumors contain various other cell types as a minor component (2 cm ± positive retroperitoneal nodes. Includes extension to capsule of liver/spleen Distant metastasis excluding peritoneal metastasis Pleural effusion with positive cytology Hepatic and/or splenic parenchymal metastasis, metastasis to extraabdominal organs (including inguinal lymph nodes and lymph nodes outside of the abdominal cavity)

a

Content in parentheses referring to tubes pertains to fallopian tube carcinoma. FIGO = International Federation of Gynecology and Obstetrics. Data from Prat J and FIGO Committee on Gynecologic Oncology: Staging classification for cancer of the ovary, fallopian tube, and peritoneum, Int J Gynaecol Obstet. 2014 Jan;124(1):1–5.

Women with relapsed ovarian cancer did not live longer by starting chemotherapy earlier based on a rising CA125 level compared with delaying treatment until symptoms developed. The group monitored with CA125 tests received 5 more months of chemotherapy overall, whereas women who were diagnosed and treated later for clinically evident recurrence had higher quality-of-life measures (Rustin, 2010). TABLE 35-6. Distribution of Epithelial Ovarian Cancer by FIGO Stage (n = 4825 patients) FIGO Stage

Percent

I II III IV

28 â•⁄8 50 13

FIGO = International Federation of Gynecology and Obstetrics. Data from Heintz APM, Odicino F, Maisonneuve P, et al: Carcinoma of the ovary. FIGO 26th Annual Report on the Results of Treatment in Gynecological Cancer, Int J Obstet Gynecol 92006 Nov;95 Suppl 1:S161–S92.

Whether suspected by examination, CA125 level elevation, or new symptoms, recurrent disease must be confirmed with the aid of imaging. Of modalities, CT is initially most helpful to identify intraperitoneal disease.

■⌀ Management of Advanced Ovarian Cancer Approximately two thirds of patients will have stage III-IV disease, and sequenced multimodality therapy offers the most successful outcomes (Earle, 2006). Ideally, surgical cytoreduction is initially performed to remove all gross disease and is followed by six courses of platinum-based chemotherapy. However, some women are not appropriate candidates for primary surgery due to their medical condition, and others will have unresectable tumor. Additionally, one randomized trial concluded that initial treatment with chemotherapy followed by interval debulking surgery might achieve equivalent results (Vergote, 2010). To effectively balance all clinical factors, each patient is individually assessed before initiating treatment.

Primary Cytoreductive Surgery Residual Disease.╇ Since the initial report by Griffiths (1975) suggested the clinical benefits of debulking, its value has been largely assumed. Numerous retrospective studies have

Epithelial Ovarian Cancer

Surgical Approach to Cytoreductive Surgery.╇ In general, a vertical incision is recommended to provide access to the entire abdomen. Women with advanced disease do not require peritoneal washings or cytologic assessment of fluid, but often several liters of ascites will need to be evacuated to improve visualization. Next, the abdomen is carefully explored to quickly determine if optimal debulking is feasible. It is preferable to perform a limited surgical procedure rather than extensive debulking if it is obvious that bulky tumors will be left behind. If hysterectomy and BSO is not possible, a biopsy of the ovary and sampling of the endometrium by dilatation and curettage is performed to confirm an ovarian primary and exclude the possibility of widely metastatic uterine papillary serous carcinoma. However, if disease is resectable, then surgery should begin with the least complicated procedure. Often, an infracolic omentectomy can be easily performed and extended (i.e., gastrocolic), as needed, to encompass the disease. A frozen section analysis can then be requested to confirm the presumed diagnosis of epithelial ovarian cancer. The

pelvis is assessed next. Usually, an extrafascial type I abdominal hysterectomy and BSO is sufficient. However, when the tumor is confluent or invading the rectosigmoid, an en bloc resection, low anterior resection, or modified posterior pelvic exenteration may be required. These and other surgeries mentioned in this section are described and illustrated in Chapter 46 (p. 1134). Patients with abdominal tumor nodules measuring 98%

Yolk Sac Tumor

Immature Teratoma

61% 39%

72% 28%

93% 64–91%

98% 73–88%

Sources for survival figures are referenced within the text.

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SECTION 4

Yolk Sac Tumors

Other Primitive Germ Cell Tumors

These tumors account for 10 to 20 percent of all malignant ovarian germ cell tumors. These lesions were previously called endodermal sinus tumors, but the terminology has been revised. One third of individuals are premenarchal at the time of initial presentation. Involvement of both gonads is rare, and the other ovary is usually involved with metastatic disease only when there are other metastases in the peritoneal cavity. Grossly, these tumors form solid masses that are more yellow and friable than dysgerminomas. They are often focally necrotic and hemorrhagic, with cystic degeneration and rupture. The microscopic appearance of yolk sac tumors is often diverse. The most common appearance, the reticular pattern, reflects extraembryonic differentiation, with the formation of a network of irregular anastomosing spaces that are lined by primitive epithelial cells. Schiller-Duval bodies are pathognomonic when present (Fig. 36-5). These characteristically have a single papilla, which is lined by tumor cells and contains a central vessel. Alpha-fetoprotein is commonly produced. As a result, yolk sac tumors usually contain cells that stain immunohistochemically for AFP, and serum levels can serve as a reliable tumor marker in posttreatment surveillance. Yolk sac tumors are the deadliest malignant ovarian germ cell tumor type. As a result, all patients are treated with chemotherapy regardless of stage. Fortunately, more than half present with stage I disease, corresponding to a 5-year disease-specific survival rate of approximately 93 percent (Chan, 2008). Disadvantageously, yolk sac tumors have a greater propensity for rapid growth, peritoneal spread, and distant hematogenous dissemination to the lungs. Accordingly, individuals with stage II-IV disease have a 5-year survival rate ranging from 64 to 91 percent. Of tumor recurrences, most will occur within the first year, and treatment is usually ineffective (Cicin, 2009).

The rarest subtypes of nondysgerminomatous tumors are typically mixed with other more common variants and usually are not found in pure form. Embryonal Carcinoma.╇ Patients diagnosed with embryonal carcinoma are characteristically younger, with a mean age of 14 years, than those having other types of germ cell tumors. Epithelial cells resembling those of the embryonic disc form these primitive tumors. The solid disorganized sheets of large anaplastic cells, glandlike spaces, and papillary structures are distinctive and allow easy identification of these rare tumors (Ulbright, 2005). Although dysgerminomas are the most common germ cell tumor resulting from malignant transformation of gonadoblastomas in individuals with dysgenetic gonads, occasionally embryonal “testicular” tumors may also originate (LaPolla, 1990). Embryonal carcinomas typically produce hCG, and 75 percent also secrete AFP. Polyembryoma.╇ These rare tumors characteristically contain many embryolike bodies. Each has a small central “germ disc” positioned between two cavities, one mimicking an amnionic cavity and the other a yolk sac. Syncytiotrophoblast giant cells are frequent, but elements other than the embryoid bodies should constitute less than 10 percent of the tumor for the “polyembryoma” designation to be used. Conceptually, these tumors may be viewed as a bridge between the primitive (dysgerminoma) and differentiated (teratoma) germ cell tumor types. For this reason, polyembryomas are often considered to be the most immature of all teratomas (Ulbright, 2005). Serum AFP or hCG levels or both may be elevated in these individuals due to the yolk sac and syncytial components, respectively (Takemori, 1998). Choriocarcinoma.╇ Primary ovarian choriocarcinoma arising from a germ cell appears similar to gestational choriocarcinoma with ovarian metastases, which is discussed in Chapter 37 (p. 785). The distinction is important because nongestational tumors have a poorer prognosis (Corakci, 2005). The detection of other germ cell components indicates nongestational choriocarcinoma, whereas a concomitant or proximate pregnancy suggests a gestational form (Ulbright, 2005). Clinical manifestations are common and result from high hCG levels produced by these rare tumors. These elevated levels may induce sexual precocity in prepubertal girls or heavy, irregular bleeding in reproductive-aged women (Oliva, 1993).

Mixed Germ Cell Tumors

FIGURE 36-5╇ Schiller-Duval body. This structure consists of a central capillary surrounded by tumor cells, present within a cystic space that may be lined by flat to cuboidal tumor cells. When present, the Schiller-Duval body is pathognomonic for yolk sac tumor, although they are conspicuous in only a minority of cases. In any given case, Schiller-Duval bodies may be few in number, absent, or have atypical morphologic features. (Used with permission from Dr. Kelley Carrick.)

Ovarian germ cell tumors have a mixed pattern of cellular differentiation in 25 to 30 percent of cases, although the incidence of these tumors has also declined by approximately 30 percent over the past few decades (Smith, 2006). Dysgerminoma is the most common component and is typically seen with yolk sac tumor or immature teratoma or both. The frequency of bilateral ovarian involvement depends on the presence or absence of a dysgerminoma component and increases when it is present. However, treatment and prognosis are determined by the nondysgerminomatous component (Low, 2000). For this reason, elevated serum hCG and particularly AFP levels in a woman

Ovarian Germ Cell and Sex Cord-Stromal Tumors

Immature Teratomas Due to a 60-percent increased incidence during the past few decades, immature teratomas are now the most common variant and account for 40 to 50 percent of all malignant ovarian germ cell tumors (Chan, 2008; Smith, 2006). They are composed of tissues derived from the three germ layers: ectoderm, mesoderm, and endoderm. The presence of immature or embryonal structures, however, distinguishes these tumors from the much more common and benign mature cystic teratoma (dermoid cyst). Bilateral ovarian involvement is rare, but 10 percent have a mature teratoma in the contralateral ovary. Tumor markers are often not elevated unless the immature teratoma is mingled with other germ cell tumor types. Alpha-fetoprotein, cancer antigen 125 (CA125), CA19-9, and carcinoembryonic antigen (CEA) may be helpful in some cases (Li, 2002). With gross external inspection, these tumors are large, rounded or lobulated, soft or firm masses. They frequently perforate the ovarian capsule and invade locally. The most frequent site of dissemination is the peritoneum and much less commonly the retroperitoneal lymph nodes. With local invasion, surrounding adhesions commonly form and are thought to explain the lower rates of torsion with this tumor compared with that of its benign mature counterpart (Cass, 2001). On cut surface, the interior is typically solid with intermittent cystic areas, but occasionally the reverse is seen, with solid nodules present only in the cyst wall (Fig. 36-6). Solid parts may correspond to the immature elements, cartilage, bone, or a combination of these. Cystic areas are filled with hair and with serous fluid, mucinous fluid, or sebum. Microscopic examination reveals a disorderly mixture of tissues. Of the immature elements, neuroectodermal tissues almost always predominate and are arranged as primitive tubules and sheets of small, round, malignant cells that may be

A

associated with glia formation. The diagnosis is usually difficult to confirm during frozen section analysis, and most tumors are confirmed only on final pathologic review (Pavlakis, 2009). Tumors are graded 1 to 3 primarily by the amount of immature neural tissue they contain. O’Connor and Norris (1994) analyzed 244 immature teratomas and noted significant inconsistencies in grade assignment by different observers. For this reason, they proposed changing the system to two grades: low (previous grades 1 and 2) and high (previous grade 3). This practice, however, has not been universally accepted. In general, survival is predicted most accurately by stage and by histologic grade of the tumor. For example, almost three quarters of immature teratomas are stage I at diagnosis and have a 5-year survival rate of 98 percent (Chan, 2008). Those with stage IA grade 1 immature teratomas have an excellent prognosis and do not require adjuvant chemotherapy (Bonazzi, 1994; Marina, 1999). Patients with stage II-IV disease have a 5-year survival rate ranging from 73 to 88 percent (Chan, 2008). Unilateral salpingo-oophorectomy is the standard care for these and other malignant germ cell tumors in reproductive-aged women. Beiner and colleagues (2004), however, treated eight women with early-stage immature teratoma with ovarian cystectomy and adjuvant chemotherapy and noted no recurrences. Immature teratomas may be associated with mature tissue implants studding the peritoneum that do not increase the stage of the tumor or diminish the prospect of survival. However, these implants of mature teratomatous elements, even though benign, are resistant to chemotherapy and can enlarge during or after chemotherapy. Termed the growing teratoma syndrome, these implants require second-look surgery and resection to exclude recurrent malignancy (Zagame, 2006).

Malignant Transformation of Mature Cystic Teratomas (Dermoid Cysts) These rare tumors are the only germ cell variants that typically develop in postmenopausal women. Malignant areas are

B

FIGURE 36-6╇ Immature teratoma. A. This opened surgical specimen shows characteristic solid and cystic architecture. As in mature teratomas, hair and other skin elements are often found. B. Immature teratomas contain a disorderly mixture of mature and immature tissues derived from the three germ cell layers—ectoderm, mesoderm, and endoderm. Of the immature elements, immature neuroepithelium is the most common. Here, immature neuroepithelial cells arranged in rosettes lie within a background of mature neural tissue. (Used with permission from Dr. Kelley Carrick.)

CHAPTER 36

with a presumed pure dysgerminoma should prompt a search for other germ cell components by a more extensive histologic evaluation (Aoki, 2003).

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SECTION 4 FIGURE 36-7╇ This opened surgical specimen reveals squamous cell carcinoma malignant transformation within a mature cystic teratoma.

usually found as small nodules in the cyst wall or a polypoid mass within the lumen after removal of the entire mature cystic teratoma (Pins, 1996). Squamous cell carcinoma is most common and is found in approximately 1 percent of mature cystic teratomas (Fig. 36-7). Platinum-based chemotherapy with or without pelvic radiation is most often used for adjuvant treatment of early-stage disease (Dos Santos, 2007). However, regardless of treatment received, patients with advanced disease do poorly (Gainford, 2010). Other uncommon types of malignant features may include basal-cell carcinomas, sebaceous tumors, malignant melanomas, adenocarcinomas, sarcomas, and neuroectodermal tumors. Moreover, endocrine-type neoplasms such as struma ovarii (teratoma composed mainly of thyroid tissue) and carcinoid may also be found within mature cystic teratomas.

■⌀ Treatment Surgery A vertical abdominal incision is traditionally recommended if ovarian malignancy is suspected. However, increasingly, investigators with advanced endoscopic skills have noted laparoscopy to be a safe and effective alternative for women with smaller ovarian masses and apparent stage I disease (Shim, 2013). If present, ascites is evacuated and sent for cytologic evaluation. Otherwise, washings of the pelvis and paracolic gutters are collected for analysis prior to manipulation of the intraperitoneal contents. The entire peritoneal cavity is systematically inspected. The ovaries are assessed for size, tumor involvement, capsular rupture, external excrescences, and adherence to surrounding structures. Fertility-sparing USO is performed in all reproductive-aged women diagnosed with malignant ovarian germ cell tumors, as this conservative approach in general does not adversely affect survival (Chan, 2008; Lee, 2009). Following USO, blind biopsy or wedge resection of a normal-appearing contralateral ovary is not recommended. For those who have completed childbearing, hysterectomy with bilateral salpingo-oophorectomy

(BSO) is appropriate (Brown, 2014b). In either case, following removal of the affected ovary, surgical staging by laparotomy or laparoscopy proceeds as previously described for epithelial ovarian cancer (Chap. 35, p. 748) (Gershenson, 2007a). Because of tumor dissemination patterns, lymphadenectomy is most important for dysgerminomas, whereas staging peritoneal and omental biopsies are particularly valuable for yolk sac tumors and immature teratomas (Kleppe, 2014). Cytoreductive surgery is recommended for advanced-stage malignant ovarian germ cell tumors if it can be accomplished with minimal residual disease (Bafna, 2001; Nawa, 2001; Suita, 2002). The same general principles for debulking are applied as described for epithelial ovarian cancer. Because of the exquisite chemosensitivity of most malignant germ cell tumors, however, neoadjuvant chemotherapy is a reasonable option for patients thought to be unresectable (Talukdar, 2014). Many women will be referred to an oncologist after USO for a tumor that was clinically confined to the excised ovary. For such patients, if initial surgical staging was incomplete, options may include a second surgery to complete primary staging, regular surveillance, or adjuvant chemotherapy. Unfortunately, few data support a preferred approach. Because of its minimally invasive qualities, laparoscopy is a particularly attractive option for delayed surgical staging following primary excision and has been shown to accurately detect those women who require chemotherapy (Leblanc, 2004). Surgical staging following primary excision, however, is less important for scenarios in which chemotherapy will be administered regardless of surgical findings such as clinical stage I yolk sac tumors and high-grade clinical stage I immature teratomas (Stier, 1996). In such patients, reassurance of no abnormalities by CT imaging is often sufficient prior to proceeding with adjuvant chemotherapy (Gershenson, 2007a).

Surveillance Patients with malignant ovarian germ cell tumors are followed by careful clinical, radiologic, and serologic surveillance every 3 months for the first 2 years after therapy completion (Dark, 1997). Ninety percent of recurrences develop within this time frame (Messing, 1992). Second-look surgery at the completion of therapy is not necessary in women with completely resected disease or in those individuals with advanced tumor that does not contain teratoma. However, incompletely resected immature teratoma is the one circumstance among all types of ovarian cancer in which patients clearly benefit from second-look surgery and excision of chemorefractory tumor (Culine, 1996; Rezk, 2005; Williams, 1994).

Chemotherapy Stage IA dysgerminomas and stage IA grade 1 immature teratomas do not require additional chemotherapy. More advanced disease and all other histologic types of malignant ovarian germ cell tumors have historically been treated with combination chemotherapy after surgery (Suita, 2002; Tewari, 2000). However, there is a strong trend toward exploring the feasibility of surgery followed by close surveillance in pediatric and adolescent girls (Billmire, 2014). Because chemotherapy remains effective when used at the time of relapse, some investigators are attempting to identify additional low-risk, early-stage subgroups that

Ovarian Germ Cell and Sex Cord-Stromal Tumors

Radiation Chemotherapy has replaced radiation as the preferred adjuvant treatment for all types of malignant ovarian germ cell tumors. This transition was prompted primarily by the exquisite sensitivity of these tumors to either modality, but higher likelihood of retained ovarian function using chemotherapy (Solheim, 2015). Patients treated with radiotherapy are also much more likely to develop a second cancer within 10 years (Solheim, 2014). Occasional situations may still exist in which radiotherapy is considered, such as palliation of a germ cell tumor that has demonstrated resistance to chemotherapy.

Relapse At least four courses of BEP chemotherapy is the preferred treatment for recurrent ovarian germ cell tumors in women initially managed with surgery alone. Patients who achieved a sustained clinical remission of greater than 6 months after completing BEP or another platinum-based chemotherapy regimen may be treated again with BEP. Because their tumors are generally more responsive, these “platinum-sensitive” patients have a much better prognosis. However, women who do not achieve remission with BEP chemotherapy or relapse within a few months (fewer than 6) are considered “platinum-resistant,” and treatment options are limited. Chemorefractory cases with dysgerminoma or immature teratoma appear to have a better outcome than other subtypes, and surgical salvage aimed at achieving no residual disease may benefit some patients (Li, 2007). Another option for this group is vincristine, dactinomycin, and cyclophosphamide (VAC) (Gershenson, 1985). Other potentially active drugs include paclitaxel, gemcitabine, and oxaliplatin (Hinton, 2002; Kollmannsberger, 2006). Second-look procedures with surgical debulking have a limited role because of the inherent chemosensitivity of these recurrent tumors. Chemorefractory immature teratomas are notable exceptions (Munkarah, 1994). Growth or persistence of a tumor after chemotherapy does not necessarily imply progression of malignancy, but these masses should still be resected (Geisler, 1994).

■⌀ Prognosis Malignant ovarian germ cell tumors have an excellent overall prognosis (see Table 36-3) (Solheim, 2013, 2014). Moreover, the number of cases with distant and unstaged disease has dramatically declined, suggesting that germ cell tumors are being

diagnosed earlier. In addition, the survival rates have significantly improved for all subtypes, especially with the demonstrated efficacy of cisplatin-based combination therapy (Smith, 2006). Histologic cell type, elevated serum marker levels, surgical stage, and the amount of residual disease at initial surgery are the major variables affecting prognosis (Murugaesu, 2006; Smith, 2006). Typically, pure dysgerminomas recur within 2 years and are highly treatable (Vicus, 2010). However, for nondysgerminomatous tumors, outcome after relapse is poor, and fewer than 10 percent of patients achieve long-term survival (Murugaesu, 2006). Most women treated with fertility-sparing surgery, with or without chemotherapy, will resume normal menses and are able to conceive and bear children (Gershenson, 2007b; Zanetta, 2001). In addition, none of the reported studies has noted an increased rate of birth defects or spontaneous abortion in those treated with chemotherapy (Brewer, 1999; Low, 2000; Tangir, 2003; Zanetta, 2001).

■⌀ Management During Pregnancy Persistent adnexal masses are detected in 1 to 2 percent of all pregnancies. These neoplasms are usually seen during routine obstetric sonographic examination, but occasionally a dramatically elevated maternal serum alpha-fetoprotein (MSAFP) level is the presenting sign of a malignant germ cell tumor (Horbelt, 1994; Montz, 1989). Mature cystic teratomas (dermoid cysts) make up one third of tumors resected during pregnancy. In contrast, dysgerminomas account for only 1 to 2 percent of such neoplasms but still are the most common ovarian malignancy during pregnancy. Development of other germ cell tumors is rare (Shimizu, 2003). Initial surgical management including surgical staging is the same as for the nonpregnant woman (Horbelt, 1994; Zhao, 2006). Fortunately, very few patients have advanced disease necessitating radical dissection for cytoreduction. The decision to administer chemotherapy during pregnancy is controversial. Malignant ovarian germ cell tumors have the propensity to grow rapidly, and delaying treatment until after delivery is potentially hazardous. Treatment with BEP appears to be safe during pregnancy, but some reports have speculated that fetal complications are possible (Elit, 1999; Horbelt, 1994). For this reason, some advocate postponing treatment until the puerperium (Shimizu, 2003). Unfortunately, there are no results from large studies to resolve this dilemma. Although BEP administration may be delayed until the puerperium for completely resected dysgerminomas, patients with nondysgerminomatous tumors (mainly yolk sac tumors and immature teratomas) and incompletely resected disease warrant strong consideration of chemotherapy during pregnancy.

OVARIAN SEX CORD-STROMAL TUMORS Sex cord-stromal tumors (SCSTs) are a heterogeneous group of rare neoplasms that originate from the ovarian matrix. Cells within this matrix have the potential for hormone production, and nearly 90 percent of hormone-producing ovarian tumors are SCSTs. As a result, individuals with these tumors typically present with signs and symptoms of estrogen or androgen excess.

CHAPTER 36

may be observed postoperatively and thereby avoid treatmentrelated toxicity (Bonazzi, 1994; Cushing, 1999; Dark, 1997). However, before this strategy can be incorporated into general practice, additional large studies are needed. The standard regimen is a 5-day course of bleomycin, etoposide, and cisplatin (BEP) given every 3 weeks (Gershenson, 1990; Williams, 1987). Modified 3-day BEP combinations are also safe and effective (Chen, 2014; Dimopoulos, 2004). Carboplatin and etoposide, given in three cycles, has shown promise as an alternative for selected patients (Williams, 2004). For women with incompletely resected disease, at least four courses of BEP are usually recommended (Williams, 1991).

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Surgical resection is the primary treatment, and SCSTs are generally confined to one ovary at the time of diagnosis. Moreover, most have an indolent growth pattern and low malignant potential. For these reasons, few patients ever require platinum-based chemotherapy. Although recurrent disease often responds poorly to treatment, patients may live for many years because of characteristically slow tumor progression. The overall prognosis of ovarian SCSTs is excellent—primarily due to early-stage disease at diagnosis and curative surgery. The scarcity of these tumors, however, limits the understanding of their natural history, treatment, and prognosis.

■⌀ Epidemiology SCSTs account for 3 to 5 percent of ovarian malignancies (Ray-Coquard, 2014). These tumors are more than twice as likely to develop in black women for reasons that are unclear (Quirk, 2005). In contrast with epithelial ovarian cancers or malignant germ cell tumors, ovarian SCSTs typically affect women of all ages. This range contains a unique bimodal distribution that reflects inherent tumor heterogeneity. For example, juvenile granulosa cell tumors, Sertoli-Leydig cell tumors, and sclerosing stromal tumors are found predominantly in prepubertal girls and women within the first three decades of life (Schneider, 2005). Adult granulosa cell tumors commonly develop in older women, at an average age in the mid-50s (van Meurs, 2013). There are no proven risk factors for SCSTs. However, in a hypothesis-generating case-control study, Boyce and coworkers (2009) observed that obesity as a hyperestrogenic state was independently associated, whereas parity, smoking, and oral contraceptive use were protective. The etiology of SCSTs is largely unknown. However, a single, recurrent FOXL2 gene mutation (402C>G) is present in virtually all adult-type granulosa cell tumors. Thus, mutant FOXL2 appears to be a highly specific event in the pathogenesis of these rare tumors (Schrader, 2009; Shah, 2009). The other major finding is that women with a germline DICER1 mutation are predisposed to developing SCSTs (Heravi-Moussavi, 2012). Otherwise, there is no known inherited predisposition for the development of these tumors, and familial cases are rare (Stevens, 2005). However, ovarian SCSTs do develop in association with several defined hereditary disorders at a frequency that exceeds mere chance. Associated disorders include Ollier disease, which is characterized by multiple benign but disfiguring cartilaginous neoplasms, and Peutz-Jeghers syndrome, characterized by intestinal hamartomatous polyps (Stevens, 2005).

■⌀ Diagnosis

TABLE 36-4. â•„Tumor Markers for Ovarian Sex CordStromal Tumors with Malignant Potential Granulosa cell tumors (adult and juvenile) Sertoli-Leydig cell tumors Sex cord tumor with annular tubules Steroid cell tumors not otherwise specified

Inhibin A and B; estradiol (not as reliable) Inhibin A and B; occasionally alpha-fetoprotein Inhibin A and B Steroid hormones elevated pretreatment

mild hirsutism that rapidly progresses to frank virilization should prompt evaluation to exclude these tumors. The classic presentation is a postmenopausal woman with rapidly evolving stigmata of androgen excess and a complex adnexal mass. Abdominal pain or a mass palpable by the patient herself are other telling signs and symptoms (Chan, 2005). The size of SCSTs varies widely, but most women have a palpable abdominal or pelvic mass during examination regardless of their age. A fluid wave and other physical findings suggestive of advanced disease, however, are rare.

Laboratory Testing Elevated circulating levels of testosterone or androstenedione or both are strongly suggestive of an ovarian SCST in a woman with signs and symptoms of virilization. Clinical hyperandrogenism is more likely to be idiopathic or related to polycystic ovarian syndrome, but serum testosterone levels >150 g/dL or dehydroepiandrosterone sulfate (DHEAS) levels >8000 g/L strongly suggest the possibility of an androgen-secreting tumor (Carmina, 2006). In most instances, tumor marker studies are not obtained preoperatively, because the diagnosis of ovarian SCST is often not suspected. When the diagnosis is confirmed, the appropriate tumor markers may be drawn during or following surgery (Table 36-4).

Imaging The gross appearances of SCSTs range from large multicystic masses to small solid masses—effectively precluding a specific radiologic diagnosis. Granulosa cell tumors often sonographically demonstrate semisolid features but are not reliably discernible from epithelial tumors (Fig. 36-8) (Sharony, 2001). In addition, the endometrium may be thickened from increased tumor estrogen production. Although CT or MR imaging has been used to clarify indeterminate sonograms, there is no definitive radiologic study to diagnose these tumors (Jung, 2005).

Patient Findings

Diagnostic Procedures

Isosexual precocious puberty is the presenting sign in more than 80 percent of prepubertal girls ultimately diagnosed with an ovarian SCST (Kalfa, 2005). Adolescents often report secondary amenorrhea. As a result, these young individuals presenting with endocrinologic symptoms tend to be diagnosed at earlier stages. Abdominal pain and distention are other common complaints in this age group (Schneider, 2003a). In adult women, heavy, irregular bleeding and postmenopausal bleeding are the most frequent symptoms. In addition,

Patients with an ovarian mass suspicious for malignancy based on clinical and sonographic findings require surgical resection for definitive tissue diagnosis, staging, and treatment. Sonographically or CT-guided percutaneous biopsy has no role. Moreover, diagnostic laparoscopy or laparotomy with visual assessment of the adnexal mass alone is inadequate. Thus, excision and pathologic evaluation are necessary. Following removal, ovarian SCSTs can usually be distinguished histologically from germ cell tumors, epithelial ovarian cancers, or other

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spindle-cell neoplasms by immunostaining for inhibin (Cathro, 2005; Schneider, 2005).

A

Preoperatively, patients with a potentially malignant ovarian SCST are ideally referred to a gynecologic oncologist for evaluation. Most ovarian SCSTs, however, are diagnosed by generalist gynecologists following resection of a seemingly benign but complex mass in a woman with a CA125 level that is typically normal, if known beforehand. The initial surgery is often performed in a community-based hospital and without adequate staging. In this setting, prior to referral, histologic results should be reviewed and confirmed by an experienced pathologist. Following referral to a gynecologic oncologist, surgical staging may be indicated.

■⌀ Pathology Classification Ovarian SCSTs arise from sex cord and mesenchymal cells of the embryonic gonad (Chap. 18, p. 407). Granulosa and Sertoli cells develop from the sex cords and thus from the coelomic epithelium. In contrast, theca cells, Leydig cells, and fibroblasts are derived from the mesenchyme. The primitive gonadal stroma possesses sexual bipotentiality. Therefore, developing tumors may be composed of a male-directed cell type (Sertoli or Leydig cell) or a female-directed cell type (granulosa or theca cell). Although distinct categories of SCSTs have been defined, mixed tumors are relatively common (Table 36-5). For example, ovarian granulosa cell tumors may have admixed Sertoli components. Similarly, tumors that are predominantly Sertoli or B

TABLE 36-5. â•„Modified WHO Classification of Ovarian Sex Cord-Stromal Tumors Pure stromal tumors Fibroma/fibrosarcoma Thecoma Sclerosing stromal tumor Leydig cell tumor Steroid cell tumor Pure sex cord tumors Granulosa cell tumor â•… Adult type â•… Juvenile type Sertoli cell tumor Sex cord tumor with annular tubules C

FIGURE 36-8╇ Adult granulosa cell tumor. A. Abdominal sonography displays a large adnexal mass with solid and cystic areas. With application of color Doppler, thick vascular septa are seen. B. Computed tomographic (CT) scan of the same tumor. C. The tumor was opened after excision, and again its mixed architecture is noted. (Used with permission from Dr. Christa Nagel.)

Mixed sex cord-stromal tumors Sertoli-Leydig cell tumors Sex cord-stromal tumors, NOS NOS = not otherwise specified; WHO = World Health Organization. Adapted with permission from Kurman RJ, Carcangiu ML, Herrington CS, et al (eds): WHO Classification of Tumours of Female Reproductive Organs, 4th ed. Lyon, International Agency for Research on Cancer, 2014.

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■⌀ Role of the Generalist

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Sertoli-Leydig cells may contain minor granulosa cell elements. These mixed tumors are believed to arise from a common lineage with variable differentiation and do not represent two concurrent separate entities (McKenna, 2005; Vang, 2004).

Histologic Grading Ovarian granulosa cell tumors are universally considered to have malignant potential, but most other SCST subtypes do not have definitive criteria for clearly defining benign and malignant. Attempts to grade these tumors using nuclear characteristics or mitotic activity counts have produced inconsistent results (Chen, 2003).

Patterns of Growth and Spread The natural history of SCSTs in general differs greatly from that of epithelial ovarian carcinomas. For example, most of these tumors have low malignant potential. They are typically unilateral and remain localized, retain hormone-secreting functions, and infrequently relapse. Recurrences tend to be late and usually develop in the abdomen or pelvis (Abu-Rustum, 2006). Bone metastases are rare (Dubuc-Lissoir, 2001).

Granulosa Cell Tumors Adult Granulosa Cell Tumors.╇Seventy percent of ovarian SCSTs are granulosa cell tumors (Colombo, 2007). These tumors are formed by cells believed to arise from those surrounding the germinal cells within ovarian follicles. There are two clinically and histologically distinct types: the adult form, which makes up 95 percent of cases, and the juvenile type, accounting for 5 percent. With adult granulosa cell tumor, most women are diagnosed after age 30, and the average age approximates 55 years. Heavy, irregular menstrual bleeding and postmenopausal bleeding are common and reflect prolonged exposure of the endometrium to estrogen. Related to this estrogen excess, coexisting pathology such as endometrial hyperplasia or adenocarcinoma has been found in 25 to 30 percent of patients with adult granulosa cell tumor (van

A

Meurs, 2013). Similarly, breast enlargement and tenderness are frequent associated complaints, and secondary amenorrhea has been reported (Kurihara, 2004). Alternatively, symptoms may stem from the mass of the ovary rather than from hormones produced (Ray-Coquard, 2014). An enlarging and potentially hemorrhagic tumor can cause abdominal pain and distention. Acute pelvic pain may suggest adnexal torsion, or tumor rupture with hemoperitoneum can mimic ectopic pregnancy. During surgery, if an adult granulosa cell tumor is confirmed, tumor markers may be requested. Of these, inhibin B seems to be more accurate than inhibin A, frequently being elevated months before clinical detection of recurrence (Mom, 2007). The diagnostic value of these markers, however, is often hampered by their physiologically broad normal ranges (Schneider, 2005). Estradiol also has limited use in surveillance. This is particularly true for the younger patient wishing to preserve fertility and having the contralateral ovary left in situ. Grossly, adult granulosa cell tumors are large and multicystic and often exceed 10 to 15 cm in diameter (see Fig. 36-8). The surface is frequently edematous and unusually adhered to other pelvic organs. For this reason, more extensive dissection is typically required than for epithelial ovarian cancers or malignant germ cell tumors. During excision, inadvertent rupture and intraoperative bleeding from the tumor itself is also common. The interior of the tumor is highly variable. Solid components may predominate with large areas of hemorrhage and necrosis. Alternatively, it can be cystic, with numerous locules filled with serosanguinous or gelatinous fluid (Colombo, 2007). Microscopic examination shows predominately granulosa cells with pale, grooved, “coffee bean” nuclei. The characteristic microscopic feature is the Call-Exner body—a rosette arrangement of cells around an eosinophilic fluid space (Fig. 36-9). Adult granulosa cell tumors are low-grade malignancies that typically demonstrate indolent growth. Ninety-five percent are unilateral, and 70 to 90 percent are stage I at diagnosis (Table 36-6). The 5-year survival for patients with stage I disease is 90 to 95 percent (Colombo, 2007; Zhang, 2007). However, 15 to

B

FIGURE 36-9╇ Adult granulosa cell tumor. A. Cells are typically crowded and contain scant, pale cytoplasm. Their elongated nuclei may have a longitudinal fold or groove that gives them a “coffee bean” appearance. B. Call-Exner bodies are identified by their rosette appearance. (Used with permission from Dr. Raheela Ashfaq.)

Ovarian Germ Cell and Sex Cord-Stromal Tumors TABLE 36-6. â•„Stage and Survival of Common Ovarian Sex Cord-Stromal Tumors Sertoli-Leydig Cell

Stage at diagnosis I II-IV

70–90% 10–20%

97% 2–3%

Five-year survival Stage I Stage II–IV

90–95% 30–50%

90–95% 10–20%

Sources for survival figures are referenced within the text. 25 percent of stage I tumors will eventually relapse. The median time to recurrence is 5 to 6 years, but may be several decades (Abu-Rustum, 2006; East, 2005). Advantageously, these indolent tumors usually progress slowly thereafter, and the median length of survival after relapse is another 6 years. Advanced tumor stage and residual disease are poor prognostic factors (Al Badawi, 2002; Sehouli, 2004). Patients with stage II-IV tumors have a 5-year survival rate of 30 to 50 percent (Malmstrom, 1994; Miller, 1997; Piura, 1994). Cellular atypia and mitotic count may help in determining the prognosis but are difficult to reproducibly quantify (Miller, 2001). Juvenile Granulosa Cell Tumors.╇These rare neoplasms develop primarily in children and young adults, and approximately 90 percent are diagnosed before puberty (Colombo, 2007). The mean age at diagnosis is 13 years, but patient ages range from newborn to 67 years (Young, 1984). Juvenile granulosa cell tumors are sometimes associated with Ollier disease or with Maffucci syndrome, which is characterized by endochondromas and hemangiomas (Young, 1984; Yuan, 2004). In affected females, estrogen, progesterone, and testosterone levels may be elevated and lead to suppression of gonadotropins. As a result, menstrual irregularities or amenorrhea are common. Prepubertal girls typically display isosexual precocious puberty, which is characterized by breast enlargement and development of pubic hair, vaginal secretions, and other secondary sexual characteristics. These tumors infrequently secrete androgens, but in such cases may induce virilization. Despite these endocrinologic signs, a delayed diagnosis of juvenile granulosa cell tumors in pre- and postpubertal girls is common and associated with a higher risk of peritoneal tumor spread (Kalfa, 2005). In addition to hormonal changes, individuals may display tumor effects. For example, older patients usually seek medical attention for abdominal pain or swelling. Preoperative rupture with resulting hemoperitoneum may create acute abdominal symptoms in 5 to 10 percent of cases (Colombo, 2007). Ascites is present in 10 percent (Young, 1984). Juvenile granulosa cell tumors are grossly similar to the adult-type tumor and display variable solid and cystic components. They can attain significant size and have an average diameter of approximately 12 cm. Microscopically, cytologic features that distinguish these tumors from the adult type are their rounded, hyperchromatic nuclei without “coffee-bean”

Thecoma-Fibroma Group Thecomas.╇ These are relatively common SCSTs and are rarely malignant. Thecomas are unique because they typically develop in postmenopausal women in their mid-60s and develop infrequently before age 30. These solid tumors are among the most hormonally active of the SCSTs and usually produce excess estrogen. As a result, the primary signs and symptoms are abnormal vaginal bleeding or pelvic mass or both. Many women also present with concurrent endometrial hyperplasia or adenocarcinoma (Aboud, 1997). These tumors are composed of lipid-laden stromal cells that are occasionally luteinized. Half of these luteinized thecomas are either hormonally inactive or androgenic with the potential for inducing masculinization. Thecomas are solid tumors whose cells resemble the theca cells that normally surround the ovarian follicles (Chen, 2003). Because of this texture, these tumors appear sonographically as solid adnexal masses and may mimic extrauterine leiomyomas. Bilateral ovarian involvement and extraovarian spread are rare. Fortunately, ovarian thecomas are clinically benign, and surgical resection is curative. Fibromas-Fibrosarcomas.╇ Fibromas are also relatively common, hormonally inactive SCST variants that usually occur in perimenopausal and menopausal women (Chechia, 2008). These solid, generally benign ovarian neoplasms arise from the spindled stromal cells that form collagen. Most fibromas are found incidentally during pelvic or sonographic examination. They are round, oval, or lobulated solid tumors associated with free fluid or less commonly, with frank ascites and possess minimal to moderate vascularization (Paladini, 2009). Perhaps 1 percent of women present with Meigs syndrome, which is a triad of pleural effusion, ascites, and a solid ovarian mass (Siddiqui, 1995). Pleural effusions are usually rightsided, and these, as well as accompanying ascites, are typically transudative and resolve after tumor resection (Majzlin, 1964). Despite this association of ascites with benign fibromas, when ascites and a pelvic mass coexist, evaluation is based on an assumption of malignancy. The prognosis following excision of fibromas is that for any benign tumor. However, 10 percent will demonstrate increased cellularity and varying degrees of pleomorphism and mitotic activity that indicate a tumor better characterized as having low malignant potential. In 1 percent of cases, malignant transformation to fibrosarcoma is found. Sclerosing Stromal Tumors.╇These tumors are rare and account for less than 5 percent of SCSTs. The average patient age is approximately 20 years, and 80 percent develop before

CHAPTER 36

Adult Granulosa Cell

grooves. Call-Exner bodies are rare, but often there is a theca cell component (Young, 1984). Prognosis is excellent, and the 5-year survival rate is 95 percent. Similar to adult-type tumors, 95 percent of juvenile granulosa cell tumors are unilateral and stage I at diagnosis (Young, 1984). However, the juvenile type is more aggressive in advanced stages, and the time to relapse and death is much shorter. Recurrences typically develop within 3 years and are highly lethal. Later recurrences are unusual (Frausto, 2004).

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age 30. Sclerosing stromal tumors are clinically benign and typically unilateral. Menstrual irregularities and pelvic pain are both frequent symptoms (Marelli, 1998). Ascites is seldom encountered (unlike fibromas), and sclerosing stromal tumors are hormonally inactive (unlike thecomas). Tumor size ranges from microscopic to 20 cm. Histologically, the presence of pseudolobulation of cellular areas separated by edematous connective tissue, increased vascularity, and prominent areas of sclerosis are distinguishing features.

Sertoli-Stromal Cell Tumors Sertoli Cell Tumors.╇ Ovarian Sertoli cell tumors are rare and account for less than 5 percent of all SCSTs. The mean patient age at diagnosis is 30 years, but ages range from 2 to 76 years. One quarter of patients present with estrogenic or androgenic manifestations, but most tumors are clinically nonfunctional. Sertoli cell tumors are typically unilateral, solid, and yellow and measure 4 to 12 cm in diameter. Derived from the cell type that gives rise to the seminiferous tubules, these tumor cells often organize into histologically characteristic tubules (Young, 2005). Sertoli cell tumors, however, may also mimic many different tumors, and immunostaining in these cases is invaluable to confirm the diagnosis. More than 80 percent are stage I at diagnosis, and most are clinically benign. Moderate cytologic atypia, brisk mitotic activity, and tumor cell necrosis are indicators of greater malignant potential and are found in 10 percent of individuals with stage I disease and most of those with stage II-IV tumors. The risk of recurrence is higher when these features are identified (Oliva, 2005). Sertoli-Leydig Cell Tumors.╇Sertoli-Leydig cell tumors comprise only 5 to 10 percent of ovarian SCSTs (Zhang, 2007). Their incidence mirrors that of Sertoli cell tumors, and the average age is 25 years. Although Sertoli-Leydig cell tumors have been identified in children and postmenopausal females, more than 90 percent develop during the reproductive years. These tumors frequently produce sex-steroid hormones, most commonly androgens. As a result, frank virilization develops in one third of affected women, and another 10 percent have clinical manifestations of androgen excess (Young, 1985). Menstrual disorders are also common. Accordingly, SertoliLeydig cell tumors are suspected preoperatively in a patient with a unilaterally palpable adnexal mass and with androgenic manifestations. For these women, an elevated serum testosteroneto-androstenedione ratio further suggests the diagnosis. Although these hormonal effects frequently develop, one half of patients will have nonspecific abdominal mass symptoms as their only presenting complaint. Associated ascites is infrequent (Outwater, 2000). Thyroid abnormalities also coexist with Sertoli-Leydig cell tumors at a frequency that exceeds mere chance. These tumors tend to be large at the time of excision with an average diameter greater than 10 cm, but ranges from 1 to 50 cm have been reported. In most cases, Sertoli-Leydig cell tumors appear yellow and lobulated. Tumors can be solid, partially cystic, or completely cystic, and they may or may not have polypoid or vesicular structures in their interior (Fig. 36-10).

A

B

C

FIGURE 36-10╇ Sertoli-Leydig cell tumor (SLCT). A. SLCTs show variable gross features depending on the degree of differentiation and presence of heterologous elements. This opened surgical specimen has a predominantly solid cut surface with focal cysts, variegated yellow-brown color, and foci of hemorrhage. B. Well-differentiated SLCT composed of hollow tubules admixed with clusters of mature Leydig cells. C. This intermediate differentiated SLCT contains solid tubules, which are thought to resemble those of the fetal testis. (Used with permission from Dr. Katja Gwin.)

Ovarian Germ Cell and Sex Cord-Stromal Tumors

Sex Cord Tumors with Annular Tubules This tumor accounts for 5 percent of SCSTs and is characterized by ring-shaped tubules and distinctive cellular elements that are histologically intermediate between Sertoli-cell and granulosa cell tumors. There are two clinically distinct types. One third are clinically benign and develop in patients with Peutz-Jeghers syndrome (PJS). These tumors are typically small, multifocal, calcified, bilateral, and diagnosed incidentally. Fifteen percent of PJS-associated cases will also develop adenoma malignum of the cervix, which is a rare, extremely well-differentiated adenocarcinoma. In contrast, two thirds of tumors are not associated with PJS. These masses are usually larger, unilateral, and symptomatic and carry a clinical malignancy rate of 15 to 20 percent (Young, 1982).

Steroid Cell Tumors Fewer than 5 percent of SCSTs are steroid cell tumors. The average age at diagnosis is the mid-20s, but patients can present at virtually any age. These tumors are composed entirely or predominantly of cells that resemble steroid hormone-secreting cells and are categorized according to the histologic composition of these cells. Stromal luteomas are clinically benign tumors that by definition lie completely within the ovarian stroma. They are usually seen in postmenopausal women. Estrogenic effects are common, but occasional individuals have androgenic manifestations. Leydig cell tumors are also benign and typically are seen in postmenopausal women. They are distinguished microscopically by rectangular, crystal-like cytoplasmic inclusions, termed crystals of Reinke. Leydig cells secrete testosterone, and these tumors are usually associated with androgenic effects. Steroid cell tumors not otherwise specified (NOS) are the most common subtype within this group and typically present in younger reproductive-aged women. Some of these cases may represent large stromal luteomas that have grown to reach the ovarian surface or Leydig-cell tumors in which Reinke crystals cannot be identified. These tumors are typically associated

with androgen excess, but estrogen or cortisol overproduction (i.e., Cushing syndrome) has also been reported. One third of �steroid cell tumors NOS are clinically malignant and have a dismal prognosis (Oliva, 2005).

Unclassified Sex Cord-Stromal Tumors Unclassified tumors account for 5 percent of SCSTs and have no clearly predominant pattern of testicular (Sertoli cells) or ovarian (granulosa cells) differentiation. These ill-defined tumors are especially common during pregnancy due to alterations in their usual clinical and pathologic features (Young, 2005). They may be estrogenic, androgenic, or nonfunctional. The prognosis is similar to that of granulosa cell tumors and Sertoli-Leydig cell tumors of similar degrees of differentiation.

Gynandroblastomas These are the rarest type of ovarian SCST. Patients present at a mean age of 30 years and typically have menstrual irregularities or evidence of hormonal excess. The tumors are characterized by intermingled granulosa cells and tubules of Sertoli cells. Theca or Leydig cells or both may also be present in varying degrees. Gynandroblastomas have low malignant potential, and only one death has been reported (Martin-Jimenez, 1994).

■⌀ Treatment Surgery The mainstay of treatment for patients with an ovarian SCST is complete surgical resection. This group shows relative insensitivity to adjuvant chemotherapy or radiation. Thus, operative goals are to establish a definitive tissue diagnosis, determine the extent of disease, and also remove all grossly visible tumors in those infrequent patients with advanced-stage disease. Moreover, during preoperative planning, clinicians should consider the patient’s age and desire for future fertility. Hysterectomy with BSO is performed for those who have completed childbearing, whereas fertility-sparing USO with preservation of the uterus and remaining ovary may be appropriate in the absence of obvious disease spread to these organs (Zanagnolo, 2004). Endometrial sampling is performed, especially if fertility-sparing surgery is planned in women with granulosa cell tumors or thecomas. This is because many of these patients will have coexisting endometrial hyperplasia or adenocarcinoma that may affect the decision for hysterectomy. Minimally invasive laparoscopic surgery has a variety of relevant applications. For some, the diagnosis of SCST may not be discovered until the mass is laparoscopically removed and sent for frozen section analysis. Laparoscopic surgical staging can then proceed. When the diagnosis is not made until the final pathology report is confirmed postoperatively, laparoscopic staging may be proposed to determine whether metastatic disease is present. This can reduce the morbidity of a second operation (Shim, 2013). Surgical staging is essential to determine the extent of disease and the need for adjuvant therapy in most individuals with potentially malignant SCST subtypes (Fig. 36-11). That said, only approximately 20 percent of cases have complete staging (Abu-Rustum, 2006; Brown, 2009). More recent data Â�suggest

CHAPTER 36

Microscopically, these morphologically diverse tumors contain cells resembling epithelial and stromal testicular cells in varying proportions. The five subtypes of differentiation (well, intermediate, poor, retiform, and heterologous) have considerable overlap. Well-differentiated tumors are all clinically benign (Chen, 2003; Young, 2005). Overall, 15 to 20 percent of Sertoli-Leydig cell tumors are clinically malignant. Prognosis depends predominantly on the stage and degree of tumor differentiation in these malignant variants. For example, Young and Scully (1985) performed a clinicopathologic analysis of 207 cases and identified stage I disease in 97 percent. The 5-year survival rate for patients with stage I disease exceeds 90 percent (Zaloudek, 1984). Malignant features were observed in approximately 10 percent of tumors with intermediate differentiation and in 60 percent of poorly differentiated tumors. Retiform and heterologous elements are seen only in intermediate or poorly differentiated Sertoli-Leydig cell tumors and typically are associated with poorer prognosis. Overall, the 2 to 3 percent of patients with stage II-IV disease have a dismal prognosis (Young, 1985).

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stage II-IV disease warrants postoperative treatment. In general, SCSTs display less sensitivity to chemotherapy than other ovarian malignancies, but most women at high Staging required risk for disease progression can be treated successfully with adjuvant platinum-based chemotherapy (van Meurs, 2014). The 5-day bleomycin, etoposide, and cisplatin (BEP) regimen is the most widely Thecoma used first-line chemotherapy combination Fibroma Sclerosing stromal tumor (Gershenson, 1996; Homesley, 1999). For Staging not Gynandroblastoma completely resected disease, three courses required Sertoli-Leydig cell tumor (well-differentiated) given every 3 weeks are sufficient. Four cycles Sex cord tumor with annular tubules are recommended for patients with incom(associated with PJS) pletely resected tumor (Homesley, 1999). In addition to BEP, taxanes have demonFIGURE 36-11╇ Staging of sex cord-stromal tumors. PJS = Peutz-Jeghers syndrome. strated activity against ovarian SCSTs, and combination paclitaxel and carboplatin chemotherapy shows promising results (Brown, 2004, 2005). that, due to surface and hematogenous routes of spread, the To determine the most effective regimen, a prospective ranstandard ovarian cancer procedure can be modified. Pelvic domized study is currently underway, comparing paclitaxel washings, exploration of the abdomen, peritoneal biopsies, and and carboplatin to BEP in those with newly diagnosed ovarpartial omentectomy remain important. However, the utility ian SCSTs (GOG protocol #264). Unfortunately, the relaof routine pelvic and paraaortic lymphadenectomy has been tive scarcity of women who have ovarian SCST and receive increasingly challenged. In a study of 262 ovarian SCSTs, chemotherapy limits the ability to conduct large randomized none of the 58 patients undergoing nodal dissection had posistudies. tive nodes (Brown, 2009). Additionally, performing a lymphadenectomy has not been shown to improve survival rates in Radiation those with SCSTs (Chan, 2007). Postoperative radiation therapy currently has a limited role in Surgical removal of hormone-producing SCSTs results in an the management of ovarian SCSTs. There is some evidence immediate drop in elevated preoperative sex-steroid hormone indicating a prolonged survival in at least some women with levels. Physical manifestations of these elevated levels, however, newly diagnosed disease who received whole-abdominal radiopartially or completely resolve more gradually. therapy (Wolf, 1999). However, chemotherapy is usually the Granulosa cell tumor (adult or juvenile) Fibrosarcoma Sertoli-Leydig cell tumor (intermediate and poorly differentiated) Sex cord tumor with annular tubules (independent of PJS) Steroid-cell tumors

Surveillance

In general, women with stage I ovarian SCSTs have an excellent prognosis following surgery alone and usually can be followed at regular intervals without the need for further treatment (Schneider, 2003a). Surveillance includes a general physical and pelvic examination, serum marker level testing, and imaging as clinically indicated.

Chemotherapy The decision to administer postoperative therapy depends on various factors (Fig. 36-12). Although typically treated solely with surgery, malignant stage I ovarian SCSTs may require adjuvant chemotherapy when large tumor size, high mitotic index, capsular excrescences, tumor rupture, incomplete staging, or equivocal pathology results are noted. Women with one or more of these suspicious features are thought to be at higher risk of relapse and are considered for platinum-based chemotherapy (Schneider, 2003b). In addition,

Low-risk disease: Stage IA

No adjuvant therapy Fertility-sparing surgical approach in selected patients

Intermediate-risk disease: Higher-risk stage I (tumor rupture, large size, high mitotic rate, positive cytology, surface involvement, incompletely staged) Any stage II

Consider postoperative adjuvant chemotherapy: bleomycin, etoposide, cisplatin (BEP) × 3 cycles

High-risk disease: Stage III Stage IV

Postoperative adjuvant chemotherapy: BEP (3 cycles if completely resected, 4 cycles if residual disease)

Recurrent disease

Consider secondary debulking if technically feasible and prolonged disease-free interval; followed by BEP or paclitaxel or If not surgical candidate, chemotherapy with BEP, paclitaxel, or other salvage regimen.

FIGURE 36-12╇ Postoperative treatment of sex cord-stromal tumors.

Ovarian Germ Cell and Sex Cord-Stromal Tumors

Relapse The management of recurrent ovarian SCST depends on the clinical circumstances. Secondary surgical debulking is strongly considered due to the indolent growth pattern, the typically long disease-free interval after initial treatment, and the inherent insensitivity to chemotherapy (Crew, 2005; Powell, 2001). Platinum-based combination chemotherapy is the primary treatment chosen for recurrent disease with or without surgical debulking (Uygun, 2003). Of regimens, BEP is most frequently administered because it has the highest known response rate (Homesley, 1999). Paclitaxel is another promising agent that was evaluated as a single agent in a phase II Gynecologic Oncology Group trial (GOG protocol #187). There is no standard treatment for women who have progressive disease despite aggressive surgery and platinum-based chemotherapy. Bevacizumab (Avastin) demonstrated a 17-percent response rate in a Phase II trial (GOG protocol #251) (Brown, 2014a). Vincristine, actinomycin D, and cyclophosphamide (VAC) regimen has limited activity (Ayhan, 1996; Zanagnolo, 2004). Hormonal therapy is minimally toxic, but the clinical experience with this approach is extremely limited (Hardy, 2005). Medroxyprogesterone acetate and the gonadotropinreleasing hormone (GnRH) agonist leuprolide acetate (Lupron) have each demonstrated activity in halting the growth of recurrent ovarian SCSTs (Fishman, 1996; Homesley, 1999). GnRH antagonists, however, may not be as effective (Ameryckx, 2005). In addition to traditional drugs, discovery of the FOXL2 402C>G mutation occurring exclusively in all adult granulosa cell tumors may lead to the development of targeted therapies for women with advanced or recurrent disease. Currently, FOXL2 as a transcription factor does not represent a pharmacologic target. Further insights into its function and downstream effects may identify molecular alterations in these tumors that can be targeted (Kobel, 2009).

■⌀ Prognosis In general, ovarian SCSTs portend a much better prognosis than epithelial ovarian carcinomas chiefly because most women with SCSTs are diagnosed with stage I disease. Stage II-IV tumors are rare, but women with these cancers have a poor prognosis similar to their counterparts with epithelial disease. Unfortunately, improvements in survival rates have not been observed in ovarian SCSTs during the past few decades (Chan, 2006). Of the clinical factors affecting prognosis, surgical stage and residual disease are the most important (Lee, 2008; Zanagnolo, 2004). Further, in a Surveillance, Epidemiology and End Results (SEER) database study, Zhang and colleagues (2007) performed a multivariate analysis of 376 women with SCSTs. They concluded that age younger than 50 years was also an independent predictor of an improved survival rate.

■⌀ Management During Pregnancy Ovarian SCSTs are rarely detected during pregnancy (Okada, 2004). In a California population-based study of more than 4 million obstetric patients, one granulosa cell tumor was diagnosed among 202 women with an ovarian malignancy (Leiserowitz, 2006). Granulosa cell tumors are most common, but only 10 percent are diagnosed during pregnancy (Hasiakos, 2006). One third of pregnant women with SCSTs are incidentally diagnosed at cesarean delivery, one third has abdominal pain or swelling, and the remainder may present with hemoperitoneum, virilization, or vaginal bleeding (Young, 1984). Surgical management should be the same as for the nonpregnant woman. For most, conservative management with USO and staging is the primary procedure, but hysterectomy and BSO may be indicated in selected circumstances (Young, 1984). Postoperative chemotherapy is typically withheld until after delivery because SCSTs have an indolent growth pattern.

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primary postoperative treatment because it is generally better tolerated, more widely accessible, and easier to administer. Radiation is best reserved for palliation of local symptoms (Dubuc-Lissoir, 2001).

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Gestational Trophoblastic Disease EPIDEMIOLOGY AND RISK FACTORS.

. . . . . . . . . . . . .

HYDATIDIFORM MOLE (MOLAR PREGNANCY). . DIAGNOSIS.

. . . .

780

. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

782

TREATMENT.

. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

GESTATIONAL TROPHOBLASTIC NEOPLASIA. .

783

. . . . .

784

. . . . . . . . . . . . . . . . . .

785

. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

786

HISTOLOGIC CLASSIFICATION. . DIAGNOSIS.

779

TREATMENT.

. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

REFERENCES. .

. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

788 791

Gestational trophoblastic disease (GTD) refers to a spectrum of interrelated but histologically distinct tumors originating from the placenta (Table 37-1). These diseases are characterized by a reliable tumor marker, which is the β-subunit of human chorionic gonadotropin (β-hCG), and have varied tendencies for local invasion and spread. Gestational trophoblastic neoplasia (GTN) refers to the subset of GTD that develops malignant sequelae. These tumors require formal staging and typically respond favorably to chemotherapy. Most commonly, GTN develops after a molar pregnancy but may follow any gestation. The prognosis for most GTN cases is TABLE 37-1. â•„Modified WHO Classification of GTD Molar pregnancies Hydatidiform mole â•…Complete â•…Partial Invasive mole Trophoblastic tumors Choriocarcinoma Placental site trophoblastic tumor Epithelioid trophoblastic tumor GTD = gestational trophoblastic disease; WHO = World Health Organization. Modified with permission from Kurman RJ, Carcangiu ML, Herrington CS, et al (eds): WHO Classification of Tumours of Female Reproductive Organs, 4th ed. Lyon, International Agency for Research on Cancer, 2014.

excellent, and patients are routinely cured, even with widespread metastases. The outlook for preservation of fertility and for successful subsequent pregnancy outcomes is equally bright (Vargas, 2014; Wong, 2014). Accordingly, although GTD is uncommon, because the opportunity for cure is great, clinicians should be familiar with its presentation, diagnosis, and management.

EPIDEMIOLOGY AND RISK FACTORS The incidence of GTD has remained fairly constant at approximately 1 to 2 per 1000 deliveries in North America and Europe (Drake, 2006; Loukovaara, 2005; Lybol, 2011). Although historically higher incidence rates have been reported in parts of Asia, some of this disparity may reflect discrepancies between population-based and hospital-based data collection (Chong, 1999; Kim, 2004; Matsui, 2003). Improved socioeconomic conditions and dietary changes may be partly responsible as well. That said, certain Southeast Asian populations as well as Hispanics and Native Americans living in the United States do have increased incidences (Drake, 2006; Smith, 2003; Tham, 2003). Maternal age at the upper and lower extremes carries a higher risk of GTD (Altman, 2008; Loukovaara, 2005). This association is much greater for complete moles, whereas the risk of partial molar pregnancy varies relatively little with age. Moreover, compared with the risk in those aged 15 years or younger, the degree of risk is much greater for women 45 years (1 percent) or older (17 percent at age 50) (Savage, 2010; Sebire, 2002a). One explanation relates to ova from older women having higher rates of abnormal fertilization. Similarly, older paternal age has been associated with increased risk (La Vecchia, 1984; Parazzini, 1986). A history of prior unsuccessful pregnancies also increases the risk of GTD. For example, previous spontaneous abortion at least doubles the risk of molar pregnancy (Parazzini, 1991). More significantly, a personal history of GTD increases the risk of developing a molar gestation in a subsequent pregnancy at least 10-fold. The frequency in a subsequent conception is approximately 1 percent, and most cases mirror the same type of mole as the preceding pregnancy (Garrett, 2008; Sebire, 2003). Furthermore, following two episodes of molar pregnancy, 23 percent of later conceptions result in another molar gestation (Berkowitz, 1998). For this reason, women with a prior history of GTD should undergo firsttrimester sonographic examination in subsequent pregnancies. Familial molar pregnancies, however, are rare (Fallahian, 2003). Of other risk factors, combination oral contraceptive (COC) pill use has been associated with an increased risk of GTD. Specifically, prior COC use approximately doubles the risk, and longer duration of use also correlates positively with risk (Palmer, 1999; Parazzini, 2002). Moreover, women who

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SECTION 4 A

B

FIGURE 37-1╇ A. Complete hydatidiform mole. These moles classically have swollen enlarged villi, some of which show cistern formation, that is, central cavitation within the large villi (black asterisks). Seen diffusely throughout the placenta, these villous changes create the vesicles noted grossly in complete moles (see Fig. 37-3). Complete moles also typically show trophoblastic proliferation (yellow asterisk), which may be focal or widespread. (Used with permission from Dr. Erika Fong.) B. Normal term placenta showing smaller, nonedematous villi and absence of trophoblastic proliferation. (Used with permission from Dr. Kelley Carrick.)

used COCs during the cycle in which they conceived have a higher risk in some but not all studies (Costa, 2006; Palmer, 1999). Many of these associations, however, are weak and could be explained by confounding factors other than causality (Parazzini, 2002). Some epidemiologic characteristics differ markedly between complete and partial moles. For example, vitamin A deficiency and low dietary intake of carotene are associated only with an increased risk of complete moles (Berkowitz, 1985, 1995; Parazzini, 1988). Partial moles have been linked to higher educational levels, smoking, irregular menstrual cycles, and obstetric histories in which only male infants are among the prior live births (Berkowitz, 1995; Parazzini, 1986).

HYDATIDIFORM MOLE (MOLAR PREGNANCY) Hydatidiform moles are abnormal pregnancies characterized histologically by aberrant changes within the placenta. Classically, the chorionic villi in these placenta show varying

degrees of trophoblast proliferation and edema of the stroma within villi (Fig. 37-1). Hydatidiform moles are categorized as either complete hydatidiform moles or partial hydatidiform moles (Table 37-2). Chromosomal abnormalities play an integral role in hydatidiform mole development.

■⌀ Complete Hydatidiform Mole These molar pregnancies differ from partial moles with regard to their karyotype, their histologic appearance, and their clinical presentation. First, complete moles typically have a diploid karyotype, and 85 to 90 percent of cases are 46,XX. The chromosomes, however, in these pregnancies are entirely of paternal origin, and thus, the diploid set is described as diandric. Specifically, complete moles are formed by androgenesis, in which the ovum is fertilized by a haploid sperm that then duplicates its own chromosomes after meiosis (Fig. 37-2) (Fan, 2002; Kajii, 1977). The ovum fails to contribute chromosomes. Most of these moles are 46,XX, but dispermic fertilization of a single ovum, that is, simultaneous fertilization by two sperm, can produce a 46,XY karyotype (Lawler, 1987). Although

TABLE 37-2. â•„Features of Hydatidiform Moles Feature

Complete Mole

Partial Mole

Karyotype

46,XX or 46,XY

69,XXX or 69,XXY

Pathology Fetus/embryo Villous edema Trophoblastic proliferation p57Kip2 immunostaining

Absent Diffuse Can be marked Negative

Present Focal Focal and minimal Positive

Clinical presentation Typical diagnosis Postmolar malignant sequelae

Molar gestation 15%

Missed abortion 4–6%

Gestational Trophoblastic Disease

46,XX

46,XX

Cell duplication

23,X Paternal Chromosome Duplication

Paternal Chromosomes Only

46,XX

A

69,XXY 23,Y 23,Y 23,X 23,X

23,X 23,X

69,XXY

Triploid 69, XXY Cells Maternal and Paternal Chromosomes

Dispermy 69,XXY

B

FIGURE 37-2╇ A. A 46,XX complete mole may be formed if a 23,X-bearing haploid sperm penetrates a 23,X-containing haploid egg whose genes have become “inactive.” Paternal chromosomes then duplicate to create a 46,XX diploid chromosomal complement solely of paternal origin. Alternatively, this same type of inactivated egg can be fertilized independently by two sperm, either 23,X- or 23,Y-bearing, to create a 46,XX or 46,XY chromosomal complement, again of paternal origin only. B. Partial moles may be formed if two sperm, either 23,X- or 23,Y-bearing, both fertilize a 23,X-containing haploid egg, whose genes have not been inactivated. The resulting fertilized egg is triploid. Alternatively, a similar haploid egg may be fertilized by an unreduced diploid 46,XY sperm.

nuclear DNA is entirely paternal, mitochondrial DNA remains maternal in origin (Azuma, 1991). Microscopically, complete moles display enlarged, edematous villi and abnormal trophoblastic proliferation. These changes diffusely involve the entire placenta (see Fig. 37-1). Macroscopically, these changes transform the chorionic villi into clusters of vesicles with variable dimensions. Indeed, the name hydatidiform mole literally stems from this “bunch of grapes” appearance. In these pregnancies, no fetal tissue or amnion is produced. As a result, this mass of placental tissue completely fills the endometrial cavity (Fig. 37-3). Clinically, the presentation of a complete mole has changed considerably. In the 1960s and 1970s, more than half of affected patients had anemia and uterine sizes in excess of that predicted for their gestational age. In addition, hyperemesis gravidarum, preeclampsia, and theca-lutein cysts developed in approximately one quarter of women (Soto-Wright, 1995). As described in Chapter 9 (p. 219), theca-lutein cysts develop with prolonged exposure to luteinizing hormone (LH) or β-hCG (Fig. 37-4). These cysts range in size from 3 to 20 cm, and most regress with falling β-hCG titers after molar evacuation. If such cysts are present, and especially if they are bilateral, the risk of postmolar GTN is increased.

Complete moles, however, infrequently present today with these traditional signs and symptoms (Mangili, 2008). As a result of β-hCG testing and sonography, the mean gestational age at evacuation currently approximates 12 weeks, compared with 16 to 17 weeks in the 1960s and 1970s (Drake, 2006; Soto-Wright, 1995). A large proportion of patients are asymptomatic at diagnosis (Joneborg, 2014). For the remainder, vaginal bleeding remains the most common presenting symptom, and β-hCG levels are often greater than expected. One quarter of women will present with uterine size greater than dates, but the incidence of anemia is less than 10 percent. Moreover, hyperemesis gravidarum, preeclampsia, and symptomatic theca-lutein cysts are now rare (Soto-Wright, 1995). Currently, these sequelae typically develop chiefly in patients without early prenatal care who present with a more advanced gestational age and markedly elevated serum β-hCG levels. Last, plasma thyroxine levels are often increased in women with complete moles, but clinical hyperthyroidism is infrequent. In these circumstances, serum free thyroxine levels are elevated as a consequence of the thyrotropin-like effect of β-hCG (Chap. 15, p. 335).

■⌀ Partial Hydatidiform Mole

These moles differ from complete hydatidiform moles clinically, genetically, and histologically. The degree and extent of trophoblastic proliferation and villous edema are decreased compared with those of complete moles. Moreover, most partial moles contain fetal tissue and amnion, in addition to placental tissues. As a result, patients with partial moles typically present with signs and symptoms of an incomplete or missed abortion. Many women will have vaginal bleeding. However, because trophoblastic proliferation is slight and only focal, uterine enlargement in excess of gestational

FIGURE 37-3╇ Photograph of a complete hydatidiform mole. Note the grapelike fluid-filled clusters of chorionic villi. (Used with permission from Dr. Sasha Andrews.)

CHAPTER 37

Maternal Chromosome Inactivation

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Gynecologic Oncology

SECTION 4 FIGURE 37-4╇ Transvaginal sonogram of multiple theca-lutein cysts within one ovary of a woman with a complete molar pregnancy. Bilateral, multiple simple cysts are characteristic findings.

FIGURE 37-5╇ Transverse sonographic view of a uterus with a complete hydatidiform mole. The classic “snowstorm” appearance is created by the multiple placental vesicles. The mole completely fills this uterine cavity, and calipers are placed on the outer uterine borders.

age is uncommon. Similarly, preeclampsia, theca-lutein cysts, hyperÂ�thyroidism, or other dramatic clinical features are rare. Preevacuation β-hCG levels are typically much lower than those for complete moles and often do not exceed 100,000 mIU/mL. For this reason, partial moles are often not identified until after a histologic review of a curettage specimen. Partial moles have a triploid karyotype (69,XXX, 69,XXY, or less commonly 69,XYY) that is composed of one maternal and two paternal haploid sets of chromosomes (see Fig. 37-2) (Lawler, 1991). The coexisting fetus present with a partial mole is nonviable and typically has multiple malformations with abnormal growth (Jauniaux, 1999).

(Johns, 2005; Lindholm, 1999; Sebire, 2001). Consequently, diagnosis in early gestations is usually difficult. Often, the diagnosis commonly is not made until after histologic review of the abortal specimen. In unclear cases with a live fetus and a desired pregnancy, fetal karyotyping to identify a triploid fetal chromosomal pattern can clarify the diagnosis and management.

■⌀ Diagnosis Clinical Assessment In reproductive-aged women with vaginal bleeding, diagnoses may include gynecologic causes of bleeding and complications of first-trimester pregnancy. The trophoblast of molar pregnancies produce β-hCG, and elevated hormone levels reflect their proliferation. Accordingly, initial urine or serum β-hCG measurement and transvaginal sonography are invaluable in guiding evaluation. Because of these, first-trimester diagnosis of hydatidiform mole is now common. Although β-hCG levels are helpful, the diagnosis of molar pregnancy is more frequently found sonographically. Most firsttrimester complete moles demonstrate a complex, echogenic, intrauterine mass containing many small cystic spaces, which reflect swollen chorionic villi. Fetal tissues and amnionic sac are absent (Fig. 37-5) (Benson, 2000). In contrast, sonographic features of a partial molar pregnancy include a thickened, hydropic placenta with a concomitant fetus (Zhou, 2005). However, there are diagnostic limitations. For example, βhCG levels in early molar pregnancies may not always be elevated in the first trimester (Lazarus, 1999). Moreover, sonography can lead to a false-negative diagnosis if performed at very early gestational ages, before the chorionic villi have attained their characteristic vesicular pattern. Studies show that only 20 to 30 percent of patients may have sonographic evidence to indicate a partial mole

Histopathology The histopathologic changes typical of hydatidiform moles are listed in Table 37-2. But, in early pregnancy, it may be difficult to distinguish among these and a hydropic abortus. Hydropic abortuses are pregnancies formed by the traditional union of one haploid egg and one haploid sperm but are pregnancies that have failed. Their placentas display hydropic degeneration, in which villi are edematous and swollen, and thus mimic some villous features of hydatidiform moles (Fig. 37-6). Although no single criterion distinguishes these three, complete moles generally have two prominent features: (1) trophoblastic proliferation and (2) hydropic villi. In gestations younger than 10 weeks, however, hydropic villi may not be apparent, and molar stroma may still be vascular (Paradinas, 1997). As a result, identification of early complete moles must rely on more subtle histologic abnormalities, supplemented by immunohistochemical and molecular diagnostic techniques. Partial moles are optimally diagnosed when three or four major diagnostic criteria are demonstrated: (1) two populations of villi, (2) enlarged, irregular, dysmorphic villi (with trophoblast inclusions), (3) enlarged, cavitated villi (≥3 to 4 mm), and (4) syncytiotrophoblast hyperplasia/atypia (Chew, 2000). Good diagnostic reproducibility can still be achieved in most circumstances using these histologic distinctions of complete and partial mole.

Ancillary Techniques Histopathologic evaluation can be enhanced by immunohistochemical staining for p57 expression and by molecular genotyping. p57KIP2 is a nuclear protein whose gene is paternally imprinted and maternally expressed. This means that the gene product is produced only in tissues containing a maternal

Gestational Trophoblastic Disease

Complete mole

Partial mole

Hydropic changes

CHAPTER 37

H&E

p57

FIGURE 37-6╇ Composite diagram of differences among normal hydropic abortuses and partial or complete hydatidiform moles. The first row shows typical appearances after hematoxylin and eosin (H&E) staining. The second row shows results after p57 staining. p57 is a nuclear protein whose gene product is produced only in tissues containing a maternal allele. After immunostaining for p57, note the positive (brown) staining in the villi of the partial hydatidiform mole and normal hydropic abortus. This contrasts to the absent staining for p57 in the complete mole (only blue counterstain is seen). (Used with permission from Drs. Kelley Carrick and Raheela Ashfaq.)

allele. Because complete moles contain only paternal genes, the p57KIP2 protein is absent in complete moles, and tissues do not pick up this stain (Merchant, 2005). In contrast, this nuclear protein is strongly expressed in normal placentas, in spontaneous pregnancy losses with hydropic degeneration, and in partial hydatidiform moles (Castrillon, 2001). Accordingly, immunostaining for p57KIP2 is an effective means to isolate complete mole from the diagnostic list. For distinction of a partial mole from a nonmolar hydropic abortus, both of which express p57, molecular genotyping can be used. Molecular genotyping determines the parental source of polymorphic alleles. Thereby, it can distinguish among a diploid diandric genome (complete mole), a triploid diandric-monogynic genome (partial mole), or biparental diploidy (nonmolar abortus) (Ronnett, 2011).

■⌀ Treatment Suction curettage is the preferred method of evacuation regardless of uterine size in patients who wish to remain fertile (American College of Obstetricians and Gynecologists, 2014; Tidy, 2000). Nulliparous women are not given prostanoids to ripen the cervix since these drugs can induce uterine contractions and might increase the risk of trophoblastic embolization to the pulmonary vasculature (Seckl, 2010). Hysterectomy is rarely recommended unless the patient wishes surgical sterilization or is approaching menopause (Elias, 2010). Symptomatic theca-lutein ovarian cysts are an unusual finding and tend to regress after molar evacuation. In extreme cases, these may be aspirated, but oophorectomy is not performed except when torsion leads to extensive ovarian infarction (Mungan, 1996).

783

Prior to surgery, patients are evaluated for associated medical complications. Fortunately, thyroid storm from untreated hyperthyroidism, respiratory insufficiency from trophoblastic emboli, and other severe coexisting conditions are rare. Because of the tremendous vascularity of these placentas, blood products should be available prior to the evacuation of larger moles, and adequate infusion lines established. At the beginning of the evacuation, the cervix is dilated to admit a 10- to 12-mm plastic suction curette. As aspiration of molar tissues ensues, intravenous oxytocin is given. At our institution, 20 units of synthetic oxytocin (Pitocin) are mixed with 1 L of crystalloid and infused at rates to achieve uterine contraction. In some cases, intraoperative sonography may be indicated to help reduce the risk of uterine perforation and assist in confirming complete evacuation. Finally, a thorough, gentle curettage is performed. Following curettage, because of the possibility of partial mole and its attendant fetal tissue, Rh immune globulin is given to nonsensitized Rh D-negative women. Rh immune globulin, however, may be withheld if the diagnosis of complete mole is certain (Fung Kee, 2003).

■⌀ Postmolar Surveillance Gestational trophoblastic neoplasia develops after evacuation in 15 percent of patients with complete moles (Golfier, 2007; Wolfberg, 2004). Despite the trend of diagnosing these abnormal pregnancies at earlier gestational ages, this incidence has not declined (Seckl, 2004). Of those women who develop GTN, three quarters have locally invasive molar disease and the

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SECTION 4

remaining one quarter develop metastases. In contrast, GTN develops in only 4 to 6 percent of patients with partial moles following evacuation (Feltmate, 2006; Lavie, 2005). Malignant transformation into metastatic choriocarcinoma does occur after partial mole evacuation, but this is rare (0.1 percent) (Cheung, 2004; Seckl, 2000). No pathologic or clinical features at presentation accurately predict which patients will ultimately develop GTN. Because of the trophoblastic proliferation that characterizes these neoplasms, serial serum β-hCG levels following molar evacuation can be used to effectively monitor patients for GTN development. Therefore, postmolar surveillance with serial quantitative serum β-hCG levels is the standard. Titers are monitored following uterine evacuation at least every 1 to 2 weeks until they become undetectable. After undetectable β-hCG levels are achieved, subsequent monthly levels are drawn during 6 months of surveillance for all patients with a molar gestation (Sebire, 2007). However, poor compliance with prolonged monitoring has been reported— especially among indigent women and certain ethnic groups in the United States (Allen, 2003; Massad, 2000). A single blood sample demonstrating an undetectable level of β-hCG following molar evacuation is sufficient to exclude the possibility of progression to GTN in most patients. Thus, some women, especially those with a partial mole, may be safely discharged from routine surveillance once an undetectable value is achieved (Lavie, 2005; Wolfberg, 2004). Shortened surveillance could enable women to attempt a subsequent pregnancy sooner. However, GTN may still rarely develop after an hCG level has returned to normal, potentially leading to increased morbidity (Kerkmeijer, 2007; Sebire, 2007). When pregnancies occur during the monitoring period, the resulting normal β-hCG production can hinder detection of postmolar progression to GTN (Allen, 2003). But other than complicating the monitoring schedule, these pregnancies fortunately are otherwise uneventful (Tuncer, 1999). To prevent difficulties with interpretation, women are encouraged to use effective contraception until achieving a β-hCG titer 40 years, previous history of molar pregnancy, or

an excessively high β-hCG titer prior to evacuation. That said, few women are ultimately assigned to this group. Moreover, due to the risks of increased drug resistance, delayed treatment of GTN, and toxic side effects, this practice cannot currently be recommended (American College of Obstetricians and Gynecologists, 2014; Fu, 2012). Prophylactic chemotherapy is not routinely offered in the United States and Europe. However, a single dose of dactinomycin has been shown to reduce the incidence of postmolar GTN in certain populations. For example, in one randomized trial, 60 Thai women who had high-risk complete moles were assigned to receive either prophylactic dactinomycin or placebo at the time of evacuation (Limpongsanurak, 2001). Adjuvant chemotherapy reduced the incidence of GTN from 50 percent to 14 percent, but toxicity was significant. As a result, prophylactic chemotherapy is generally used only in those countries with limited resources to reliably monitor patients after evacuation (Uberti, 2009).

■⌀ Ectopic Molar Pregnancy The true incidence of GTD developing outside the uterine cavity approximates 1.5 per 1 million births (Gillespie, 2004). More than 90 percent of suspected cases will reflect an overdiagnosis of florid extravillous trophoblastic proliferation in the fallopian tube (Burton, 2001; Sebire, 2005b). As with any ectopic pregnancy, initial management usually involves surgical removal of the conceptus and histopathologic evaluation.

■⌀ Coexistent Fetus At times, a twin pregnancy can consist of a hydatidiform mole and a coexisting fetus. The estimated incidence is 1 per 20,000 to 100,000 pregnancies (Fig. 37-7). Sebire and associates (2002b) described the outcome of 77 twin pregnancies, each composed of a complete mole and a healthy cotwin. Of this group, 24 women chose to have an elective termination, and 53 continued their pregnancies. Twenty-three gestations spontaneously aborted at less than 24 weeks, two were terminated due to severe preeclampsia, and 28 pregnancies lasted at least 24 weeks—resulting in 20 live births. The authors demonstrated that coexisting complete moles and healthy cotwin pregnancies have a high risk of spontaneous abortion, but approximately 40 percent result in live births. The risk of progression to GTN was 16 percent in first-trimester terminations and not significantly higher (21 percent) in women who continued their pregnancies. Because the risk of malignancy is unchanged with advancement of gestational age, pregnancy continuation may be allowed, provided that severe maternal complications are controlled and fetal growth is normal. Importantly, these cases should be distinguished early from a single partial molar pregnancy with its abnormal associated fetus. Fetal karyotyping to confirm a normal fetal chromosomal pattern is also recommended (Marcorelles, 2005; Matsui, 2000).

GESTATIONAL TROPHOBLASTIC NEOPLASIA This term primarily encompasses pathologic entities that are characterized by aggressive invasion of the endometrium and

Gestational Trophoblastic Disease

■⌀ Histologic Classification Invasive Mole

Complete mole

Normal placenta

FIGURE 37-7╇ Photograph of placentas from a twin pregnancy with one normal twin and with a complete mole. The complete mole (left) shows the characteristic vesicular structure. The placenta on the right appears grossly normal. A transverse section through the border between these two is shown (inset). (Used with permission from Drs. April Bleich and Brian Levenson.)

myometrium by trophoblast cells. Histologic categories include common tumors such as the invasive mole and gestational choriocarcinoma, as well as the rare placental-site trophoblastic tumor and epithelioid trophoblastic tumor. Although these histologic types have been characterized, in most cases of GTN, no tissue is available for pathologic study. Instead, GTN is diagnosed based on elevated β-hCG levels and managed clinically. Gestational trophoblastic neoplasia typically develops with or follows some form of pregnancy. Most cases follow a hydatidiform

A

This common manifestation of GTN is characterized by whole chorionic villi that accompany excessive trophoblastic overgrowth and invasion (Fig. 37-8). These tissues penetrate deep into the myometrium, sometimes to involve the peritoneum, adjacent parametrium, or vaginal vault. Such moles are locally invasive but generally lack the pronounced tendency to develop widespread metastases typical of choriocarcinoma. Invasive moles originate almost exclusively from a complete or a partial hydatidiform mole (Sebire, 2005a).

Gestational Choriocarcinoma

This extremely malignant tumor contains sheets of anaplastic trophoblast and prominent hemorrhage, necrosis, and vascular invasion (see Fig. 37-8). However, formed villous structures are characteristically absent. Gestational choriocarcinoma initially invades the endometrium and myometrium but tends to develop early blood-borne systemic metastases (Fig. 37-9). Most cases develop following evacuation of a molar pregnancy, but these tumors may also follow a nonmolar pregnancy. Specifically, gestational choriocarcinoma develops in approximately 1 in 30,000 nonmolar pregnancies. Two thirds of such cases follow term pregnancies, and one third develop after a spontaneous abortion or pregnancy termination. One

B

FIGURE 37-8╇ A. An invasive mole contains whole villi that invade locally. The arrow marks one villus invading deeply into the adjacent myometrium. (Used with permission from Dr. Ona Faye-Peterson.) B. Choriocarcinoma is a biphasic tumor characterized by intermediate trophoblast and cytotrophoblast (asterisk), intimately admixed with multinucleate syncytiotrophoblast (S). Choriocarcinoma is a vascular tumor, typically with prominent hemorrhage, as evidenced by the abundant blood in the background. (Used with permission from Dr. Kelley Carrick.)

CHAPTER 37

mole. Rarely, GTN develops after a live birth, miscarriage, or termination. Occasionally, the antecedent gestation cannot be confirmed with certainty. Many of the reported nonmolar cases may actually represent disease originating from an unrecognized early mole (Sebire, 2005a).

785

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Gynecologic Oncology

SECTION 4 FIGURE 37-9╇ Computed-tomography (CT) scan of choriocarcinoma invading the uterus.

review of 100 patients with nonmolar gestational choriocarcinoma reported that 62 presented after a live birth, 6 after a live birth preceded by a molar pregnancy, and 32 after a nonmolar abortion (Tidy, 1995). Vaginal bleeding was the most common symptom in all groups. For this reason, abnormal bleeding for more than 6 weeks following any pregnancy warrants evaluation with β-hCG testing to exclude a new pregnancy or GTN. When choriocarcinoma is diagnosed after a live birth, the antecedent pregnancy usually proceeded normally to term. One case series collected between 1964 and 1996 showed that in 89 percent of cases, the preceding pregnancy had produced an uncomplicated live birth (Rodabaugh, 1998). Hydrops, while a notable complication in the remaining fetuses in this earlier series, was not observed in a more recent cohort compiled between 1996 and 2011 (Diver, 2013). Occasionally, unanticipated choriocarcinoma is detected in an otherwise normalappearing placenta at delivery. More commonly, however, the diagnosis of choriocarcinoma is delayed for months due to subtle signs and symptoms. Most patients present with intermenstrual bleeding, and high β-hCG levels are detected (Lok, 2006). Less frequently, the diagnosis is made in an asymptomatic woman by an incidental positive pregnancy test (Diver, 2013). In part because of the typical delay to diagnosis, choriocarcinomas following term pregnancies are associated with high-risk features and a higher mortality rate than GTN following nonmolar abortions. Death rates range from 10 to 15 percent (Diver, 2013; Lok, 2006; Rodabaugh, 1998; Tidy, 1995). In contrast to this gestational choriocarcinoma, primary “nongestational” choriocarcinoma is an ovarian germ cell tumor (Chap. 36, p. 764). Although rare, ovarian choriocarcinoma has a histologic appearance identical to that of gestational choriocarcinoma. It is in part distinguished by the lack of a preceding pregnancy (Lee, 2009).

Placental-site Trophoblastic Tumor This tumor consists predominantly of intermediate trophoblasts at the placental site. It is a rare GTN variant with unique disease behavior. Placental-site trophoblastic tumor (PSTT) can follow

any type of pregnancy but develops most commonly following a term gestation (Papadopoulos, 2002). Typically, patients have irregular bleeding months or years after the antecedent pregnancy, and the diagnosis is not entertained until endometrial sampling has been performed (Feltmate, 2001). PSTT tends to infiltrate only within the uterus, disseminates late in its course, and produces low β-hCG levels (van Trommel, 2013). Of interest, an elevated proportion of free β-subunit can help to discriminate it from other GTN types if the endometrial biopsy is equivocal (Cole, 2008; Harvey, 2008). When this tumor does spread, the pattern mirrors that of gestational choriocarcinoma. Metastases often spread to the lungs, liver, or vagina (Baergen, 2006). Hysterectomy is the primary treatment for nonmetastatic PSTT due to its relative insensitivity to chemotherapy. In particularly motivated patients, fertility-sparing procedures have mixed results (Feltmate, 2001; Machtinger, 2005; Papadopoulos, 2002; Taylor, 2013b). Metastatic PSTT has a much poorer prognosis than its postmolar GTN counterparts. As a result, aggressive combination chemotherapy is indicated. EMA/EP regimens of etoposide, methotrexate, and dactinomycin (actinomycin D) that alternate with etoposide and cisplatin (Platinol) are considered the most effective (Newlands, 2000). Radiation, however, may also have a role. The overall 10-year survival is 70 percent, but patients with metastases, especially stage IV disease, have a much poorer prognosis (Hassadia, 2005; Hyman, 2013; Schmid, 2009).

Epithelioid Trophoblastic Tumor This rare trophoblastic tumor is distinct from gestational choriocarcinoma and PSTT. The preceding pregnancy event may be remote, or in some cases, a prior gestation cannot be confirmed (Palmer, 2008). Epithelioid trophoblastic tumor develops from neoplastic transformation of chorionic-type intermediate trophoblast. Microscopically, this tumor resembles PSTT, but the cells are smaller and display less nuclear pleomorphism. Grossly, epithelioid trophoblastic tumor grows in a nodular fashion rather than the infiltrative pattern of PSTT (Shih, 1998). Hysterectomy is again the primary treatment due to presumed chemoresistance and since the diagnosis is usually confirmed in advance by endometrial biopsy. More than one third of patients will present with metastatic disease and demonstrable chemoresistance to multiagent therapy, which portends a poor prognosis (Davis, 2015; Palmer, 2008).

■⌀ Diagnosis Most GTN cases are clinically diagnosed, using β-hCG evidence to identify persistent trophoblastic tissue (Table 37-3). Tissue is infrequently available for pathologic diagnosis, unless a diagnosis of placental-site or nongestational tumor is being considered. As a result, most centers in the United States diagnose GTN on the basis of rising β-hCG values or a persistent plateau of β-hCG values for at least 3 weeks. Unfortunately, uniformity is lacking in the definition of a persistent plateau. Additionally, the diagnostic criteria are less stringent in the United States than in Europe. This is partly because of concern that some patients may be lost to follow-up if stricter criteria are used.

Gestational Trophoblastic Disease

787

TABLE 37-3. â•„FIGO Criteria for Gestational Trophoblastic Neoplasia Diagnosis

β-hCG = beta human chorionic gonadotropin; FIGO = International Federation of Gynecology and Obstetrics. Data from FIGO Oncology Committee: FIGO staging for gestational trophoblastic neoplasia 2000. Int J Gynaecol Obstet 2002 Jun;77(3):285–287. When serologic criteria for GTN are met, a new intrauterine pregnancy is excluded using β-hCG levels that are correlated with sonographic findings. This is done especially if there has been a long delay in monitoring of serial β-hCG levels or noncompliance with contraception or both.

■⌀ Assessment Patients with GTN undergo a thorough pretreatment assessment to determine disease extent. The initial evaluation may be limited to pelvic examination, chest radiograph, and pelvic sonography or abdominopelvic computed tomography (CT) scanning. Although approximately 40 percent of patients will have micrometastases not otherwise visible on chest radiography, chest CT is not needed because these small lesions do not affect outcome (Darby, 2009; Garner, 2004). However, pulmonary lesions identified on chest radiograph should prompt CT of the chest and magnetic resonance (MR) imaging of the brain. Fortunately, central nervous system involvement is rare in the absence of neurologic symptoms or signs (Price, 2010). Positron emission tomography (PET) may occasionally be useful to evaluate occult choriocarcinoma or relapse from previously treated GTN when conventional imaging is equivocal or fails to identify metastatic disease (Dhillon, 2006; Numnum, 2005).

■⌀ Staging Gestational trophoblastic neoplasia is anatomically staged based on a system adopted by the International Federation of Gynecology and Obstetrics (FIGO) (Table 37-4 and Fig. 37-10). Patients at low risk for therapeutic failure are distinguished from those at high risk by using the modified prognostic scoring system of the World Health Organization (WHO) (Table 37-5). About 95 percent of patients will have a WHO score of 0 to 6 and will be considered to have low-risk disease (Sita-Lumsden, 2012). The remainder will have a score of 7 or higher and be assigned to the high-risk GTN

group. For the most accurate description of affected patients, the Roman numeral corresponding to FIGO stage is separated by a colon from the sum of the risk factor scores, for example, stage II:4 or stage IV:9. This description best reflects disease behavior (Ngan, 2004). Women with high-risk scores are more likely to have tumors that are resistant to single-agent chemotherapy. They are therefore treated initially with combination chemotherapy. Although patients with stage I disease infrequently have a highrisk score, those with stage IV disease invariably have a high-risk score. Women diagnosed with FIGO stage I, II, or III GTN have a survival rate approaching 100 percent (Lurain, 2010).

Nonmetastatic Disease Invasive moles arising from complete molar gestations make up most nonmetastatic GTN cases. Approximately 12 percent of complete moles develop locally invasive disease after evacuation, compared with only 4 to 6 percent of partial moles. Epithelioid trophoblastic tumor and PSTT are other rare causes of nonmetastatic GTN. Locally invasive trophoblastic tumors may perforate the myometrium and lead to intraperitoneal bleeding (Mackenzie, 1993). Alternatively, vaginal hemorrhage can follow tumor erosion into uterine vessels, or necrotic tumor may involve the uterine wall and serve as a nidus for infection. Fortunately, the prognosis is typically excellent for all types of nonmetastatic disease despite these possible manifestations.

Metastatic Disease Choriocarcinomas originating from complete molar gestations account for most cases of metastatic GTN. Three to 4 percent of complete moles develop metastatic choriocarcinoma after evacuation. This event is rare following any other type of molar or nonmolar gestation. Choriocarcinomas have a propensity for distant spread and should be suspected in any woman of reproductive age with metastatic disease from an unknown primary (Tidy, 1995). Moreover, because of this tendency,

TABLE 37-4. â•„FIGO Anatomic Staging of GTN Stage

Characteristics

╇ I II III IV

Disease confined to the uterus GTN extends outside of the uterus but is limited to the genital structures (adnexa, vagina, broad ligament) GTN extends to the lungs, with or without known genital tract involvement All other metastatic sites

FIGO = International Federation of Gynecology and Obstetrics; GTN = gestational trophoblastic neoplasia. Reproduced with permission from FIGO Committee on Gynecologic Oncology: Current FIGO staging for cancer of the vagina, fallopian tube, ovary, and gestational trophoblastic neoplasia. Int J Gynaecol Obstet 2009 Apr;105(1):3–4.

CHAPTER 37

β-hCG level plateau persists in four measurements during a period of 3 weeks or longer (days 1, 7, 14, and 21) β-hCG level rise in 3 weekly consecutive measurements or longer, over a period of 2 weeks or more (days 1, 7, and 14) β-hCG level remains elevated for 6 months or more Histologic diagnosis of choriocarcinoma

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or cerebral involvement is encountered almost exclusively in patients who have had an antecedent nonmolar pregnancy and a protracted delay in tumor diagnosis (Newlands, 2002; Savage, 2015b). These women may present with associated hemorrhagic events. Virtually all patients with hepatic or cerebral metastases have concurrent pulmonary or vaginal involvement or both. Great caution is used in attempting excision of any metastatic disease site due to the risk of profuse hemorrhage. Thus, this practice is almost uniformly avoided except in extenuating circumstances of life-threatening brainstem herniation or chemotherapy-resistant disease.

■⌀ Treatment Surgery Most patients diagnosed with postmolar GTN have persistent tumor confined to the endometrial cavity and are treated primarily with chemotherapeutic agents. Repeat dilatation and curettage is generally avoided to prevent morbidity and mortality caused by uterine perforation, hemorrhage, infection, uterine adhesions, and anesthetic complications (American College of Obstetricians and Gynecologists, 2014). Accordingly, second evacuations are not typically performed in the United States unless patients have persistent uterine bleeding and substantial amounts of retained molar tissue. Repeat uterine curettage is a more standard part of postmolar GTN management in Europe. This practice reduces both the number of patients needing any further treatment and the number of courses in those who do require chemotherapy (Pezeshki, 2004; van Trommel, 2005). A second evacuation followed by continued surveillance, however, is a less attractive option, even for poorly compliant patients, than single-agent chemotherapy (Allen, 2003; Massad, 2000). Hysterectomy may play several roles in GTN treatment. First, it may be performed to primarily treat PSTT, epithelioid trophoblastic tumors, or other chemotherapy-resistant disease. Second, severe uncontrollable vaginal or intraabdominal bleeding may necessitate hysterectomy as an emergency procedure (Clark, 2010). Because of these more extreme indications,

FIGURE 37-10╇ International Federation of Gynecology and Obstetrics (FIGO) staging of gestational trophoblastic neoplasia.

chemotherapy is indicated whenever choriocarcinoma is diagnosed histologically. Although many patients are largely asymptomatic, metastatic GTN is highly vascular and prone to severe hemorrhage either spontaneously or during biopsy. Heavy menstrual bleeding is a common presenting symptom. The most common sites of spread are the lungs (80 percent), vagina (30 percent), pelvis (20 percent), liver (10 percent), and brain (10 percent) (Fig. 37-11). Patients with pulmonary metastases typically have asymptomatic lesions identified on routine chest radiograph and infrequently present with cough, dyspnea, hemoptysis, pleuritic chest pain, or signs of pulmonary hypertension (Seckl, 1991). In patients with early development of respiratory failure that requires intubation, the overall outcome is poor. Hepatic

TABLE 37-5. â•„Modified WHO Prognostic Scoring System as Adapted by FIGO Scores

0

1

2

4

Age (yr) Antecedent pregnancy Interval months from index pregnancy Pretreatment serum β-hCG (mIU/mL) Largest tumor size (including uterus) Site of metastases Number of metastases Previous failed chemotherapy drugs

2. Continue warfarin

Protocol for direct oral anticoagulant 1–2 days before surgery Stop agent: dabigatran 2 days prior; apixaban and rivaroxaban 1 day prior 1 day after surgery Start agent Protocol for antiplatelet agents 7 days before surgery 1 day after surgery

Stop aspirin or clopidogrel Start agent 12–24 hours after surgery

INR = international normalized ratio; LMWH = low-molecular-weight heparin; UFH = unfractionated heparin. Data from Committee opinion no 610: chronic antithrombotic therapy and gynecologic surgery, Obstet Gynecol 2014 Oct;124(4):856-862; Douketis J, Bell AD, Eikelboom J, et al: Approach to the new oral anticoagulants in family practice: Part 2: addressing frequently asked questions, Can Fam Physician 2014 Nov;60(11):997–1001.

CHAPTER 39

Condition

832

Aspects of Gynecologic Surgery

SECTION 5

Although warfarin antagonizes all vitamin K-dependent clotting factors, newer direct oral anticoagulants (DOACs) inhibit specific factors. The three currently licensed medications are dabigatran (Pradaxa), which targets factor IIa (thrombin), and rivaroxaban (Xarelto) and apixaban (Eliquis), which target factor Xa. Because of their recent introduction, few studies provide recommendations for their perioperative management (KozekLangenecker, 2014). The pharmacologic half-life is 14 hours for dabigatran and 9 hours for rivaroxaban and apixaban (Schaden, 2010). Thus, in women with normal preoperative creatinine clearance, stopping rivaroxaban and apixaban 24 hours prior to surgery and halting dabigatran 48 hours prior to surgery is reasonable. The withdrawal time is doubled if the creatinine clearance is 90 seconds and an INR >2 suggest possible overdosing (Lindahl, 2011). Also for dabigatran, thrombin time testing is more sensitive and normal values exclude significant anticoagulant effect. However, the turnaround time with this specific test can be long. For emergent surgery, the DOACs have no antidote, and management of life-threatening bleeding remains empirical. Fortunately, anticoagulant effects rapidly dissipate because of the drugs’ short half-lives. Indirect evidence suggests that recombinant factor VIIa (NovoSeven) or a prothrombin complex concentrate may be helpful (Ageno, 2012). Last, antiplatelet agents such as aspirin and clopidogrel (Plavix) may increase surgical bleeding. These are generally stopped 7 days prior to surgery (American College of Obstetricians and Gynecologists, 2014b).

Postoperative Management After surgery, heparin, either UFH or LMWH, is restarted 12 to 24 hours after major surgery (see Table 39-3). Oral warfarin therapy is started concurrently as several days are required to regain therapeutic levels (Harrison, 1997; White, 1994). Once the INR ranges between 2 and 3, then heparin is discontinued. DOACs are typically restarted 24 hours following surgery. Antiplatelet agents may be resumed 12 to 24 hours following surgery. In all cases, agents are begun only after surgical hemostasis is confirmed.

ENDOCRINE EVALUATION ■⌀ Hyperthyroidism and Hypothyroidism The pathophysiologic stress of surgery can exacerbate endocrine conditions such as thyroid dysfunction, diabetes mellitus, and adrenal insufficiency. Of these, both hyper- and hypothyroidism have anesthetic and metabolic derangements unique to each disease state. Nevertheless, management goals for each aim to achieve a euthyroid state before surgery. Hyperthyroidism carries the risk of developing thyroid storm perioperatively. Moreover, airway compromise is a risk in those

with goiter. Thus, during physical examination, tracheal deviation is sought. In addition to thyroid function tests, an ECG and serum electrolyte levels can help predict signs of preexisting metabolic stress. Patients are encouraged to maintain their usual medications at prescribed dosages until the day of surgery. Newly diagnosed hypothyroidism generally does not require preoperative therapy other than thyroid hormone replacement. Exceptions include cases of severe disease with signs of cardiac depression, electrolyte irregularities, and hypoglycemia.

■⌀ Diabetes Mellitus Long-term complications of diabetes mellitus may include vascular, neurologic, cardiac, and renal dysfunction. Thus, a vigilant preoperative risk assessment for these in affected women is essential. In addition, increased postoperative morbidity rates have been linked with poor preoperative glycemic control. Specifically, glucose levels >200 mg/dL and hemoglobin A1c levels >7 are both associated with significantly increased rates of postoperative wound infection (Dronge, 2006; Trick, 2000). At minimum, diabetic patients undergoing major surgical procedures benefit from three diagnostic tests—serum electrolyte levels, urinalysis, and ECG. These screen for metabolic disturbances, undiagnosed nephropathy, and unrecognized cardiac ischemia, respectively. In general, stress induced by surgery and anesthesia elevates catecholamine levels, relative insulin deficiency, and hyperglycemia (Devereaux, 2005). Although glycemic responses vary with surgery, overt hyperglycemia is avoided to minimize postoperative complications related to dehydration, electrolyte abnormalities, diminished wound healing, and even ketoacidosis in type 1 diabetics (Jacober, 1999). However, fluctuations in oral intake and metabolic needs make optimal glycemic control labor intensive. Moreover, clear evidence for glucose targets are lacking. As a result, most providers aim for glucose readings below 200 mg/dL (Table 39-4) (Finney, 2003; Garber, 2004; Hoogwerf, 2006). Table 39-5 and Figure 39-4 summarize perioperative recommendations set forth by Jacober and coworkers (1999) based on disease severity.

■⌀ Adrenal Insufficiency Inadequacy of the hypothalamic-pituitary-adrenal (HPA) axis due to secondary suppression from chronic steroid use can lead to perioperative hypotension. Despite this physiologic understanding, controversy surrounds perioperative corticosteroid supplementation. Corticosteroid users who undergo minor surgical procedures or who use lower doses are generally assumed not to be at risk for adrenal suppression, and additional corticosteroid therapy is not recommended. The value of perioperative supplementation remains an area of chronic debate (Bromberg, 1991; Marik, 2008). Systematic reviews of the literature regarding perioperative supplemental doses of corticosteroids find no evidence to support additional supratherapeutic “stress doses.” Instead, patients should continue their usual daily dose (Kelly, 2013; Marik, 2008). Close hemodynamic monitoring is performed to look for volume-refractory hypotension, at which time stress-dose corticosteroids are initiated for presumed secondaryÂ�

Preoperative Considerations

833

TABLE 39-4. Sliding-Scale Insulin Order Examplea Increment Formula

Calculation

Short-Acting Insulin, units

╇╇ 0–11.0 (0–200) 11.1–14.0 (201–250) 14.1–17.0 (251–300) 17.1–20.0 (301–350) 20.1–23.0 (251–400) 23.1–26.0 (401–450) >26.0 (>450)

0 1 × (TDI/30) 2 × (TDI/30) 3 × (TDI/30) 4 × (TDI/30) 5 × (TDI/30) Call physician

0 1 × (120/30) 2 × (120/30) 3 × (120/30) 1 × (120/30) 5 × (120/30) Call physician

â•⁄0 â•⁄4 â•⁄4 12 16 20 Call physician

a

Example uses a preoperative total daily insulin dose (TDI) of 120 units. For convenience, conversions of millimoles per liter to milligrams per deciliter are approximate. Reproduced with permission from Jacober SJ, Sowers JR: An update on perioperative management of diabetes. Arch Intern Med 1999 Nov 8;159(20):2405–2411. b

adrenal insufficiency. Of note, Marik and Varon (2008) observed that patients receiving corticosteroids due to primary hypothalamic-pituitary-adrenal axis disease require stress doses in the perioperative period. One regimen is hydrocortisone, 100 mg administered IV every 8 hours and titrated to reduced doses as the patient improves.

DIAGNOSTIC TESTING GUIDELINES In the absence of a clinical indication, a rote panel of preoperative tests does not enhance the safety or quality of care. Roizen and colleagues (2000) noted that nearly half of abnormalities found on routine preoperative testing were ignored by clinicians. Moreover, multiple studies have documented the inefficiency of hematologic tests for obtaining clinically significant diagnoses (Kaplan, 1985; Korvin, 1975). Most importantly, diagnostic testing has not been shown to outperform a clinical history and physical examination (Rucker, 1983). Thus, in the absence of changes in clinical status, diagnostic tests found to be normal 4 to 6 months prior to surgery may be used as “preoperative tests.” In patients managed this way, MacPherson and coworkers (1990) found that fewer than 2 percent had significant changes during the course of 4 months. Codified guidelines for preoperative testing have not been crafted in the United States. However, in the United Kingdom, the National Institute for Health and Clinical Excellence

(NICE) has indications for such testing. Complete documents are available at: http://www.nice.org.uk/guidance/cg3.

INFORMED CONSENT Obtaining informed consent is a process and not merely a medical record document (Lavelle-Jones, 1993; Nandi, 2006). This conversation between a clinician and patient enhances a woman’s awareness of her diagnosis and contains a discussion of medical and surgical care alternatives, procedure goals and limitations, and surgical risks. Multimedia decision support tools, such as photographs, pamphlets, and educational videos, can augment the discussion (Coulter, 2007; Stacey, 2014). When informed consent cannot be obtained from the patient, an independent surrogate should be identified to represent the patient’s best interest and wishes (American College of Obstetricians and Gynecologists, 2012). Ultimately, written documentation of the entire process serves as a historical record of a patient’s understanding and agreement within the medical records. Despite a clinician’s recommendations, an informed patient may decline a particular intervention. A woman’s decisionmaking autonomy must be respected, and a clinician documents informed refusal in the medical record. Appropriate documentation includes: (1) a patient’s refusal to consent to the recommended intervention, (2) notation that the value of the intervention has been explained to the patient, (3) a

TABLE 39-5. Perioperative Management of Diabetes Mellitus by Disease Type Disease

Preoperative Management

Postoperative Management

Type 2 DM treated with diet alone

No additional care with PRN subcutaneous regular insulin for AM hyperglycemia Discontinue all agents on the day of surgery

PRN subcutaneous regular insulin

Type 2 DM treated with oral hypoglycemic agents Type 1or 2 DM treated with insulin

See Figure 39-3

Supplemental subcutaneous insulin until return of normal diet, at which time preoperative therapy can be reinstituted Sliding-scale insulin (see Table 39-4)

DM = diabetes mellitus; PRN = as needed. Data from Jacober SJ, Sowers JR: An update on perioperative management of diabetes. Arch Intern Med 1999 Nov 8;159(20):2405–2411.

CHAPTER 39

Blood Glucose, mmol/L (mg/dL)b

834

Aspects of Gynecologic Surgery

Short procedure early morning

SECTION 5 Short procedure late morning

Short procedure afternoon

Complex procedure

Delay diabetes regimen

Oral agents

Hold oral agents

Single dose of insulin

2/3 total daily dose

2 or 3 doses of insulin

1/2 total morning dose

MDI

1/3 morning dose

Insulin pump

Basal rate only

Oral agents

Hold oral agents

Single dose of insulin

1/2 total daily dose

2 or 3 doses of insulin

1/3 total morning dose

MDI

1/3 morning, lunch doses

Insulin pump

Basal rate only

Oral agents

Hold oral agents

Insulin

Continuous IV insulin

FIGURE 39-4╇ Perioperative management recommendations for surgical patients with diabetes mellitus. IV = intravenous; MDI = multiple doses of short-acting insulin. (Reproduced with permission from Jacober SJ, Sowers JR: An update on perioperative management of diabetes. Arch Intern Med 1999 Nov 8;159(20):2405–2411.)

patient’s reasons for refusal, and (4) a statement describing the health consequences as described to the patient.

INFECTION PROPHYLAXIS Appropriate antibiotic prophylaxis can significantly reduce hospital-acquired infections following gynecologic surgery. Selection recommendations are summarized in Table 39-6. Decisions regarding the choice, timing, and duration of antibiotic prophylaxis are guided by the intended procedure and the anticipated organisms to be encountered (Chap. 3, p. 76). Typically, a single dose of antibiotics is given at anesthesia induction. Additional doses are considered in cases with blood loss >1500 mL or with duration longer than 3 hours. For obese individuals, a higher antibiotic dose is suggested (American College of Obstetricians and Gynecologists, 2014a). Recommendations do not support subacute bacterial endocarditis prophylaxis prior to GI or GU surgeries, as noted on page 828.

GASTROINTESTINAL BOWEL PREPARATION Mechanical bowel preparation was previously advocated if the risk for colon injury was high. This supposedly prevented bowel anastomosis leaks from passage of hard feces and reduced fecal and bacterial loads to lower wound infection rates (Barker, 1971; Nichols, 1971). Multiple studies, however, question routine mechanical bowel preparation (Duncan, 2009; Platell, 1997). Güenaga and coworkers (2011) performed a review of trials to determine the effectiveness of such preparation on morbidity and mortality rates in colorectal surgery. They found no evidence to support the perceived benefit from mechanical bowel preparation. Similar results have been found with laparoscopic surgery and pelvic floor procedures (Ballard, 2014; Muzii, 2006). Moreover, bowel preparation does not decrease microbial contamination of the peritoneal cavity and subcutis after elective open colon surgery (Fa-Si-Oen, 2005).

Preoperative Considerations

835

TABLE 39-6. Antimicrobial Prophylactic Regimens by Procedurea Antibiotic

Dose (single dose)

Hysterectomy

1. Cefazolin

1 g or 2 gc IV

Urogynecology procedures

2. Clindamycind PLUS Gentamicin or Quinolonee or Aztreonam

600 mg IV

3. Metronidazoled PLUS Gentamicin or Quinolonee

500 mg IV

f

b

Laparoscopy : diagnostic or operative Laparotomy Hysteroscopy: diagnostic or operative Hysterosalpingogram or chromotubation IUD insertion Endometrial biopsy Induced abortion dilatation and evacuation

None None None Doxycyclineg None None Doxycycline

Urodynamics

Metronidazole None

1.5 mg/kg IV 400 mg IV 1g IV

1.5 mg/kg IV 400 mg IV

100 mg orally, twice daily

100 mg orally 1 hour before and 200 mg orally after surgery or 500 mg orally twice daily for 5 d

a

A convenient time to administer antibiotic prophylaxis is just before anesthesia induction. Acceptable alternatives include cefotetan, cefoxitin, cefuroxime, or ampicillin-sulbactam. c A 2-g dose is recommended in women with a body mass index >35 or weight >100 kg or 220 lb. d Antimicrobial agents of choice in women with a history of immediate hypersensitivity to penicillin. e Ciprofloxacin, levofloxacin, or moxifloxacin. f For total laparoscopic hysterectomy, prophylaxis is given. g If patient has a history of pelvic inflammatory disease or procedure demonstrates dilated fallopian tubes. No prophylaxis is indicated for a study without dilated tubes. IV = intravenously; IUD = intrauterine device. Reproduced with permission from ACOG Committee on Practice Bulletins–Gynecology: ACOG practice bulletin No. 104: antibiotic prophylaxis for gynecologic procedures, Obstet Gynecol. 2009 May;113(5):1180–1189. b

Although its routine use should be limited, mechanical bowel preparation may be elected for certain advanced laparoscopic surgeries or for female pelvic reconstructive procedures involving the posterior vaginal wall and anal sphincter. In these cases, evacuation of rectal stool provides additional operating space and undistorted anatomy. Moreover, following sphincteroplasty, preoperative evacuation typically delays stooling and allows initial healing. Various regimens exist: (1) low-residue or clear liquid diets the day(s) prior to surgery, (2) oral cathartics such as 240 mL of senna extract (Senokot, X-Prep) or 240 mL of magnesium citrate, (3) sodium phosphate enemas (Fleet), (4) oral phosphates (Visicol, Fleet Phospho-soda), or (5) oral polyethylene glycol (PEG) solutions (GoLYTELY, NuLYTELY, HalfLytely).

THROMBOEMBOLISM PREVENTION Prophylaxis against VTE ranks in the top 10 patient safety practices recommended by the Agency for Healthcare Research and Quality (AHRQ) and the National Quality Forum (Kaafarani, 2011). In the United States alone, the annual incidence of deepvein thrombosis (DVT) and pulmonary thromboembolism are estimated to approach 600,000, with more than 100,000 deaths each year (Beckman, 2010). Ten to 30 percent of those diagnosed with VTE die within 1 month of diagnosis. National recommendations for prophylaxis against VTE follow a riskbased approach. The Caprini score is a tool validated using a large sample of general, vascular, and urologic surgery patients (Table 39-7) (Gould, 2012). Despite not being validated in gynecologic surgery, the patient populations are similar enough

CHAPTER 39

Procedure

836

Aspects of Gynecologic Surgery TABLE 39-7. Caprini Risk Assessment Model

SECTION 5

1 Point

2 Points

3 Points

5 Points

Age 41–60 yr Minor surgery BMI >25 kg/m2 Swollen legs Varicose veins Pregnancy or postpartum Recurrent spontaneous abortion COC or HRT use Sepsis 72 hr Immobilizing plaster cast Central venous access

Age ≥75 yr Prior VTE Family history of VTE Factor V Leiden Prothrombin 20210A Lupus anticoagulant Anticardiolipin antibodies Elevated serum homocysteine Heparin-induced thrombocytopenia Other thrombophilia

Stroke 30 Normal color Normal Alert

Normal Raised 100–120 Slow (>2 sec) Normal 20–30 Pale Pale Anxious or aggressive

Reduced Reduced (thready) Slow (>2 sec) Tachypnea (>20/min) 10–20 Pale Pale Anxious, aggressive, or drowsy

Very low Very low, unrecordable >120 (thready) Undetectable Tachypnea (>20/min) 0–10 Pale and cold Ashen Drowsy, confused, or unconscious

Reproduced with permission from Baskett PJ: ABC of major trauma. Management of hypovolaemic shock, BMJ 1990 Jun 2;300(6737):1453–7.

Intraoperative Considerations

■⌀ Red Blood Cell Replacement Clinical Assessment The decision to administer RBCs is complex and must balance the risks of transfusion with needs for adequate tissue oxygenation. Assessment includes hemoglobin level, vital signs, patient age, risks for further blood loss, and underlying medical conditions, especially cardiac disease. These needs will vary depending on the clinical setting. Accordingly, no specific hemoglobin threshold dictates when RBCs are administered. Consensus guidelines suggest that in those without significant cardiac disease, transfusion to a hemoglobin level above 10 g/dL is rarely indicated (Carless, 2010). If hemoglobin levels acutely drop to 6 g/dL, transfusion almost always is required (Madjdpour, 2006). Hemoglobin levels between 6 and 10 g/dL are more problematic, and patient factors and risk for continued hemorrhage dictate therapy (American Society of Anesthesiologists, 2015). In one randomized study of 838 critically ill patients, one group of euvolemic patients received transfusion when their hemoglobin levels fell below 7 g/dL. These individuals

fared better than those transfused at an earlier threshold (hemoglobin below 10 g/dL), excepting those with significant cardiac disease (Hébert, 1999).

Transfusion When the possible need for transfusion is present, an order for a type and screen informs blood bank personnel that blood products may be required and initiates two tests to characterize a patient’s RBCs. The first evaluation, termed typing, mixes commercially available standardized controls with a patient’s blood sample to determine her ABO type and Rh phenotype. The second test, or screen, combines a patient’s plasma sample with control RBCs that express clinically significant RBC antigens. If a patient has formed antibodies to any of these specific RBC surface antigens, then agglutination or hemolysis of the sample is seen. However, if blood is needed immediately and a full screen is not possible, then ABO type-specific blood or O-negative blood may be used. Typing and screening require approximately 45 minutes for completion and are valid for 3 days in patients who do receive transfusion. In those who are not transfused, the validity is considerably longer and typically is determined by individual blood banks. Alternatively, an order to type and crossmatch blood products alerts blood bank personnel to designate specific units of blood solely for one individual’s use. Those specific units are tested against the patient’s for specific antigen reactions. Previously, whole-blood transfusion was used commonly to provide RBCs, coagulation factors, and plasma proteins. This largely has been replaced by component therapy. Packed RBCs are the primary product used for most clinical situations and are prepared by removing most of the supernatant plasma during centrifugation. One unit of packed RBCs contains the same red cell mass as 1 unit of whole blood at approximately half the volume and twice the hematocrit (70 to 80 percent). One unit of packed RBCs raises the hematocrit approximately 3 volume percent in an adult or increases the hemoglobin level of a 70-kg individual by 1 g/dL (Table 40-7) (Gorgas, 2004). With severe hemorrhage that is anticipated to require ≥10 RBC units, massive transfusion protocols that combine units of packed RBCs, platelets, and plasma in 1:1:1 ratios are effective (McDaniel, 2014).

Complications Despite numerous tests for compatibility, adverse reactions to blood products can develop. An acute or delayed hemolytic transfusion reaction, febrile nonhemolytic transfusion reaction, allergic reaction, infection, or associated lung injury are among these. First, acute hemolytic transfusion reaction involves acute immune-mediated hemolysis usually from destruction of transfused RBCs by patient antibodies. This most commonly results from ABO incompatibility. Symptoms begin within minutes or hours of transfusion and may include chills, fever, urticaria, tachycardia, dyspnea, nausea and vomiting, hypotension, and chest and back pain. In addition, these reactions can lead to acute tubular necrosis or disseminated intravascular coagulopathy, and treatment is directed to these serious complications. If acute hemolysis is suspected, transfusion is halted immediately. A sample of the patient’s blood is sent with the remaining donor unit for evaluation in the blood bank. In patients

CHAPTER 40

commonly, and their composition is described in Chapter 42 (p. 908). For moderate hemorrhage, both perform equally well as fluid replacements (Healey, 1998). Although crystalloids have an immediate effect to expand intravascular volume, a portion will extravasate into extracellular tissues. Thus, in the setting of hemorrhage, crystalloid volume is administered in a 3:1 ratio to blood lost (Moore, 2004). Clinically, urine output of 0.5 mL/kg/per hour or 30 mL or more per hour, heart rate less than 100 beats per minute, and systolic blood pressure greater than 90 mm Hg may be used as general indicators of volume improvement. If rapid crystalloid infusion fails to correct hypotension or tachycardia, then RBC transfusion usually is prudent. In addition to or as an alternative to crystalloid solutions, colloids may be used for volume expansion. These fluids have higher molecular weights than crystalloids. As a result, a greater portion remains intravascular and is not lost to extracellular extravasation. Despite this perceived advantage, studies comparing survival rates when crystalloids or colloids are administered find no superiority with colloids but greater expense (Perel, 2013). Intraoperative fluid management strategies broadly fall into categories of liberal (sometimes thought of as fixed volume), restrictive, or goal directed. Of these, evidence from colorectal and trauma surgery is now more supportive of restrictive management. Less bowel edema, quicker return of bowel function, and fewer pulmonary complications are all purported benefits (Chappell, 2008; Joshi, 2005). Restrictive strategies generally use colloid to replace blood loss in a 1:1 ratio, unless red cell transfusion is indicated. Crystalloids are then used to replace urine and insensible losses 1:1. In contrast, liberal strategies rely on large volumes of crystalloid. Last, goal directed therapy refers to using a monitoring device (such as an arterial line) and administering fluids to achieve a goal (such as maximizing stroke volume). Patients with severe comorbid conditions undergoing major procedures may benefit from this strategy (Chappell, 2008).

865

866

Aspects of Gynecologic Surgery TABLE 40-7. Characteristics of Blood Components

SECTION 5

Component

Volume, mL

Content

Clinical Response

PRBCs Platelets â•… Random-donor unit â•… Single-donor collection

180–200

RBCs

â•⁄50–70 200–400

5.5 × 1010 platelets 3.0 × 1011 platelets

FFP

200–250

Cryoprecipitate

â•⁄10–15

Coagulation factors, including fibrinogen, proteins C and S, antithrombin Fibrinogen, factor VIII, vWF

Increases Hb 1 g/dL and Hct 3% Increases platelet count: 5–10 × 109/L >10 × 109/L within 1 hr and >7.5 × 109/L within 24 hr posttransfusion Increases coagulation factors ∼2%

Increases fibrinogen level 0.1 g/L

FFP = fresh-frozen plasma; Hct = hematocrit; Hb = hemoglobin; PRBCs = packed red blood cells; RBCs = red blood cells; vWF = von Willebrand factor. Reproduced with permission from Kasper DL, Fauci AS, Longo DL, et al: Harrison’s Principles of Internal Medicine, 19th ed. New York: McGraw-Hill; 2015. with significant hemolysis, laboratory values will be altered. Specifically, serum haptoglobin levels will be lowered; serum lactate dehydrogenase and bilirubin levels will be increased; and serum and urine hemoglobin levels will be elevated. Serum creatinine and electrolyte levels and coagulation studies additionally are ordered. To prevent renal toxicity, diuresis is prompted with intravenous crystalloids and administration of furosemide or mannitol. Alkalinization of urine may prevent precipitation of hemoglobin within the renal tubules, and therefore, intravenous bicarbonate also may be given. In contrast to acute hemolytic transfusion reaction, delayed hemolytic transfusion reactions may develop days or weeks later. Patients often lack acute symptoms, but lowered hemoglobin levels, fever, jaundice, and hemoglobinemia may be noted. Clinical intervention typically is not required in these cases. Febrile nonhemolytic transfusion reaction is characterized by chills and a greater than 1°C rise in temperature and is the most common transfusion reaction. Blood transfusion typically is stopped to exclude a hemolytic reaction, and treatment is supportive. For patients with a previous history of febrile reaction, premedication with an antipyretic such as acetaminophen prior to transfusion is reasonable. Last, an allergic reaction can follow an antibody-mediated response to donor plasma proteins. Urticaria alone may develop during transfusion and typically is not associated with serious sequelae. The transfusion does not need to be stopped, and treatment with an antihistamine, such as diphenhydramine (Benadryl) 50 mg orally or intramuscularly, usually suffices. Rarely, an anaphylactic reaction may complicate transfusion, and treatment follows that for classic anaphylaxis (Table 27-2, p. 596). Infectious complications associated with packed RBC transfusion are uncommon. The risk for transmission of HIV and hepatitis B and C virus has diminished over the past decade, and bacterial contamination now stands as a greater infection risk. In addition, emerging infection concerns include transmission of West Nile virus, transfusion-transmitted virus (TTV), hepatitis G, EpsteinBarr virus, and Creutzfeldt-Jakob disease (Luban, 2005). Transfusion-related acute lung injury (TRALI) is an infrequent but serious complication of blood component therapy

that is similar clinically to acute respiratory distress syndrome (ARDS). Symptoms develop within 6 hours of transfusion and may include extreme respiratory distress, frothy sputum, hypotension, fever, and tachycardia. Noncardiogenic pulmonary edema with diffuse bilateral pulmonary infiltrates on chest radiography is characteristic (Toy, 2005). Treatment of TRALI is supportive and focuses on oxygenation and blood pressure support (Silliman, 2005; Swanson, 2006).

■⌀ Platelet Replacement For patients with moderate hemorrhage, RBC transfusion typically is sufficient, but for patients with severe hemorrhage, platelet transfusion also may be indicated. Platelets may be acquired from a single individual during plateletpheresis and are termed single-donor platelets. Alternatively, platelets may be derived from random units of whole blood and are referred to as random-donor platelets. Fewer platelets are harvested from a unit of whole blood compared with the amount removed during donor plateletpheresis. Specifically, a single-donor platelet dose contains at least 3 × 1011 platelets in 250 to 300 mL of plasma, and this approximates the dose from six random-donor platelet concentrates. Each random-donor platelet concentrate contain 5.5 × 1010 platelets suspended in approximately 50 mL of plasma. Each concentrate transfused should raise the platelet count by 5 to 10 × 109/L, and the usual therapeutic dose is one platelet concentrate per 10 kg of body weight. Five to six concentrates provide a typical adult dose. Donor plasma must be compatible with recipient erythrocytes because a few RBCs are invariably transfused along with the platelets. Only platelets from D-negative donors should be given to D-negative recipients. Surgical patients with bleeding usually require platelet transfusion if the platelet count is less than 50 × 109/L and rarely require therapy if it is greater than 100 × 109/L (American Society of Anesthesiologists, 2015). With counts between 50 and 100 × 109/L, the decision to provide platelet transfusion is based on a patient’s risk for additional significant bleeding.

Intraoperative Considerations

■⌀ Factor Replacement

ADJACENT ORGAN SURGICAL INJURY ■⌀ Lower Urinary Tract Sound anatomic knowledge, adequate operating exposure, meticulous technique, and surgical experience are essential to avoid surrounding organ injury during pelvic surgery. The lower gastrointestinal and urinary tracts are closely related to the female reproductive organs, and disease processes, anatomic distortion, and adverse operating conditions can increase their injury risk. Iatrogenic damage to the lower urinary tract is common, and up to 75 percent of ureter or bladder injuries sustained during gynecologic surgery occur during hysterectomy (Walters, 2007). Most injuries have no antecedent risk factors, but highrisk elements are ideally sought preoperatively. These include compromised visibility from large pelvic masses, hemorrhage, pregnancy, obesity, inadequate incision, suboptimal retraction, and poor lighting. Additionally, scarring or anatomic distortion from cervical and broad ligament leiomyomas, malignancy, endometriosis, pelvic organ prolapse, and prior pelvic infection, surgery, or radiation are risks (Brandes, 2004; Francis, 2002). Patients who sustain surgical injury to the bladder or ureter suffer significantly greater morbidity. In one case-control study, women with injury to the lower urinary tract during abdominal hysterectomy had significantly greater operative time, estimated blood loss, blood transfusion rates, febrile morbidity, and postoperative stay length than their respective controls (Carley, 2002).

■⌀ Bladder Injury Cystotomy is common and complicates approximately 0.3 to 11 per 1000 benign gynecologic surgeries, especially urogyneco-

■⌀ Urethral Injury The female urethra is rarely injured during gynecologic surgery, but cystoscopy, urethral diverticulum repairs, antiincontinence operations, and possibly anterior colporrhaphy are at-risk procedures. Repair is completed with 3-0 or 4-0 absorbable suture in an interrupted fashion and in multiple layers, if possible. Similar to cystotomy, a Foley catheter is typically placed

CHAPTER 40

Fresh-frozen plasma (FFP) is one option for factor replacement and is prepared from whole blood or by plasmapheresis. It is stored frozen, and approximately 30 minutes are required for it to thaw. One unit contains all coagulation factors, including 2 to 5 mg/mL of fibrinogen in 250 mL of volume. Recommended FFP dosing is 15 mL/kg. Fresh-frozen plasma is used commonly as first-line hemostatic therapy in massive hemorrhage because it replaces multiple coagulation factors. It is considered in a bleeding woman with a fibrinogen level below 1.0 g/L or with abnormal prothrombin and partial thromboplastin times. Another option, cryoprecipitate, is prepared from fresh-frozen plasma and contains fibrinogen, factor VIII, von Willebrand factor, factor XIII, and fibronectin. Cryoprecipitate was developed and used originally for treatment of hemophilia A and von Willebrand disease. However, specific factor concentrates are now available for these disorders, and thus, the clinical indications for cryoprecipitate are limited. Fresh-frozen plasma provides all coagulation factors and is favored in severe hemorrhage over cryoprecipitate. However, cryoprecipitate is an excellent source of fibrinogen and may be indicated if fibrinogen levels persist below 1.0 g/L despite administration of fresh-frozen plasma, such as in disseminated intravascular coagulopathy (DIC). The dose of cryoprecipitate is usually 2 mL/kg of body weight, and each unit contains approximately 15 mL volume. One unit typically increases the fibrinogen level by 10 mg/dL (Erber, 2006).

logic procedures and hysterectomy (Gilmour, 2006; Mathevet, 2001). In sum, depending on the procedure, the bladder may be at greater risk during: (1) initial abdominal entry when incising the anterior parietal peritoneum, (2) dissection within the space of Retzius, (3) vaginal epithelium dissection during anterior colporrhaphy, or (4) hysterectomy when dissecting in the vesicocervical space, entering the anterior vagina, or suturing the vaginal cuff. With hysterectomy, bladder injury traditionally has been associated more often with the vaginal hysterectomy, but some data suggest that laparoscopic procedures pose the greatest risk (Francis, 2002; Frankman, 2010; Harris, 1997). Preventatively, clear identification of the bladder, gentle retraction, meticulous surgical technique, sharp dissection, and maintenance of a drained bladder intraoperatively are standard principles. Cystotomy is suspected if a Foley bulb, bloody urine, or urine leaking into the operative field is seen. During laparoscopy, the Foley bag may also distend with gas from the pneumoperitoneum. For diagnosis, retrograde instillation of sterile milk through a catheter confirms injury and delineates its full extent. This is superior to methylene blue and indigo carmine dyes, as infant formula does not stain surrounding tissues and is readily available. In addition, small defects can be difficult to identify and repair if the tissues surrounding the defect become dye stained. Prior to repair, cystoscopy is indicated for any bladder base injury to assess ureteral patency. In addition, the full extent of injury can be defined, and the bladder can be evaluated for additional injuries or intravesical sutures. If bladder distension cannot be maintained during cystoscopy or if the patient is not in dorsal lithotomy, the ureteral orifices can also be evaluated grossly through the cystotomy site. If the cystotomy is small, suprapubic teloscopy, which is described in Chapter 45, is also an option, or the cystotomy can be extended to allow evaluation. Repair during the primary surgery is preferred and lowers risks of later vesicovaginal fistula formation. Principles of repair include injury delineation; wide mobilization of surrounding tissues; tension-free, multilayered, watertight closure; and adequate postoperative bladder drainage (Utrie, 1998). Suture identified in the bladder is cut, as persistence can lead to cystitis, stone formation, or both. Needle-stick and subcentimeter lacerations can be managed conservatively. Larger defects may be closed in two or three layers with a running stitch using 3-0 absorbable or delayed-absorbable suture (Fig. 40-32). The first layer inverts the mucosa into the bladder, and subsequent layers reapproximate the bladder muscularis and serosa. In the area of the trigone, the ureters are typically stented first, and the repair may be performed with interrupted sutures to avoid ureteral kinking (Popert, 2004). Postoperatively, continuous bladder drainage is continued for 7 to 10 days (Utrie, 1998). Evidence is conflicting regarding the use of prophylactic antibiotics for the expected duration of catheterization, and thus remains at the provider’s discretion.

867

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Aspects of Gynecologic Surgery

Diagnosis

SECTION 5 FIGURE 40-32╇ Cystotomy repair. The primary layer inverts the bladder mucosa with running or interrupted sutures of 3-0 delayedabsorbable or absorbable suture. Second and possibly a third layer approximate the bladder muscularis to reinforce the incision closure. (Reproduced with permission from Cunningham FG, Vandorsten JP, Gilstrap LC: Operative Obstetrics, 2nd ed. New York: McGraw-Hill; 2002.)

postoperatively for 7 to 10 days, with antibiotic prophylaxis provided at the surgeon’s discretion (Francis, 2002).

■⌀ Ureteral Injury This is uncommon in benign gynecologic surgery, and the incidence approximates 0.2 to 7.3 per 1000 surgeries. For hysterectomy, the highest rate of ureteral injury is linked with laparoscopic hysterectomy, and the lowest with vaginal hysterectomy (Gilmour, 2006). Other associated procedures include operations for pelvic organ prolapse, incontinence, malignancy, or endometriosis (Patel, 2009; Utrie, 1998). The ureter is 25 to 30 cm long, and its anatomy is described in Chapter 38 (p. 816). Gynecologic ureteral injury typically occurs in the distal third and includes transection, ligation, kinking, and crushing (Brandes, 2004; Utrie, 1998). Trauma to the outer sheath can also disrupt ureteral blood supply. Of these, the ureter more often is transected or kinked, and each accounts for approximately 40 percent of injuries. During hysterectomy, the most common trauma site is at the level of the uterine artery and accounts for 80 percent of injuries (Ibeanu, 2009). The ureter is also vulnerable near the pelvic brim during adnexectomy and at the distal uterosacral ligaments. Mechanisms of injury include clamping or suturing with the ureter poorly visualized. Thermal insult or devascularization may lead to stricture or leak. Injury prevention measures include preoperative risk evaluation and if indicated, intravenous pyelography (IVP) or computed tomography (CT). Ureteral stenting assists with intraoperative recognition but does not necessarily prevent injury. As with bladder injury, the best prevention is sound intraoperative technique and direct visualization of the peristalsing ureter. Also, the ureter may be felt to “snap” if palpated and stretched along its course on the broad ligament’s medial leaf. However, vessels, adipose tissue, and peritoneal folds can mimic this.

Iatrogenic injury ideally is diagnosed early, as immediate repair is associated with improved outcomes and less patient morbidity (Neuman, 1991; Sakellariou, 2002). Damage may be seen directly or identified during intraoperative cystoscopy. Intravenous administration of indigo carmine or methylene blue can aid cystoscopic evaluation, with observation of blue-stained urine from the ureteral orifices. This is described fully in Section 45-1 of the atlas (p. 1057). However, use of the latter may increase given current indigo carmine shortages. With these dyes, blue effluent is usually seen in 5 to 10 minutes. Failure to see dye after 30 to 40 minutes mandates further evaluation with either IVP or ureteral catheterization. Unfortunately, normal-appearing findings at cystoscopy do not guarantee ureteral integrity, as nonobstructive, partially obstructive, or late ureteral injuries may be unrecognized. Diagnosing injury shortly after surgery is challenging, as patient symptoms may be attributable to other causes. Thus, thorough patient evaluation and a high clinical suspicion are crucial. Renal damage may begin 24 hours after obstruction and can be irreversible in 1 to 6 weeks (Walter, 2002). Symptoms usually develop about 48 hours after surgery, and fever, abdominal pain, flank pain, and watery discharge may be among these. Findings can include leukocytosis, elevated blood urea nitrogen level, and ileus. Prolonged skin or vaginal drainage suggests a urinary leak, and high creatinine levels in these fluids are diagnostic of urine. Serum creatinine measurement may or may not be helpful. In one retrospective study of 187 patients, a 24-hour postoperative change 0.2 mg/dL has been associated with obstruction, the authors recommended repeating a creatinine measurement and renal imaging for persistent elevation above this level (Walter, 2002). With elevated serum creatinine levels, calculation of the fractional excretion of sodium (FENa) or assessment of urine sodium levels may also help clarify the renal injury source as prerenal, intrarenal, or postrenal, as described in Chapter 42 (p. 916). Sonography, CT, or magnetic resonance (MR) imaging will help identify hydronephrosis, urinoma, or abscess. Lack of contrast in the distal ureter on delayed CT images confirms total obstruction (Armenakas, 1999). IVP can also help localize injury. However, IV contrast can be nephrotoxic, and thus CT with contrast may be a less than ideal choice for those with already elevated creatinine levels. Retrograde pyelography with fluoroscopic guidance and attempted retrograde ureteral stent placement can be considered in cases where suspicion remains high, and IVP is contraindicated or has equivocal findings. All of these imaging modalities can be used to diagnose injury in both the early and late postoperative periods.

Treatment The best repair method depends on the location, extent, time from surgery, and mechanism of injury. Expert assistance from a urogynecologist, gynecologic oncologist, or urologist may be prudent. The ureter can be repaired by stenting, reimplantation, or end-to-end reanastomosis. For low-grade sheath injuries from clamping or suturing, removal of the insult and stent placement

Intraoperative Considerations

■⌀ Universal Cystoscopy Lower urinary tract injury is poorly detected by direct visualization, and rates range from 7 to 12 percent for ureteral trauma and approximate 35 percent for bladder damage (Vakili, 2005). To increase early diagnosis, universal intraoperative cystoscopy has been advocated, and detection rates are near 96 percent (Ibeanu, 2009; Vakili, 2005; Visco, 2001). Proponents argue that the procedure is cost-effective, carries minimal risk, and prevents both postoperative morbidity and liability. Opponents cite overall low rates of injury, imperfect detection rates, increased costs, credentialing problems, and a need for Â�training

(Patel, 2009). Using a decision analysis model, one study estimated that routine cystoscopy was cost-effective when ureteral injury rates were above 1.5 percent for abdominal hysterectomy and 2 percent for vaginal and laparoscopically assisted hysterectomy (Visco, 2001). Cystoscopy is currently indicated for urogynecologic procedures, but there are no strict recommendations for other routine gynecologic procedures, including hysterectomy (American College of Obstetricians and Gynecologists, 2013; Patel, 2009). At present, the decision remains at the surgeon’s discretion. Some have elected selective cystoscopy, or cystoscopy restricted to patients with risk factors or when intraoperative events make injury more likely.

■⌀ Bowel Injury Injury to the bowel infrequently complicates gynecologic surgery, and rates are 30, 50 kg Body Wt

Parenteral (mg)

Oral (mg)

Duration (h)

10

30

—

Children and Adults 92 percent represent adequate oxygenation, however, a PaO2 measurement by arterial blood gas will most accurately assess a patient with hypoxic respiratory

failure. In addition to bedside findings, chest radiography typically shows linear densities in the lower lung fields. Classically, atelectasis is associated with low-grade fevers. However, Mavros and colleagues (2011) reviewed eight studies with a total of 998 patients and found no association between atelectasis and postoperative fever. Prevention using lung expansion therapies is described in Chapter 39 (p. 827), and these can be used for treatment as well. Atelectasis is usually temporary (up to 2 days) and selflimited, and it rarely slows patient recovery or hospital discharge (Platell, 1997). Its importance mainly lies in its clinical similarity to PE and pneumonia. Thus, in women with risks for these more life-threatening complications, atelectasis may ultimately be a diagnosis of exclusion.

■⌀ Hospital-acquired Pneumonia This is the second most common nosocomial infection in the United States and carries high associated morbidity and mortality rates (Tablan, 2004). Its incidence in surgical patients varies and ranges from 1 to 19 percent depending on surgical procedure and hospital surveyed (Kozlow, 2003). With these infections, bacterial pathogens most typically include aerobic gram-negative bacilli, such as Pseudomonas aeruginosa, Escherichia coli, Klebsiella pneumoniae, and Acinetobacter species. Clinically, pneumonia is diagnosed if chest radiography reveals a new or progressive radiographic infiltrate and if two of three clinical features (leukocytosis, fever >38°C, or purulent secretions) are present. Broad-spectrum antibiotic regimens are recommended for hospital-acquired pneumonia treatment (Table 42-3). If aspiration is highly suspected, specific treatment

TABLE 42-3. Empiric Antibiotic Therapy for Hospitalacquired Pneumoniaa Regimen Options

Dosage

Cefepime or ceftazidime or Imipenem or meropenem or Piperacillin–tazobactam PLUS Aminoglycoside â•…Gentamicin â•…Tobramycin â•…Amikacin or Quinolone â•…Levofloxacin â•…Ciprofloxacin

2 g every 8 hr

a

1 g every 8 hr 4.5 g every 6 hr

7 mg/kg/d 7 mg/kg/d 20 mg/kg/d 750 mg daily 400 mg every 8 hr

In patients with late-onset disease or risk factors for multidrug-resistant pathogens. Adapted with permission from American Thoracic Society: Guidelines for the management of adults with hospitalacquired, ventilator-associated, and healthcare-associated pneumonia. Am J Respir Crit Care Med 2005 Feb 15; 171(4):388–416.

CHAPTER 42

hot flashes to headaches or sudden mood swings. In these women, estrogen replacement therapy is considered for those without contraindications (Chap. 22, p. 494). For women completing surgery for endometriosis, a progestin may be added for those with residual disease, as discussed in Chapter 10 (p. 243).

911

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Aspects of Gynecologic Surgery

HAP, VAP or HCAP suspected

SECTION 5

Obtain lower respiratory tract (LRT) sample for culture & microscopy

Unless there is both a low clinical suspicion for pneumonia & negative microscopy of LRT sample, begin empiric antimicrobial therapy

Days 2 & 3: check culture results & assess clinical response: temperature, WBC, chest radiography, oxygenation, purulent sputum, hemodynamic changes, & organ function

Clinical improvement at 48–72 hours

No

Cultures −

Yes

Cultures +

Cultures −

Cultures +

Consider stopping De-escalate antibiotics, Search for other pathogens, Adjust antibiotic therapy; antibiotics if possible. Treat selected complications, other search for other pathogens, patients for 7–8 days diagnoses, or other complications, other diagnoses, & reassess sites of infection or other sites of infection

FIGURE 42-1╇ Algorithm describes management strategies for hospital-acquired pneumonia. HAP = hospital-acquired pneumonia; HCAP = health care-associated pneumonia; VAP = ventilator-associated pneumonia; WBC = white blood cells. (Reproduced with permission from American Thoracic Society: Guidelines for the management of adults with hospital-acquired, ventilator-associated, and healthcare-associated pneumonia. Am J Respir Crit Care Med 2005 Feb 15;171(4):388–416.)

for anaerobes with metronidazole or clindamycin is considered. An algorithm supported by the American Thoracic Society is shown in Figure 42-1. Preventive steps include substituting oral endotracheal and orogastric tubes in place of nasal tubes; elevating the head of the bed 30 to 45 degrees, particularly during feeding; and removing subglottic secretions in those unable to clear these (American Thoracic Society, 2005; Ferrer, 2010).

■⌀ Pulmonary Embolism If venous thromboembolism (VTE) is suspected, evaluation begins with clinical examination and risk estimation. Wells and colleagues (1995) described one of the most widely used pretest probability assessments for DVT (Table 42-4). When indicated, duplex sonography is highly sensitive for detecting proximal leg DVTs, with a false-negative rate of 0 to 6 percent (Gottlieb, 1999). For PE, because symptoms may reflect other cardiopulmonary pathology, clinicians often initially elect chest radiography and electrocardiogram (ECG). The radiograph is typically abnormal but nonspecific, and findings can include atelectasis, elevated hemidiaphragm, cardiomegaly, and small pleu-

ral effusions (Worsley, 1993). ECG may display tachycardia or may reflect right heart strain by showing a large S wave in lead  I, a Q wave in lead III, and inverted T wave in lead III (Stein, 1991). If suspicion for PE remains, then computed tomographic angiography (CTA) or less frequently, ventilation/perfusion (V/Q) scanning is ordered. These serve as alternatives to the invasive gold standards—pulmonary angiography or contrast venography. Acute management of VTE involves anticoagulation with intravenous unfractionated heparin or subcutaneous low-molecular-weight heparin (Tables 42-5 and 42-6). After achieving adequate anticoagulation, oral vitamin K antagonists such as warfarin are initiated. To avoid paradoxical hypercoagulability, heparin is continued for at least 5 days after the initiation of warfarin (Houman Fekrazad, 2009). Once the international normalized ratio (INR) reaches a therapeutic range of 2 to 3, then heparin is stopped. Long term, anticoagulation therapy duration is dictated by clinical and patient circumstances. For those with a provoked first DVT or PE, anticoagulants are recommended for 3 months. Provocateurs include surgery, exogenous estrogen, or local trauma. Extended therapy is preferred for both those with unprovoked VTE or with second VTE,

Postoperative Considerations TABLE 42-6. Characteristics of Some Low-MolecularWeight Heparins

Major Points

Minor Points

Name (Brand Name)

Dose

Cancer Immobilization Recent major surgery Thigh or calf tenderness Calf swelling Family history of DVT

Recent trauma to symptomatic leg Unilateral edema Erythema Dilated superficial veins Hospitalized in last 6 months

Enoxaparin (Lovenox)

1 mg/kg every 12 hr 1.5 mg/kg daily 175 IU/kg daily 100 IU/kg every 12 hr 200 IU/kg daily

Tinzaparin (Innohep) Dalteparin (Fragmin) IU = international units.

Clinical Probability High >3 major points and no alternative diagnosis >2 major points and >2 minor points + no alternative diagnosis Low 1 major point + >2 minor points + has an alternative diagnosis 1 major point + >1 minor point + no alternative diagnosis 0 major points + >3 minor points + has an alternative diagnosis 0 major points + >2 minor points + no alternative diagnosis Moderate All other combinations

syndrome. This is a pathophysiologic continuum from mild pulmonary insufficiency to dependence on high inspired oxygen concentrations and mechanical ventilation. The theory that multiple insults lead to postoperative ARDS offers insight into modifiable intra- and postoperative alveolar damage prevention (Litell, 2011; Warner, 2000). Intraoperative strategies minimize lung trauma by keeping airway pressure and tidal volumes within set limits and by avoiding repeated alveolar opening and closing (Hemmes, 2013). Other measures strive to prevent infection, limit IV fluid volumes, and avoid blood product transfusion (Güldner, 2013).

Adapted with permission from Wells PS, Hirsh J, Anderson DR, et al: Accuracy of clinical assessment of deepvein thrombosis. Lancet 1995 May 27;345(8961):1326–1330.

■⌀ Myocardial Infarction

unless the risk of bleeding is high, in which case, treatment is halted at 3 months. For those with concurrent cancer, therapy is extended regardless of bleeding risk (Kearon, 2012).

■⌀ Acute Respiratory Distress Syndrome Acute lung injury that causes a form of severe permeability pulmonary edema and ARF is termed acute respiratory distress

CARDIAC COMPLICATIONS Postoperative myocardial infarction (MI) is rare, and its generally reported incidence ranges from nearly 1 percent to as high as 37 percent among patients with surgery within 3 months following an MI (Mangano, 1990; Tinker, 1978). Declines in oxygen supply and increased demand classically underlie this coronary ischemia. Events that decrease oxygen supply include hypotension, lowered coronary perfusion, or poor carrying capacity caused by anemia. Increased afterload, tachycardia, and increased cardiac contractility can raise myocardial oxygen demands.

TABLE 42-5. Parkland Hospital Protocol for Continuous Heparin Infusion for Patients with Venous Thromboembolism Initial Heparin Dose: __ units IV push (recommended 80 units/kg rounded to nearest 100, maximum 7500 units), then __ units/hr by infusion (recommended 18 units/kg/hr rounded to nearest 50). Infusion Rate Adjustments—based on partial thromboplastin time (PTT): PTT (sec)a Interventionb Baseline Infusion Rate Changec 100 Stop infusion 60 minutes ↓by 3 units/kg/hr a

PTT goal 55–84. Rounded to nearest 100. c Rounded to nearest 50. b

CHAPTER 42

TABLE 42-4. Pretest Probability for Deep-Vein Thrombosis

913

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Aspects of Gynecologic Surgery

SECTION 5

Most patients with postoperative MI do not have classic symptoms of chest pain or pressure. These are in part masked by postoperative analgesics (Muir, 1991). Dyspnea is the most common complaint and may be accompanied by acute cardiac failure or hemodynamic instability. ECG changes of postoperative MI tend to be less well defined, and most demonstrate a non-Q wave variant (Badner, 1998). CK isoenzyme (CK-MB) abnormalities are seen within 6 hours, and cardiac troponin I and T are highly specific later for diagnosis of MI (Zimmerman, 1999). Postoperative MI treatment differs from that of nonsurgical patients, and its main tenets focus on shifting the oxygen delivery and utilization balance. Special attention is given to arrhythmia correction and hemodynamic status improvement. Ideally, these patients are cared for in a unit that provides intense monitoring, cardiopulmonary support, and cardiology consultation.

■⌀ Hypertension This is frequently encountered both preoperatively and postoperatively. As standard definitions are lacking, the reported incidence ranges from 3 to 90 percent, depending on the thresholds set and the type of surgery. Patients with poorly controlled hypertension preoperatively tend to have more blood pressure lability compared with normotensive patients or those with well-controlled hypertension. In general, a diastolic blood pressure greater than 110 mm Hg preoperatively best predicts those who will have postoperative hypertension issues. Several possible triggers may raise blood pressures in the first 24 hours after surgery. First, abrupt withdrawal of β-blocker or of centrally acting sympatholytic agents such as clonidine can cause rebound hypertension. Pain and bladder distention may also contribute. Later in postoperative recovery, sympathetic hyperactivity may stem from inadequate pain management or from alcohol withdrawal. Last, return of excess interstitial fluid back into the vascular space may create fluid overload and hypertension.

Two approaches have been described for blood pressure treatment: fixed thresholds and relative changes from baseline. Charlson and colleagues (1990) demonstrated increased rates of postoperative cardiac and renal complications when the mean blood pressure rose 20 percent or more compared with preoperative levels. Given the paucity of good evidence, it is reasonable to initiate treatment if mean blood pressure readings rise by this percentage. With acute blood pressure management, the mean blood pressure should not be lowered by more than 20 percent or to a level less than 160/100 mm Hg.

GASTROINTESTINAL COMPLICATIONS ■⌀ Postoperative Nausea and Vomiting This is one of the most common complaints following surgery, and its incidence ranges from 30 to 70 percent in high-risk patients (Møller, 2002). Those at risk for postoperative nausea and vomiting (PONV) include females, nonsmokers, those with prior motion sickness or prior PONV, and those with extended surgeries (Apfelbaum, 2003). A multimodal approach to prevention is recommended (Apfel, 2004). Currently, combinations of 4 to 8 mg of dexamethasone prior to anesthesia induction are followed, toward the end of surgery, by less than 1 mg of droperidol (Inapsine) and 4 mg of ondansetron (Zofran). This pretreatment significantly reduces symptoms by 25 percent. However, if symptoms develop within 6 hours of surgery, antiemetics from a different pharmacologic class than previously administered are considered (Habib, 2004). Persistent nausea may benefit from combining agents from different classes (Table 42-7).

■⌀ Bowel Function and Diet Resumption Normal GI function requires synchronized motility, mucosal transport of nutrients, and evacuation reflexes (Nunley, 2004).

TABLE 42-7. Commonly Used Medications for Nausea and Vomiting Medication (Brand Name)

Usual Dosage

Antihistamines Diphenhydramine (Benadryl) Hydroxyzine (Atarax, Vistaril) Meclizine (Antivert) Benzamides Metoclopramide (Reglan) Trimethobenzamide (Tigan) Phenothiazines Prochlorperazine (Compazine) Promethazine (Phenergan) Serotonin Antagonists Ondansetron (Zofran) Granisetron (Kytril) Dolasetron (Anzemet)

Every 6 hr 25–50 mg 25–100 mg 25–50 mg Every 6 hr 5–15 mg 250 mg Every 6 hr 5–10 (25 PR) mg 12.5–25 mg 8 mg every 8 hr 2 mg daily 100 mg daily

Route(s) IM, IV, PO IM, PO PO IM, IV, PO IM, PO, PR IM, IV, PO, PR IM, IV, PO, PR IV, PO IV, PO IV, PO

IM = intramuscular; IV = intravenous; PO = orally; PR = per rectum.

Postoperative Considerations

■⌀ Ileus Postoperative ileus (POI) is a transient impairment of GI activity that leads to abdominal distention, hypoactive bowel sounds, nausea and vomiting related to GI gas and fluid accumulation, and delayed passage of flatus or stool (Livingston, 1990). The genesis of POI is multifactorial. First, bowel manipulation during surgery leads to production of contributory factors. These include: (1) neurogenic factors related to sympathetic overactivity, (2) hormonal factors related to the release of hypothalamic corticotropin-releasing hormone (CRH), which plays a key role in the stress response, and (3) inflammatory factors (Tache, 2001). Second, perioperative opioid use also increases POI rates. Thus, in selecting opiates, clinicians balance the beneficial analgesia produced by central opioid receptor binding against the GI dysfunction that results from peripheral receptor binding effects (Holzer, 2004). No single treatment defines POI management. Electrolyte repletion and IV fluids to reestablish euvolemia are traditional. In contrast, routine nasogastric tube (NGT) decompression to promote bowel rest has been challenged by multiple prospective randomized trials. A metaanalysis including nearly 5240 patients found routine NGT decompression unsuccessful and inferior to its selective use in symptomatic patients. Specifically, patients without NGTs had significantly earlier return of normal bowel function and decreased risks of wound infection and ventral hernia (Nelson, 2007). Additionally, tube-related discomfort, nausea, and hospital stays were reduced. For these reasons, postoperative NGTs are recommended only for symptomatic relief of abdominal bloating and recurrent vomiting (Nunley, 2004). Gum chewing after laparotomy as a preventive modality for POI has been the focus of several small but randomized studies.

In these, sugarless gum is usually chewed 15 to 30 minutes at least three times daily. In evaluations, this practice is associated with earlier improvement in bowel motility markers (Ertas, 2013; Jernigan, 2014). However, compared with placebo, gum chewing achieves these goals on average only several hours earlier (Li, 2013).

■⌀ Bowel Obstruction Obstruction of the small intestines may be partial or complete and can result from adhesions following intraabdominal surgery, infection, or malignancy. Of these, surgical adhesions are the most common cause (Krebs, 1987; Monk, 1994). Small bowel obstruction (SBO) develops following 1 to 2 percent of total abdominal hysterectomies, and nearly 75 percent of obstructions are complete (Al-Sunaidi, 2006). Obstruction may be remote from surgery, and the mean interval between primary intraabdominal procedure and SBO approximates 5 years (Al-Took, 1999). Initial SBO management is similar to that for POI, but distinguishing between the two is important to prevent serious SBO sequelae. During SBO, the bowel lumen dilates proximal to the obstruction, and decompression may develop distally. Bacterial overgrowth in the proximal small bowel can promote bacterial fermentation and worsening dilation. The bowel wall also becomes edematous and dysfunctional (Wright, 1971). Progressive increases in bowel pressure compromise perfusion to the intestinal segment and can ultimately lead to ischemia or rupture (Megibow, 1991). Clinical signs that may help distinguish SBO from POI include tachycardia, oliguria, and fever. Physical examination may reveal abdominal distention, high-pitched bowel sounds, and an empty rectal vault during digital examination. Last, leukocytosis with a neutrophil dominance should alert to possible coexistent bowel ischemia. Computed tomography (CT) scanning is the primary imaging tool to identify SBO. Water-soluble contrast can safely help identify the cause and severity of an obstruction. Gastrografin, the most commonly used water-soluble dye, is a mixture of sodium amidotrizoate and meglumine amidotrizoate and may aid resolution of small bowel edema due to its high osmotic pressure. Gastrografin is also theorized to enhance smooth muscle contractility (Assalia, 1994). Although the use of oral Gastrografin does appear to reduce hospital length of stay, it has no therapeutic benefit in adhesion-related SBO (Abbas, 2007). Treatment of SBO varies with the degree of obstruction. For partial obstruction, feedings are held, IV fluids and antiemetics are initiated, and an NGT is placed for significant nausea and vomiting. Continued surveillance monitors for signs of bowel ischemia. Symptoms in most cases of partial SBO improve within 48 hours. In contrast, for most of those with complete bowel obstruction, surgery to relieve the obstruction is indicated. Colonic obstruction is rare following gynecologic surgery but carries a high mortality rate (Krstic, 2014). The colon can be obstructed by intrinsic lesions such as colon cancer or diverticulitis-related strictures or can be compressed by a

CHAPTER 42

However, following intraabdominal surgery, dysfunction of enteric neural activity typically disrupts normal propulsion. Activity first returns in the stomach and is noted typically within 24 hours. The small intestine also exhibits contractile activity within 24 hours after surgery, but normal function may be delayed for 3 to 4 days (Condon, 1986; Dauchel, 1976). Rhythmic colonic motility resumes last, at approximately 4 days following intraabdominal surgery (Huge, 2000). Passage of flatus characteristically marks this return of function, and stool passage usually follows in 1 to 2 days. Postoperative feeding is most effective when started early. It improves wound healing, promotes gut motility, decreases intestinal stasis, raises splanchnic blood flow, and stimulates reflexes that elicit GI hormone secretion to shorten postoperative ileus (Anderson, 2003; Braga, 2002; Correia, 2004; Lewis, 2001). The decision to initiate “early feeding” with liquids or with solid food has been studied prospectively (Jeffery, 1996). In patients who were given solid food as the first postoperative meal, the number of calories and amount of protein consumed on the first postoperative day were higher. In addition, the number of patients requiring diet changes to NPO (nil per os) was not statistically different (7.5 percent in regular diet and 8.1 percent in the clear diet groups). The improved tolerance and better palatability of solids makes this a reasonable option.

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pelvic mass or foreign body, such as a retained surgical sponge. An enlarged cecum found on an abdominal radiograph requires further evaluation by either a barium enema or colonoscopy. Immediate intervention is necessary when the cecal diameter exceeds 10 to 12 cm to minimize perforation risks.

■⌀ Diarrhea Transient episodes of postoperative diarrhea are not uncommon after major gynecologic surgery as the GI tract returns to its baseline motility and function. Protracted episodes and excessive amounts of diarrhea almost always stem from infection and warrant further evaluation. Stool samples are examined for ova and parasites, cultured for bacteria, and assayed for Clostridium difficile toxin. Of potential etiologies, broad-spectrum antibiotics can impair normal GI flora growth and thereby promote C difficile toxin-associated pseudomembranous colitis. If toxin is identified, oral metronidazole or vancomycin is initiated and continued for 10 to 14 days after diarrhea resolution (Cohen, 2010). Regardless of the pathogen, aggressive fluid and electrolyte replacement is critical to prevent further aberrations that can delay recovery.

URINARY COMPLICATIONS ■⌀ Oliguria Prerenal Oliguria Postoperative oliguria is defined as urine production less than 0.5 mL/kg/hr. Oliguria can be caused by a prerenal, intrarenal, or postrenal insult, and a systematic approach typically allows differentiation among these. Prerenal oliguria is a physiologic response to hypovolemia, and coexistent tachycardia and orthostatic hypotension usually reflect this volume depletion. Causes of postoperative hypovolemia are varied and include acute hemorrhage, vomiting, severe diarrhea, and inadequate intraoperative volume replacement. In response to hypovolemia, the renin-angiotensin system is activated, and antidiuretic hormone (ADH) is released to prompt reabsorption of sodium and water by the renal tubules. Prerenal oliguria is the result of this sequence. Treatment focuses on volume replacement. Thus, an accurate assessment of the patient’s fluid deficit is critical. Tallying estimated surgical blood loss and data from the intraoperative fluid logs kept by the anesthesiologist will help begin the calculations. Insensible loss during laparotomy approximates 150 mL/hr.

Intrarenal Oliguria

■⌀ Nutrition The primary goals of postoperative nutrition are to improve immune function, promote wound healing, and minimize metabolic disturbances. Despite the additional stress in the immediate postoperative period, underfeeding is accepted for a brief period (Seidner, 2006). Table 42-8 offers a summary of basic immediate postoperative metabolic needs. However, extended protein calorie restriction in a surgical patient can lead to impaired wound healing, diminished cardiac and pulmonary function, bacterial overgrowth within the GI tract, and other complications that increase hospital stays and patient morbidity (Elwyn, 1975; Kinney, 1986; Seidner, 2006). If substantial oral caloric intake is delayed for 7 to 10 days, nutritional support is warranted. In the absence of contraindications, enteral nutrition is preferred to a parenteral route, especially when infectious complications are compared (Kudsk, 1992; Moore, 1992). Other advantages of enteral nutrition include fewer metabolic disturbances and lower cost (Nehra, 2002).

Ischemic injury can lead to necrosis of the renal tubules and decreased filtration. This damage may be more common in a prerenal setting, in which the renal tubules are more vulnerable to insult from nephrotoxic agents such as NSAIDs, aminoglycosides, and contrast media. In many cases, intrarenal and prerenal oliguria can be differentiated by calculating the fractional excretion of sodium (FENa). Using sodium (Na+) and creatinine (Cr) levels from both serum and urine, this is defined as: (Urine Na+/plasma Na+) ÷ (Urine Cr/plasma Cr). A ratio 3 indicates an intrarenal insult. Another difference is urine sodium levels. In prerenal oliguria, the level is typically 80 mEq/L.

Postrenal Oliguria The most common cause of postrenal oliguria is urinary catheter obstruction. In those without a catheter, urinary retention is most

TABLE 42-8. Postoperative Nutritional Requirements Nutritional Requirements BEE in women Total calories Glucose Protein

Recommendations 65.5 + 1.9 (height in cm) + 9.6 (weight in kg) - 4.7 (age in years) 100% to 120% BEE 50–70% total caloric intake. Maintain blood glucose level 1500 mL) Maintain intraoperative normothermia Postoperative Maintain serum glucose levels 5 cm, and intraligamental location (Sizzi, 2007). Accounting for these factors, a surgeon’s expertise is the most important factor in determining approach to myomectomy.

■⌀ Consent Myomectomy can cause significant bleeding that requires transfusion. Moreover, uncontrolled hemorrhage or extensive myometrial injury during tumor removal may necessitate hysterectomy. Patients are also counseled regarding the risk of conversion to an open procedure, which ranges from 2 to 8 percent (American College of Obstetricians and Gynecologists, 2014a). Postoperatively, serosal adhesions can form and leiomyomas can recur. In some series, the risk of leiomyoma recurrence after laparoscopic myomectomy appears to be higher than in conventional myomectomy (Dubuisson, 2000; Fauconnier, 2000). As one explanation, with laparoscopic myomectomy, small, deep intramural leiomyomas may be missed because a surgeon’s tactile sensation is diminished. The use of electrosurgical energy on the uterus and challenges of laparoscopic multilayer hysterotomy closure also heighten concerns regarding uterine rupture during a subsequent pregnancy (Hurst, 2005; Parker, 2010; Sizzi, 2007). Women undergoing myomectomy who do plan to have future pregnancies are counseled regarding the possible need for cesarean delivery based on the extent of myometrial disruption during the myomectomy.

■⌀ Patient Preparation Hematologic Status and Tumor Size.╇ Many preparatory steps prior to myomectomy address associated patient anemia, anticipated intraoperative blood loss, and tumor size. First, many women who undergo this surgery are often anemic secondary to associated menorrhagia. Correction prior to surgery may include oral iron therapy, gonadotropin-releasing hormone (GnRH) agonist administration, or both. In anticipation of blood loss, a CBC and type and crossmatch for packed red blood cells is obtained. Autologous blood donation or cell saver devices may be considered if great blood loss is expected. In addition, uterine artery embolization may be performed the morning of surgery for large uteri to minimize blood loss. However, this is most often used prior to laparotomy for significantly sized uteri. GnRH agonists may be considered to decrease leiomyoma size, lower intraoperative blood loss, and decreased adhesion rates. However, loss of pseudocapsule planes around the tumors and greater risk of recurrence due to missed smaller leiomyomas is the trade-off. A fuller evidence-based discussion of these same preoperative options is found in Section 43-10 (p. 945).

Prophylaxis Few studies have addressed the benefits of preoperative antibiotic use. Iverson and coworkers (1996), in their analysis of 101 open myomectomy cases, found that although 54 percent of patients received prophylaxis, infectious morbidity was not lowered compared with patients in whom antibiotics were not used. In cases of myomectomy performed for infertility, because of the potential for tubal adhesions associated with pelvic infection, antibiotic prophylaxis is commonly used. For those in whom prophylaxis is planned, 1 g of a first- or second-generation cephalosporin is appropriate (Iverson, 1996; Periti, 1988; Sawin, 2000). The risk of bowel injury with this procedure is low, and bowel preparation is typically not required unless extensive adhesions are anticipated. Because the risk of conversion to hysterectomy is present, vaginal preparation immediately prior to surgical draping is performed. With laparoscopic gynecologic surgery, the decision to provide VTE prophylaxis factors patient- and procedure-related VTE risks (Gould, 2012). Thus, if longer operating times are anticipated or preexisting VTE risks are present, then prophylaxis as outlined in Table 39-8 (p. 836) is reasonable.

INTRAOPERATIVE ■⌀ Instruments Many instruments required for laparoscopic myomectomy are found in a standard laparoscopy instrument set. However, a laparoscopic injection needle may be required for vasopressin injection, and a suction irrigation system is frequently needed to remove blood following tumor enucleation. A myoma screw or tenaculum is helpful to create needed tissue tension and countertension for enucleation. After tumor excision, removal may be accomplished by several techniques described on page 1031. Thus, required endoscopic bags or morcellators are assembled preoperatively.

■⌀ Surgical Steps ➊╇ Anesthesia and Patient Positioning.╇ As with most laparoscopic procedures, the patient is placed in low dorsal lithotomy position in booted support stirrups after adequate general anesthesia has been delivered. A bimanual examination is completed to determine uterine size to aid port placement. Because of the risk of hysterectomy and because colpotomy may be used for tumor removal, both the vagina and abdomen are surgically prepared. A Foley catheter is

Minimally Invasive Surgery

➋╇ Trocar and Laparoscope Insertion.╇ Primary and accessory trocars are placed as described in Chapter 41 (p. 889). Port placement is customized to assist uterine manipulation, leiomyoma excision, and hysterotomy repair. Depending on uterine height, the primary port may need to be placed supraumbilically. In general, a distance of at least 4 cm above the level of the fundus is helpful to provide a global view of the uterus. Typically, at least three accessory ports are required. If use of an electric morcellator is planned, one of the cannulas should be at least 12 mm to accommodate the morcellator. After the abdomen is safely entered, a diagnostic laparoscopy is performed, and the serosal uterine surface should be inspected to identify leiomyomas to be removed. Correlating with preoperative imaging, the surgeon selects the optimal uterine incision to minimize myometrial disruption and to remove the maximum number of tumors thorough one incision.

➌╇ Use of Vasopressin.╇8-Arginine vaso-

pressin (Pitressin) is a sterile, aqueous solution of synthetic vasopressin. It is effective

in limiting uterine blood loss during myomectomy because of its ability to cause vascular spasm and uterine muscle contraction. Compared with placebo, vasopressin injection has been shown to significantly decrease blood loss during myomectomy (Frederick, 1994). Each vial of vasopressin is standardized to contain 20 pressor units/mL. Suitable doses for myomectomy include 20 U diluted in a range from 30 to 100 mL of saline (Fletcher, 1996; Iverson, 1996). Vasopressin is typically injected along the planned serosal incision(s), between the myometrium and leiomyoma capsule (Fig. 44-8.1). A laparoscopic needle placed through one of the accessory ports or a 22-gauge spinal needle placed directly through the abdominal wall is suitable for injection. Needle aspiration prior to injection is imperative to avoid intravascular injection of this potent vasoconstrictor. The anesthesiologist is informed of vasopressin injection, as a sudden increase in patient blood pressure may potentially occur following injection. Blanching at the injection site is common. The plasma half-life of this agent is 10 to 20 minutes. For this reason, injection of vasopressin is discontinued 20 minutes prior to uterine repair to allow evaluation of bleeding from myometrial incisions (Hutchins, 1996). The main risks associated with local vasopressin injection result from inadvertent intravascular infiltration and include transient increases in blood pressure, bradycardia, atrioventricular block, and pulmonary edema (Hobo, 2009; Tulandi, 1996). For these

FIGURE 44-8.1╇ Vasopressin injection beneath serosa.

reasons, patients with a medical history of cardiac or pulmonary disease may be poor candidates for vasopressin use.

➍╇ Serosal Incision.╇Because of postop-

erative adhesion formation risks, surgeons minimize the number of serosal incisions and attempt to place incisions on the anterior uterine wall. Tulandi and colleagues (1993) found for open myomectomy that posterior wall incisions result in a 94-percent adhesion formation rate compared with a 55-percent rate for anterior incisions. After vasopressin injection, hysterotomy may be performed using a Harmonic scalpel, monopolar electrode, or laser. For most patients, an anterior midline vertical uterine incision allows removal of the greatest number of leiomyomas through the fewest incisions. The length should accommodate the approximate diameter of the largest tumor. The incision depth should afford access to all leiomyomas (Fig. 44-8.2).

➎╇ Tumor Enucleation.╇ Once the hysterotomy is created, the myometrium will generally retract, and the first leiomyoma may be grasped with a laparoscopic single-toothed tenaculum. Alternatively, a leiomyoma screw can also retract tissue to create tension between the myometrium and mass (Fig. 44-8.3). Using a blunt tool or suction-irrigator tip, blunt dissection of the pseudocapsule surrounding the leiomyoma frees the tumor from the

FIGURE 44-8.2╇ Serosal incision overlying leiomyoma.

CHAPTER 44

inserted. A uterine manipulator may also be placed, including one that will allow chromotubation at the procedure’s end (p. 881). If planned, indigo carmine or methylene blue dye is mixed with 50 to 100 mL of sterile saline for injection through the cervical cannula.

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SECTION 6 FIGURE 44-8.3╇ Tumor enucleation.

adjacent myometrium. Areas requiring sharp dissection from the myometrium may be freed with any of the electrosurgical instruments that were used for the uterine incision.

➏╇ Bleeding.╇ Hemorrhage during myo-

mectomy primarily develops during tumor enucleation and positively correlates with preoperative uterine size, total weight of leiomyomas removed, and operating time (Ginsburg, 1993). Approximately two to four main arteries feed each leiomyoma and enter the tumor at unpredictable sites. For this reason, surgeons must watch for these vessels, coagulate them prior to transection when possible, and be ready to immediately fulgurate remaining bleeding vessels (Fig. 44-8.4). To avoid myo-

FIGURE 44-8.4╇ Coagulation of vascular attachments between the leiomyoma and the myometrium. metrial damage, the surgeon applies electrosurgical energy only when necessary.

➐╇ Myometrial Closure.╇ Following removal

of all tumors, redundant serosa may be excised. Laparoscopic suturing techniques described in Chapter 41 (p. 897) are used during incision reapproximation. The same general principles of myometrial closure for abdominal myomectomy are employed during laparoscopic myomectomy. In one method, for deep myometrial closure, a needle driver can be used with 0-gauge delayedabsorbable suture on a CT-2 needle in a continuous running fashion. Smaller internal myometrial incisions are closed first. The primary incision(s) is then closed in layers to

improve hemostasis and prevent hematoma formation (Fig. 44-8.5). A gauge of sufficient strength to prevent breakage during muscle approximation is selected, typically 0 to 2-0 gauge. Alternatively, barbed sutures can close myometrial defects during laparoscopic myomectomy. These obviate the need for knot tying and yield consistent wound opposition (Einarsson, 2010; Greenberg, 2008).

➑╇ Serosal Closure.╇ Closure of the sero-

sal incision using a running suture line with 4-0 or 5-0 gauge monofilament delayedabsorbable suture may help to limit adhesion formation (Fig. 44-8.6). Moreover, absorbable adhesion barriers have been shown to reduce the incidence of adhesion formation following myomectomy and may be introduced through laparoscopic ports (Ahmad, 2008). However, no substantial evidence documents that adhesion barrier use improves fertility, decreases pain, or prevents bowel obstruction (American Society for Reproductive Medicine, 2013).

➒╇ Tissue Extraction.╇Once amputated, the myomas must be removed, and options include minilaparotomy, colpotomy, and tissue morcellation. These are fully described in Section 44-10 (p. 1031) and illustrated in Chapter 41 (p. 896). ➓╇ Laparoscopically Assisted MyomeÂ�

FIGURE 44-8.5╇ Myometrial closure.

ctomy (LAM).╇Another MIS technique that may allow for safe and efficient myomectomy is LAM. The procedure is initiated as described above, and abdominal cavity assessment, uterine inspection, and incision of the serosa and myometrium are performed

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FIGURE 44-8.7╇ Tumor enucleation during laparoscopically assisted myomectomy. FIGURE 44-8.6╇ Serosal closure. laparoscopically. To aid in the laparoscopically challenging steps of myomectomy, LAM offers a hybrid approach. Specifically, tumor enucleation and uterine closure are completed through a 2- to 4-cm minilaparotomy incision placed suprapubically. With this, the pneumoperitoneum and visualization through the laparoscope are lost. Instead, application of a wound retraction system such as the Alexis or Mobius retractor provides visual access to the operative field. The uterus and leiomyoma are brought to the surface of the anterior abdominal wall and through the laparotomy incision. The tumors are then enucleated and divided through this incision (Fig. 44-8.7). This open incision also allows for conventional suturing techniques and aids suturing of large defects that require a multilayer closure (Fig. 44-8.8).

Advantages include decreased operative time, technical simplicity, improved tactile sensation to detect deep intramural leiomyomas, and easier removal of very large tumors (Prapas, 2009; Wen, 2010). Disadvantages stem mainly from the larger abdominal wall incision.

POSTOPERATIVE Following abdominal myomectomy, postoperative care follows that for any major laparoscopic surgery. Hospitalization typically varies from 0 to 1 days, and febrile morbidity and return of normal bowel function usually dictate this course (Barakat, 2011). Postoperative activity in general can be individualized, although vigorous exercise is usually delayed until 4 weeks after surgery.

FIGURE 44-8.8╇ Myometrial closure during laparoscopically assisted myomectomy.

■⌀ Fever Febrile morbidity of greater than 38.0°C is common following myomectomy (Iverson, 1996; LaMorte, 1993; Rybak, 2008). Purported causes include atelectasis, myometrial incisional hematomas, and factors released with myometrial destruction. Although fever is common following myomectomy, pelvic infection is not. LaMorte and colleagues (1993) noted only a 2-percent rate of pelvic infection in their analysis of 128 open myomectomy cases.

■⌀ Subsequent Pregnancy There are no clear guidelines as to the timing of pregnancy attempts following myomectomy. Darwish and colleagues (2005) performed sonographic examinations on 169 patients following open myomectomy. Following myometrial indicators, they concluded that wound healing is usually completed within 3 months. There are no clinical trials that address the issue of uterine rupture and therefore route of delivery of pregnancies occurring after myomectomy (American College of Obstetricians and Gynecologists, 2014a). Management of these cases requires sound clinical judgment and individualization of care. In general, large incisions or those entering the endometrial cavity favor cesarean delivery.

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44-9 SECTION 6

Laparoscopic Hysterectomy Several laparoscopic techniques have been developed for hysterectomy and vary depending on the degree of laparoscopic dissection versus vaginal surgery required to remove the uterus (Garry, 1994). These include: • Diagnostic laparoscopy prior to vaginal hysterectomy (VH) • Vaginal hysterectomy assisted by laparoscopy, that is, lysis of adhesions and/or excision of endometriosis prior to VH • Laparoscopically assisted vaginal hysterectomy (LAVH): laparoscopic dissection down to, but not including, uterine artery transection • Laparoscopic hysterectomy (LH): laparoscopic dissection, including uterine artery transection, but completion of hysterectomy vaginally • Total laparoscopic hysterectomy (TLH): complete laparoscopic excision of the uterus. The laparoscopic approach offers advantages over traditional total abdominal hysterectomy (TAH). These include significant lower analgesia requirements, shorter hospital stays, rapid recovery, greater patient satisfaction, and lower rates of wound infection and hematoma formation (Kluivers, 2007; Schindlbeck, 2008). Disadvantageously, surÂ� gical time is lengthened, although the learning curve may be a factor. TLH offers fewer advantages compare with VH. Thus, in most cases, TLH should be an alternative to TAH (American College of Obstetricians and Gynecologists, 2011; Marana, 1999; Nieboer, 2009). For all the hysterectomy types described in the following sections, plans for concurrent bilateral salpingo-oophorectomy (BSO) or for prophylactic salpingectomy are individualized. A detailed discussion of the surgical BSO is found in Chapter 43 (p. 951), whereas the advantages of risk-reducing salpingectomy are outlined in Chapter 35 (p. 738).

PREOPERATIVE ■⌀ Patient Evaluation A thorough pelvic examination and history reveal factors that help determine the optimal surgical route. Poor candidates for a vaginal approach include patients with minimal uterine descent, extensive abdominal or pelvic adhesions, a large uterus not amenable

to tissue extraction methods, adnexal pathology, and a restricted vaginal vault or contracted pelvis. Patients with these findings are generally considered for TAH and also for TLH (Schindlbeck, 2008). Of factors, uterine size and mobility are important. There is no agreed-upon size that precludes LH. However, a wide bulky uterus with minimal mobility may make it difficult to visualize vital structures, to manipulate the uterus during surgery, and to remove it vaginally. Once a patient has been deemed eligible for a laparoscopic approach, the same preoperative evaluation as for abdominal hysterectomy applies (Section 43-12, p. 950).

■⌀ Consent Similar to an open approach, possible risks of hysterectomy include increased blood loss and need for transfusion, unplanned adnexectomy, and injury to other pelvic organs, especially bladder, ureter, and bowel. The ureters are also at greater risk during LH compared with other hysterectomy approaches (Harkki-Siren, 1997, 1998). Kuno and colleagues (1998) evaluated ureteral catheterization to prevent such injury but found no benefit. Complications related specifically to laparoscopy include injury to the major vessels, bladder, and bowel during trocar placement (Chap. 41, p. 877). The risk of conversion to an open procedure is also discussed. In general, conversion to laparotomy may be necessary if exposure and organ manipulation is limited or if bleeding is encountered that cannot be controlled laparoscopically. Concurrent salpingectomy during hysterectomy may be considered to lower future rates of some epithelial ovarian cancers. For this, complete rather than partial salpingectomy is preferred. Operating time is minimally lengthened, but complication rates are not increased. Notably, the American College of Obstetricians and Gynecologists (2015) has emphasized that the planned route of hysterectomy should not be changed to complete prophylactic salpingectomy.

■⌀ Patient Preparation A blood sample is typed and crossmatched for potential transfusion. If considered, bowel preparation prior to laparoscopy may assist with colon manipulation and pelvic anatomy visualization by evacuating the rectosigmoid. Alternatively, enemas prior to surgery may be as effective for this goal. Antibiotic prophylaxis is administered within the hour prior to skin incision, and appropriate antibiotic options are listed in Table 39-6 (p. 835). Overall, the likelihood of VTE

during laparoscopic hysterectomy is significantly reduced when compared to abdominal hysterectomy (Barber, 2015). Thus, the decision to provide VTE prophylaxis should factor patient- and procedure-related VTE risks (Gould, 2012). If longer operating times are anticipated, conversion to laparotomy is a concern, or preexisting VTE risks are present, then prophylaxis as outlined in Table 39-8 (p. 836) is reasonable.

INTRAOPERATIVE ■⌀ Instruments Vessel occlusion is an important component of any hysterectomy. For this, suitable instruments include monopolar or bipolar instruments, Harmonic scalpel, stapling devices, traditional sutures, and suturing devices. Several of these can be used for dissection and hemostasis. The Harmonic scalpel is frequently used for its ability to cut with minimal smoke plume and little surrounding thermal tissue damage, although it should only be used to seal vessels up to 5 mm. Several advanced bipolar devices also offer improved vessel sealing. With various instruments, vessels measuring up to 5 mm (LigaSure, Gyrus Plasma Kinetic) and up to 7 mm (ENSEAL) can be coagulated with minimal thermal spread (Lamberton, 2008; Landman, 2003; Smaldone, 2008).

■⌀ Surgical Steps ➊╇ Anesthesia and Patient Positioning.╇ For most women, these procedures are performed in an inpatient setting under general anesthesia. The patient is placed in a low dorsal lithotomy position in booted support stirrups. A bimanual examination is completed to determine uterine size and shape to aid port placement. The abdomen and vagina are surgically prepared, a Foley catheter is inserted, and orogastric or nasogastric tube is placed. Uterine manipulators can assist with visualization. These are considered in cases in which anatomic distortion is anticipated or in those with large uteri.

➋╇ Initial Steps.╇The introductory steps for LH mirror that for other laparoscopic procedures (Chap. 41, p. 889). The number of ports and their caliber may vary, but in general, LH requires a 5- to 12-mm optical port placed at the level of the umbilicus or higher for larger uteri. Left upper quadrant entry is considered in cases of suspected periumbilical adhesions. For larger uteri, if the uterine fundus is close to or above the level of the umbilicus, the optical port is placed approximately 3 to 4 cm above the fundus for optimal viewing.

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CHAPTER 44

FIGURE 44-9.2╇ Uteroovarian ligament transection.

FIGURE 44-9.1╇ The ureter is first identified. With ovarian conservation, the round ligament is transected, and the fallopian tube is then grasped for transection. Two or three accessory ports are also placed through the lower abdominal wall. Specifically, two ports are positioned beyond the lateral borders of the rectus abdominis muscle, whereas a third may be positioned centrally and cephalad to the uterine fundus.

➌╇ Pelvic Evaluation.╇With the ports

and laparoscope inserted and the patient in Trendelenburg position, a blunt laparoscopic probe can aid organ manipulation. The pelvis and abdomen are visually explored. At this point, the decision is made whether to continue with LH or convert to laparotomy. If needed, adhesions are lysed to restore normal anatomy. The bowel is displaced from the pelvis into the abdomen to expand available operating space and viewing.

then is extended caudally and cephalad along the length of the ureter. Through this peritoneal window, the ureter is identified, and peristalsis should be noted (Fig. 44-9.1) (Parker, 2004).

➎╇ Round Ligament Transection.╇The

proximal round ligament is grasped and divided.

➏╇ Ovarian Conservation.╇If ovarian preÂ� servation is planned, proximal portions of

the fallopian tube and uteroovarian ligament are also desiccated and transected (Figs. 44-9.1 and 44-9.2). With this, the tube and ovary are freed from the uterus and can be placed in the ovarian fossa.

➐╇ Oophorectomy.╇ If removal of the

ovaries is desired, the IP ligament is grasped and pulled up and away from retroperitoneal structures. The presence and path of the ureter is identified. The IP ligament is isolated and dissected away from the ureteral course. The pedicle is coagulated, desiccated, or stapled, and then divided (Fig. 44-9.3).

➑╇ Broad Ligament Incision.╇Following transection of the round ligament, the leaves of the broad ligament fall open and

➍╇ Ureter Identification.╇ Irrigating fluids

and CO2 used for insufflation can, with time, create edema of the peritoneum and hinder viewing of retroperitoneal structures. For this reason, the ureters are identified early. The ureters can often be seen easily beneath the pelvic peritoneum, or the peritoneum may be open to identify these. In such situations, the peritoneum medial to the infundibulopelvic (IP) ligament is grasped and tented using atraumatic forceps and incised with scissors. Hydrodissection techniques may be employed. The opening in the peritoneum

FIGURE 44-9.3╇ Infundibulopelvic ligament transection.

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SECTION 6 FIGURE 44-9.4╇ Anterior leaf of broad ligament incised caudally. loose gauzy connective tissue is found between these leaves. The anterior leaf is incised sharply (Fig. 44-9.4). This incision is directed caudally and centrally to the midline above the vesicouterine fold. The posterior leaf requires incision caudally to the level of the uterosacral ligament. The loose areolar tissue separating the anterior and posterior leaves is dissected as well. Ultimately, opening the broad ligament provides access to lateral uterine anatomy, which is important for subsequent uterine artery ligation.

➒╇ Bladder Flap Development.╇After

broad ligament incision bilaterally, the vesicouterine fold is grasped with atraumatic forceps, elevated away from the underlying bladder, and incised (Fig. 44-9.5). This exposes connective tissue between the bladder and underlying uterus in the vesicouterine space. Loosely attached connections can be bluntly divided by gently pushing against the cervix and caudally to move the bladder caudad (Fig. 44-9.6). Denser tissue in the vesicouterine space is better divided sharply. With this, the tissue is elevated, and the

FIGURE 44-9.6╇ Bladder moved caudally.

FIGURE 44-9.5╇ Vesicouterine fold incised. scissors are kept close to the surface of the cervix to minimize inadvertent cystotomy risk. As this tissue is dissected, the vesicouterine space is opened. Electrosurgery may be needed to coagulate small bleeding vessels. Creating cephalad traction on the uterus with the uterine manipulator may also help with this dissection. Development of this space allows the bladder to be moved caudally and off the lower uterus and upper vagina. This mobilization of the bladder is necessary for final colpotomy and uterus removal. Of the hysterectomy types, MIS approaches have the highest risk of bladder injury, and injury occurs most frequently to the dome during this sharp or blunt dissection (Harkki, 2001). This risk is increased if prior cesarean delivery or endometriosis has left scarring.

➓╇ Uterine Artery Transection.╇After

the uterine arteries are identified, the areolar connective tissue surrounding them is grasped, placed on tension, and incised. This

skeletonizing of the vessels leads to superior occlusion of the uterine artery and vein. The arteries then are then coagulated and transected (Fig. 44-9.7). Alternatively, surgeons may elect to terminate the laparoscopic portion prior to uterine artery transection and complete artery ligation from a vaginal approach (LAVH). ╇ Vaginal Hysterectomy.╇With LH, after the uterine arteries are transected, the surgical approach is converted to that for vaginal hysterectomy and is completed as outlined in Section 43-13 (p. 957). In this transition, the patient is repositioned from low dorsal lithotomy to standard lithotomy position. ╇ Abdominal Inspection.╇After vaginal completion of the hysterectomy, attention is redirected to laparoscopic inspection of the pelvis for signs of bleeding. Before returning to the abdomen, surgeons will replace their

FIGURE 44-9.7╇ Uterine artery coagulation.

Minimally Invasive Surgery

POSTOPERATIVE Following LH, patient recovery mirrors that for vaginal hysterectomy. In general, compared with those undergoing abdominal hysterectomy, LH patients have faster return of normal bowel function, easier ambula-

tion, and decreased analgesia requirements. A clear liquid diet can be initiated the day of surgery and advanced quickly as tolerated. Postoperative complications in general mirror those for abdominal hysterectomy with the exception that superficial surgical site infection rates are lower.

CHAPTER 44

surgical gloves. Copious irrigation of the abdominopelvic cavity and confirmation of hemostasis is performed. During this inspection, intraabdominal pressures are lowered to better identify sources of bleeding. The laparoscopic procedure is terminated as outlined in Section 44-1 (p. 1005).

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Laparoscopic Supracervical Hysterectomy Laparoscopic supracervical hysterectomy (LSH) differs from total laparoscopic hysterectomy (TLH) in that the uterine corpus is amputated, but the cervix remains. Once freed, the corpus either is delivered through a posterior colpotomy or minilaparotomy incision or undergoes enclosed morcellation. Advantageously, the uterosacral and cardinal ligaments, which are important to pelvic support, are retained. It is also an excellent alternative for cases complicated by extensive scarring. Specifically, adhesions between the bladder and the lower uterine segment in the vesicouterine space or those in the cul-de-sac may make removal of the cervix difficult. Related to this, ureteral and bladder injury rates are decreased by avoiding difficult dissection. Certain contraindications to preserving the cervix are excluded prior to selecting supracervical hysterectomy. Examples include Pap test findings of high-grade cervical dysplasia; endometrial hyperplasia with atypia or endometrial cancer; or a patient at risk for noncompliance with routine cervical cancer screening.

PREOPERATIVE ■⌀ Patient Evaluation A thorough pelvic examination and history reveal factors that help determine the optimal surgical route. Uterine size and mobility are important, although there is no agreed-upon size that precludes LSH. That said, a large bulky uterus with minimal mobility may be difficult to adequately manipulate, may limit exposure during surgery, and may be challenging to extract. Once a patient has been deemed eligible for a laparoscopic approach, the same preoperative evaluation as for an abdominal hysterectomy applies (Section 43-12, p. 950).

LSH. As a result, the risk of cyclic long-term bleeding is a potential consequence. Rates quoted in early studies are as high as 24 percent but are lower in more recent investigations and range from 5 to 10 percent (Okaro, 2001; Sarmini, 2005; Schmidt, 2011; van der Stege, 1999). Techniques that resect more of the lower uterine and proximal endocervical tissue appear to decrease these long-term bleeding risks (Schmidt, 2011; Wenger, 2005). In some case, secondary excision of the cervical stump may later be required. Termed trachelectomy, this excision may be indicated if refractory long-term bleeding or significant subsequent cervical neoplasia develops postoperatively. Trachelectomy has the additional indication for residual persistent infection, although this is more anecdotal and not quoted with a consistent incidence. Overall rates of trachelectomy appear to mimic the bleeding rates above and are on a downward trend. The risk of conversion to an open procedure is also discussed. In general, conversion to laparotomy may be necessary if exposure and organ manipulation are limited or if bleeding is encountered that cannot be controlled with laparoscopic tools and techniques.

■⌀ Patient Preparation A blood sample is typed and crossmatched for potential transfusion. If considered, bowel preparation prior to laparoscopy may assist with colon manipulation and pelvic anatomy visualization by evacuating the rectosigmoid. Enemas prior to surgery may be as effective for this goal. Antibiotic prophylaxis is administered within the hour prior to skin incision, and appropriate antibiotic options are listed in Table 39-6 (p. 835). With laparoscopic gynecologic surgery, the

decision to provide VTE prophylaxis factors patient- and procedure-related VTE risks (Gould, 2012). Thus, if longer operating times are anticipated, conversion to laparotomy is a concern, or preexisting VTE risks are present, then prophylaxis as outlined in Table 39-8 (p. 836) is reasonable.

INTRAOPERATIVE ■⌀ Instruments During cervical amputation, blunt scissors, Harmonic scalpel, laser, or monopolar needle or scissors may be used to excise the corpus. Vessel occlusion is an important component of any hysterectomy. For this, suitable instruments include monopolar or bipolar instruments, Harmonic scalpel, stapling devices, traditional sutures, and suturing devices. Many of these instruments may not be readily available in all operating suites, and desired tools should be requested prior to surgery. After tumor excision, removal may be accomplished by several techniques described in Steps 3, 4, and 5. Thus, required endoscopic bags or morcellators are assembled preoperatively.

■⌀ Surgical Steps ➊╇ Initial Steps.╇ The initial surgical steps for LSH mirror those for LH, including coagulation of the uterine vessels as described in Section 44-9, Steps 1 through 10 (p. 1026). ➋╇ Uterine Amputation.╇The corpus is

amputated from the cervix at a point just below the internal cervical os and superior to the uterosacral ligaments (Fig. 44-10.1). To limit the possibility of residual endometrium, the incision is conical and extends

■⌀ Consent Similar to an open approach, possible risks of LSH include blood loss and need for transfusion, unplanned adnexectomy, and injury to other pelvic organs, especially bladder, ureter, and bowel. Complications related specifically to laparoscopy include injury to the major vessels, bladder, and bowel during trocar placement (Chap. 41, 877). Postoperatively, endometrium within the lower uterine segment may be retained with

FIGURE 44-10.1╇ Incision initiated above uterosacral ligaments.

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FIGURE 44-10.2╇ Incision extended posteriorly. down into the cervix (Figs. 44-10.2 through 44-10.4). Following amputation, adjunctive coring or ablation of the endocervical canal also may be performed to decrease the risk of postoperative cyclic bleeding (Fig. 44-10.5).

➌╇ Tissue Extraction.╇Once amputated, the uterine corpus must be removed, and options include minilaparotomy, colpotomy, and enclosed morcellation. Although

FIGURE 44-10.4╇ Excision completion.

FIGURE 44-10.3╇ Cone-shape incision extended anteriorly. described here for the uterine corpus, these methods translate to surgical removal of other specimens. First, for smaller specimens, a minilaparotomy incision ranging from 1 to 4 cm can be made to extract the corpus. Typically, a small Pfannenstiel incision is made, although a small midline vertical incision is also suitable. Both incisions are illustrated in Chapter 43 (p. 927).

For larger uteri, the addition of a tissue retrieval bag and self-retaining retractor can create a closed environment for manual morcellation. For this, a retrieval bag is initially placed into the abdomen. The bag containing the excised specimen is then brought to the surface and is fanned open outside and around the minilaparotomy incision. A selfretaining circular retractor is placed into the bag’s interior and simultaneously opened within the incision (see Fig. 44-8.7). This creates a closed environment where the specimen can be sharply divided manually with scissors or knife. Long-term data on safety and efficacy are not currently available.

FIGURE 44-10.5╇ Endocervical canal coagulated.

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SECTION 6

terior colpotomy can be created similar to that for vaginal hysterectomy and shown in Figure 41-27 (p. 896). To enter the posterior cul-de-sac, attention is turned to the vagina, and handheld retractors are placed to expose the cervix and posterior fornix. The uterine manipulator is used to anteflex the uterus, and an Allis clamp is placed on the posterior vaginal wall 2 to 3 cm from the posterior cervicovaginal junction. The Allis clamp is pulled downward to create tension across the posterior vaginal wall. The posterior vaginal vault is then cut with curved Mayo scissors, and the cul-de-sac of Douglas is entered. Alternatively, a colpotomy may be created laparoscopically by incising the posterior cul-de-sac with a monopolar instrument, a harmonic scalpel, or Endo Shears near the cervicovaginal junction. A uterine manipulator is used to reflect the uterus anteriorly to create space for the colpotomy, and a sponge stick may be used vaginally to help delineate the space. As Figure 41-28 illustrates, care is taken to avoid damage to the rectosigmoid and to the ureters, which lie lateral to the planned colpotomy. With colpotomy, pneumoperitoneum is lost immediately. If a laparoscopic instrument is already holding the specimen, this can be passed through the colpotomy and removed vaginally. For larger uteri, the addition of a tissue retrieval bag during tissue extraction can create a closed environment for scissor morcellation (Fig. 41-29). This reduces the risk of inadvertent tissue dissemination during fragmentation, although long-term safety data are needed (Cohen, 2014; Einarsson, 2014). Following extraction, the vaginal incision is closed with interrupted stitches or a running suture line using 0-gauge delayedabsorbable suture. If colpotomy is used for specimen removal, a single prophylactic dose of antibiotics is administered. Suitable agents are listed in Table 39-6 (p. 835).

➎╇ Morcellation.╇ A third method, enclosed power morcellation, is still being studied. For this, a large containment bag that can house the insufflation gas, can conform to the abdominal cavity, and can flatten against the intraperitoneal organs is introduced into the abdomen. Once in the abdomen, it is unfolded to allow the specimen and gas to be contained. Depending on the pathology, the bag may be

FIGURE 44-10.6╇ Uterine corpus morcellation. exteriorized through one abdominal port or incision or may function simply as a liner that catches any disseminated tissue during power or manual morcellation (Einarsson, 2014). During power morcellation, the corpus specimen is grasped securely with a toothed instrument such as a tenaculum and brought to the anterior abdominal wall. Because of the potential for surrounding organ injury, morcellators should not be moved toward the grasped tissue, but rather, those tissues should be brought to it (Fig. 44-10.6) (Milad, 2003). Importantly, the morcellator tip is always kept in laparoscopic view. A peeling rather than coring technique is used to pare down the mass. During this, the tenaculum holding the corpus is drawn up into the morcellator cylinder and well past the edge of the morcellating blade. This avoids metal-tometal contact, which dulls the blade. In cases of prolonged morcellation, such as with large uteri, the blade may dull. For this, the generator allows a reverse in the blade’s rotary direction. Improved cutting is usually restored with this step and generally offers enough blade life to complete the procedure. Following morcellation, the gas is released, and bag and tissue fragments are removed.

Limitations of currently available retrieval bags involve pouch size, working aperture diameter, tensile strength of the bag, and bag permeability.

➏╇ Hemostasis.╇ Points of bleeding are

coagulated, and the surgeon may elect to reapproximate the anterior vesical and posterior cul-de-sac peritoneum to cover the cervical stump using 2-0 or 0-gauge delayedabsorbable suture. Alternatively, absorbable adhesion barriers (Interceed, Seprafilm) can be placed at the hemostatic surgical stump.

➐╇ Laparoscopy Final Steps.╇Completion of the procedure follows that for general laparoscopic procedures (p. 1005).

POSTOPERATIVE Advantages of laparoscopy include a rapid return to normal diet and activities. With supracervical hysterectomy, there is no vaginal cuff that requires extended healing. Sexual intercourse, however, is delayed for 2 weeks following surgery to allow adequate internal healing.

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44-11

Total laparoscopic hysterectomy (TLH) is similar to LAVH, LSH, and LH with the exception that the procedure is completed entirely from a laparoscopic approach. After detachment, the specimen is removed vaginally or by tissue extraction techniques described on page 1031. If all factors are equal, vaginal hysterectomy is considered for women undergoing hysterectomy. Ideal candidates for TLH are those not suitable for vaginal hysterectomy (American College of Obstetricians and Gynecologists, 2011). As such, TLH is viewed as a less invasive alternative to TAH. Compared with TAH, TLH benefits include rapid recovery, shorter hospitalizations, fewer minor complications of the wound or abdominal wall, and less blood loss (Nieboer, 2009; Walsh, 2009). These benefits are dependent on a learning curve and may not be readily apparent (Schindlbeck, 2008). Moreover, longer operative times and higher rates of urinary tract injuries are negative balancing factors.

PREOPERATIVE ■⌀ Patient Evaluation A thorough pelvic examination and history reveal factors that help determine the optimal surgical route. Uterine size and mobility are important, although there is no agreedupon size that precludes TLH. That said, a wide bulky uterus with minimal mobility may be difficult to adequately manipulate, may limit exposure during surgery, and may be challenging to extract. Once a patient has been deemed eligible for a laparoscopic approach, the same preoperative evaluation as for an abdominal hysterectomy applies (Section 43-12, p. 950).

■⌀ Consent Similar to an open approach, possible risks of this procedure include increased blood loss and need for transfusion, unplanned adnexectomy, and injury to other pelvic organs, especially bladder, ureter, and bowel. Complications related to laparoscopy include entry injury to the major vessels, bladder, and bowel (Chap. 41, p. 877). The ureters are also at greater risk during laparoscopic hysterectomies compared with other hysterectomy approaches (Harkki-Siren, 1998). Kuno and colleagues (1998) evaluated the

■⌀ Patient Preparation A blood sample is typed and crossmatched for potential transfusion. If considered, bowel preparation prior to laparoscopy may assist with colon manipulation and pelvic anatomy visualization by evacuating the rectosigmoid. Alternatively, enemas prior to surgery may be as effective for this goal. Antibiotic prophylaxis is administered within the hour prior to skin incision, and appropriate antibiotic options are listed in Table 39-6 (p. 835). With laparoscopic gynecologic surgery, the decision to provide VTE prophylaxis factors patient and procedure-related VTE risks (Gould, 2012). Thus, if longer operating times are anticipated, conversion to laparotomy is a concern, or preexisting VTE risks are present, then prophylaxis as outlined in Table 39-8 (p. 836) is indicated.

PREOPERATIVE ■⌀ Instruments The same instruments that are used for the LH or LSH can be used for this procedure. In addition, a uterine manipulator that has a cupping device for delineating the cervicovaginal junction is helpful for colpotomy and also for final tissue extraction. If these are not available, a low-cost alternative is a right-angle retractor to delineate the anterior and posterior fornices for colpotomy.

■⌀ Surgical Steps ➊╇ Anesthesia and Patient Positioning.╇ For most women, TLH is performed as an inpatient procedure under general anesthesia. The patient is placed in low dorsal lithotomy position in booted support stirrups. A bimanual examination is completed to determine uterine size and shape to aid port placement. The abdomen and vagina are surgically prepared, a Foley catheter is inserted, and an orogastric or nasogastric tube is placed.

➋╇ Uterine Manipulator.╇ A uterine manipÂ� ulator with its attached cervical cup (VCare or KOH Cup with RUMI manipulator) is placed vaginally to assist uterine manipulation and delineate the cervicovaginal junction for colpotomy. To accomplish placement, the

cervical diameter and thickness are assessed. From this information, the manipulatorcup size, which is small, medium, or large, is selected. To permit manipulator insertion, the cervical os is dilated to accept a no. 8 cervical dilator. The uterus is also sounded to determine cavity depth for correct manipulator placement. The surgeon tests the balloon at the manipulator’s end for patency by filling it with air via a port at the opposite end. Once again deflated, it is passed through the cervical os to the fundus and then reinflated to hold the manipulator in place (Fig. 44-11.1A). Two stay sutures of 0-gauge delayed-absorbable suture are placed at 6 and 12 o’clock or at 3 and 9 o’clock, depending on surgeon preference. To securely anchor the cup and cervix, stitches enter the ectocervix and exit just lateral to the endocervix. Each suture end is then passed through openings in the cup base (Fig. 44-11.1B). They are then tied firmly to the cervix on the outside face of the cup (Fig. 44-11.1C). Once in position, the proximal rim of the cup will delineate the cervicovaginal junction. With the VCare, the blue vaginal cup is then advanced to join the interior cup and is locked in place by a locking knob at the manipulator’s distal end (Fig. 44-11.1D). If the KOH Cup is used, then a pneumo-occluding balloon is positioned behind the colpotomy cup.

➌╇ Initial Laparoscopic Steps.╇ The introÂ�

ductory steps for LH mirror those for other laparoscopic procedures (Chap. 41, p. 889). The number of trocars and their caliber may vary, but in general, TLH requires a 5- to 12-mm optical port, usually at the umbilicus, and two or three accessory ports placed through the lower abdominal wall. Specifically, two trocars are placed beyond the lateral borders of the rectus abdominis muscle, whereas a third may be positioned centrally and cephalad to the uterine fundus. Left upper quadrant entry is considered for initial entry in cases with suspected periumbilical adhesions.

➍╇ Pelvic Evaluation.╇ With the cannulas and laparoscope inserted and the patient in Trendelenburg position, a blunt laparoscopic probe aids bowel displacement. The pelvis and abdomen are thoroughly explored. At this point, the decision to continue with TLH or convert to laparotomy is made. If necessary, adhesions are lysed to restore normal anatomy. ➎╇ Ureter Identification.╇ Irrigating fluids

and CO2 used for insufflation can with time create edema of the peritoneum and hinder visualization of structures beneath it. For this reason, the ureters are identified early. The ureters are often easily seen retroperitoneally, or the peritoneum may be opened to locate

CHAPTER 44

Total Laparoscopic Hysterectomy

use of ureteral catheterization to prevent such injury but found no benefit. The risk of conversion to an open procedure is also discussed. In general, conversion to laparotomy may be necessary if exposure and organ manipulation is limited or if bleeding is encountered that cannot be controlled with laparoscopic tools and techniques.

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SECTION 6 A

B

C

monopolar hook, or plasma kinetic needle point. Prior to incision, the uterine manipulator is pushed cephalad to allow the cervical cupping device to displace the ureters laterally and expose the optimal location for colpotomy. Additionally, dissection within the vesicouterine space should be sufficient to mobilize the bladder caudad and away from the planned colpotomy site. With these preparatory steps completed, colpotomy is begun by placing the incising tool at the posterior cervicovaginal junction, which is delineated by the cervical cup. If a colpotomy cup is not used, a simple tool such as a right-angle retractor or sponge on a stick placed vaginally in the posterior fornix can also assist with delineating the cervicovaginal junction. The posterior vaginal wall is opened first (Fig. 44-11.3). By extending this incision, the uterosacral ligament is next transected (Fig. 44-11.4). The opposite uterosacral ligament is then divided close to the cervix. Last, the anterior colpotomy incision is created (Fig. 44-11.5). To minimize twisting and specimen disorientation, the lateral vaginal cuff points are transected last (Fig. 44-11.6). Hemostasis is generally maintained using this technique. To prevent vaginal tissue thermal damage and subsequent cuff dehiscence, surgeons use the minimum necessary amount of electrosurgery on the vaginal cuff.

➒╇ Removal of Uterus.╇The uterus is removed intact through the vaginal vault using the manipulator, unless uterine size limits this (Fig. 44-11.7). In the case of large uteri, the uterus is removed using tissue extraction techniques described on page 1031. ➓╇ Repair of the Vaginal Cuff.╇ The cuff is

closed laparoscopically with a running closure of absorbable suture, with interrupted figureof-eight sutures, or with a suturing device. For this, delayed-absorbable material is preferred, D and the uterosacral ligament is incorporated FIGURE 44-11.1╇ Uterine manipulator placement. A. Manipulator tip inserted into uterine into the closure for vaginal cuff support (Fig. cavity. B. Balloon tip inflated (left). Colpotomy cup sutured to cervix (right). C. Colpotomy 44-11.8). If traditional suture is used, one cup sutured in place. D. Blue pneumo-occluding cup advanced and locked in place. must maintain tension to sufficiently close the cuff. If using barbed suture, the procedure is modified by manufacturer’s recomthem. In such situations, the peritoneum 44-9, Steps 5 through 10 (p. 1027). These mendations to loosen stitch tension between medial to the infundibulopelvic (IP) ligament steps include transection of the round ligathe approximated cuff tissues. Moreover, is grasped and tented using atraumatic forment, conservation or excision of the adnexa, if barbed suture is used, it is recommended ceps and incised with scissors. An irrigating caudad displacement of the bladder, and to throw at least two bites in the opposite probe is used to force water beneath and elecoagulation of the uterine vessels. direction to the original direction of suture vate the peritoneum for easier incision. The ➐╇ Cardinal Ligament Transection.╇ line closure to maintain tissue tension. For opening in the peritoneum then is extended example, if closure is performed from right Following uterine artery coagulation, the cara short distance caudally and cephalad over to left, the surgeon will reach the far left end dinal ligaments are transected on each side to the suspected path of the ureter. Through this and then will place two additional stitches in reach the level of the uterosacral attachments peritoneal window, the ureter is identified the left-to-right direction prior to final suture (Fig. 44-11.2). (see Fig. 44-9.1, p. 1027) (Parker, 2004). cutting. It is advisable to cut the suture flush with the tissue to decrease bowel damage ➏╇ Round Ligament, Adnexa, and ➑╇ Colpotomy.╇ Incision at the cervicovaginal junction may be performed with Uterine Artery.╇ The initial steps for TLH risk from the barbed end. Confirmation of Harmonic scalpel, monopolar scissors, mirror those for LH, described in Section full-thickness closure is necessary to prevent

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FIGURE 44-11.2╇ Cardinal ligament incised. later cuff dehiscence. Alternatively, for those less proficient with laparoscopic suturing, the cuff may be closed vaginally after removal of the uterus as described in Section 43-13 (p. 961).

FIGURE 44-11.3╇ Posterior colpotomy. After cuff closure, irrigation and confirmation of hemostasis is performed. Intra� abdominal pressures are lowered during this inspection to better identify sources of bleeding.

╇ Laparoscopy Final Steps.╇ Completion of this operation follows that for diagnostic laparoscopy (p. 1005).

POSTOPERATIVE The advantages of a laparoscopic approach include a rapid return to normal diet and activities. Generally, the evening of the surgery, the Foley catheter is removed, diet is

FIGURE 44-11.4╇ Right uterosacral ligament transected, and colpotomy extended toward the left.

FIGURE 44-11.5╇ Anterior colpotomy.

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SECTION 6 FIGURE 44-11.7╇ Uterus and manipulator removal.

FIGURE 44-11.6╇ Joining anterior and posterior colpotomy incisions.

FIGURE 44-11.8╇ Vaginal cuff closure.

advanced, and the patient is allowed to ambulate. Oral analgesics are quickly adopted in place of parenteral options. The usual precautions for abdominal hysterectomy in regard to limitation of stress on the abdominal cavity by heavy lifting are followed. Delay of sexual activity mirrors that for abdominal hysterectomy, which is typically 6 weeks. Vaginal cuff dehiscence is a serious postoperative complication that more frequently follows laparoscopic hysterectomy approaches compared with VH or TAH (Agdi, 2009; Walsh, 2007). In most cases, the precipitating event is sexual activity in premenopausal women and increased intraabdominal pressure coupled with a weak, atrophic vagina in postmenopausal women (Lee, 2009). Patients present with vaginal bleeding or evisceration. Typical treatment includes debridement of vaginal cuff edges, reapproximation with delayed-absorbable suture, and administration of antibiotic prophylaxis. However, compromised bowel may require more extensive surgeries to repair. Preventatively, sound initial surgical technique strives to minimize electrosurgical damage during colpotomy creation and limit undue desiccation of the vaginal cuff. Approximation of all tissue planes, particularly full-thickness closure of the vaginal wall, should also be ensured. Reapproximation includes an adequate amount of viable tissue that is free of thermal effect. In addition, a two-layer closure may have an advantage over a single-layer figure-of-eight closure (Jeung, 2010).

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44-12 CHAPTER 44

Diagnostic Hysteroscopy Hysteroscopy allows an endoscopic view of the endometrial cavity and tubal ostia. Indications are varied and include evaluation of abnormal uterine bleeding, infertility, or a sonographically identified uterine cavity mass Contraindications to surgery include pregnancy and current reproductive tract infection.

PREOPERATIVE ■⌀ Consent Risks with diagnostic hysteroscopy are infrequent. Those described in Chapter 41 (p. 903) include uterine perforation and volume overload. Gas embolism is rare.

■⌀ Patient Preparation Infectious and VTE complications following hysteroscopic surgery are also rare. Accordingly, prophylaxis is typically not required (American College of Obstetricians and Gynecologists, 2013c, 2014b).

INTRAOPERATIVE ■⌀ Surgical Steps ➊╇ Anesthesia and Patient Positioning.╇ Diagnostic hysteroscopy can be performed in an outpatient setting under local anesthesia with or without intravenous sedation. Alternatively, a day-surgery setting and general anesthesia may be selected. The patient is placed in standard lithotomy position, the vagina is surgically prepared, and the bladder is drained. Because diagnostic hysteroscopy is a short procedure with little if any blood loss, CO2 or saline is typically selected for uterine distention. Trendelenburg positioning should be avoided to prevent the risk of gas embolism.

➋╇ Hysteroscope Assembly.╇For assem-

bly, the hysteroscope is placed within its outer sheath and locked into place. The light source is then attached to the endoscope. By convention, during hysteroscope insertion, the light source is kept pointing toward the floor. The distention media tubing port is attached to a port that typically lies 180 degrees away from the light source connection.

➌╇ Hysteroscope Introduction.╇ For most diagnostic hysteroscopic procedures, cervical

FIGURE 44-12.1╇ Hysteroscopic photograph of normal tubal ostia. (Used with permission from Dr. Kevin Doody.)

dilatation is not required to admit the 4- to 5-mm hysteroscope. Uterine sounding is not recommended by many because information regarding uterine depth and cavity inclination is provided by direct visualization during hysteroscope insertion. Moreover, the sound may disrupt the endometrium. This may alter endometrial anatomy prior to inspection and may cause obscuring bleeding. For diagnostic purposes, a hysteroscope equipped with a 0-, 12-, or 30-degree forward oblique-view lens is suitable. A singletoothed tenaculum is placed on the anterior cervical lip, the flow of distention medium is begun, and the hysteroscope is introduced into the endocervical canal. Pressure exerted by the medium opens the endocervical canal and allows entry of the hysteroscope. If using an angled lens, the surgeon should keep in mind that a panoramic image with a dark hole directly in the middle of the view is incorrect. The desired image would have the cervical canal at the bottom of the monitor if the light cord is directed downward, thus implying that the hysteroscope is in fact in the center of the cervical canal (Fig. 41-37, p. 902).

➍╇ Hysteroscopic Evaluation.╇As the hysteroscope is inserted, the endocervical canal is examined for abnormalities. Upon entering the cavity, the hysteroscope is held at the distal portion of the cavity to allow a panoramic evaluation. Systematically, the hysteroscope is moved to the fundus and then to the left and right to permit inspection of the tubal ostia (Fig. 44-12.1). If an angled lens is employed, the hysteroscope may remain just beyond the internal cervical os and the light cord moved in a 180-degree rotational arc to obtain a global assessment of the endometrial cavity. Some surgeons also advocate keeping the hysteroscope in the cav-

ity, evacuating it of distention medium, and evaluating the cavity in this decompressed stage. This helps identify lesions that may have been obliterated or flattened by the increased pressure of the distention medium.

➎╇ Specific Procedures.╇Following com-

plete cavity inspection, if specific lesions are identified, they are typically biopsied under direct visualization with hysteroscopic forceps. If intrauterine device (IUD) removal is planned, most are grasped by the string or stem with hysteroscopic grasping forceps and are easily extracted as the entire hysteroscope is removed. However, embedded or fragmented devices may require removal in pieces. In these instances, a sturdy portion of the IUD is firmly grasped and traction on the forceps is exerted toward the vagina. For cases in which the IUD is deeply embedded, laparoscopy can assist in identifying uterine perforation and in determining whether the device is best removed hysteroscopically or laparoscopically.

➏╇ Procedure Completion.╇At the end of the procedure, the flow of distending medium is stopped, and the hysteroscope and then tenaculum are removed. A critical step at this point, and throughout the procedure, is to note the amount of distention fluid used and the amount retrieved. These values are used to calculate the fluid deficit, which is included in the operative report.

POSTOPERATIVE Patient recovery is typically rapid and without complication and mirrors that following dilatation and curettage. Diet and activities may be resumed as desired by the patient. Spotting or light bleeding is not uncommon and typically stops within days.

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44-13 SECTION 6

Hysteroscopic Polypectomy Indications for endometrial polyp removal include abnormal uterine bleeding, infertility, and risk of malignant transformation (Chap. 8, p. 188). Hysteroscopic excision of these growths may be completed by incision of the polyp base with hysteroscopic scissors or resectoscope loop, avulsion of the polyp with hysteroscopic forceps, or retrieval using suction and morcellation. Of these, the resectoscope and morcellator offer the most versatility in managing lesions, both large and small.

PREOPERATIVE ■⌀ Patient Evaluation In many women undergoing polypectomy, preoperative transvaginal sonography or saline infusion sonography examinations have been completed. Information regarding the size, number, and location of polyps is reviewed prior to surgery. Rarely, MR imaging may be indicated to fully distinguish a presumed polyp from a submucous leiomyoma. This often helps determine if myomectomy is instead required.

■⌀ Consent The complication rates for this procedure are low and mirror that for hysteroscopy in general (Chap. 41, p. 903). Thus, bleeding, infection, and uterine perforation, and rare fluid overload and gas embolism are described.

excise small to large growths. For smaller polyps, polyp forceps may also be used through the 5F channel of the operative port.

➍╇ Resection.╇ Medium flow is begun, and

Selection.╇ Hysteroscopic morcellation may be performed with a physiologic saline solution. However, if a monopolar resectoscope is used, then a nonelectrolyte solution is required. Because of the risks for hyponatremia with sorbitol and glycine, many prefer 5-percent mannitol. Alternatively, selection of a bipolar resecting system (Versapoint) allows performance within an isotonic electrolyte medium. The basics of medium selection are further described in Chapter 41 (p. 903). As with any hysteroscopic procedure, fluid volume deficits are calculated and noted regularly during surgery.

the resectoscope is inserted into the endocervical canal under hysteroscopic visualization. Upon entering the cavity, a panoramic inspection is completed to identify the location and number of polyps. The resectoscope loop is then extended to reach behind the polyp. Electrosurgical current is applied as the loop is retracted toward the cervix to cut the polyp base. During resection, the loop should remain in view. The freed polyp is then grasped and delivered through the cervical os. This is similar to myoma excision, shown on page 1041. In cases in which the polyp is large, several passes with the loop electrode may be required for complete excision. Passes begin at the polyp tip and progress until the base is reached. The uterus is not emptied after each pass. This practice maintains visualization of the polyp and minimizes the gas embolism and perforation risks associated with multiple introductions and reintroductions of instruments into the cavity. Instead, resected segments are allowed to float within the cavity as resection continues. Once the entire polyp is excised, then the fragments are collected on a Telfa sheet as they flow out of the cavity along with the distending medium. For larger polyps, the number of floating fragments will accrue. Thus, the cavity may need to be emptied prior to complete resection to permit an unobstructed view during resection.

➌╇ Cervical Dilatation.╇ The larger diameter of an 8- or 10-mm resectoscope or morcellator typically requires dilatation up to

➎╇ Morcellation.╇ As with loop resection, distention medium flow is begun, and the morcellation unit is inserted. During morcellation,

■⌀ Surgical Steps ➊╇ Anesthesia and Patient Positioning.╇ Although simple polypectomy procedures under local analgesia in an office setting have been described, most cases are outpatient procedures performed under general or regional anesthesia. The complexity of fluid management, particularly with the use of hypotonic fluids, warrants a degree of safety that can be best provided in the operating suite. Following adequate anesthesia administration, the patient is placed in standard lithotomy position, the vagina is surgically prepared, and a Foley catheter is inserted.

➋ ╇ Media

■⌀ Patient Preparation As with most hysteroscopic procedures, polypectomy is ideally performed during the follicular phase of the menstrual cycle, when the endometrial lining is thinnest and polyps would be most easily identified. Preoperative endometrial biopsy is optional but is generally considered part of abnormal uterine bleeding evaluation for those with endometrial cancer risks (Chap. 8, p. 184). Preoperative antibiotics or VTE prophylaxis is typically not required (American College of Obstetricians and Gynecologists, 2013c, 2014b).

INTRAOPERATIVE ■⌀ Instruments A resectoscope with a 90-degree loop electrode is ideal for polyp excision. Alternatively, an intrauterine morcellator has a hollow cannula that is attached to suction and can quickly

9 mm with Pratt or similar dilators (Chap. 43, p. 967).

FIGURE 44-13.1╇ Hysteroscopic polypectomy.

Minimally Invasive Surgery

➏╇ Control of Bleeding.╇Bleeding sites may be coagulated with the same resection

loop using a coagulating current. Alternatively, for heavy bleeding, a Foley catheter balloon may be inflated to tamponade vessels. This can be left in for several hours depending on bleeding severity. This is later removed, and vaginal bleeding is reassessed.

➐╇ Instrument Removal.╇ The resectoscope

or morcellator is removed, and the surgical specimen is sent for pathologic evaluation. At the end of the procedure, the flow of distending medium is stopped, and the hysteroscope

and then tenaculum are removed. A critical step at this point, and throughout the procedure, is to note the amount of distention fluid used and retrieved to calculate the fluid deficit.

POSTOPERATIVE Recovery following polypectomy is rapid, is typically without complication, and follows that for other hysteroscopic procedures (p. 1037).

CHAPTER 44

it is important to work from the polyp tip toward the base (Fig. 44-13.1). Moreover, the mass is kept between the morcellator opening and the optics of the camera. The morcellator also has suction action. This can be used to clear blood, tissue debris, and clots during resection of large growths. Better visual acuity and the continuous retrieval of the tissue are two of the advantages to this approach.

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Atlas of Gynecologic Surgery

44-14 SECTION 6

Hysteroscopic Myomectomy For symptomatic women with submucous leiomyomas, hysteroscopic resection of these tumors may provide relief of symptoms in most cases. Candidates may include those with abnormal uterine bleeding, with dysmenorrhea, or with infertility in which leiomyomas are suspected to be contributory. Tumors selected for resection should be either submucous or intramural with a prominent submucous component. During surgery, pedunculated submucous leiomyomas may be excised similarly to polyps (p. 1038). However, tumors with an intramural component require resection with a resectoscope, morcellator, or laser.

PREOPERATIVE ■⌀ Patient Evaluation Hysteroscopic myomectomy is a safe and effective option for most women. Contraindications to surgery, however, include pregnancy, potential endometrial cancer, current reproductive tract infection, and medical conditions sensitive to fluid volume overload. Specific leiomyoma characteristics such as great size, large number, and greater degree of intramural penetration can increase the technical difficulty, complication rate, and clinical failure rate of this procedure (Di Spiezio Sardo, 2008). Thus, prior to resection, women typically undergo transvaginal sonography, saline infusion sonography (SIS), or hysteroscopy to evaluate leiomyoma characteristics. Alternatively, MR imaging can also accurately document uterine anatomy, but its expense and availability may limit its routine use. During the evaluation by SIS or hysteroscopy, leiomyomas may be grouped according to criteria developed by Wamsteker and associates (1993) and adopted by the European Society for Gynaecological Endoscopy (ESGE). Class 0: complete submucosal location Class I: greater than 50-percent submucosal component Class II: some submucosal involvement but greater than 50-percent myometrial component. These criteria help predict which leiomyomas are suitable for hysteroscopic resection. A more recent classification has also been proposed by Lasmar and coworkers (2005, 2011). Similar to the ESGE system, their evaluation

grades the degree of tumor penetration into the myometrium. But, in addition, larger tumor size, wider tumor base, tumors in the upper portion of the cavity, or those found along the lateral wall receive higher scores. For higher scores, a nonhysteroscopic technique may be the safest and most successful. Large or predominantly intramural tumors decrease clinical success rates, increase surgical risks, and increase the need for more than one surgical session to complete resection. For these reasons, many choose to resect only type 0 and I tumors and those measuring less than 3 cm (Vercellini, 1999; Wamsteker, 1993). More recent studies have reported resection of larger leiomyomas, although many need a two-step procedure and require a longer recovery (Camanni, 2010).

■⌀ Consent Complications of this procedure mirror that for hysteroscopy in general, and rates of 2 to 3 percent have been reported. Hysteroscopic myomectomy is associated with a greater risk of uterine perforation. This complication may follow cervical dilatation, but more frequently results during aggressive resection into the myometrium. Because of this risk, women are also consented for laparoscopy to assess and treat uterine or abdominal organ damage if perforation occurs. Additionally, patients planning to seek pregnancy should be aware of possible intrauterine adhesion formation following resection and of rare uterine rupture during subsequent pregnancies (Batra, 2004; Howe, 1993). During hysteroscopic myomectomy, distending medium is absorbed through venules that are opened during myometrial resection. Media is also absorbed across the peritoneum as the fluid flows in a retrograde direction through the fallopian tubes. Thus, resection of type I or II tumors or removal of large leiomyomas may be halted due to advancing fluid volume deficits. Patients are counseled that a second surgery may be required to finish resections in these cases. Fortunately, because of newer hysteroscopic morcellating tools, operating times and thus fluid deficits are decreased, even with large tumors. Last, myomectomy is effective treatment, but 15 to 20 percent of patients will eventually require reoperation. This may be hysterectomy or repeat hysteroscopic resection at a later time for either persistent or recurrent symptoms (Derman, 1991; Hart, 1999).

■⌀ Patient Preparation GnRH agonists can preoperatively shrink leiomyomas to enable resection of large tumors or allow patients to rebuild their red

cell mass before surgery (Chap. 9, p. 208). However, disadvantages include preoperative hot flashes, difficulty in cervical dilatation, increased risk of laceration or perforations, and reduced intracavitary volume, which limits instrument mobility. Thus, GnRH agonist use is individualized. To allow easier cervical dilatation and resectoscope insertion, misoprostol (Cytotec) can aid cervical softening. This practice is supported in some but not all studies, and postmenopausal women may benefit less from this pretreatment (Ngai, 1997, 2001; Oppegaard, 2008; Preutthipan, 2000). Commonly used dosing options include 200 or 400 μg vaginally or 400 μg orally once 12 to 24 hours prior to surgery. Common side effects include cramping, uterine bleeding, or nausea. Another alternative for cervical preparation prior to dilation is the use of dilute vasopressin (0.05 units/ mL). Twenty milliliters of diluted vasopressin can be injected in divided doses intracervically at 4 and 8 o’clock. This method has the advantage of working rapidly at the time of surgery if the need for preoperative preparation was not anticipated (Phillips, 1997). Precautions with this potent vasocontrictor are outlined in Step 3 on page 1023. Although the risk of postoperative infection is low, because pelvic infections can have devastating effect on future fertility, most recommend antibiotic prophylaxis prior to extensive hysteroscopic resections, as with myomectomy. Suitable agents are found in Table 39-6 (p. 835).

■⌀ Concurrent Ablation In those women with menorrhagia and with no desire for future fertility, endometrial ablation may be concurrently performed (p. 1043) (Loffer, 2005). However, because leiomyoma resection alone resolves abnormal bleeding in most women, we do not routinely perform concomitant endometrial ablation unless the patient desires hypomenorrhea.

INTRAOPERATIVE ■⌀ Instruments Hysteroscopic myomectomy can be performed using a resectoscope or hysteroscopic morcellator. Both procedures are described.

■⌀ Surgical Steps ➊╇ Anesthesia and Patient Positioning.╇ For most cases, hysteroscopic myomectomy is an outpatient procedure performed under general anesthesia. The patient is placed in standard lithotomy position, the vagina is surgically prepared, and a Foley catheter is inserted.

Minimally Invasive Surgery

➏╇ Morcellation.╇ Morcellators

currently available include Hologic’s MyoSure, Smith & Nephew’s TruClear system, and Boston Scientific’s Symphion system. In general, sharp moving blades are contained within a hollow, rigid tube. By means of a vacuum source connected to the hollow tube, tissue is suctioned into the window opening at the device tip and is shaved off by the moving blade (Fig 44-14.2). Suction also removes morcellated tissue fragments through the device cylinder and allows collection for pathologic analysis. In retrospective comparisons, hysteroscopic morcellation is faster than resectoscopy

FIGURE 44-14.1╇ Hysteroscopic resection.

➋╇ Medium Selection.╇ The choice of distending medium is dictated by the resecting tool used. Resection using a morcellator, bipolar electrosurgical loop, or laser can be performed in saline solution. Alternatively, cases using a monopolar electrosurgical loop require an electrolyte-free solution. Solution differences are discussed in Chapter 41 (p. 903). ➌╇ Cervical Dilatation.╇ Using Pratt or other suitable dilators, the surgeon dilates the cervix as shown in Chapter 43 (p. 967).

A

➍╇ Instrument Insertion.╇ The distending medium flow is begun, and the resectoscope or morcellator is inserted into the endocervical canal under direct visualization. Upon entering the endometrial cavity, a panoramic inspection is first performed to identify and assess leiomyomas. ➎╇ Resection.╇ The electrosurgical unit is

set to a continuous-wave mode (cutting). The resectoscope loop is advanced to lie behind the leiomyoma, and electric current is applied before the loop contacts the tissue. To minimize thermal injury and perforation, current is applied only as the loop is retracted and not when it is being extended. During resection, the loop should remain in view. Upon contact, the loop electrode is retracted toward the resectoscope (Fig. 44-14.1). To ensure a clean cut and complete excision of the shaved strip, current is not stopped until the entire loop is retracted. The shaved strip

B

C

FIGURE 44-14.2╇ Hysteroscopic morcellator. A. Morcellator blade retracted. Suction draws tissue into the fluted opening. B. Blade partially advanced. The blade rapidly rotates as it is advanced and retracted. C. Blade is fully advanced and slices tissue drawn into the opening.

CHAPTER 44

of smooth muscle floats within the endometrial cavity. This shaving process is repeated serially toward the myoma’s base until the tumor is removed. Although strips can be removed from the cavity after each pass, this results in a repetitive loss of uterine distention. Repeated removal and reinsertion of a resectoscope increases the risk of perforation, gas embolism, and fluid intravasation. Thus in most cases, pushing removed strips to the fundus will help to adequately clear the operative field. However, if the view becomes obstructed, a pause in resection may be required to remove these strips.

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Atlas of Gynecologic Surgery

SECTION 6

and appears easier to perform. It is associated with fewer fluid-related complications and has a shorter learning curve compared with conventional resectoscopy (Emanuel, 2005).

fully monitored throughout the procedure. The final fluid deficit is noted in the operative report.

➐╇ Intramural

ing myomectomy and will often cease as the myometrium fibers contract due to the reduction in intracavitary volume. Vessels that are more actively bleeding may be coagulated with the edge of the resecting loop, and the electrosurgical unit set to a modulating (coagulating) current. At times, a ball electrode may be required to increase the surface area over which current is delivered. Global endometrial ablation offers a similar treatment in the case of multiple bleeding sites but is not suitable for patients desiring fertility. Rarely, bleeding may be poorly controlled with electrosurgical tools. In such cases, mechanical pressure applied to bleeding vessels by a Foley balloon inflated with 5 to 10 mL of saline may be required. This

Leiomyomas.╇ During removal of leiomyomas with an intramural component, uterine perforation risks are increased if resection extends below the level of the normal myometrium. Therefore, when resection reaches this level, the surgeon should pause and wait for the surrounding myometrium to contract around the now smaller tumor. This delivers deeper portions of the leiomyoma into the uterine cavity. Diminishing the intrauterine pressure, by decreasing the fluid inflow pressure, can also help to deliver the myoma.

➑╇ Fluid Volume Deficit.╇Because of the hypervolemia risk during hysteroscopic myomectomy, fluid volume deficits are care-

➒╇ Hemostasis.╇ Bleeding is common dur-

can be left in for several hours depending on bleeding severity. The catheter is later removed, and vaginal bleeding is reassessed.

POSTOPERATIVE Recovery following myomectomy is quick and typically without complication. Patients may resume diet and activities as tolerated. Spotting or light bleeding may follow surgery for 1 to 2 weeks. For patients desiring pregnancy, conception may be attempted in the menstrual cycle after the resection, unless the leiomyoma was broadbased or had a significant intramural component. In these patients, barrier contraception is advised for three cycles. For women who fail to conceive or continue to have abnormal bleeding following resection, postoperative hysterosalpingography or hysteroscopy is recommended to evaluate for intrauterine synechiae.

Minimally Invasive Surgery

44-15

Endometrial ablation broadly describes a group of hysteroscopic procedures that destroys or resects the endometrium and leads to eumenorrhea. For many women, ablation serves as a minimally invasive and effective treatment of abnormal uterine bleeding. Within the ablation group, techniques are defined as first- or second-generation depending on their temporal introduction into use and the need for hysteroscopic skills. First-generation tools require advanced hysteroscopic skills and longer operating times and can be associated with distention medium complications, such as volume overload. These techniques include endometrial vaporization with the neodymium:yttriumaluminum-garnet (Nd-YAG) laser, rollerball electrosurgical desiccation, and endometrial resection by resectoscope. Comparing first-generation methods, it appears that all three produce similar outcomes in terms of bleeding and patient satisfaction. However, resection methods have been associated with more surgical complications, and thus desiccation methods may be preferred for women without intracavitary lesions (Lethaby, 2002; Overton, 1997). To reduce risks and required specialized training of these early ablative tools, secondgeneration nonresectoscopic methods have been introduced during the past 10 years. These tools use various modalities to destroy the endometrium but do not require direct hysteroscopic guidance. Modalities include thermal energy, cryosurgery, electrosurgery, and microwave energy.

PREOPERATIVE ■⌀ Patient Evaluation Prior to ablation, complete evaluation of abnormal uterine bleeding should be completed. Accordingly, the possibility of pregnancy, endometrial hyperplasia or endometrial cancer, and active pelvic infection is excluded. During evaluation of bleeding, transvaginal sonography (TVS), saline infusion sonography (SIS), and hysteroscopy may be used solely or in combination (Chap. 8, p. 188). However, many second-generation ablation techniques require a normal endometrial cavity, and endometrial pathology, if identified, can be treated concurrently by several of these ablative methods. Thus, SIS and hysteroscopy are more sensitive than TVS for focal lesions, and either is preferred

■⌀ Consent Patients selecting ablation should be aware of success rates relative to other treatment options for abnormal bleeding (Chap. 8, p. 197). In general, rates of decreased menstrual flow range from 70 to 80 percent and of amenorrhea, from 15 to 35 percent (Sharp, 2006). Eumenorrhea, rather than amenorrhea, is considered the treatment goal. Therefore, a patient should not undergo ablation if guaranteed amenorrhea is desired. In addition, endometrial ablation effectively destroys the endometrium and is contraindicated in those who desire future fertility. Endometrial tissue has tremendous regenerative capabilities. Therefore, premenopausal women are counseled before surgery regarding the need for adequate postoperative contraception. If pregnancy does occur, complications after ablation include prematurity, abnormal placentation, and perinatal morbidity. For this reason, many providers recommend concomitant tubal sterilization at the time of endometrial ablation (American College of Obstetricians and Gynecologists, 2013b). However, in women with tubal sterilization, cornual hematometra or postablation tubal sterilization syndrome (PATSS) can develop from bleeding from regenerated or remnant endometrium. With cornual hematometra, blood is trapped between the postoperative cornual synechiae. With PATSS, blood collects between the occluded proximal tubal stump and synechiae to cause proximal hematosalpinx. Both conditions cause associated cyclic pain. Hysterectomy is commonly required for resolution (McCausland, 2002). Following ablation, later evaluation of the endometrium for recurrent abnormal bleeding can be challenging. Namely, a Pipelle may not reach remnant endometrium, and endometrial stripe measurements may be less accurate. The American Society for Reproductive

Medicine (2008) advises against endometrial ablation in postmenopausal women because excluding malignancy in these women can be more difficult. Women with risks for endometrial cancer pose similar sampling challenges. Complications associated with ablation mirror those with operative hysteroscopy, although the risk of fluid volume overload is avoided with second-generation tools.

■⌀ Patient Preparation During hysteroscopic surgeries, bacteria in the vagina may gain access to the upper reproductive tract and peritoneal cavity. However, postablation infection is rare, and preoperative prophylactic antibiotics are generally not indicated. Because the endometrium can thicken from only a few millimeters in the early proliferative phase to deeper than 10 mm in the secretory phase, all first-generation techniques and some of the second-generation ones are ideally performed in the early proliferative phase. Otherwise, drugs that induce endometrial atrophy such as GnRH agonists, combination oral contraceptives, or progestins may be used for 1 to 2 months prior to surgery. Alternatively, curettage may be performed immediately prior to ablation.

INTRAOPERATIVE ■⌀ Surgical Steps ➊╇ Anesthesia and Patient Positioning.╇ Endometrial ablation is typically a day-surgery procedure, performed under general anesthesia. Some studies state that secondgeneration techniques may be satisfactorily completed in an outpatient setting with intravenous sedation, local anesthetic blockade, or both (Sambrook, 2010; Varma, 2010). The patient is placed in dorsal lithotomy position, and the perineum and vagina are surgically prepared.

➋╇ Selection of Distending Medium.╇ With first-generation procedures, distending medium is required and selected based on the destructive energy used as described in Chapter 41 (p. 903). In general, saline may be used for laser and bipolar electrical current, whereas monopolar tools require nonelectrolyte solutions.

➌╇ Neodymium: Yttrium-Aluminum-GarÂ�

net Laser.╇ Introduced in the 1980s, the NdYAG laser was the first ablative tool. Under direct hysteroscopic observation and uterine distention with saline, a Nd-YAG laser fiber touches the endometrium and is dragged across the endometrial surface. This creates furrows of photocoagulated tissue that are 5 to 6 mm deep (Garry, 1995; Goldrath, 1981).

CHAPTER 44

Endometrial Ablation Procedures

for preoperative evaluation. In addition, several second-generation techniques are not appropriate for large endometrial cavities. Thus, uterine depth is also assessed preoperatively by uterine sounding or sonography. Myometrial thinning from prior uterine surgery may increase the risk of damage to surrounding viscera during ablation. Therefore, women with prior transmural uterine surgery are evaluated for type and location of uterine scar. A history of prior classical cesarean delivery or of abdominal or laparoscopic myomectomy may be considered a relative contraindication to ablation. Some experts advocate the sonographic evaluation of myometrial thickness to determine whether a patient is a candidate for ablation, although no specific thickness has been established (American College of Obstetricians and Gynecologists, 2013b).

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Atlas of Gynecologic Surgery ➍╇ Transcervical Resection of the

SECTION 6

Endometrium (TCRE).╇ In addition to less expense, because of the larger loop diameter, TCRE can be completed more quickly than laser fiber ablation. The shorter procedure duration can reduce the risk of excess media absorption. This method uses a resectoscope with monopolar or bipolar electrical current to excise strips of endometrium. The resection technique is similar to that described for hysteroscopic myomectomy (p. 1040). The excised tissue strips are sent for pathologic evaluation. In cases with concurrent intrauterine pathology such as endometrial polyps or submucous leiomyomas, TCRE can excise these lesions in addition to the endometrium. However, TCRE has been associated with higher rates of perforation, especially at the cornua, where the myometrium is thinner. For this reason, many use a rollerball electrosurgical electrode in combination with TCRE, with the rollerball used in the cornua (Oehler, 2003).

➎╇ Rollerball.╇ A 2- to 4-mm ball-shaped or barrel-shaped electrosurgical electrode can be rolled across the endometrium as an effective means of vaporizing the tissue (Vancaillie, 1989). Advantages to rollerball ablation compared with TCRE include shorter operating time, less fluid absorption, and lower perforation rates. Unfortunately, it is not effective in the treatment of intracavitary lesions, and pathology specimens are not obtained.

FIGURE 44-15.1╇ ThermaChoice III Uterine Balloon Therapy System. (©Ethicon, Inc. Reproduced with permission.) Some studies, however, have demonstrated successful use in patients with submucosal leiomyomas (Soysal, 2001). Another limitation is the required pharmacologic thinning prior to thermal ablation. Alternatively, mechanical thinning can be accomplished with dilatation and curettage prior to ablation.

➐╇ Hysteroscopic Thermal Ablation.╇ Several second-generation ablation procedures require a normal uterine cavity. However, the HydroThermAblator (HTA) system allows treatment of the endometrium concurrent with submucous leiomyomas, polyps, or abnormal uterine anatomy. Another advantage of this system is that it is

performed under direct hysteroscopic visualization, allowing the surgeon to observe the endometrium being destroyed. However, the risk of external burns from circulating hot water appears to be higher using this method compared other second-generation methods (Della Badia, 2007). This tool is designed to ablate the endometrial lining of the uterus by heating an uncontained saline solution to a temperature of 90°C and recirculating it through the uterus for 10 minutes (Fig. 44-15.2). Spill through the fallopian tubes is avoided because hydrostatic pressure during the procedure remains below 55 mm Hg, which is well below pressures needed to open the tubes to the peritoneal

➏╇ Thermal Balloon Ablation.╇Several

thermal balloon ablation systems are now currently used worldwide (Fig. 44-15.1). Of these, only the ThermaChoice III Uterine Balloon Therapy System is approved for use in the United States. Other balloon systems available in other countries include the Cavaterm Plus system or the Thermablate Endometrial Ablation System. The ThermaChoice III Uterine Balloon Therapy System is a software-controlled device designed to destroy endometrial tissue using thermal energy. After cervical dilation to 5.5 mm, the Thermachoice device is inserted into the uterine cavity. Once inside the cavity, a 5-percent dextrose and water solution is instilled into a disposable silicone balloon at the tip and heated to coagulate the endometrium. During the treatment, the contained fluid within the balloon is circulated to maintain a temperature of 87°C (186°F) for 8 minutes. The balloon can be introduced without hysteroscopic assistance into the uterine cavity, and when inflated, it conforms to the cavity contour. All hot-liquid balloon devices require no advanced hysteroscopic skills, and complication rates are low (Gurtcheff, 2003; Vilos, 2004). One disadvantage is the requirement for an anatomically normal uterine cavity.

FIGURE 44-15.2╇ Hysteroscopic thermal ablation.

Minimally Invasive Surgery

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CHAPTER 44

FIGURE 44-15.3╇ Impedance-controlled electrocoagulation.

cavity. Similarly, the water seal created between the hysteroscope and internal cervical os prevents leakage of fluid into the vagina. For this reason, care is taken not to dilate the cervix to a diameter greater than 8 mm. Initially, a hysteroscope is inserted into the 7.8-mm diameter disposable HTA sheath. This combination is introduced into the endometrial cavity to enable viewing while roomtemperature saline is instilled into the uterine cavity. The fluid flow is then gradually heated and circulated to treat the endometrium. At the completion of the treatment phase, cool saline replaces the heated fluid, and the instrument is then removed (Glasser, 2003).

➑╇ Impedance-controlled ElectrocoaguÂ�

la�tion.╇ The NovaSure endo�metrial ablation system consists of a high-frequency (radiofrequency) bipolar electrosurgical generator and a single-use, fan-shaped device constructed of metal mesh. The mesh fan is designed to contour to the shape of the endometrial cavity. During treatment, an attachment provides suction to draw the endometrium and myometrium up against the mesh electrode for improved contact and to remove generated vapor (Fig. 44-15.3). The treatment time of 2 minutes results in desiccation of the endometrium. An advantage of this system is that it does not require preoperative endometrial preparation. Although Food and Drug Administration (FDA) approval studies evaluated the system in normal �uterine

FIGURE 44-15.4╇ Cryoablation.

� cavities, it has been used successfully in patients with small submucosal leiomyomas and polyps (Sabbah, 2006).

➒╇ Cryoablation.╇ In addition to ther-

mal damage, endometrial ablation can be achieved with extreme cold using the Her Option cryoablation system. Similar to the physics of cervical cryotherapy, gases compressed under pressure with this unit can generate temperatures of –100° to –120°C at the cryoprobe tip to produce an iceball. As an iceball grows, its leading edge advances through tissue, and cryonecrosis develops in those tissues reaching temperatures below –20°C (Chap. 43, p. 989). The Her Option cryoablation system contains a metal probe, which is covered by a 5.5-mm disposable cryoprobe. After dilatation of the cervix, the cryoprobe’s 1.4-inch cryotip is placed against one side of the endometrial cavity and advanced to one uterine cornu (Fig. 44-15.4). Concurrent transabdominal sonography is required to ensure accurate cryotip placement and surveillance of the increasing iceball diameter, which is seen as an enlarging hypoechoic area. The first freeze is terminated after 4 minutes or sooner, if the advancing iceball reaches to within 3 mm of the uterine serosa. The cryotip is allowed to warm, is moved from the cornu, and is redirected into the contralateral cornu. A second freeze is performed for 6 minutes or less based on iceball advancement.

➓╇ Microwave Ablation.╇ The microwave endometrial ablation (MEA) technique uses microwave energy to destroy the endometrium. During the procedure, a microwave probe is inserted until the tip reaches the uterine fundus. Once placed, the probe tip is maintained at 75° to 80°C and moved slowly from side to side. Microwave energy is spread with a maximum penetration of 6 mm over the entire uterine cavity surface. Speed is an advantage, with the entire treatment completed in 2 to 3 minutes (Cooper, 1999). Due to complications of bowel burns in patients without evidence of uterine perforation, to obtain FDA approval, the manufacturers of the MEA system recommend preoperative myometrial thickness assessment to document at least a 10-mm thickness throughout the uterus (Glasser, 2009; Iliodromiti, 2011). MEA was FDA-approved in 2003, but Microsulis discontinued worldwide sales of the MEA device in 2011.

POSTOPERATIVE Advantages to endometrial ablation include rapid patient recovery and low incidence of complications. Patients may resume normal diet and activities as tolerated. Patients may expect light bleeding or spotting during the first postoperative days as necrotic endometrial tissue is shed. A serosanguinous discharge follows for 1 week and is replaced by a profuse and watery discharge for another 1 to 2 weeks.

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Atlas of Gynecologic Surgery

■⌀ Consent

44-16 SECTION 6

Transcervical Sterilization Hysteroscopic sterilization is a minimally invasive, transcervical method to perform surgical sterilization. Currently, only two forms of transcervical sterilization are approved by the FDA. These are the Essure Permanent Birth Control system and Adiana Permanent Contraception system (Chap. 5, p. 117). However, the Adiana System is no longer manufactured, although not because of safety or efficacy concerns. Essure employs a coil device, termed a microinsert, which is inserted into the proximal section of each fallopian tube. Once in place and released from its delivery catheter, the microinsert expands to anchor itself within the fallopian tube (Fig. 44-16.1). Over time, synthetic fibers within the microinsert incite a chronic inflammatory response and a local tissue ingrowth from the surrounding tube. This ingrowth leads to complete tubal lumen occlusion, which is documented by hysterosalpingography (HSG) at 3 months following surgery. As with any permanent birth control method, candidates should be confident in their decision for sterilization. Contraindications include pregnancy or pregnancy termination within the prior 6 weeks, recent pelvic infection, known tubal occlusion, and for Essure, allergy to radiographic contrast medium or nickel.

PREOPERATIVE ■⌀ Patient Evaluation Pregnancy is excluded prior to sterilization using a serum or urine β-hCG test.

For many women, hysteroscopic sterilization is a safe and effective method of birth control. Efficacy rates are comparable with current laparoscopic sterilization rates, although long-term data are limited (Magos, 2004). With proper placement, Essure appears to have similar or superior contraceptive efficacy compared with other methods of sterilization (Levy, 2007). Effective bilateral tubal occlusion or insert placement may not be possible in all patients due to tubal ostium stenosis or spasm or an inability to visualize the ostia (Cooper, 2003). Rates of successful placement average 88 to 95 percent (Kerin, 2003; Ubeda, 2004). In general, complications of transcervical sterilization are similar to those of hysteroscopy. However, rates of fluid volume overload are low because in most cases procedure lengths are short (15 to 30 minutes) and opening of endometrial vascular channels is minimal. Uterine or tubal perforation has been noted. Rates approximate 1 to 2 percent, and in most cases, these are clinically insignificant (Cooper, 2003; Kerin, 2003). A perforated Essure insert may need to be removed from the peritoneal cavity to prevent complications. Chronic pelvic pain and insert erosion or migration can also occur.

■⌀ Patient Preparation Because menstrual bleeding and a thick endometrium can impair identification of tubal ostia, this procedure is typically performed during the early proliferative phase of the menstrual cycle. This also decreases the chance of an unidentified luteal-phase pregnancy. Preoperative analgesia may be considered and typically consists of a nonsteroidal antiinflammatory drug given 30 to 60 minutes

before the procedure. Prophylactic antibiotics are not required.

INTRAOPERATIVE ■⌀ Instruments The Essure system is disposable and comes individually wrapped. It contains a handle, delivery catheter, release catheter, delivery wire, and microinserts. Each microinsert is attached to the end of a delivery wire, which is housed within a release catheter. In turn, the release catheter is surrounded by a delivery catheter.

■⌀ Surgical Steps ➊╇ Anesthesia and Patient Positioning.╇ Transcervical sterilization can be performed in an outpatient setting under local anesthesia with or without intravenous sedation. Alternatively, a day-surgery setting using general anesthesia may be selected. The patient is placed in the standard lithotomy position, and the vagina is surgically prepared.

➋╇ Media Selection.╇For the Essure system, electrosurgery is not required, and therefore, 0.9-percent saline is commonly used to avoid the increased expense and risk of hyponatremia associated with nonelectrolyte solutions. As with any hysteroscopic procedure, accurate calculation of fluid volume deficits during the procedure is essential. The final deficit is recorded within the operative note. ➌╇ Hysteroscope Insertion.╇ Vaginal retracÂ�

tors or speculum provides access to the cervix, and a tenaculum may be used for adequate cervical traction to insert the hysteroscope. Depending on the diameter of the operative hysteroscope, standard cervical dilatation may or may not be required. A 12- to 30-degree hysteroscope is preferred to provide easy visualization of the cornua, and a 5F operating channel is needed.

➍╇ Essure Microinsert Delivery.╇Requisite

FIGURE 44-16.1╇ Microinsert placement and ingrowth of tissue.

for completion of the procedure, both tubal ostia must be visualized. To begin delivery, the outermost catheter of the system, the delivery catheter, is threaded through the operating channel of the hysteroscope. Its tip is inserted into one tubal ostium. This delivers the tightly coiled, collapsed insert into the ostium. The delivery catheter is then retracted into the Essure device handle, and an inner cannula, which is the release catheter, is now seen. As the release catheter is retracted, the microinsert begins to uncoil. Ideally, if correctly placed, three to eight coils of the microinsert trail into the endometrial cavity (Fig. 44-16.2). As a final step, a guide

Minimally Invasive Surgery

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CHAPTER 44

FIGURE 44-16.3╇ Hysterosalpingography displaying correct Essure microinsert placement. (Reproduced with permission from Bayer.) FIGURE 44-16.2╇ Hysteroscopic photograph of Essure microinsert coils within the tubal ostium. (Reproduced with permission from Bayer.) wire that is attached to the distal end of the microinsert is detached and retracted. These steps are repeated at the opposite ostium.

POSTOPERATIVE Patients typically resume normal diet and activity within the first 24 hours following surgery. Cramping is common within the first few days, and light spotting or bleeding may be noted during the week following surgery. To document complete tubal occlusion, HSG is performed at 3 months following

insertion (Fig. 44-16.3). Until this time, an alternative method of contraception should be used. Rarely, in those with correct placement, tubal occlusion may not be complete at 3 months, and a second HSG at 6 months may be required to document sterilization. Of note, although Essure microinserts are radiopaque with fluoroscopy, the Adiana silicone implant is not visible. Microinserts can be expelled. Thus, if no Essure device is identified during HSG or if 18 or more of its coils are seen trailing into the uterine cavity, then the microinsert should be replaced or

an alternative method of contraception used (Magos, 2004). Essure microinserts conduct thermal energy, and this is factored into future surgery across the proximal fallopian tube. Also, synechiae after endometrial ablation can obscure Essure HSG. Thus, ablation and Essure insertion are not performed concurrently. However, following HSG confirmation, Novasure, HTA, and Thermachoice III are thermal methods that can be performed with Essure inserts in place (Aldape, 2013). Last, MR imaging can safely be completed in those with Essure inserts.

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44-17 SECTION 6

Hysteroscopic Septoplasty Most uterine septa form from incomplete regression of the medial portion of the müllerian ducts during their fusion (Fig. 44-17.1) (Chap. 18, p. 406). These septa rarely result in infertility. However, they have been associated with malpresentation and increased rates of first- and second-trimester spontaneous abortion. This serves as the main indication for septoplasty. Before the popularity of operative hysteroscopy, septoplasty was performed abdominally and with a hysterotomy incision. Fortunately, hysteroscopic septoplasty affords MIS with decreased morbidity to the patient and uterus. Septoplasty refers to central division of the septum in a caudad-to-cephalad direction, generally with the use of hysteroscopic scissors. Bleeding is minimal due to the relative avascularity of the septum’s fibroelastic tissue, which retracts upon incision. Septum resection is performed for broader, larger septa that have wider bases. A loop resectoscope or morcellator may be preferred for this.

pregnancy and active pelvic infection, and these should be excluded.

■⌀ Consent Hysteroscopic septoplasty is a safe and effective treatment for recurrent pregnancy loss, and postoperative live birth rates approximate 85 percent (Fayez, 1987). In general, complications mirror those for operative hysteroscopy, although the risk of uterine perforation appears increased. For this reason, concurrent laparoscopy in some cases is recommended to help inform a surgeon as to the proximity of the uterine serosa. As the hysteroscope nears the fundal serosa, transillumination of the hysteroscopic light indicates the potential for uterine perforation. Accordingly, a patient may also be consented for concurrent diagnostic laparoscopy as outlined on page 1003.

■⌀ Patient Preparation Infectious and VTE complications following hysteroscopic surgery are rare. Accordingly, preoperative antibiotics or VTE prophylaxis is typically not required (American College of Obstetricians and Gynecologists, 2013c, 2014b). Misoprostol may be used preoperatively to ease cervical dilatation (p. 901).

INTRAOPERATIVE PREOPERATIVE ■⌀ Patient Evaluation Diagnosis of a septate uterus follows guidelines outlined in Chapter 18 (p. 422) and includes HSG, SIS, and transvaginal sonography. Because of the frequent association between renal and müllerian anomalies, intravenous pyelography is also performed. Finally, although a septate uterus is associated with infertility and pregnancy loss, evaluation for other causes of these two conditions is completed prior to septum excision. Contraindications to septoplasty include

■⌀ Instruments Septum incision or resection can be completed using hysteroscopic scissors, resectoscope loop, Nd-YAG laser, or mechanical morcellators. Selection is according to septum dimensions and surgeon preference.

■⌀ Surgical Steps ➊╇ Anesthesia and Patient Positioning.╇ Hysteroscopic septoplasty is typically a daysurgery procedure performed under general anesthesia. A woman is placed in standard

lithotomy position, the vagina is surgically prepared, and a Foley catheter inserted. If surveillance laparoscopy is planned, then the abdomen is also prepared.

➋╇ Medium Selection.╇The choice of distending medium is dictated by the incising tool used. Sharp incision with scissors, Nd:YAG laser, or bipolar instrument is commonly selected and can be performed in any liquid medium. Monopolar technology will require a hypotonic nonconductive medium. ➌╇ Concurrent Laparoscopy.╇ If planned concurrently, placement of the laparoscope follows the steps described in Chapter 41 (p. 889). ➍╇ Cervical Dilatation.╇A tenaculum is placed on the anterior cervical lip. Using a Pratt or other suitable dilator, the surgeon serially dilates the cervix. ➎╇ Instrument Insertion.╇ The distending medium flow is begun, and the operative hysteroscope is inserted into the endocervical canal under direct visualization. Upon entering the endometrial cavity, a panoramic inspection is first performed to identify the septum. ➏╇ Septum Incision.╇ If scissors are used, a

surgeon attempts to keep the line of incision in the anteroposterior midline. Transection begins caudally, at the septum apex, and continues cephalad toward the fundus. Bites with the scissors are taken bilaterally and are directed toward the horizontal midline (Fig. 44-17.2). During incision of the septum, drifting from the vertical midline is common. Incisions typically drift posteriorly in an anteverted uterus and anteriorly in a retroverted one. Thus, a surgeon may pause and reorient periodically. During septoplasty, incision rather than complete resection of the septum is sufficient. Septal stumps are retracted into the myometrium as the septum is transected. In most cases, the septum is relatively avascular, and cutting at its midpoint causes little bleeding. Signs that transection is complete include increasing tissue vascularity, serosal transillumination of the hysteroscope at the uterine fundus, and reaching a level in line with the tubal ostia.

➐╇ Septum Resection.╇ In some cases, the

FIGURE 44-17.1╇ Hysteroscopic photograph of uterine septum. The dark uterine cavity is seen on either side.

FIGURE 44-17.2╇ Septum incision.

septum is broad, wide, and difficult to simply incise. Thus, to achieve the desired uterine cavity, a surgeon must completely excise or resect the septum. In general, scissors may be used, but in some instances, vaporizing electrodes, loop electrodes, or morcellators are more useful. Instruments are selected according to surgeon skill and preference.

Minimally Invasive Surgery

POSTOPERATIVE Recovery following septoplasty is rapid and typically without complication. Light bleed-

ing or spotting may last 1 week or more. Patients may resume normal diet and activities as desired. Following resection, symptoms such as dysmenorrhea ultimately are greatly decreased. To stimulate endometrial proliferation and prevent adhesion reformation, oral estrogen administration has proved effective. Although several regimens can be used, we prescribe 2 mg of estradiol, orally for 30 days.

Attempts at conception are delayed for 2 to 3 months following surgery. If septum resection appeared incomplete at the time of surgery or if recurrent miscarriage or amenorrhea develops, then postoperative HSG or a second hysteroscopy may be performed. Complete removal of the septum or adhesiolysis may be required (p. 1052). With subsequent pregnancy, if the myometrium was not entered, cesarean delivery is required only for obstetric indications.

CHAPTER 44

➑╇ Procedure Completion After incision completion, the hysteroscope and tenaculum are removed. The final fluid deficit is noted in the operative report. Final steps of laparoscopy, if performed, follows those outlined in Chapter 41 (p. 1005).

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44-18 SECTION 6

Proximal Fallopian Tube Cannulation Proximal fallopian obstruction may results from pelvic inflammatory disease, intratubal debris, congenital malformations, tubal spasm, endometriosis, tubal polyps, and salpingitis isthmica nodosa. It is generally diagnosed during evaluation of infertility when documentation of tubal patency is sought. Therapeutic options have the goal of a successful pregnancy. Therefore, approaches to occlusion in this portion of the tube include tubal cannulation, surgical tubocornual anastomosis, and in vitro fertilization (IVF) (Kodaman, 2004). During cannulation, attempts are made to flush debris from within the tubes and perform chromotubation. Proximal fallopian tube cannulation may be used to treat up to 85 percent of proximal tubal obstructions, but the occlusion may recur following the surgery. It may be performed as an outpatient radiologic procedure using fluoroscopy (Papaioannou, 2003). Alternatively, cannula placement may be completed with hysteroscopic guidance (Confino, 2003). If a hysteroscopic approach is selected, laparoscopy is typically used concurrently. This allows evaluation and treatment of both proximal and distal tubal disease and provides identification of tubal perforation by the cannulating guide wire if this occurs.

PREOPERATIVE

assessed by concurrent laparoscopic examination of the perforated tube. In most cases, patients with combined proximal and distal tubal disease are best managed with IVF. As discussed in Chapter 9 (p. 224), hydrosalpinges, when present, can lower IVF success rates and are typically removed. Thus, consideration of and consent for salpingectomy should accompany plans for proximal tubal cannulation.

concurrent laparoscopy is typically an outpatient procedure performed under general anesthesia. The patient is placed in standard lithotomy position, the abdomen and vagina are surgically prepared, and a Foley catheter is inserted.

■⌀ Patient Preparation

➌╇ Laparoscopy.╇ The laparoscope is inserted

The risk of pelvic infection is low. However, because adhesions following such infection can have damaging effects on fallopian tube health, patients are given either a first- or second-generation cephalosporin prior to surgery. In addition, misoprostol may be used preoperatively to aid cervical softening and hysteroscope insertion.

INTRAOPERATIVE ■⌀ Instruments Fallopian tubes may be cannulated with a catheter system displayed in Figure 44-18.1. This system contains an outer cannula, inner cannula, and inner guide wire. The preset bend of the outer cannula aids placement of both the inner cannula and guide wire into the tubal ostium. Once the inner cannula has been threaded into the proximal fallopian tube, the guide wire is removed. The inner cannula, now emptied of the guide wire, can be used to flush debris from the fallopian tube and allow chromotubation, which is visualized laparoscopically (Fig. 19-9, p. 441).

■⌀ Surgical Steps

■⌀ Patient Evaluation

➊╇ Anesthesia and Patient Positioning.╇

Proximal tubal occlusion is typically identified with HSG during evaluation of female infertility. To avoid disrupting an early pregnancy, preoperative β-hCG testing is warranted in most patients. Although this procedure may be performed at any time during the menstrual cycle, the early proliferative phase offers the advantage of a thinner endometrium to allow easy identification of tubal ostia and avoids disruption of an early luteal-phase pregnancy.

Hysteroscopic tubal cannulation with

➋╇ Medium Selection.╇ No electrosurgery

is required for tubal cannulation, thus saline is the preferred medium. as described in Chapter 41 (p. 889).

➍╇ Cervical Dilatation.╇ Because a smaller

diameter operative hysteroscope is required for tubal cannulation, cervical dilatation may not be required. If needed, it is performed as described in Chapter 43 (p. 967).

➎╇ Hysteroscope Insertion.╇ The flow of saline is begun, and a 0- or 30-degree hysteroscope is inserted. A panoramic inspection of the entire cavity is performed, and the tubal ostia are identified.

➏╇ Tubal Cannulation.╇ The catheter sys-

tem is threaded through an operating port of the hysteroscope. Under direct visual guidance, the outer catheter is advanced and placed at one of the tubal ostia. The inner catheter is then threaded approximately 2 cm into the proximal fallopian tube (Fig. 44-18.2). The guide wire is removed.

➐╇ Tubal Flushing.╇The inner catheter is

flushed with water-soluble dye. Indigo carmine dye or methylene blue can be diluted and used. However, current indigo carmine shortages may favor methylene blue use. Either agent is diluted into 50 to 100 mL of sterile saline for injection. The laparoscope is positioned to allow inspection of the distal tube to note the presence or absence of dye spill.

■⌀ Consent In addition to general complications associated with hysteroscopy and laparoscopy, patients undergoing proximal tubal cannulation are informed of the small risk of tubal perforation. Fortunately, because the guide wire measures only 0.5 mm in diameter, tubal damage is rarely significant and can be

FIGURE 44-18.1╇ Hysteroscopic tubal cannulation catheter.

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1051

If ➑╇ Concurrent Procedures.╇

distal tubal adhesions are noted, laparoscopic lysis of adhesions may be concurrently performed.

Completion.╇ Following cannulation, the hysteroscope and cervical tenaculum are removed. Laparoscopy is completed as described in Chapter 41 (p. 1005).

POSTOPERATIVE

FIGURE 44-18.2╇ Tubal cannulation.

Recovery from hysteroscopic tubal cannulation and laparoscopy is typically quick and uncomplicated. Patients may resume diet, activity, and attempts at conception as desired.

CHAPTER 44

➒╇ Procedure

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44-19 SECTION 6

Lysis of Intrauterine Adhesions Intrauterine adhesions, also called synechiae, may develop following uterine curettage (Fig. 44-19.1). Less commonly, they may result from pelvic radiation, tuberculous endometritis, or endometrial ablation. The presence of these adhesions, also termed Asherman syndrome, may lead to hypo- or amenorrhea, pelvic pain, and infertility or pregnancy loss. Treatment goals include surgical recreation of normal intrauterine anatomy and prevention of adhesion reformation. Surgery involves hysteroscopic transection rather than excision of adhesions. Thus, thin adhesions can usually be lysed using only gentle blunt force from the hysteroscopic sheath. However, dense adhesions usually require hysteroscopic division with scissors or laser. Postsurgical pregnancy and live delivery rates are markers of surgical success, and these rates vary depending on the thickness of adhesions and degree of cavity obliteration. For this reason, various adhesion classification systems are useful to help predict the success of adhesiolysis for a given woman (Al-Inany, 2001).

PREOPERATIVE ■⌀ Patient Evaluation Although hysteroscopy and saline infusion sonography (SIS) can both accurately identify adhesions, HSG is preferred initially,

because it allows concurrent assessment of tubal patency. However, after adhesions have been noted, diagnostic hysteroscopy is recommended to assess the thickness and density of these bands (Fayez, 1987). Additionally, completion of fertility assessment, including semen analysis and assessment of ovulation, is recommended prior to surgery to help predict chances of conception following the procedure.

■⌀ Consent In general, hysteroscopic adhesiolysis is an effective tool to correct menstrual disorders and improve fertility in women with uterine adhesions (Valle, 2003). Although overall cumulative delivery rates in those with no other fertility factors ranges from 60 to 70 percent, lower rates generally are associated with more severe disease (Pabuccu, 1997; Zikopoulos, 2004). In addition, pregnancies following surgery may be complicated by placental implantation abnormalities or by preterm labor (Dmowski, 1969; Pabuccu, 2008). The complications mirror those for operative hysteroscopy. However, the risk of uterine perforation may be increased. For this reason, patients should also be consented for diagnostic laparoscopy.

■⌀ Patient Preparation Infectious and VTE complications following hysteroscopic surgery are rare. Accordingly, preoperative antibiotics or VTE prophylaxis is typically not required (American College of Obstetricians and Gynecologists, 2013c, 2014b). Additionally, intraoperative intracervical dilute vasopressin or preoperative misoprostol may be used to soften the cervix and ease dilatation (Chap. 41, p. 901).

INTRAOPERATIVE ■⌀ Surgical Steps ➊╇ Anesthesia and Patient Positioning.╇ Hysteroscopic lysis of adhesions is typically a day-surgery procedure performed under general anesthesia. The patient is placed in standard lithotomy position, the vaginal is surgically prepared, and a Foley catheter inserted.

➋╇ Medium Selection.╇ The choice of dis-

tending medium is dictated by the tool used. Sharp transection with scissors, Nd:YAG laser, or bipolar instrument can be performed in any liquid medium. However, thick adhesions often require resection rather than division, and they are severed close to the myometrium. Thus, the potential for creation of large denuded areas and fluid intravasation is great. Accordingly for many surgeons, 0.9-percent saline is preferred because hyponatremia less likely if fluid overload does develop.

➌╇ Concurrent Laparoscopy.╇ There is an increased risk of uterine perforation in those with more severe obliteration of the cavity. Thus, adjunctive laparoscopy may guide surgeons as to instrument proximity to the uterine serosa. The decision to use a laparoscope is individualized, and its placement follows the steps described in Chapter 41 (p. 889). ➍╇ Cervical Dilatation.╇Using Pratt or

other suitable dilators, the surgeon serially dilates the cervix as described in Chapter 43 (p. 967).

➎╇ Instrument Insertion.╇The

distending medium flow is begun, and the operative hysteroscope is inserted into the endocervical canal under direct visualization. Upon entering the endometrial cavity, a panoramic inspection is first performed to identify adhesions.

➏╇ Approach to Lysis.╇ In general, a systematic approach to adhesiolysis begins with either blunt or sharp disruption of the most central adhesions and moves gradually to reach the most lateral. The size and qualities of adhesions may vary. Thin endometrial adhesions can usually be disrupted with gentle blunt force from the hysteroscopic sheath alone. More commonly, myofibrous and fibrous adhesions are denser and may require complete resection. Adhesiolysis is continued until the endometrial cavity is restored to normal and the tubal ostia are seen. Importantly, procedures may require termination prior to this, if significant fluid volume deficits are reached. FIGURE 44-19.1╇ Hysteroscopic photograph of intrauterine adhesions. (Used with permission from Dr. Kevin Doody.)

➐╇ Chromotubation.╇ At completion of adhesiolysis, transcervical chromotubation

Minimally Invasive Surgery and greater pregnancy rates in women using the balloon. If a Foley balloon is placed, antibiotic prophylaxis with either doxycycline 100 mg orally twice daily or other appropriate antibiotic is recommended.

➑╇ Mechanical Uterine Cavity DistenÂ�

Recovery from hysteroscopic resection is rapid and typically without complication. Patients may resume normal activities and diet as tolerated. To stimulate endometrial proliferation and prevent reformation of adhesions, oral estrogen administration has proved effective. Although several regimens can be used, we

tion.╇ This option has been used to prevent treated areas from adhering following surgery. Either a copper IUD, placed for 3 months, or an 8F pediatric Foley catheter balloon, used for 10 days, may be chosen. In a comparison of the two, Orhue and colleagues (2003) noted fewer new adhesions

POSTOPERATIVE

prescribe 2 mg of estradiol, orally for 30 days following adhesiolysis. Conjugated equine estrogen (Premarin) 1.25 mg may also be used. Following IUD insertion, 6 to 8 weeks of oral estrogen supplementation is given. New adhesions can form following adhesiolysis. In their early stages, these bands are thinner and thus more amenable to successful resection. For this reason, another hysteroscopy or HSG is typically performed at 3 months following the initial resection. If significant new adhesions are found, a second surgical lysis of adhesions is planned. To allow adequate uterine healing, attempts at pregnancy by the patient are delayed for 2 to 3 months.

CHAPTER 44

is performed to document tubal patency. Chromotubation may be performed by injecting dye into the uterine cavity through a uterine manipulator during simultaneous laparoscopy. Alternatively, tubal cannulation as described previously may be performed to establish tubal patency (p. 1050).

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REFERENCES SECTION 6

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Chan LM, Westhoff CL: Tubal sterilization trends in the United States. Fertil Steril 94(1):1, 2010 Cohen SL, Einarsson JI, Wang KC, et al: Contained power morcellation within an insufflated isolation bag. Obstet Gynecol 124(3):491, 2014 Confino E: Tubal Catheterization and falloposcopy. In Bieber EJ, Loffer FD (eds): Hysteroscopy, Resectoscopy, and Endometrial Ablation. Boca Raton, Parthenon Publishing Group, 2003, p 113 Cooper JM, Carignan CS, Cher D, et al: Microinsert nonincisional hysteroscopic sterilization. Obstet Gynecol 102:59, 2003 Cooper KG, Bain C, Parkin DE: Comparison of microwave endometrial ablation and transcervical resection of the endometrium for treatment of heavy menstrual loss: a randomised trial. Lancet 354:1859, 1999 Dabirashrafi H: Complications of laparoscopic ovarian cauterization. Fertil Steril 52:878, 1989 Darwish AM, Nasr AM, El Nashar DA: Evaluation of postmyomectomy uterine scar. J Clin Ultrasound 33:181, 2005 Della Badia C, Nyirjesy P, Atogho A: Endometrial ablation devices: review of a manufacturer and user facility device experience database. J Minim Invasive Gynecol 14:436, 2007 Derman SG, Rehnstrom J, Neuwirth RS: The long-term effectiveness of hysteroscopic treatment of menorrhagia and leiomyomas. Obstet Gynecol 77:591, 1991 Di Spiezio Sardo A, Mazzon I, Bramante S, et al: Hysteroscopic myomectomy: a comprehensive review of surgical techniques. Hum Reprod Update 14(2):101, 2008 Dmowski WP, Greenblatt RB: Asherman’s syndrome and risk of placenta accreta. Obstet Gynecol 34:288, 1969 Donesky BW, Adashi EY: Surgically induced ovulation in the polycystic ovary syndrome: wedge resection revisited in the age of laparoscopy. Fertil Steril 63:439, 1995 Doss BJ, Jacques SM, Qureshi F, et al: Extratubal secondary trophoblastic implants: clinicopathologic correlation and review of the literature. Hum Pathol 29:184, 1998 Dubuisson JB, Fauconnier A, Babaki-Fard K, et al: Laparoscopic myomectomy: a current view. Hum Reprod Update 6:588, 2000 Einarsson JI, Cohen SL, Fuchs N, et al: In-bag morcellation. J Minim Invasive Gynecol 21(5): 951, 2014 Einarsson JI, Vellinga TT, Twijnstra AR, et al: Bidirectional barbed suture: an evaluation of safety and clinical outcomes. JSLS 14(3):381, 2010 Emanuel MH, Wamsteker K: The Intra Uterine Morcellator: a new hysteroscopic operating technique to remove intrauterine polyps and myomas. J Minim Invasive Gynecol 12:62, 2005 Farquhar C, Brown J, Marjoribanks J, et al: Laparoscopic drilling by diathermy or laser for ovulation induction in anovulatory polycystic ovary syndrome. Cochrane Database Syst Rev 6:CD001122, 2012 Farquhar CM: The role of ovarian surgery in polycystic ovary syndrome. Best Pract Res Clin Obstet Gynaecol 18:789, 2004 Fauconnier A, Chapron C, Babaki-Fard K, et al: Recurrence of leiomyomata after myomectomy. Hum Reprod Update 6:595, 2000 Fayez JA, Mutie G, Schneider PJ: The diagnostic value of hysterosalpingography and hysteroscopy in infertility investigation. Am J Obstet Gynecol 156:558, 1987 Fedele L, Bianchi S, Tozzi L, et al: Intramesosalpingeal injection of oxytocin in conservative laparoscopic treatment for tubal

pregnancy: preliminary results. Hum Reprod 13:3042, 1998 Fletcher H, Frederick J, Hardie M, et al: A randomized comparison of vasopressin and tourniquet as hemostatic agents during myomectomy. Obstet Gynecol 87:1014, 1996 Franchi M, Ghezzi F, Beretta P, et al: Microlaparoscopy: a new approach to the reassessment of ovarian cancer patients. Acta Obstet Gynaecol Scand 79:427, 2000 Franklin RR: Reduction of ovarian adhesions by the use of Interceed. Ovarian Adhesion Study Group. Obstet Gynecol (3):335, 1995 Frederick J, Fletcher H, Simeon D, et al: Intramyometrial vasopressin as a haemostatic agent during myomectomy. BJOG 101:435, 1994 Garry R, Reich H, Liu CY: Laparoscopic hysterectomy: definitions and indications. Gynaecol Endosc 3:1, 1994 Garry R, Shelley-Jones D, Mooney P, et al: Six hundred endometrial laser ablations. Obstet Gynecol 85:24, 1995 Ginsburg ES, Benson CB, Garfield JM, et al: The effect of operative technique and uterine size on blood loss during myomectomy: a prospective, randomized study. Fertil Steril 60:956, 1993 Giuliani A, Panzitt T, Schoell W, et al: Severe bleeding from peritoneal implants of trophoblastic tissue after laparoscopic salpingostomy for ectopic pregnancy. Fertil Steril 70:369, 1998 Glasser MH: Practical tips for office hysteroscopy and second-generation “global” endometrial ablation. J Minim Invasive Gynecol 16(4):384, 2009 Glasser MH, Zimmerman JD: The Hydro ThermAblator system for management of menorrhagia in women with submucous myomas: 12- to 20-month follow-up. J Am Assoc Gynecol Laparosc 10:521, 2003 Goldrath MH, Fuller TA, Segal S: Laser photovaporization of endometrium for the treatment of menorrhagia. Am J Obstet Gynecol 140:14, 1981 Gooden MD, Hulka JF, Christman GM: Spontaneous vaginal expulsion of Hulka clips. Obstet Gynecol 81:884, 1993 Gould MK, Garcia DA, Wren SM, et al: Prevention of VTE in nonorthopedic surgical patients: Antithrombotic Therapy and Prevention of Thrombosis, 9th ed: American College of Chest Physicians Evidence-Based Clinical Practice Guidelines. Chest 141(2 Suppl):e227S, 2012 Greenberg JA, Einarsson JI: The use of bidirectional barbed suture in laparoscopic myomectomy and total laparoscopic hysterectomy. J Minim Invasive Gynecol 15(5):621, 2008 Greenblatt EM, Casper RF: Adhesion formation after laparoscopic ovarian cautery for polycystic ovarian syndrome: lack of correlation with pregnancy rate. Fertil Steril 60:766, 1993 Gürgan T, Kisnisci H, Yarali H, et al: Evaluation of adhesion formation after laparoscopic treatment of polycystic ovarian disease. Fertil Steril 56(6):1176, 1991 Gürgan T, Urman B, Aksu T, et al: The effect of short-interval laparoscopic lysis of adhesions on pregnancy rates following Nd:YAG laser photo-coagulation of polycystic ovaries. Obstet Gynecol 80(1):45, 1992 Gurtcheff SE, Sharp HT: Complications associated with global endometrial ablation: the utility of the MAUDE database. Obstet Gynecol 102:1278, 2003 Harkki P, Kurki T, Sjoberg J, et al: Safety aspects of laparoscopic hysterectomy. Acta Obstet Gynaecol Scand 80:383, 2001 Harkki-Siren P, Sjoberg J, Makinen J, et al: Finnish national register of laparoscopic hysterectomies:

Minimally Invasive Surgery uate the viability of hysteroscopic surgical treatment—preliminary report. J Minim Invasive Gynecol 12(4):308, 2005 Lasmar RB, Xinmei Z, Indman PD, et al: Feasibility of a new system of classification of submucous myomas: a multicenter study. Fertil Steril 95(6):2073, 2011 Lee CK, Hansen SL: Management of acute wounds. Surg Clin North Am 89(3):659, 2009 Lethaby A, Hickey M: Endometrial destruction techniques for heavy menstrual bleeding: a Cochrane review. Hum Reprod 17:2795, 2002 Levy B, Levie MD, Childers ME: A summary of reported pregnancies after hysteroscopic sterilization. J Minim Invasive Gynecol 14(3):271, 2007 Liu CD, McFadden DW: Laparoscopic port sites do not require fascial closure when nonbladed trocars are used. Am Surg 66(9):853, 2000 Loffer FD: Improving results of hysteroscopic submucosal myomectomy for menorrhagia by concomitant endometrial ablation. J Minim Invasive Gynecol 12(3):254, 2005 Magos A, Chapman L: Hysteroscopic tubal sterilization. Obstet Gynecol Clin North Am 31:705, 2004 Malacova E, Kemp A, Hart R, et al: Long-term risk of ectopic pregnancy varies by method of tubal sterilization: a whole-population study. Fertil Steril 101(3):728, 2014 Malkawi HY, Qublan HS: Laparoscopic ovarian drilling in the treatment of polycystic ovary syndrome: how many punctures per ovary are needed to improve the reproductive outcome? J Obstet Gynaecol Res 31:115, 2005 Marana R, Busacca M, Zupi E, et al: Laparoscopically assisted vaginal hysterectomy versus total abdominal hysterectomy: a prospective, randomized, multicenter study. Am J Obstet Gynecol 180:270, 1999 Marana R, Luciano AA, Muzii L, et al: Reproductive outcome after ovarian surgery: suturing versus nonsuturing of the ovarian cortex. J Gynecol Surg 7:155, 1991 Mazdisnian F, Palmieri A, Hakakha B, et al: Office microlaparoscopy for female sterilization under local anesthesia: a cost and clinical analysis. J Reprod Med 47:97, 2002 McCausland AM, McCausland VM: Frequency of symptomatic cornual hematometra and postablation tubal sterilization syndrome after total rollerball endometrial ablation: a 10-year follow-up. Am J Obstet Gynecol 186(6):1274, 2002 Mercorio F, Mercorio A, Di Spiezio Sardo A, et al: Evaluation of ovarian adhesion formation after laparoscopic ovarian drilling by second-look minilaparoscopy. Fertil Steril 89(5):1229, 2008 Milad MP, Sokol E: Laparoscopic morcellatorrelated injuries. J Am Assoc Gynecol Laparosc 10:383, 2003 Mosesson MW: The roles of fibrinogen and fibrin in hemostasis and thrombosis. Semin Hematol 29(3):177, 1992 Muzii L, Bianchi A, Croce C, et al: Laparoscopic excision of ovarian cysts: is the stripping technique a tissue-sparing procedure? Fertil Steril 77:609, 2002 Naether OG, Fischer R, Weise HC, et al: Laparoscopic electrocoagulation of the ovarian surface in infertile patients with polycystic ovarian disease. Fertil Steril 60:88, 1993 Ngai SW, Chan YM, Ho PC: The use of misoprostol prior to hysteroscopy in postmenopausal women. Hum Reprod 16:1486, 2001 Ngai SW, Chan YM, Liu KL, et al: Oral misoprostol for cervical priming in non-pregnant women. Hum Reprod 12(11):2373, 1997

Nieboer TE, Johnson N, Lethaby A, et al: Surgical approach to hysterectomy for benign gynaecological disease. Cochrane Database Syst Rev 3:CD003677, 2009 Oehler MK, Rees MC: Menorrhagia: an update. Acta Obstet Gynaecol Scand 82:405, 2003 Okaro EO, Jones KD, Sutton C: Long term outcome following laparoscopic supracervical hysterectomy. BJOG 108:1017, 2001 Oppegaard KS, Nesheim BI, Istre O, et al: Comparison of self-administered vaginal misoprostol versus placebo for cervical ripening prior to operative hysteroscopy using a sequential trial design. BJOG 115(5):663, 2008 Orhue AA, Aziken ME, Igbefoh JO: A comparison of two adjunctive treatments for intrauterine adhesions following lysis. Int J Gynaecol Obstet 82:49, 2003 Overton C, Hargreaves J, Maresh M: A national survey of the complications of endometrial destruction for menstrual disorders: the MISTLETOE study (Minimally invasive surgical techniques— Laser, endothermal or endoresection). BJOG 104:1351, 1997 Pabuccu R, Atay V, Orhon E, et al: Hysteroscopic treatment of intrauterine adhesions is safe and effective in the restoration of normal menstruation and fertility. Fertil Steril 68:1141, 1997 Pabuccu R, Onalan G, Kaya C, et al: Efficiency and pregnancy outcome of serial intrauterine device-guided hysteroscopic adhesiolysis of intrauterine synechiae. Fertil Steril 90(5):1973, 2008 Palter SF: Microlaparoscopy under local anesthesia and conscious pain mapping for the diagnosis and management of pelvic pain. Curr Opin Obstet Gynecol 11:387, 1999 Papaioannou S, Afnan M, Girling AJ, et al: Diagnostic and therapeutic value of selective salpingography and tubal catheterization in an unselected infertile population. Fertil Steril 79:613, 2003 Parker WH: Total laparoscopic hysterectomy and laparoscopic supracervical hysterectomy. Obstet Gynecol Clin North Am 31:523, 2004 Parker WH, Einarsson J, Istre O, et al: Risk factors for uterine rupture after laparoscopic myomectomy. J Minim Invasive Gynecol 17(5):551, 2010 Pati S, Cullins V: Female sterilization: evidence. Obstet Gynecol Clin North Am 27:859, 2000 Penfield AJ: The Filshie clip for female sterilization: a review of world experience. Am J Obstet Gynecol 182:485, 2000 Periti P, Mazzei T, Orlandini F, et al: Comparison of the antimicrobial prophylactic efficacy of cefotaxime and cephazolin in obstetric and gynaecological surgery: a randomised multi-centre study. Drugs 35:133, 1988 Peterson HB, Xia Z, Hughes JM, et al: The risk of pregnancy after tubal sterilization: findings from the U.S. Collaborative Review of Sterilization. Am J Obstet Gynecol 174:1161, 1996 Peterson HB, Xia Z, Wilcox LS, et al: Pregnancy after tubal sterilization with bipolar electrocoagulation. U.S. Collaborative Review of Sterilization Working Group. Obstet Gynecol 94:163, 1999 Phillips DR, Nathanson HG, Milim SJ, et al: The effect of dilute vasopressin solution on the force needed for cervical dilatation: a randomized controlled trial. Obstet Gynecol 89(4):507, 1997 Prapas Y, Kalogiannidis I, Prapas N: Laparoscopy vs laparoscopically assisted myomectomy in the management of uterine myomas: a prospective study. Am J Obstet Gynecol 200(2):144.e1, 2009

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a review and complications of 1165 operations. Am J Obstet Gynecol 176:118, 1997 Harkki-Siren P, Sjoberg J, Tiitinen A: Urinary tract injuries after hysterectomy. Obstet Gynecol 92:113, 1998 Harrison MS, DiNapoli MN, Westhoff CL: Reducing postoperative pain after tubal ligation with rings or clips: a systematic review and meta-analysis. Obstet Gynecol 124(1):68, 2014 Hart R, Molnar BG, Magos A: Long-term followup of hysteroscopic myomectomy assessed by survival analysis. BJOG 106:700, 1999 Hobo R, Netsu S, Koyasu Y, et al: Bradycardia and cardiac arrest caused by intramyometrial injection of vasopressin during a laparoscopically assisted myomectomy. Obstet Gynecol 113(2 Pt 2):484, 2009 Howe RS: Third-trimester uterine rupture following hysteroscopic uterine perforation. Obstet Gynecol 81:827, 1993 Hurst BS, Matthews ML, Marshburn PB: Laparoscopic myomectomy for symptomatic uterine myomas. Fertil Steril 83:1, 2005 Hutchins FL Jr: A randomized comparison of vasopressin and tourniquet as hemostatic agents during myomectomy. Obstet Gynecol 88:639, 1996 Iliodromiti S, Murage A: Multiple bowel perforations requiring extensive bowel resection and hysterectomy after microwave endometrial ablation. J Minim Invasive Gynecol 18(1):118, 2011 Iverson RE Jr, Chelmow D, Strohbehn K, et al: Relative morbidity of abdominal hysterectomy and myomectomy for management of uterine leiomyomas. Obstet Gynecol 88:415, 1996 Jeung IC, Baek JM, Park EK, et al: A prospective comparison of vaginal stump suturing techniques during total laparoscopic hysterectomy. Arch Gynecol Obstet 282(6):631, 2010 Kerin JF, Cooper JM, Price T, et al: Hysteroscopic sterilization using a micro-insert device: results of a multicentre phase II study. Hum Reprod 18:1223, 2003 Kesby GJ, Korda AR: Migration of a Filshie clip into the urinary bladder seven years after laparoscopic sterilisation. BJOG 104:379, 1997 Kluivers KB, Hendriks JC, Mol BW, et al: Quality of life and surgical outcome after total laparoscopic hysterectomy versus total abdominal hysterectomy for benign disease: a randomized, controlled trial. J Minim Invasive Gynecol 14(2):145, 2007 Kodaman PH, Arici A, Seli E: Evidence-based diagnosis and management of tubal factor infertility. Curr Opin Obstet Gynecol 16:221, 2004 Kuno K, Menzin A, Kauder HH, et al: Prophylactic ureteral catheterization in gynecologic surgery. Urology 52:1004, 1998 Lajer H, Widecrantz S, Heisterberg L: Hernias in trocar ports following abdominal laparoscopy: a review. Acta Obstet Gynaecol Scand 76:389, 1997 Lamberton GR, Hsi RS, Jin DH, et al: Prospective comparison of four laparoscopic vessel ligation devices. J Endourol 22(10):2307, 2008 LaMorte AI, Lalwani S, Diamond MP: Morbidity associated with abdominal myomectomy. Obstet Gynecol 82:897, 1993 Landman J, Kerbl K, Rehman J, et al: Evaluation of a vessel sealing system, bipolar electrosurgery, harmonic scalpel, titanium clips, endoscopic gastrointestinal anastomosis vascular staples and sutures for arterial and venous ligation in a porcine model. J Urol 169(2):697, 2003 Lasmar RB, Barrozo PR, Dias R, et al: Submucous myomas: a new presurgical classification to eval-

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Preutthipan S, Herabutya Y: Vaginal misoprostol for cervical priming before operative hysteroscopy: a randomized, controlled trial. Obstet Gynecol 96:890, 2000 Rybak EA, Polotsky AJ, Woreta T, et al: Explained compared with unexplained fever in postoperative myomectomy and hysterectomy patients. Obstet Gynecol 111(5):1137, 2008 Sabbah R, Desaulniers G: Use of the NovaSure Impedance Controlled Endometrial Ablation System in patients with intracavitary disease: 12-month follow-up results of a prospective, single-arm clinical study. J Minim Invasive Gynecol 13:467, 2006 Sambrook AM, Jack SA, Cooper KG: Outpatient microwave endometrial ablation: 5-year followup of a randomised controlled trial without endometrial preparation versus standard day surgery with endometrial preparation. BJOG 117(4):493, 2010 Sarmini OR, Lefholz K, Froeschke HP: A comparison of laparoscopic supracervical hysterectomy and total abdominal hysterectomy outcomes. J Minim Invasive Gynecol 12(2):121, 2005 Sawin SW, Pilevsky ND, Berlin JA, et al: Comparability of perioperative morbidity between abdominal myomectomy and hysterectomy for women with uterine leiomyomas. Am J Obstet Gynecol 183:1448, 2000 Schindlbeck C, Klauser K, Dian D, et al: Comparison of total laparoscopic, vaginal and abdominal hysterectomy. Arch Gynecol Obstet 277(4):331, 2008 Schmidt T, Eren Y, Breidenbach M: Modifications of laparoscopic supracervical hysterectomy technique significantly reduce postoperative spotting. J Minim Invasive Gynecol 18, 81, 2011 Schytte T, Soerensen JA, Hauge B, et al: Preoperative transcervical analgesia for laparoscopic sterilization with Filshie clips: a doubleblind, randomized trial. Acta Obstet Gynaecol Scand 82:57, 2003 Seifer DB: Persistent ectopic pregnancy: an argument for heightened vigilance and patient compliance. Fertil Steril 68:402, 1997 Sharp HT: Assessment of new technology in the treatment of idiopathic menorrhagia and uterine leiomyomata. Obstet Gynecol 108(4):990, 2006 Sizzi O, Rossetti A, Malzoni M, et al: Italian multicenter study on complications of laparoscopic myomectomy. J Minim Invasive Gynecol (4): 453, 2007

Smaldone MC, Gibbons EP, Jackman SV: Laparoscopic nephrectomy using the EnSeal Tissue Sealing and Hemostasis System: successful therapeutic application of nanotechnology. JSLS 12(2):213, 2008 Soderstrom RM, Levy BS, Engel T: Reducing bipolar sterilization failures. Obstet Gynecol 74:60, 1989 Soysal ME, Soysal SK, Vicdan K: Thermal balloon ablation in myoma-induced menorrhagia under local anesthesia. Gynecol Obstet Invest 51:128, 2001 Spandorfer SD, Sawin SW, Benjamin I, et al: Postoperative day 1 serum human chorionic gonadotropin level as a predictor of persistent ectopic pregnancy after conservative surgical management. Fertil Steril 68:430, 1997 Strowitzki T, von Wolff M: Laparoscopic ovarian drilling (LOD) in patients with polycystic ovary syndrome (PCOS): an alternative approach to medical treatment? Gynecol Surg 2:71, 2005 Tan BL, Chong HC, Tay EH: Migrating Filshie clip. Aust N Z J Obstet Gynaecol 44:583, 2004 Toaff R, Toaff ME, Peyser MR: Infertility following wedge resection of the ovaries. Am J Obstet Gynecol 124:92, 1976 Tulandi T, Beique F, Kimia M: Pulmonary edema: a complication of local injection of vasopressin at laparoscopy. Fertil Steril 66:478, 1996 Tulandi T, Guralnick M: Treatment of tubal ectopic pregnancy by salpingotomy with or without tubal suturing and salpingectomy. Fertil Steril 55:53, 1991 Tulandi T, Murray C, Guralnick M: Adhesion formation and reproductive outcome after myomectomy and second-look laparoscopy. Obstet Gynecol 82:213, 1993 Ubeda A, Labastida R, Dexeus S: Essure: a new device for hysteroscopic tubal sterilization in an outpatient setting. Fertil Steril 82:196, 2004 Valle RF: Intrauterine adhesion. In Bieber EJ, Loffer FD (eds): Hysteroscopy, Resectoscopy, and Endometrial Ablation. Boca Raton, Parthenon Publishing Group, 2003, p 93 Vancaillie TG: Electrocoagulation of the endometrium with the ball-end resectoscope. Obstet Gynecol 74:425, 1989 van der Stege JG, van Beek JJ: Problems related to the cervical stump at follow-up in laparoscopic supracervical hysterectomy. JSLS 3(1):5, 1999 Varma R, Soneja H, Samuel N, et al: Outpatient Thermachoice endometrial balloon ablation:

long-term, prognostic and quality-of-life measures. Gynecol Obstet Invest 70(3):145, 2010 Vercellini P, Zaina B, Yaylayan L, et al: Hysteroscopic myomectomy: long-term effects on menstrual pattern and fertility. Obstet Gynecol 94:341, 1999 Vilos GA: Hysteroscopic and nonhysteroscopic endometrial ablation. Obstet Gynecol Clin North Am 31:687, 2004 Visco AG, Advincula AP: Robotic gynecologic surgery. Obstet Gynecol 112(6):1369, 2008 Walsh CA, Sherwin JR, Slack M: Vaginal evisceration following total laparoscopic hysterectomy: case report and review of the literature. Aust N Z J Obstet Gynaecol 47(6):516, 2007 Walsh CA, Walsh SR, Tang TY, et al: Total abdominal hysterectomy versus total laparoscopic hysterectomy for benign disease: a meta-analysis. Eur J Obstet Gynecol Reprod Biol 144(1):3, 2009 Wamsteker K, Emanuel MH, de Kruif JH: Transcervical hysteroscopic resection of submucous fibroids for abnormal uterine bleeding: results regarding the degree of intramural extension. Obstet Gynecol 82:736, 1993 Wen KC, Chen YJ, Sung PL, et al: Comparing uterine fibroids treated by myomectomy through traditional laparotomy and 2 modified approaches: ultraminilaparotomy and laparoscopically assisted ultraminilaparotomy. Am J Obstet Gynecol 202(2):144.e1, 2010 Wenger JM, Spinosa JP, Roche B, et al: An efficient and safe procedure for laparoscopic supracervical hysterectomy. J Gynecol Surg 21(4): 155, 2005 Wiseman DM, Trout JR, Franklin RR, et al: Metaanalysis of the safety and efficacy of an adhesion barrier (Interceed TC7) in laparotomy. J Reprod Med 44(4):325, 1999 Wiskind AK, Toledo AA, Dudley AG, et al: Adhesion formation after ovarian wound repair in New Zealand White rabbits: a comparison of ovarian microsurgical closure with ovarian nonclosure. Am J Obstet Gynecol 163:1674, 1990 Wrigley LC, Howard FM, Gabel D: Transcervical or intraperitoneal analgesia for laparoscopic tubal sterilization: a randomized, controlled trial. Obstet Gynecol 96:895, 2000 Zikopoulos KA, Kolibianakis EM, Platteau P, et al: Live delivery rates in subfertile women with Asherman’s syndrome after hysteroscopic adhesiolysis using the resectoscope or the VersaPoint system. Reprod Biomed Online 8:720, 2004

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CHAPTER 45

Surgeries for Pelvic Floor Disorders

45-1: Diagnostic and Operative Cystoscopy and Urethroscopy. . . . . 45-2: Burch Colposuspension.

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45-3: Tension-free Vaginal Tape. . . . . .

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45-4: Transobturator Tape Sling. . . . . . . . . .

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45-13: Anterior Colporrhaphy. .

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45-16: Perineorrhaphy. .

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45-17: Abdominal Sacrocolpopexy.. . .

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45-18: Minimally Invasive Sacrocolpopexy.. . . . . . . . .

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45-1

Diagnostic and Operative Cystoscopy and Urethroscopy During gynecologic surgery, the lower urinary tract may be injured. Thus, diagnostic cystoscopic evaluation is often warranted following procedures in which the bladder and ureters

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45-21: Sacrospinous Ligament Fixation.. . .

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45-9. Urethral Diverticulum Repair. .

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45-12: Sacral Neuromodulation. .

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45-19: Vaginal Uterosacral Ligament Suspension. . . . . .

45-20: Abdominal Uterosacral Ligament Suspension. . . . . . . . . 1110

45-15. Posterior Colporrhaphy. . .

. . . . .

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45-11: Martius Bulbocavernosus Fat Pad Flap. 1083

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45-6: Urethral Bulking Injections. . . . . . . . . . . . 45-8: Midurethral Sling Release. . . . .

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. . . . . . . .

45-14: Abdominal Paravaginal Defect Repair. .

45-5: Pubovaginal Sling. .

45-7: Urethrolysis.

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45-10: Vesicovaginal Fistula Repair.. . . . . . .

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45-22: McCall Culdoplasty. .

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45-23: Abdominal Culdoplasty Procedures. . 45-24: Colpocleisis. 45-25: Anal Sphincteroplasty..

45-26: Rectovaginal Fistula Repair.. . . . . . References. .

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have been placed at risk. Additionally, operative cystoscopy is within the scope of many gynecologists for the passage of ureteral stents, lesion biopsy, and foreign-body removal. Of these, ureteral stenting may be indicated to delineate the ureter’s course during cases with abnormal pelvic anatomy or to assess ureteral patency following gynecologic surgery. Rigid and flexible cystoscopes are available, although in gynecology, a rigid scope is typically used. A cystoscope is composed of an outer sheath, bridge, endoscope, and obturator. The sheath contains one port for

fluid infusion and a second port for fluid egress. For office cystoscopy, a sheath measuring 17F affords greater comfort. However, for operative cases, a 21F or wider-diameter cystoscope is preferred to allow rapid fluid infusion and easier instrument and stent passage. The sheath’s end tapers, and in women- with a narrow urethral meatus, an obturator can be placed inside the sheath to create a rounded tip for smooth introduction. In selected instances, gentle dilation of the external urethral opening using narrow cervical dilators is needed prior to sheath introduction. The next piece,

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toscopy is performed to document ureteral patency, ½ to 1 ampule of indigo carmine is administered intravenously prior to the procedure to aid visualization of urine jets. Less commonly, methylene blue may be used instead but carries the risk of methemoglobinemia in patients with glucose-6-phosphate dehydrogenase deficiency. However, its use may increase given current shortages of indigo carmine (American Urogynecologic Society, 2014a).

➍╇ Cystoscopy.╇ The anterior urethral wall

0 degree

30 degree

70 degree

FIGURE 45-1.1╇ Cystoscopic optical views. the bridge, attaches to the proximal portion of the sheath and allows coupling between the endoscope and sheath. Additional ports are present on the bridge and are generally used to introduce stents or instruments. Several endoscope viewing angles are available and include 0-, 30-, and 70-degree optical views (Fig. 45-1.1). Zero-degree endoscopes are used for urethroscopy. For cystoscopy, a 70-degree endoscope is superior for providing the most comprehensive view of the lateral, anterior, and posterior walls; trigone; and ureteral orifices. To achieve a comparable view, a 30-degree endoscope requires additional manipulation. However, a 30-degree endoscope does offer advantages and allows surgeons greater flexibility as it can be used for either urethroscopy or cystoscopy during a given examination. For operative cystoscopic cases in which instruments are passed down the sheath, a 30-degree endoscope should be used because with 0- and 70-degree endoscopes, operative instruments generally lie outside the field of view.

standard lithotomy position with the legs positioned in stirrups. For office cystoscopy, 2-percent lidocaine jelly is instilled into the urethra 5 to 10 minutes prior to cystoscope insertion. For operative procedures, an additional 50 mL of 4-percent lidocaine solution may be instilled via catheter into the bladder. The perineum and urethral meatus are surgically prepared prior to urethral manipulation.

➋╇ Distention Media.╇The bladder must

be adequately distended to fully visualize all surfaces, and for diagnostic purposes, saline or sterile water is suitable. To ensure adequate medium flow, an infusion bag is elevated significantly above the level of the symphysis. The volume needed may vary but is reached when bladder walls are not collapsing inward. Overdistending the bladder is also avoided as it may result in temporary urinary retention. If the bladder is distended beyond its capacity, excess fluid will leak out the urethral meatus and around the cystoscope rather than rupturing the bladder, which is rare.

is sensitive, and discomfort may result if the sheath’s tapered edge is directed anteriorly. Thus, the sheath is inserted into the urethral meatus with the bevel directed posteriorly. Immediately following insertion into the external urethral opening, medium flow is begun. The cystoscope is advanced toward the bladder under direct visualization. Often, in women with anterior wall prolapse, the urethra slopes downward, and the scope tip is similarly directed. During the procedure, the cystoscope can be steadied with one hand holding the sheath near the urethral meatus (Fig. 45-1.2).

➎╇ Bladder Inspection.╇Upon entry into

the bladder, the cystoscope is slowly withdrawn until the bladder neck is identified. The cystoscope is then advanced and rotated 180 degrees so that the light-source cable is pointing down. In this position, an air bubble is noted at the dome, which provides orientation for the remainder of the cystoscopic examination. When a 70- or 30-degree scope is used, the cystoscope is angled upward to view this bubble. To maintain orientation during rotation, the camera is held static while the light cord and cystoscope are rotated (Fig. 45-1.3). As the distended bladder assumes a spherical shape, it is systematically inspected on each side from apex to internal urethral opening. First, to view the entire left side of the bladder, the cystoscope and light cable are rotated

PREOPERATIVE Prior to office cystoscopy, urinary tract infection (UTI) is excluded to avoid upper tract infection. If diagnostic cystoscopy is performed properly, complications are rare. Of these, infection is the most common and results from the significant incidence of bacteriuria following cystoscopy.

INTRAOPERATIVE ■⌀ Surgical Steps ➊╇ Anesthesia and Patient Positioning.╇ Cystoscopy may be performed in low or

FIGURE 45-1.2╇ Cystoscope steadied during procedure.

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➑╇ To Exclude Ureteral Obstruction.╇ A

approximately 90 degrees in a clockwise fashion. The surgeon’s left hand is used to prevent awkward hand crossing. To examine the bladder wall from 12 to 3 o’clock positions, the cystoscope is initially angled upward and then pans down to the 3 o’clock position, at which point the scope is parallel to the floor. Next, inspection from 3 to 6 o’clock requires gradual downward angling of the cystoscope. The left ureteral orifice is generally found at the 5 o’clock position, approximately 3 to 4 cm proximal to the internal urethral opening. During bladder inspection, especially the base or posterior wall, digital elevation of the anterior vaginal wall to lift the bladder floor and orifices to a more anatomically correct position is beneficial if pelvic organ prolapse is present. Moreover, accentuated angling may be needed. Once the left orifice is noted, further subtle clockwise rotation of the cystoscope along the interureteric ridge permits isolation of the right ureteral orifice. The cystoscope is again rotated so that the light-source cable is again pointing downward and the bubble at the dome is again identified. For the right side, counterclockwise movement of the cystoscope and light cord with the surgeon’s right hand averts awkward hand crossing. The right wall of the bladder is then similarly examined. While horizontal to the floor, the cystoscope is withdrawn to the bladder neck and then angled downward to provide a second view of the trigone and both ureteral orifices and to document ureteral patency. Brisk urine flow, with or without indigo carmine, should be seen from each orifice. Peristalsis of the ureteral orifice alone, without flow, is insufficient to document patency. Moreover, scant flow may indicate partial ureteral obstruction and merits further evaluation. The average time to efflux approximates 10 minutes but can be longer. After 20 minutes, absent jets bilaterally more often reflect hypovolemia and resolve with fluid bolus.

Following this bolus, 10 to 20 mg of furosemide (Lasix) can be added as needed to promote diuresis. Underlying renal disease may also delay efflux. During inspection, a unilateral jet is more concerning for ureteral injury. To evaluate, the surgeon can attempt to thread a stent through the ureteral orifice and into the ureter, as described in Step 8. Repair of ureteral injury is described in Chapter 40 (p. 868).

➏╇ Operative Cystoscopy.╇ For this procedure, the operative instrument (biopsy or grasping forceps or scissors) is introduced through the operating port, until viewed at the end of the cystoscope. Prior to instrument insertion, a rubber adapter cap is positioned over the operating port to create a watertight seal with the operative instrument. Once in view, the instrument and cystoscope are moved together as a unit toward the area of interest. ❼╇ Ureteral Stenting.╇Ureteral stents may be placed at several junctures during surgery. They may be inserted at the beginning of surgery and left through its duration to define anatomy in cases in which the ureter is at high surgical risk of injury. Alternatively, they may be threaded intraoperatively to document ureteral patency and exclude injury. Finally, ureteral stents may be positioned and left in place at the conclusion of surgery if ureteral injury is suspected or identified. Duration of postoperative stenting is variable and based on indications. Ureteral stents are available in various sizes, and those ranging from 4 to 7 F are commonly used. Stents vary in length from 20 to 30 cm, and a 24-cm length is appropriate for most adults. Generally, open-ended or whistle-tip stents are used to delineate anatomy or to exclude obstruction. Double- or single-pigtail stents are used in situations that require prolonged ureteral drainage.

➒╇ To Delineate Anatomy.╇ For this pur-

pose, the stent is advanced until resistance is met, which indicates that the renal pelvis has been reached. The stent is tied securely to the transurethral catheter and drains into the cystoscopy drape. At the conclusion of surgery, the stent is removed.

➓╇ Ureteral Stenting.╇In cases in which

a ureteral stent is required postoperatively, a double-pigtail stent is used. The proximal coil of the stent prevents renal pelvis injury, and the distal coil secures placement in the bladder. For placement, a guide wire is first threaded into the ureteral orifice and passed to the renal pelvis. The pigtail stent is then placed over the guide wire and advanced by a pusher device until the distal end enters the bladder. The guide wire is removed, allowing the ends to coil in the renal pelvis and

CHAPTER 45

FIGURE 45-1.3╇ Orientation during cystoscopy is maintained by holding the camera steady while the light cord and cystoscope are rotated.

4F to 6F open-ended or whistle-tip stent is threaded through the operating channel of a 30-degree cystoscope and into the field of view. By advancing both the stent and cystoscope toward the orifice, the stent is passed into the ureteral orifice. After the stent has entered the opening, it is manually threaded and advanced. Alternatively, an Albarrán bridge may be used. This specialized bridging sheath allows deflection and guidance of a stent into an orifice. Once inserted, a stent is advanced past the level of suspected obstruction. If a stent threads easily, obstruction is excluded. In most gynecologic surgery, this would not be higher than the pelvic brim, which should be 12 to 15 cm from the ureteral orifice in adults. When passing a stent, undue pressure is avoided during advancement to avoid ureteral perforation. Efflux should be documented after stent removal. If ureteral transection or stricture is suspected from the above steps, a cone-tip ureteral catheter is inserted, and dye is injected into the distal ureter to locate extravasation or point of narrowing. This is done intraoperatively with fluoroscopic guidance. If dye flows to the renal pelvis easily and no extravasation noted, ureteral injury is unlikely. If gross blood issues from an orifice prior to ureteral manipulation, the ureter may be partially transected. Even if good efflux is noted, many insert and maintain a doubleJ stent for approximately 4 weeks. In such cases, a computed tomography (CT) urogram or renal sonogram is completed 4 to 12 weeks after stent removal to exclude stricture. After the above interrogations, absent efflux from one orifice may uncommonly reflect a long-standing unilateral nonfunctioning kidney. For this, postoperative CT and nuclear scan can be selected.

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bladder, respectively. Correct upper coil positioning is confirmed intraoperatively using fluoroscopy or plain film radiograph. Stents are usually kept for 2 to 8 weeks depending on the injury identified or suspected. They are generally removed in the office with cystoscopic guidance. ╇ Biopsy and Foreign Body Removal.╇ Mucosal lesions can be biopsied with minimal risk or discomfort to the patient. A biopsy instrument is introduced into the cystoscope’s operating port and brought into the operative field. With the instrument in view, the cystoscope is moved directly to the lesion. Biopsy is performed, and the cystoscope and instrument are withdrawn through the urethra together. In this way, a biopsy specimen is not pulled through the sheath and possibly lost. Bleeding is usually minor and will stop by itself. For brisk bleeding, electrosurgical coagulation can be used if a nonconducting solution was selected as the distention medium. As described in Chapter 41 (p. 903), electrolyte solutions such as saline cannot be used with monopolar electrosurgery. These solutions conduct current, thus dissipating the energy and thereby rendering the instrument useless. Foreign bodies, such as stones, are removed using the same technique as biopsy. The instrument is used to grasp the foreign body and then removed together with the cystoscope. ╇ Suprapubic Teloscopy.╇ This is a technique used to visualize the bladder through an abdominal approach. We have found suprapubic teloscopy to be valuable when the ureters must be assessed during a difficult cesarean delivery or during a laparotomy in which a woman has not been positioned to allow easy cystoscopic access to the urethra. The bladder is distended using the transurethral Foley catheter until the bladder wall is tense. A wide purse-string using 2-0 gauge absorbable suture is then placed

FIGURE 45-1.4╇ Suprapubic teloscopy.

at the bladder dome, taking deep bites into the bladder muscularis (Fig. 45-1.4). The two suture ends are elevated but held loosely. A small stab incision is then made in the purse-string’s center, and a cystoscope is introduced into the bladder. This incision is preferably made in the retropubic or extraperitoneal portion of the bladder dome to minimize risk of fistula formation. For suprapubic teloscopy, a 30-degree cystoscope is most effective. The two suture ends are then pulled up and held tightly to prevent the escape of distending fluid. To allow visualization of the trigone and ureteral orifices, the Foley bulb is deflated but left in place. Indigo carmine or methylene blue is given if necessary to document ureteral efflux. If the ureteral orifices still cannot be visualized, the bladder incision is extended inferiorly into the retropubic portion to allow direct visualization. At the conclusion

of teloscopy, the cystoscope is removed, and the purse-string suture is tied, closing the cystotomy.

POSTOPERATIVE Office cystoscopy does not require specific postoperative management except for prophylactic antibiotics to cover common urinary tract pathogens. At our institution, we prescribe a single perioperative dose. With operative cystoscopy, hematuria may develop, but it generally clears within a few days and is considered significant only if associated with symptomatic anemia. With long-term ureteral stenting, additional complications may include ureteral spasm, which typically presents as back pain. Stone formation and stent fragmentation are less common but can occur if length of catheterization exceeds 8 weeks.

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Abdominal antiincontinence procedures at� tempt to correct stress urinary incontinence (SUI) by stabilizing the anterior vaginal wall and urethrovesical junction in a retropubic location. Specifically, the Burch procedure, also known as retropubic urethropexy, uses the strength of the iliopectineal ligament (Cooper ligament) to stabilize the anterior vaginal wall and anchor the wall to the musculoskeletal framework of the pelvis (Fig. 38-24, p. 817). The Burch colposuspension is usually performed through a Pfannenstiel or Cherney incision. In the past 20 years, some have introduced laparoscopic approaches that use suture or mesh to affix the paravaginal tissues to Cooper ligament (Ankardal, 2004; Zullo, 2004). Compared with open Burch colposuspension, laparoscopic approaches offer similar postoperative rates of subjective cure, despite some evidence for poorer objective outcomes (Carey, 2006; Dean, 2006). Longer-term results will also define its role.

PREOPERATIVE

■⌀ Patient Preparation The American College of Obstetricians and Gynecologists (2014) recommends antibiotic prophylaxis prior to urogynecologic surgery, and appropriate choices mirror those for hysterectomy (Table 39-6, p. 835). For all patients undergoing major gynecologic surgery, thromboprophylaxis is also recommended (Table 39-8, p. 836). Bowel preparation is based on surgeon preference and on concurrent surgeries planned.

INTRAOPERATIVE ■⌀ Surgical Steps ➊╇ Anesthesia and Patient Positioning.╇ Burch colposuspension may be performed under general or regional anesthesia as an

inpatient procedure. The patient is placed supine with legs in booted support stirrups in low lithotomy position. The abdomen and vagina are surgically prepared, and a Foley catheter is inserted.

➋╇ Abdominal Incision.╇ A low Pfannenstiel or Cherney incision is performed (Section 43-2, p. 929). Surgery in the space of Retzius (retropubic space) is easier to accomplish if the incision is placed low on the abdomen, approximately 1 cm above the upper border of the pubic symphysis. If hysterectomy, culdoplasty, or other intraperitoneal procedure is planned, the peritoneum is entered and concurrent surgery completed prior to colposuspension. If the procedure is done in isolation, fascia of the anterior abdominal wall muscles and then transversalis fascia are incised, but entry into the peritoneal cavity is not required to reach the retropubic space. ➌╇ Entry into the Space of Retzius.╇ Between the lower anterior abdominal wall peritoneum and pubic bone lies an avascular plane, that is, the space of Retzius. To enter this retropubic space, the fingers of one hand gently dissect along the cephalad surface of the pubic bone. Alternatively, gentle sponge dissection can be used to open this space (Fig. 45-2.1). Loose areolar tissue is found behind the symphysis within this space and easily separates from the bone. However,

■⌀ Patient Evaluation Prior to surgery, patients undergo complete urogynecologic evaluation. Although not required for uncomplicated demonstrable SUI, urodynamic testing can help differentiate stress and urgency incontinence and assess bladder capacity and voiding patterns (Chap. 23, p. 526). Many women with SUI may also have associated pelvic organ prolapse. For this reason, other indicated pelvic reconstructive surgeries commonly accompany Burch colposuspension. A required hysterectomy does not appear to improve or worsen Burch procedure success rates (Bai, 2004; Meltomaa, 2001).

■⌀ Consent For most women with SUI, Burch colposuspension offers a safe, effective long-term treatment for incontinence. In one systematic review, overall continence rates ranged from 85 to 90 percent at 1 year and declined to 70 percent by 5 years (Lapitan, 2012). Surgical risks compare similarly with other surgeries for SUI (Green, 2005; Lapitan, 2003). Intraoperative complications are rare and may include ureteral injury, bladder or urethral

FIGURE 45-2.1╇ Entry into the space of Retzius.

CHAPTER 45

Burch Colposuspension

perforation, and hemorrhage (Galloway, 1987; Ladwig, 2004). Complications following surgery, however, are not uncommon and may include urinary tract or wound infection, voiding dysfunction, de novo urinary urgency, and pelvic organ prolapse—primarily enterocele formation (Alcalay, 1995; Demirci, 2000, 2001; Norton, 2006). Overcorrection of the urethrovesical angle has been suggested as a cause of these long-term urinary and prolapse complications.

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entry into the wrong tissue plane risks bleeding and bladder injury. Direct exposure of the back of the pubic bone ensures that the correct space has been entered. The bladder and urethra are gently pulled downward and away from the pubic bone, and the space of Retzius opens. In those with prior surgery, sharp dissection is generally required. Dissection begins with the curved tips of Metzenbaum scissors placed directly on the pubic bone and progresses dorsally until the space is exposed. Sutures can be used to control bleeding from torn paravaginal vessels. During space of Retzius dissection, the obturator canal is identified early to avoid neurovascular injury to the obturator vessels and nerves. The canal is typically found 1.5 to 2.5 cm below the upper border of the iliopectineal ligament and approximately 5 to 7 cm from the midline of the upper border of the symphysis pubis (Drewes, 2005). Accessory obturator vessels that commonly pass over Cooper ligament to enter the obturator canal are also identified. These can be lacerated during pronounced retraction to expose Cooper ligament.

➍╇ Exposing the Anterior Vaginal Wall.╇ After opening this space, fingers of the surgeon’s nondominant hand are placed intravaginally at the vagina’s midlength and just behind the pubic bone. With one on each side, the finger pads straddle the urethra and push the vagina ventrally. Working within the retropubic space and beginning at the lateral borders of the urethra, gentle downward and lateral pressure against the finger pad bluntly dissects away fat. This exposes the pearly white periurethral tissue between the arcus tendineus fascia pelvis (ATFP), which lies laterally, and urethra, which is medial. If necessary, a surgeon can use a Kittner (peanut) sponge or gauze sponge stick. Importantly, to protect the delicate urethral musculature, this dissection remains lateral to the urethra. Aggressive dissection or Burch sutures may lacerate vessels within the Santorini plexus of paravaginal veins and risk significant bleeding (Fig. 38-24, p. 817). This is easily controlled with upward pressure from the vaginal fingers. Identified vessels can then be ligated.

➎╇ Urethrovesical Junction.╇Identifying this site aids correct suture placement. To isolate the urethrovesical junction, the surgeon’s vaginal hand positions the Foley catheter balloon at the bladder neck. Undue

FIGURE 45-2.2╇ Suture placement. tension on the Foley catheter is avoided as this can drag the bladder into the operative field and increase the risk of sutures entering the bladder.

➏╇ Suture Placement.╇For exposure, the

surgeon’s vaginal finger presses upward, and the bladder neck is gently displaced by an assistant to the contralateral side by a narrow retractor. To suspend tissue, a double-armed suture of 2-0 gauge nonabsorbable material is placed laterally on each side of the urethra. A first suture is placed 1.5 to 2 cm lateral to the proximal third of the urethra. The needle point is directed toward the vaginal finger, and a thimble may be used to avoid needle-stick injury. For this suturing, a figure-of-eight stitch is used and incorporates vaginal wall while excluding epithelium. A second suture is then placed 1.5 to 2 cm lateral to the urethrovesical junction. Identical sutures are placed on the opposite side of the urethra (Fig. 45-2.2). Both ends of each suture are then placed through the nearest point of the ipsilateral iliopectineal ligament. Slack is removed from each suture, and knots are tied above the ligament. With knot securing, suture bridges are expected, and these should stabilize but not elevate the anterior vaginal wall and urethrovesical junction. The vaginal wall is stabilized approximately at the level of the distal portion of the ATFP and not significantly higher. Greater elevation of the bladder neck risks postoperative voiding dysfunction.

❼╇ Cystoscopy.╇ Following suture ligation,

cystoscopy is performed. This allows identification and removal of any errant sutures that may traverse the bladder or urethral mucosa. Moreover, it enables a surgeon to inspect the ureteral orifices and document efflux.

➑╇ Catheterization.╇ After

colposuspension, the Foley catheter may remain to drain the bladder. Alternatively, a suprapubic catheter may be placed. Investigators comparing the two have found no differences in antiincontinence procedure success rates, length of hospitalization, or rates of infection. Urethral catheterization, however, was linked with a shorter duration of catheterization but also greater patient discomfort (Dunn, 2005; Theofrastous, 2002).

➒╇ Incision Closure.╇ The anterior abdominal wall peritoneum is generally closed to prevent displacement of small bowel into the retropubic space. The remaining abdominal wall incision is closed as described in Section 43-2 (p. 930).

POSTOPERATIVE In general, recovery follows that associated with laparotomy and varies depending on concurrent surgeries and incision size. A voiding trial as described in Chapter 42 (p. 917 is performed prior to hospital discharge.

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The tension-free vaginal tape procedure (TVT) is the most commonly performed operation worldwide for stress urinary incontinence. The procedure is one of the most widely studied incontinence operations, and cure rates up to 17 years approximate 80 percent (Holmgren, 2005; Nilsson, 2013; Song, 2009). The TVT procedure has also become the prototype for a host of other incontinence operations, which include the TOT (transobturator tape), TVT-O (tension-free vaginal tape obturator), and single-incision midurethral slings (“minislings”). These are all considered midurethral slings (MUS) and are based on the concept that midurethral support is vital to continence. Tension-free vaginal tape placement is indicated for SUI that is secondary to urethral hypermobility or intrinsic sphincteric deficiency (Chap. 23, p. 522). It is used for primary cases and for women who have had prior antiincontinence procedures. During TVT, a permanent sling material is placed underneath the midurethra, traverses the periurethral tissue, passes behind the pubic bone through the space of Retzius, and exits through the anterior abdominal wall. Once positioned, tissue ingrowth ultimately holds the mesh in place. During placement, the TVT needle is directed blindly through the space of Retzius and can lacerate vessels there to create significant bleeding. A modification of the TVT, the TOT was developed to avoid hemorrhage in this space and to decrease bladder and bowel perforation risks (p. 1063). However, the TVT remains the primary standard operation for SUI. The TVT device consists of a permanent polypropylene mesh covered with a plastic sheath that is removed after the mesh is positioned. The plastic sheath is believed to prevent bacterial contamination of the mesh as it passes through the vagina and to protect the mesh from being damaged during passage. Once these plastic sheaths are removed, the mesh remains fixed in position. The mesh is attached to two metal disposable needles that are connected to a reusable metal introducer during placement. A metal catheter guide is used to displace the urethra away from the needle during the procedure.

PREOPERATIVE ■⌀ Patient Evaluation Prior to TVT procedures, a diagnosis of SUI must be made as described in Chapter 23

■⌀ Consent The consenting process for TVT should include an honest discussion of outcomes. At best, the 5-year cure rate is 85 percent, with another 10 percent significantly improved. However, some patients will develop postoperative urgency incontinence, and others will develop bothersome voiding dysfunction. Additionally, with time and aging, incontinence may recur secondary to factors not related to urethral support. As for all antiincontinence procedures, prior to surgery, the patient is provided surgical success rates from the literature and those of the individual surgeon. Moreover, the definition of “outcome success” varies from woman to woman. For example, in a patient with severe incontinence and 20 leakage episodes per day, improvement to one leakage episode every other day would be considered successful. However, in a woman with rare leakage, it may be more difficult to achieve an outcome considered satisfactory. Therefore, patient’s expectations are discussed prior to surgery. The short-term complications of the TVT procedure include incomplete bladder emptying requiring drainage with Foley catheter or intermittent self-catheterization for several days. A small percentage of patients will develop long-term urinary retention requiring reoperation for tape division or excision (p. 1072). In these women, continence rates decrease. The TVT procedure is associated with a learning curve, and urinary retention rates decline as the number of cases a physician performs accrues. Postoperatively, vaginal mesh erosion may develop as an early or late complication. This is managed by simple excision of the piece of eroding tape and vaginal wall revision. Of note, the American Urogynecologic Society (2014b) considers the mesh used for this sling to be safe and effective.

Intraoperative complications include hemorrhage, bladder perforation, and rarely, bowel injury. Major vessels are injured in less than 1 percent of cases.

■⌀ Patient Preparation The American College of Obstetricians and Gynecologists (2014) recommends antibiotic prophylaxis prior to urogynecologic procedures, and appropriate choices mirror those for hysterectomy (Table 39-6, p. 835). For all patients undergoing major gynecologic surgery, thromboprophylaxis is recommended (Table 39-8, p. 836). Bowel preparation is based on surgeon preference and mainly on concurrent surgeries planned.

INTRAOPERATIVE ■⌀ Surgical Steps ➊╇ Anesthesia and Patient Positioning.╇ The procedure was initially described as an ambulatory surgical procedure performed under local anesthesia. However, it can also be performed with regional or general anesthesia. If performed solely, TVT in most cases is a day-surgery operation. The procedure is performed in standard lithotomy position. The vagina is surgically prepared, and an 18F Foley catheter, which allows passage of a rigid catheter guide, is inserted to assist in deflection of the urethra during needle passage.

➋╇ Abdominal Incisions.╇ To begin, two

½-cm skin incisions are made at the level of the upper border of the symphysis, and each lies no further than 2 cm from the midline. More lateral placement risks ilioinguinal nerve injury (Geis, 2002).

➌╇ Vaginal Incisions.╇ A midline incision is made sharply in the vaginal epithelium and superficial vaginal muscularis beginning 1 cm proximal to the external urethral opening and is extended 1.5 to 2 cm cephalad. Allis clamps are placed on the edges of the vaginal incision for traction. Using Metzenbaum scissors, bilateral periurethral tunnels are created beneath the vaginal epithelium on either side of the urethra. These tunnels extend several centimeters toward the inferior pubic rami to allow placement of the TVT needle just behind the pubic bone. ➍╇ Catheter-guide Placement.╇A rigid guide is placed through the 18F Foley catheter. During passage of TVT needles, a surgical assistant uses the catheter guide to deflect the urethra to the contralateral side to lower urethral injury risks.

CHAPTER 45

Tension-Free Vaginal Tape

(p. 523). Importantly, in some women, SUI can be occult and masked by pelvic organ prolapse that kinks and partially obstructs the urethra. Accordingly, prolapse replacement to reestablish more normal anatomy during urodynamic testing may help unmask this potential SUI. Also of note, caution is exercised in patients who are Valsalva voiders. These women void with abdominal straining rather than with detrusor contraction and urethral relaxation. Most incontinence procedures prevent leakage by closing the urethra during cough or Valsalva maneuver. Therefore, these surgeries, when performed in women who rely on the Valsalva maneuver to urinate, will often result in voiding dysfunction. This tenet applies to all midurethral sling procedures.

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toward the abdominal wall incisions. The bladder may be perforated if excessive pressure is applied and if the needle is aimed cephalad rather than toward the abdominal wall (Fig. 45-3.3). Small changes in the position of the hand applying handle pressure can lead to bladder perforation.

➏╇ Cystourethroscopy.╇ After the needle

FIGURE 45-3.1╇ Needle placed through periurethral tunnel.

➎╇ Mesh Placement.╇The TVT needle

and mesh are attached to the introducer. The needle is placed through one of the periurethral tunnels so that its point touches the front surface of the ipsilateral pubic ramus (Fig. 45-3.1). A hand placed in the vagina then carefully guides the needle around the back of the ramus. The needle is then curved upward toward the ipsilateral abdominal incision, perforates the periurethral tissue just behind the pubic bone, and enters the

retropubic space (Rahn, 2006). During this, the needle is always directly behind the pubic bone. Pressure is applied to the introducer handle with the other hand, but the vaginal hand controls the needle’s direction. The handle of the introducer always remains parallel to the ground to avoid lateral excursion into major vessels and obturator nerve (Fig. 45-3.2). Additionally, after the needle passes around the pubic ramus and behind the symphysis, its tip is always directed

perforates the abdominal wall, the Foley and catheter guide are removed, and cystourethroscopy is performed with a 70-degree cystoscope. The bladder is distended with 200 to 300 mL of fluid, and inspection for cystotomy is completed. Generally, perforation will be obvious, and the TVT needle will be seen entering and exiting the bladder. In this situation, the needle is removed and redirected, and correct placement is confirmed by cystoscopy. Inspection of the urethra is also essential and can be performed with the same 70-degree angle scope. Alternatively, a 0-degree or 30-degree endoscope may be used. Iatrogenic trocar bladder injury, if identified intraoperatively does not appear to influence continence outcomes or increase postoperative voiding dysfunction or infection rates (Zyczynski, 2014). In contrast to bladder perforation, urethral perforation theoretically carries a risk of urethrovaginal fistula. Thus, if urethral perforation is noted, most surgeons abort the procedure and postpone until several months later. After cystoscopy, the introducer is unscrewed from the needle. The needle is brought through the abdominal wall. The needle is then cut from the mesh, and the mesh is held with a hemostat. Next, the other TVT needle is attached to the introducer and is placed on the other side of the urethra in a similar fashion. Cystourethroscopy is then repeated.

❼╇ Setting Mesh Position.╇A hemostat

A

B

FIGURE 45-3.2╇ Correct and incorrect introducer positioning. A. Dark introducer, correct position. The tip is directed in the midline to a position behind the pubic bone. The handle is parallel to the ground. B. White introducer, incorrect position. The tip is directed laterally.

or similar instrument is placed between the suburethral tissue and the tape to act as a spacer and create distance between the mesh and urethra (Fig. 45-3.4). This spacing avoids excessive mesh tension and lowers the risk for postoperative urinary retention and voiding dysfunction. Prior to sheath removal, the vaginal sulci are inspected to exclude perforation of the vaginal epithelium occurring during needle guidance. If perforated mesh is seen, the tape is removed, and the TVT needle is again passed through a newly created periurethral tunnel that lies slightly medial to the original. The vaginal perforation defect is repaired with one or two simple interrupted delayed-absorbable sutures.

➑╇ Sheath Removal.╇Once the tape is

satisfactorily positioned, an assistant then removes the plastic covering around the

Surgeries for Pelvic Floor Disorders

POSTOPERATIVE

FIGURE 45-3.3╇ Correct (dark introducer) and incorrect (light introducer) hand and introducer positioning. mesh, while the surgeon holds the mesh at the desired distance from the urethra using the spacer instrument. The plastic covering is lifted away from both sides with minimal tension to avoid mesh stretching or undue

FIGURE 45-3.4╇ Setting mesh position.

urethral elevation. With ideal positioning, a few millimeters of free space separate the suburethral tissue and mesh. The mesh is trimmed just below the skin at the abdominal incisions (Fig. 45-3.5).

Prior to discharge from a day-surgery unit, an active voiding trial is performed (Chap. 42, p. 917). If the patient fails this trial, a Foley catheter is replaced and kept for 1 to 3 days prior to a second voiding trial. Alternatively, a patient can be taught self-catheterization. This is continued until postvoid residual volumes fall below about 100 mL. Normal diet and activity can resume during the first postoperative days. Intercourse, however, is postponed until the vaginal incision is healed, usually at 6 weeks. The time to resumption of exercise and strenuous physical activity is controversial. A standard recommendation has been to delay these at least 2 months, although there are no data supporting this. However, logic would suggest that this is reasonable for adequate healing.

FIGURE 45-3.5╇ Sheath removal and tape trimming.

CHAPTER 45

➒╇ Wound Closure.╇The vaginal incision is closed in a running fashion with 2-0 gauge delayed-absorbable suture. The abdominal incisions may be closed with Dermabond or with a single interrupted 4-0 gauge delayedabsorbable skin suture.

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Transobturator Tape Sling The transobturator tape (TOT) sling procedure is a variation of the midurethral sling procedures, which began with tension-free vaginal tape (TVT) (p. 1063). With the TOT procedure, a permanent sling material is inserted bilaterally through the obturator foramen and extends underneath the midurethra. As a result, the space of Retzius is avoided and thereby minimizes the potential for associated bladder and bowel injuries. Bleeding in the space of Retzius is a primary TVT complication, and avoiding this space is an attractive TOT feature. Additionally, in patients who have had prior incontinence procedures and have scarring in the space of Retzius, bladder perforation may be averted by avoiding dissection in this space. The procedure has several important differences from TVT, and there are also several modifications of the TOT procedure itself. Several companies produce kits containing required mesh and placement needles for TOT. The two major types of TOT procedures are defined by whether needle placement begins inside the vagina and is directed outward, termed an in-to-out approach, or starts outside the vagina and is directed inward, called an out-to-in approach. Limited data do not show superiority of one over the other (Debodinance, 2007). Currently, the out-to-in technique is more commonly performed and is described here. Generally, TOT is indicated for primary SUI secondary to urethral hypermobility (Chap. 23, p. 525). In patients with SUI secondary to intrinsic sphincteric deficiency, the value of TOT is unclear, as results are conflicting and data are limited (Rechberger, 2009; Richter, 2010).

with the supporting mesh and include mesh erosion (Schimpf, 2014). Intraoperatively, there is some risk of bladder or urethral perforation, although this is believed to be significantly less than that with TVT. Inappropriate TOT trocar placement rarely can lead to significant hemorrhage or neurologic deficits if obturator nerve and vessel branches are damaged in the thigh compartment.

and is extended 2 to 3 cm cephalad. Allis clamps are placed on the edges of the vaginal incision for traction. Using Metzenbaum scissors and blunt finger dissection, bilateral periurethral tunnels are created beneath the vaginal epithelium on either side of the urethra. These tunnels extend up to and behind the ischiopubic rami.

■⌀ Surgical Steps

➌╇ Thigh Incisions.╇ A 0.5- to 1-cm entry incision is made bilaterally in the thighcrease skin (genitocrural fold), 4 to 6 cm lateral to the clitoris, and at the point where the adductor longus insertion can be palpated. This muscle arises from the superior ramus of the pubis and inserts medially at the midlength of the femur. To summarize the needle's path, insertion starts along the lateral edge of the ischiopubic ramus just below the insertion of the adductor longus tendon and arches around the ramus. During this arc, the needle sequentially penetrates the gracilis, adductor brevis, and obturator externus muscles, obturator membrane, obturator internus muscle, and periurethral endopelvic fascia and exits through the vaginal incision.

➊╇ Anesthesia and Patient Positioning.╇

➍╇ Mesh Placement.╇The TOT needle

INTRAOPERATIVE ■⌀ Instruments A TOT kit will contain two TOT needles and synthetic mesh tape. The TOT needle is designed to navigate the path from the entry point around the pubic rami to the midurethral vaginal wall incision. A plastic sheath surrounds the mesh tape and allows the mesh to be pulled into position smoothly. However, once these plastic sheaths are removed, the mesh remains fixed in position.

If performed solely, a TOT procedure in most cases is a day-surgery procedure. It is performed in standard lithotomy position under general, regional, or local anesthesia. The vagina is surgically prepared, and a Foley catheter is placed to assist in determination of urethral location.

➋╇ Vaginal Incisions.╇ A midline incision is made sharply in the vaginal epithelium and superficial muscular layer beginning 1 cm proximal to the external urethral opening

is grasped, and the tip is placed in one of the thigh incisions (Fig. 45-4.1). The tip is directed cephalad until the obturator membrane is perforated, and a “popping” sensation is felt. A vaginal finger is placed in the ipsilateral vaginal tunnel and is positioned up to and behind the ischiopubic ramus. Using the curve of the TOT needle, the surgeon then directs the needle tip to the end of his finger and passes the needle into the vagina (Fig. 45-4.2). At this time, the vaginal sulcus is inspected to exclude perforation.

PREOPERATIVE ■⌀ Patient Evaluation Evaluation and preparation prior to TOT mirrors that for TVT (p. 1063).

■⌀ Consent As with other surgeries for incontinence, the major risks of this procedure are voiding dysfunction, urinary retention, development of urgency incontinence, and failure to correct SUI. Groin and thigh pain appear to be another potential postoperative problem. Long-term complications may be associated

FIGURE 45-4.1╇ Needle introduction.

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FIGURE 45-4.3╇ Tape placement.

FIGURE 45-4.2╇ Needle passage.

If the needle has perforated the sulcus epithelium, it is removed and reinserted correctly. Next, the TOT covered mesh is attached to the needle end, and the needle retraces its original path as it is withdrawn back through the thigh incision. With this, the covered mesh is threaded into position. The mesh is then removed from the needle. The procedure is repeated on the other side (Fig. 45-4.3).

➎╇ Setting Mesh Position.╇A hemostat

or similar instrument is placed and opened between the urethra and mesh to act as a spacer and create distance between the mesh and the urethra (Fig. 45-4.4). This spacing avoids excessive urethral elevation and lowers postoperative urinary retention risks. Prior to sheath removal, the vaginal sulci are again

inspected to exclude perforation. If mesh is seen in a sulcus, the tape is removed and reinserted on the affected side.

absorbable suture or with other suitable skin closure methods (Chap. 40, p. 847).

➏╇ Sheath Removal.╇An assistant sur-

marketed as one in which cystoscopy is not necessary. However, because the bladder and urethra can be injured, we recommend postprocedural cystoscopy.

geon then removes the plastic covering of the mesh from each of the thigh incisions. Concurrently, the surgeon holds the mesh at the desired distance from the urethra using the spacer instrument. The plastic covering is removed with minimal tension to avoid mesh stretching. The mesh is trimmed just inside thigh incisions.

❼╇ Wound Closure.╇ The vaginal incision is closed in a running fashion with 2-0 gauge delayed-absorbable suture. The thigh incisions may be closed with a single interrupted subcuticular suture with 4-0 gauge delayed-

FIGURE 45-4.4╇ Setting mesh position.

➑╇ Cystourethroscopy.╇ The procedure is

POSTOPERATIVE Prior to discharge from a day-surgery unit, an active voiding trial is performed (Chap. 42, p. 917). If significant residuals persist, a Foley catheter remains. A second voiding trial can be repeated in a few days or at the surgeon’s discretion. Alternatively, a patient can be taught self-catheterization. This is continued until postvoid residuals fall below approximately 100 mL. Normal diet and activity can resume during the first postoperative days. Intercourse, however, is delayed until the vaginal incision is healed. The time to resumption of exercise and strenuous physical activity is controversial. A standard recommendation delays these at least 2 months. Data to support this are lacking, however, logic would suggest that this is reasonable to allow adequate healing.

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45-5 SECTION 6

Pubovaginal Sling Pubovaginal sling is a standard procedure for SUI. It has traditionally been used for SUI stemming from intrinsic sphincteric deficiency (Chap. 23, p. 522). In addition, this procedure may also aid patients with prior failed antiincontinence operations. It is generally not employed in a woman having her first surgery for incontinence. In the past, different materials had been used for the sling, however, autologous fascia is currently preferred. Generally, this fascia is obtained from the patient’s rectus sheath, although fascia lata from the thigh may alternatively be harvested. With this surgery, a strip of fascia is placed at the proximal urethra through the space of Retzius, and ends are secured either to each other or to the rectus fascia above the rectus abdominis muscle. In contrast to midurethral slings, which generally employ premade kits and standardized procedural steps, the technical aspects of autologous fascia pubovaginal slings have greater variability. These include size and location of harvested tissue, anchoring method of the sling to the rectus fascia, and technique for determining mesh tension across the proximal urethra. Steps for the rectus fascial sling are described here.

PREOPERATIVE ■⌀ Patient Evaluation As with other antiincontinence procedures, patients require urogynecologic evaluation,

FIGURE 45-5.1╇ Entry into the space of Retzius.

including urodynamic testing to confirm SUI and intrinsic sphincteric deficiency. Additionally, SUI often accompanies pelvic organ prolapse. Thus, the need for concurrent repair of associated prolapse is assessed prior to surgery (Chap. 24, p. 545).

■⌀ Consent In addition to general surgical risks, patients are counseled regarding the risk of recurrent incontinence, urinary retention, and voiding dysfunction following surgery (Albo, 2007). Overall, traditional slings seem to be as effective as minimally invasive slings but have higher rates of adverse effects (Rehman, 2011).

■⌀ Patient Preparation Antibiotics and thromboprophylaxis are given as outlined in Tables 39-6 and 39-8 (p. 835). Bowel preparation is based on surgeon preference and mainly on concurrent surgeries planned.

INTRAOPERATIVE ■⌀ Surgical Steps ➊╇ Anesthesia and Patient Positioning.╇ Pubovaginal sling may be performed under general or regional anesthesia as an inpatient procedure. The patient is placed in standard lithotomy position, with lower extremities positioned in candy-cane or booted support stirrups. The abdomen and vagina are surgically prepared, and a Foley catheter is inserted.

➋╇ Graft Harvest.╇ A transverse skin incision is made 2 to 4 cm above the symphysis and is

large enough to allow removal of a transverse fascial strip that measures, at minimum, 1.5 cm wide × 6 cm long. The incision is carried down through subcutaneous tissue to the fascia. The fascia to be harvested is outlined and then incised, sharply dissected away from the underlying rectus muscle bellies, and removed. Following removal, the strip is cleaned of fat and adventitial tissue. A helical stitch using 0-gauge polypropylene suture is then placed through the fascia at each end of the strip. This stitch is repeated at the other end. These sutures are not tied. The fascial incision is then closed in a running fashion with 0-gauge delayed-absorbable suture.

➌╇ Vaginal Incision.╇ At a point 2 cm prox-

imal to the external urethral orifice, a 3- to 5-cm midline vertical incision is made sharply in the anterior vaginal wall and extended cephalad. Alternatively, a U-shaped incision is made at the level of the bladder neck. Sharp and blunt dissection is used to separate the vaginal epithelium from the underlying fibromuscular layer. The space of Retzius is then entered with a combination of sharp and blunt dissection bilaterally by penetrating the periurethral connective tissue (Fig. 45-5.1). Entry into this space is confirmed by the surgeon’s finger palpating the dorsal surface of the pubic bone (Fig. 45-5.2). During entry, Santorini’s venous plexus can be lacerated, and bleeding is controlled with compression or stitches of 2-0 gauge absorbable suture.

➍╇ Fascia Placement.╇A 0.5- to 1-cm long fascial incision is made no further than 2 cm from the midline on each side. These are placed caudal to the prior harvest incision and just above the pubic bones. A long

FIGURE 45-5.2╇ Palpation of pubic bone.

Surgeries for Pelvic Floor Disorders

➏╇ Cystourethroscopy.╇ Cystoscopy is again

performed to exclude bladder or urethral perforation. In addition, excessive resistance noted during passage of the cystoscope into the bladder may suggest undue sling tension, which can lead to postoperative obstructive symptoms. If such resistance is noted, the sling is loosened.

❼╇ Vaginal Incision.╇ The vaginal incision

is closed with 2-0 gauge delayed-absorbable suture in a running fashion. A Foley catheter is left in place. In the past, suprapubic tube insertion was common practice. However, with a trend toward tying the fascial sling with less tension, the risk of prolonged urinary retention is lowered, and suprapubic drainage is therefore not typically required.

➑╇ Abdominal Incision.╇ The two prior 1-cm fascial incisions are closed with an interrupted stitch of delayed-absorbable suture. The remaining abdominal incision is closed as described in Section 43-2 (p. 930). FIGURE 45-5.3╇ Passing of dressing forceps. dressing or packing forceps or needle ligature carrier is placed into one of these incisions and from above, perforates the rectus tendon. The instrument is placed against the back of the pubic bone and advanced toward the vagina. Concurrently, the surgeon guides the instrument to his finger within the space of Retzius and advances it into and through the vaginal incision (Fig. 45-5.3). At this time, cystourethroscopy is performed to exclude bladder or urethral perforation. The suture ties at one end of the fascial strip are grasped with the perforating forceps and threaded up through the abdominal incision on one side of the urethra. With the other end of the sling, this step is repeated on the other side of the urethra. As a result, the fascial sling lies positioned below the bladder neck (Fig. 45-5.4). Usually four 2-0 gauge delayed-absorbable sutures may be used to fix the proximal and distal edges of the sling beneath the bladder neck to prevent displacement during sling positioning. Stitches are placed lateral to the urethra.

➎╇ Setting Sling Position.╇Within the laparotomy incision, sutures attached to the sling ends from each side meet and are tied together above the rectus sheath. During knot tying, a space of two to three fingerbreadths is left between the knot and fascia to pre-

vent bladder neck obstruction and urinary retention. In addition, a hemostat is placed between the suburethral tissue and the fascial sling to create distance between the sling and urethra (see Fig. 45-4.4). After the knot

POSTOPERATIVE In general, recovery follows that associated with laparotomy and is heavily dependent on incision size. A voiding trial as described in Chapter 42 (p. 917) is performed prior to hospital discharge.

FIGURE 45-5.4╇ Fascial sling placed and sutured in place on vaginal side.

CHAPTER 45

is secured, there should be no upward angulation of the urethra or bladder neck, and a few millimeters of free space should be noted between the fascial sling and the bladder neck.

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Atlas of Gynecologic Surgery

45-6 SECTION 6

Urethral Bulking Injections Injection of bulking agents into the urethral submucosa is one method available to treat SUI that results from intrinsic sphincter deficiency (ISD) (Chap. 23, p. 522). Although mechanisms are not completely clear, effectiveness may result from expansion of the urethral walls, which allows them to better approximate or coapt. As a result, intraluminal resistance to flow is increased and continence is restored. Alternatively, injections elongate the functional urethra, and this may allow more even distribution of abdominal pressures across the proximal urethra to resist opening during stress (Monga, 1997). Although traditionally recommended for treatment of SUI solely due to ISD, some evidence suggests it can be used to treat SUI resulting from combined ISD and urethral hypermobility (Bent, 2001; Herschorn, 1997; Steele, 2000). Urethral injection offers a cystoscopically assisted, minimally invasive treatment of SUI. It can be performed in an office under local anesthesia and is associated with a low risk of complications. For these reasons, it is often chosen for women who wish to avoid surgery or who are not surgical candidates due to other comorbidities. Urethral injections can be performed both peri- and transurethrally. The transurethral approach is more often used and allows for more accurate placement of the bulking agent (Faerber, 1998; Schulz, 2004). Currently available agents in the United States approved for use include autologous fat and several synthetic agents described later.

PREOPERATIVE ■⌀ Patient Evaluation Complex urodynamic testing with assessment of urethral structure and function is completed. To assess for ISD, maximum urethral closure pressure or leak point pressure are specifically evaluated (Chap. 23, p. 527). Additionally, urethral mobility is assessed.

■⌀ Consent Procedure efficacy is discussed, and success rates in general are lower than those for surgery. Specifically, 1-year rates of curing or improving SUI range from 60 to 80 percent (Bent, 2001; Corcos, 2005; Lightner, 2002, 2009; Monga, 1995). Continence

rates diminish with time, as would be intuitive, with the breakdown of collagen and fat. However, Chrouser (2004) found similar rates of decline with time even when synthetic material was compared with collagen. Accordingly, these injections are viewed as a nonpermanent treatment of SUI, and sustained continence is found in only 25 percent of patients at 5 years following injection (Gorton, 1999). One major advantage to urethral injection is its low associated risk of complications. Side effects of injection are generally transient and may include vaginitis, acute cystitis, and voiding symptoms. Of these, urinary retention for a few days postprocedure is the most frequent. Long-term retention, however, is not a significant risk. A more serious complication is persistent de novo urgency, which may develop in as many as 10 percent of women following injection (Corcos, 1999, 2005).

■⌀ Patient Preparation Prior to urethral injection, UTI and anatomic pathology such as urethral diverticula are excluded. Anecdotally, we have seen bulking agent migration into such diverticula. As noted, UTI can commonly follow urethral injection. Therefore, a single dose of an antibiotic to cover uropathogens is administered orally after procedure completion. Thromboprophylaxis is not typically required for this brief office procedure.

INTRAOPERATIVE ■⌀ Choice of Bulking Agent In the United States, currently used agents for urethral injection are carbon-coated synthetic microspheres (Durasphere), calcium hydroxylapatite particles (Coaptite), and polydimethylsiloxane (Macroplastique). These synthetic agents are effective. However, no randomized trials compare results among these three, and long-term data are lacking (Shah, 2012; Zoorob, 2012). Of agents no longer used, autologous fat provided limited success for SUI due to rapid degradation and reabsorption (Haab, 1997; Lee, 2001). A bovine collagen product (Contigen) was commonly selected, but manufacturing ceased due to an inadequate supply of medical-grade collagen. Ethylene vinyl alcohol copolymer (Uryx/Tegress) was withdrawn due to urethral erosion complications.

■⌀ Surgical Steps ➊╇ Anesthesia and Patient Positioning.╇ Urethral injection for most patients can be

performed in an office setting with cystoscopic capability. The patient is placed in the dorsal lithotomy position, the vulva is prepared and draped, and the bladder drained. Two-percent lidocaine jelly is instilled into the urethra 10 minutes prior to the procedure. If necessary, topical 20-percent benzocaine can be used as an analgesic on the vulva, and 4 mL of 1-percent lidocaine can be injected in divided doses at the 3 and 9 o’clock positions of the external urethral orifice.

➋╇ Transurethral Approach to Needle

Placement.╇ A cystoscope is positioned within the distal urethra, so that the midurethra, proximal urethra, and bladder neck are viewed simultaneously. A 22-gauge spinal needle attached to a syringe carrying the bulking agent is introduced through the cystoscopic sheath. With the bevel pointing toward the urethral lumen, the needle is directed at a 45-degree angle to the lumen and inserted through the urethral wall at the 9 o’clock position and at the level of the midurethra. After the needle tip penetrates the urethral wall, the bevel is no longer seen. The needle is then advanced parallel to the urethral lumen for 1 to 2 cm. This positions the needle at the level of the proximal urethra.

➌╇ Injection.╇ The bulking agent is injected

under constant pressure, and the submucosal lining begins to rise (Fig. 45-6.1). The needle is withdrawn slowly to bulk the proximal and midurethra. Bulking agent is administered until coaptation of the mucosa has developed (Fig. 45-6.2). In general, 1 to 2 syringes (2.5 to 5 mL) of agent are used per procedure. These steps are then repeated at the 3 o’clock position. Ideally, the number of needle holes made into the urethral wall is minimized to avoid leakage of bulking agent through these punctures. Thus, if a second syringe of agent is required to achieve coaptation, the originally positioned needle remains in place, and a second syringe of agent is attached.

➍╇ Cystoscope Removal.╇Once coapta-

tion of the mucosa is achieved, the cystoscope is removed, taking care not to advance proximal to the injection site. This avoids forceful compression of the deposited agent by the cystoscope tip and loss of coaptation.

POSTOPERATIVE Women are discharged home following their first postinjection void, and single-dose oral antibiotic prophylaxis is prescribed. Women abstain from intercourse for 10 days following injection but may otherwise resume usual activities.

Surgeries for Pelvic Floor Disorders

FIGURE 45-6.1╇ Injection of bulking agent.

FIGURE 45-6.2╇ Corresponding cystoscopic views of urethral coaptation as bulking agent is injected, as shown in Figure 45-6.1.

CHAPTER 45

If urinary retention develops, then intermittent self-catheterization is begun and continued until retention resolves. For those unable to self-catheterize, a temporary Foley catheter is placed. However, catheter placement can potentially compress deposited bulking agent and diminish urethral coaptation. Two weeks following injection, we assess treatment success. If a patient fails to achieve desired degrees of continence, additional injections are planned to improve urethral coaptation.

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45-7 SECTION 6

Urethrolysis Urethrolysis is the loosening or release of a prior urethral suspension repair. This release is used in women with urethral obstruction symptoms including urinary retention and voiding dysfunction following suspension. It can be performed either vaginally or abdominally. A vaginal approach is predominantly used. An abdominal approach, however, may afford a better opportunity to mobilize the bladder from the pubic symphysis and may also be selected in instances in which the initial surgery was performed via laparotomy. Debate exists as to the need of a concurrent antiincontinence procedure to compensate for urethral support lost with urethrolysis. However, in many cases, residual scarring prevents SUI, and our belief is to avoid repeating a second potentially obstructing procedure. Accordingly, this decision is individualized.

PREOPERATIVE ■⌀ Patient Evaluation In women with bladder neck obstruction, symptoms usually begin soon after initial surgery. Objective assessment with urodynamic testing is performed to determine the cause of voiding dysfunction and differentiate between a hypotonic bladder and obstruction. Obstruction may result from bladder neck obstruction or

FIGURE 45-7.1╇ Vaginal incision.

pelvic organ prolapse. Thus, a thorough examination for prolapse is completed.

■⌀ Consent In addition to usual surgical risks, bleeding may be a significant complication due to vascularity in the space of Retzius. Additionally, dissection of dense scarring around the urethra and bladder may place these structures at risk of laceration. Due to scar tissue reformation, initial obstruction improvement can worsen over time, as scar tissue may variably reform. In contrast, postoperative incontinence may follow deconstruction of prior antiincontinence support or from denervation injury during extensive periurethral dissection.

■⌀ Patient Preparation As with all genitourinary procedures, UTI is excluded prior to surgery. Antibiotic prophylaxis is administered prior to surgery to decrease risks of postoperative wound and urinary tract infection (Table 39-6, p. 835). Thromboprophylaxis is provided as outlined in Table 39-8 (p. 836).

INTRAOPERATIVE ■⌀ Surgical Steps—Vaginal Approach ➊╇ Anesthesia and Patient Positioning.╇ Urethrolysis may be performed under general or regional anesthesia. The patient is placed

in standard lithotomy position with lower extremities in candy-cane or booted support stirrups. The vagina is surgically prepared, and a Foley catheter is inserted into the bladder.

➋╇ Vaginal Incision.╇Traction is placed on the Foley catheter to identify the bladder neck and assess the degree of scarring. A 2- to 3-cm long incision, either vertical midline or U-shaped, is made in the anterior vaginal wall. The incision site will vary along the vaginal length depending on the location of the original sling or sutures (Fig. 45-7.1). Sharp dissection is used to separate the vaginal epithelium from underlying fibromuscular tissue and is extended bilaterally toward the inferior edge of each pubic rami. Dissection frees the urethra by dividing scar tissue or prior sling material or sutures that lie between the urethra and pubic rami (Fig. 45-7.2). If prior supporting material is identified, it may be incised or if necessary, excised. Bleeding is frequently encountered and can be controlled with direct pressure or vessel ligation. After this lateral dissection, the periurethral tissue is perforated, and the space of Retzius is entered. Careful blunt dissection within this space and at the back of the pubic symphysis will additionally mobilize the proximal urethra. Dissection is kept close to the dorsal surface of the pubic bone to avoid cystotomy in a bladder that is generally densely adhered to the pubic bone. ➌╇ Incision Closure.╇Following adequate

mobilization of the urethra, the vaginal incision

FIGURE 45-7.2╇ Periurethral dissection.

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FIGURE 45-7.3╇ Dissection in the space of Retzius.

is reapproximated with a running closure using 2-0 gauge delayed-absorbable suture.

■⌀ Surgical Steps— Abdominal Approach ➊╇ Anesthesia and Patient Positioning.╇ As with a vaginal approach, urethrolysis may be completed under general or regional anesthesia. For an abdominal approach, booted support stirrups and low lithotomy positioning are preferred. This positioning allows vaginal access for the surgeon’s hand during dissection and for cystoscopy. The abdomen and vagina are surgically prepared, and a Foley catheter is inserted into the bladder.

➋╇ Abdominal Incision.╇ A low transverse

incision is typically preferred for this procedure to permit easy access to the space of Retzius. Either Pfannenstiel or Cherney incisions are usually selected (Sections 43-2 and 43-3, p. 929). If the procedure is done in isolation, fascia of the anterior abdominal wall muscles and then transversalis fascia are incised, but entry into the peritoneal cavity is not necessary to reach the space of Retzius.

FIGURE 45-7.4╇ Intentional cystotomy to aid bladder and urethral dissection.

➌╇ Entry into the Space of Retzius.╇ The

correct plane of dissection to enter the space of Retzius lies directly behind the pubic bone. Loose areolar tissue is gently dissected downward in a mediolateral fashion with fingers or sponge, beginning immediately behind the pubic bone. If the correct plane is entered, this potential space opens easily. However, women requiring urethrolysis have typically had prior surgery within this space. As a result, tissue can be densely adhered and sharp downward dissection along the dorsal surface of the symphysis may be preferred to enter this space (Fig. 45-7.3).

➍╇ Bladder Dissection and Urethrolysis.╇ The bladder is also typically densely adhered to the back of the symphysis. Sharp dissection with the curved surface of scissors facing the symphysis is directed against the symphysis to minimize cystotomy risk. At times, however, an intentional cystotomy may be required so that a finger can be placed inside the bladder to aid dissection (Fig. 45-7.4). Sharp dissection is continued inferiorly and laterally down the inner surface of the symphysis and pubic bones to free the bladder and eventually also the proximal urethra.

Bleeding is common during dissection and may be controlled with absorbable sutures.

➎╇ Abdominal Closure.╇ The abdomen is closed in a standard fashion (Sections 43-2 or 43-3, p. 930).

POSTOPERATIVE An active bladder test is performed following catheter removal. If large residual volumes are found, intermittent self-catheterization or Foley catheter replacement is required. If cystotomy was performed, the duration of catheterization is dependent on cystotomy size and location. For example, small cystotomies in the bladder dome typically require drainage for 7 days or less. For larger cystotomies at the bladder base, however, drainage for several weeks may be needed. Antibiotic suppression is not required with this catheter use. Normal diet and activity can resume during the first postoperative days. With a vaginal approach, however, intercourse is postponed until the vaginal incision is well healed. Recovery from an abdominal approach follows that for laparotomy (Section 43-1, p. 928).

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45-8 SECTION 6

Midurethral Sling Release Symptoms of voiding obstruction may develop following urethral sling procedures, specifically TVT and TOT procedures. For most patients, postoperative urinary retention resolves in days or 1 to 2 weeks. However, voiding dysfunction requiring surgery develops in up to 3 percent and generally is identified days to weeks after surgery (Jonsson Funk, 2013; Nguyen, 2012; Richter, 2010). If obstruction is diagnosed soon after the index procedure, surgical release is performed and involves simple cutting of the sling material.

PREOPERATIVE ■⌀ Patient Evaluation and Preparation Inability to fully empty the bladder may stem from urethral obstruction or a hypotonic bladder. New-onset urinary retention after a midurethral sling procedure (TVT or TOT) is usually due to sling tightness. However, other factors can be involved, such as preexisting or de novo bladder hypotonia. Thus, prior to TVT urethrolysis, urodynamic testing is often performed to prove that symptoms are due to obstruction rather than to bladder hypotonicity. Additionally, tape may erode into the bladder or urethra in cases of obstruction, and cystoscopy allows exclusion of this complication. Perioperatively, no specific patient preparation is required, as midurethral sling release is a minor surgical procedure.

■⌀ Consent Associated with midurethral sling release, the risks of incontinence recurrence, failure to adequately relieve retention, fistula formation, and intraoperative bladder or urethral injury are discussed during consenting.

INTRAOPERATIVE ■⌀ Surgical Steps ➊╇ Anesthesia and Patient Positioning.╇ This surgery can be performed with local,

FIGURE 45-8.1╇ Mesh transection through vaginal incision. Inset top: Mesh incision and retraction. Inset bottom: Partial mesh excision.

regional, or general anesthesia as an outpatient procedure. A patient is placed in standard lithotomy position within candy-cane or booted support stirrups. The vagina is surgically prepared, and a Foley catheter is inserted.

➋ ╇ Vaginal Incision and Tape IdentiÂ�

fication.╇ A midline suburethral incision that follows the prior primary surgical incision is made sharply. Careful dissection is used to expose the sling material and to define the urethral borders. Alternatively, with prior TOT, tight tissue bands may be palpated in the sulci. In this case, the vagina can be incised at one sulcus, and the tape transected or partially excised here. Often because of increased sling tension, sling material is stretched and measures only half its expected width. Additionally, there is usually extensive tissue ingrowth into the sling material, and identification and mobilization can be difficult. Occasionally, a sling may migrate to the proximal urethra. In these instances, the vaginal incision may require cephalad extension.

➌╇ Incision of Sling Material.╇Following mobilization of the material, a hemostat is opened between the sling and urethra.

Metzenbaum scissors are used to cut the sling material. In general, incision leads to immediate retraction of sling ends (Fig. 45-8.1, top inset). If retraction does not follow, a 1-cm segment of material is then excised (see Fig. 45-8.1, bottom inset). If the sling is deeply embedded and near the urethral lumen, one to two imbricating layers are placed through the vaginal muscularis following sling excision using 2-0 or 3-0 gauge delayed-absorbable suture.

➍╇ Incision Closure.╇After vigorous irrigation, the vaginal epithelium is closed in a continuous running fashion using 2-0 gauge delayed-absorbable suture.

POSTOPERATIVE Prior to discharge, an active voiding trial is performed (Chap. 42, p. 917). If a Foley catheter remains, a second voiding trial can be repeated in a few days or at the surgeon’s discretion. If a woman is performing self-catheterization, this is continued until postvoid residuals fall below approximately 100 mL. Normal diet and activity can resume during the first postoperative days. Intercourse, however, should be postponed until the vaginal incision is healed.

Surgeries for Pelvic Floor Disorders

45-9

The approach to urethral diverticulum repair varies and depends on diverticular sac location, size, and configuration. For those near the bladder neck, partial ablation is often chosen to avoid damage to the bladder neck and continence mechanism. For midurethral diverticula, simple diverticulectomy is typically performed. For those located at the external urethral orifice, again, simple diverticulectomy is preferred to the Spence procedure. The latter is rarely performed and can alter final urethral orifice anatomy. Last, for those with a complex diverticulum that may surround the urethra, a combination of techniques may be necessary. Of these options, complete vaginal excision of the urethral diverticulum is preferred (Antosh, 2011).

PREOPERATIVE ■⌀ Patient Evaluation As described in Chapter 26 (p. 585), urethral diverticula can be difficult to diagnose due to their often varied and nonspecific presentations. Once identified, accurate information regarding diverticular anatomy is essential to surgical planning and patient counseling. Compared with transvaginal sonography or voiding cystourethrography, magnetic resonance (MR) imaging is a superior radiographic study to delineate diverticular configuration, especially with complex diverticula (Ockrim, 2009). Additionally, cystoscopy is valuable in locating sac openings along the urethral length and demonstrates high specificity, as transurethral visualization of an ostium is unlikely to be associated with other diagnoses. That said, our frequency of urethral diverticulum detection (sensitivity) was only 39 percent (Pathi, 2013). Women with diverticulum can present with urinary incontinence. In such cases, we typically perform baseline urodynamic testing but generally defer antiincontinence procedures until after postoperative reevaluation.

■⌀ Patient Preparation Any acute diverticular infection or cystitis is treated prior to surgery. Preventatively, antibiotic and venous thromboprophylaxis are given as outlined in Tables 39-6 and 39-8 (p. 835).

INTRAOPERATIVE ■⌀ Surgical Steps— Diverticulectomy ➊╇ Anesthesia and Patient Positioning.╇ Diverticulum excision is typically performed as an inpatient procedure under general or regional anesthesia. A patient is placed in standard lithotomy position within candy-

cane or booted support stirrups. The vagina is surgically prepared, and a Foley catheter containing a 10-mL balloon is placed in the bladder to assist in identifying the bladder neck.

➋╇ Cystourethroscopy.╇ This procedure

is performed at the procedure’s onset to attempt diverticular opening identification and exclude other abnormalities.

➌╇ Vaginal Incision.╇ To begin, a midline

or U-shaped incision is made on the anterior vaginal wall over the diverticulum, and the vaginal epithelium is dissected sharply off the fibromuscular layer of the vaginal wall (Fig. 45-9.1). Ample epithelium is freed to allow adequate exposure and to permit final tissue approximation without suture-line tension.

➍╇ Diverticulum Exposure.╇Next, the

fibromuscular layer of the vagina and urethra is incised with a longitudinal or transverse incision to reach the diverticular sac. Anatomically, the distal vaginal and urethral walls are fused, and it may be difficult or impossible to separate tissue planes. Thus, sharp dissection is needed to completely mobilize the diverticular sac away from the vaginal and urethral fibromuscular layer and to the level of the diverticular sac neck (Fig. 45-9.2). During dissection, the sac may be inadvertently or intentionally entered. With this, the diverticular walls can be grasped with Allis clamps to create tension across the connective tissue fibers between the diverticular

■⌀ Consent With diverticular repair, damage to urethral continence mechanism may lead to postoperative incontinence. Alternatively, urethral stricture or stenosis or urinary retention may develop depending on the extent and location of surgery. Additionally, urethrovaginal

FIGURE 45-9.1╇ Vaginal incision.

CHAPTER 45

Urethral Diverticulum Repair

fistula and bladder injury can result. Recurrence rates of 10 to 25 percent have been reported, especially with a horseshoe or circumferential configuration or previous surgical intervention (Antosh, 2011; Ingber, 2011). Failures are believed secondary to incomplete diverticulum excision. Moreover, urethral pain can persist or arise after diverticulectomy (Ockrim, 2009). Recurrent UTI can also persist. Last, with the Spence marsupialization technique, a distal diverticulum and urethral orifice are sharply opened together to form a large single meatus. Thus, external urethral orifice anatomy is usually altered, and a spraying pattern with urination may result.

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SECTION 6 Vaginal epithelium Fibromuscular layer Vaginal epithelium Fibromuscular layer

FIGURE 45-9.2╇ Diverticular sac dissection. walls and the vaginal fibromuscular layer to aid dissection. Similarly, an index finger placed within the sac can recreate sac fullness to stretch these same connective tissue fibers. Dissection is then continued until the diverticulum’s communication with the urethra is isolated. Caution and awareness of urethral location are essential to avoid damage.

FIGURE 45-9.3╇ Diverticulum excision.

➎╇ Diverticulum Excision.╇At its neck, the diverticulum is excised from the urethra (Fig. 45-9.3). ➏╇ Urethral Closure.╇ The urethral defect is closed with interrupted 4-0 gauge delayedabsorbable sutures over the Foley catheter (Fig. 45-9.4). Fibromuscular layers of the

urethra and vagina are then reapproximated off tension in two or more layers. For this closure, a vest-over-pants method with 2-0 gauge delayed-absorbable suture is preferred when possible to avoid overlapping suture lines (Fig. 45-9.5). Redundant vaginal epithelium is trimmed, and the epithelium is closed in a running fashion with 2-0 gauge delayed-absorbable suture.

■⌀ Surgical Steps—Partial Diverticular Ablation If extensive dissection is required around the trigone, consideration is given to leaving the proximal portion of the sac in place to avoid direct injury or denervation injury. In addition, ureteral stents may be beneficial during the dissection.

➊╇ Vaginal Incision.╇ Again, a midline or U-shaped incision is made on the anterior vaginal wall over the diverticulum, and the vaginal epithelium is dissected sharply off the fibromuscular layer of the vaginal wall. Ample epithelium is freed to allow adequate exposure and later defect closure off tension. The Foley catheter and balloon can be placed on gentle tension to aid in identifying the bladder and bladder neck to avoid injury. ➋╇ Diverticulum Exposure.╇ A longitudi-

FIGURE 45-9.4╇ Urethral defect closure.

nal incision is made through the fibromuscular layer to the diverticular sac, and sharp dissection is used to completely mobilize and expose the sac. The diverticulum is opened,

Surgeries for Pelvic Floor Disorders

➋╇ Marsupialization.╇ For

marsupialization, cut edges of the diverticular sac are reapproximated to the vaginal epithelium in a running pattern using 4-0 gauge delayedabsorbable suture. Ultimately, the urethral orifice is widened by this incorporation of the diverticular sac diameter.

POSTOPERATIVE FIGURE 45-9.5╇ Fibromuscular layer reapproximation.

and the communication with the urethra is identified. To avoid injury to the proximal urethra and bladder neck, the diverticular sac, but not the neck of the diverticulum, is sharply excised. As much of the sac as can be accessed is removed.

➌╇ Sac Closure.╇ The base of the sac is then sutured side to side with 3-0 gauge delayedabsorbable suture to cover the urethral defect. A second, and possibly a third, imbricating layer using the vaginal muscularis is

created with similar suture. Excess vaginal epithelium that had previously covered the diverticulum is excised. The vaginal epithelium is closed in a running fashion with a 2-0 gauge delayed-absorbable suture.

■⌀ Surgical Steps—Spence Marsupialization ➊╇ External Urethral Orifice Incision.╇ Tips of Metzenbaum scissors are inserted

Catheter management is an important aspect of postoperative care. Although no consensus guidelines exist, most experts recommend catheter placement for 5 to 7 days. Surgeries of increasing complexity may require longer duration. Antibiotic suppression is not required with this catheter use. Normal diet and activity can resume during the first postoperative days. Intercourse, however, is postponed until the vaginal incision is well healed.

CHAPTER 45

into the urethral orifice and vagina. An incision is made that incorporates and simultaneously incises the posterior urethral wall, entire thickness of the diverticulum, and distal anterior vaginal wall. By this incision, the external urethral orifice ring is opened and its communication into the diverticular sac is enlarged.

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45-10 SECTION 6

Vesicovaginal Fistula Repair Vesicovaginal fistulas may be repaired either vaginally or abdominally. A vaginal approach is preferred for most fistulas seen in the United States, which are posthysterectomy, apical fistulas. This approach offers comparable success rates, lower morbidity, and faster patient recovery. Of vaginal methods, the one most commonly performed by gynecologists is the Latzko technique. With this, surrounding vaginal epithelium is reflected away from the fistulous tract. The tract is then resected, but the portion into the bladder is not excised. This avoids a large bladder defect, which can develop with resection of even relatively small fistulas. Following excision, layered closure of the vaginal incision seals the leak. If performed for fistulas at the vaginal apex, then both anterior and posterior vaginal wall epithelia are reflected for tract access. In this location, the final layered closure simulates the steps of colpocleisis, and thus the Latzko technique for apical fistulas is often likened to a proximal partial colpocleisis (p. 1120). Alternatively, in some cases, the fistulous tract can be completely excised vaginally, and a layered repair of the bladder and then vaginal wall follows. This is preferred by many if the fistulous opening is less than 5 mm in diameter and distant from ureteral orifices. At times, an abdominal approach may be necessary for women in whom fistula location prohibits effective surgical access or in whom prior vaginal repairs have been unsuccessful. The most commonly described abdominal approach, termed the O’Conor technique, is outlined here and involves bisecting the bladder wall to enter the fistulous tract. Modifications to this as well as an extravesical approach have been described, especially during laparoscopic or robotic routes to fistula repair (Miklos, 2015). With any abdominal approach, omentum or peritoneum can be mobilized and interposed between the bladder and vagina in an attempt to prevent recurrence. One principle of fistula repair dictates that a repair be performed in noninfected and noninflamed tissues. A second states that tissue must be approximated without excess tension. Last, a multilayer, watertight closure aids reestablishment of bladder integrity. If these guidelines are followed, success rates are typically good and approximate 95 percent (Rovner, 2012). In the United States, most fistulas follow hysterectomy for benign

causes, and repair of these fistulas is associated with high cure rates. In contrast, fistulas associated with gynecologic cancer and radiation therapy may require adjunctive surgical procedures such as vascular or myocutaneous flaps. These flaps provide supportive blood supply to defects that develop in poorly vascularized or fibrotic tissue. Even with these measures, success rates are lower.

PREOPERATIVE ■⌀ Patient Evaluation Prior to repair, a fistula should be well characterized, and complex fistulas with multiple tracts or a primary or concomitant ureterovaginal fistula should be identified. Proper evaluation typically includes cystoscopy and imaging that displays the upper and lower urinary tract such as CT urography (pyelography) or intravenous pyelography (IVP) (Fig. 26-2, p. 580). Ureterovaginal fistulas are usually associated with upper tract abnormalities such as hydroureter and hydronephrosis. Therefore, normal IVP or CT findings are reassuring that ureteral involvement is absent. Additionally, this imaging complements cystoscopy in ascertaining the proximity of ureters relative to a fistula for surgical planning. In general, routine posthysterectomy vesicovaginal fistulas develop midline at the vaginal apex and usually away from the ureters, which enter the bladder at the midlength of the vagina. However, lateral fistulas raise concern for ureteral involvement or proximity. Whether or not surgery can be performed vaginally largely depends on the ability to adequately expose the fistula. Thus, during physical examination, a surgeon assesses if a fistula can be brought down into the surgical field and if a patient’s pelvis affords adequate space. Some degree of prolapse of the vaginal apex is helpful for fistula repair. However, a final decision on the repair route is sometimes made intraoperatively, when muscle relaxation from anesthesia allows better assessment of access. Additionally, tissue infection or inflammation is sought, and if it is identified, fistula repair is delayed until resolution. Fistulas recognized within a few days following hysterectomy may be repaired immediately, prior to the brisk inflammatory response. However, if surgical repair is not undertaken within a few days following the initial surgery, a delay of approximately 6 weeks is recommended to permit tissue inflammation abatement.

■⌀ Consent Fistulas may redevelop following repair, and patients are counseled that initial surgery may not be curative. With the Latzko

procedure, the vagina is moderately shortened in most cases. Thus, the risk of postoperative dyspareunia is included during surgical consenting. However, a recent study showed that fistula repair improves sexual function and quality of life, with no attributed difference between vaginal and abdominal routes (Mohr, 2014).

■⌀ Patient Preparation Immediately prior to surgery, intravenous antibiotics and thromboprophylaxis are commonly administered (Tables 39-6 and 39-8, p. 835). The necessity of bowel preparation for this procedure is unclear, and administration is individualized.

INTRAOPERATIVE ■⌀ Surgical Steps—Vaginal Repair ➊╇ Anesthesia and Patient Positioning.╇ In most cases, repair is performed with general or regional anesthesia, and postoperative hospitalization is individualized. The patient is placed in standard dorsal lithotomy position, and the vagina is surgically prepared. If ureters lie close to a fistula, ureteral stents are placed (p. 1059). Cystoscopy is required during the procedure to document ureteral patency and assess bladder integrity.

➋╇ Delineating a Fistulous Tract.╇ Initially,

the course of a fistulous tract is identified. If a tract is wide enough to accept a pediatric catheter, the tube is threaded through the fistulous tract, and the balloon is inflated within the bladder. If a tract cannot be delineated in this manner, then lacrimal duct probes, ureteral stents, or other suitable narrow dilators are used to trace the tract course and direction. Subsequently, attempts are made to dilate the tract and place a pediatric catheter.

➌╇ Exposure.╇ For repair, the fistula is

brought into the operative field. If catheterization of the tract is possible, tension on the catheter will allow this. Alternatively, four sutures can be placed in the vaginal wall surrounding the fistula and used to pull the fistula into the operative field (Fig. 45-10.1). Some advocate performing a mediolateral episiotomy to gain exposure, although this is not our practice.

➍╇ Vaginal Incision.╇ A vaginal incision is

made circumferentially approximately 1 to 2 cm around the fistulous tract (Fig. 45-10.2). Vaginal epithelium surrounding the tract is sharply mobilized laterally and away from vaginal fibromuscular wall and then excised with Metzenbaum scissors.

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FIGURE 45-10.1╇ Stay sutures in the vaginal wall improve fistula access.

➎╇ Tract Excision.╇ The fistula tract may or may not be totally excised to the level of the bladder. As noted earlier, complete tract excision creates a larger bladder defect for repair. Also, we prefer not to excise a fistulous tract lying near a ureteral orifice to avert potential ureteral injury and need for reimplantation (Blaivas, 1995).

FIGURE 45-10.2╇ Vaginal epithelium incision.

■⌀ Surgical Steps— Abdominal Repair ➊╇ Anesthesia and Patient Positioning.╇ In most cases, abdominal repair is performed under general anesthesia. The patient is placed in low lithotomy position within booted support

stirrups. With the patient’s thighs parallel to the ground and the legs separated, access to the vagina is maximized. The abdomen and vagina are surgically prepared, and a Foley catheter is inserted.

➋╇ Abdominal Incision and Bladder Entry.╇ A low transverse or midline abdominal

➏╇ Fistula Closure.╇If a tract is totally

excised, the bladder mucosa is reapproximated with 3-0 gauge delayed-absorbable suture in an interrupted or running fashion. Following this closure, the bladder is retrograde filled with at least 200 mL of fluid to exclude leaks. If a defect is found, additional reinforcing sutures are placed until a watertight repair is achieved. Regardless of whether the tract is completely or partially excised, anterior and posterior bladder and vaginal muscular layers are then approximated over the fistula site. For this, an interrupted or running suture line of 3-0 or 2-0 gauge delayed-absorbable sutures is created (Fig. 45-10.3). Beginning proximally and adding distally, sequential suture lines are layered (Fig. 45-10.4). After muscular layers of the bladder and vaginal walls are closed, the vaginal epithelium is closed in a continuous running fashion using 3-0 or 2-0 gauge delayed-absorbable suture.

❼╇ Cystoscopy.╇ Cystoscopy is again per-

formed to document ureteral patency and to inspect the incision site.

FIGURE 45-10.3╇ First-layer closure over fistula.

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Atlas of Gynecologic Surgery ➌╇ Fistulous Tract Delineation and ExÂ�

SECTION 6

cision.╇ After cystotomy, the fistula and ureteral orifices are seen from within the bladder. If the fistulous tract is near the orifices, ureteral stents are placed. From the dome, the cystotomy incision is extended over the top and then back of the bladder to reach the circular fistulous opening (Fig. 45-10.5). A lacrimal probe or catheter may be placed into the fistulous tract to delineate its course. The tract is then excised. In contrast and less commonly, if a fistula tract lies close to the trigone, extension of the bladder incision to the fistulous tract may not be desired, as the resulting bladder defect would be extensive. In these cases, the entire fistulous tract is directly excised using only the bladder dome incision. However, vascular flap interposition with this approach is limited as the bladder wall is not significantly dissected off the vaginal wall.

➍╇ Separation of the Bladder and

FIGURE 45-10.4╇ Second fibromuscular layer closure over fistula and vaginal epithelium reapproximation.

entry incision can be used. If mobilization of the omentum is anticipated, a vertical midline incision can provide greater access to the upper abdomen. A Maylard or Cherney incision may alternatively be selected (Section 43-3, p. 931). After the peritoneum is entered, the abdomen is explored, bowel is packed from the operating field, and a self-retaining abdominal wall retractor is placed. The space of Retzius is opened using the technique

FIGURE 45-10.5╇ Bladder incision.

described on page 1061. Next, a vertical midline extraperitoneal incision is made into the bladder dome. Prior to this incision, pushing the Foley balloon up or filling the bladder helps avoid grasping and then cutting the posterior bladder wall.

Vagina.╇ In cases with bladder bisection, sharp dissection is used to separate the vagina away from the bladder in the area of the fistula (Fig. 45-10.6). Scarring may be extensive, and sharp rather than blunt dissection is preferred. To assist, the rounded tip of an end-to-end anastomosis (EEA) sizer can be placed in the vagina to manipulate and accentuate the dissection plane (Fig. 46-21.4, p. 1202). The vagina is widely separated from the bladder to allow omentum or peritoneal flap placement between the two.

FIGURE 45-10.6╇ Separation of the bladder and vagina.

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FIGURE 45-10.8╇ First-layer bladder closure.

FIGURE 45-10.7╇ Vaginal closure.

➎╇ Vaginal Closure.╇ The vagina is closed in one or two layers with 2-0 gauge delayedabsorbable suture and running or interrupted stitches (Fig. 45-10.7). The EEA sizer or fingers within the vagina can accentuate the vaginotomy margins to aid closure. ➏╇ Bladder Closure.╇ The entire bisecting bladder incision is closed in two or three layers using running sutures of 3-0 gauge absorbable suture (Fig. 45-10.8). As with the vaginal approach, after the first layer, the bladder is retrograde filled with at least

200 mL, and incision-line leaks are sought. If defects are noted, additional reinforcing sutures are placed to achieve a watertight repair. During bladder closure, each subsequent layer is imbricated such that the preceding suture line is covered and tension is released (Fig. 45-10.9). If the bladder is not bisected and the fistulous tract is directly excised solely through the bladder dome cystotomy, then the muscular wall of vagina is first repaired in one or two layers as in Step 5. Second, the bladder wall at the fistula excision site is closed in one or two

FIGURE 45-10.9╇ Second-layer bladder closure.

layers using a running stitch of 3-0 absorbable suture. Next, the bladder mucosa is reapproximated with a single-layer running stitch of 3-0 absorbable suture. Last, the entry bladder dome incision is closed similarly, except the bladder mucosa is reapproximated first and followed by bladder wall closure in layers.

❼╇ Omental or Peritoneal Interposition.╇ As described in Section 46-14 (p. 1186), the omentum can be mobilized to create a J-flap. The omentum is then sutured to the anterior wall of the vagina to cover the incision

FIGURE 45-10.10╇ Omentum interposition.

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to document ureteral patency and inspect the incision site.

SECTION 6

➒╇ Incision Closure.╇ The abdominal inci-

sion is closed as described in Chapter 43 (p. 931).

POSTOPERATIVE

FIGURE 45-10.11╇ Peritoneum interposition. line (Fig. 45-10.10). This provides a tissue layer between vagina and bladder, increases vascular flow to the area, and may improve tissue healing. Alternatively, if the omentum

cannot be mobilized, peritoneum, although less vascular, can be interposed and creates another barrier layer between the bladder and vagina (Fig. 45-10.11).

The bladder is drained postoperatively to prevent overdistention and suture disruption. Either transurethral or suprapubic catheter placement will ensure adequate drainage in the immediate postoperative period. At our institution, we generally continue catheterization for at least 2 weeks following vesicovaginal fistula repair. Antibiotic suppression is not required with this catheter use.

Surgeries for Pelvic Floor Disorders

45-11

This vascular graft contains the fat pad overlying the bulbospongiosus (formerly called bulbcocavernosus) muscle and brings a supportive blood supply to repairs involving avascular or fibrotic tissue. As such, this graft is commonly used in complex urethral diverticulum excisions or in complex rectovaginal or vesicovaginal fistula repairs. However, of these indications, there is some evidence supporting successful repair of certain recurrent fistulas without vascular graft interposition (Miklos, 2015; Pshak, 2013). During graft placement, one end of the bulbocavernosus fat pad is dissected free and subsequently brought to the repair site through the primary vaginal incision. Thus, due to its anatomic origin and limited length, this fat pad, when indicated, is selected for defects involving the low to mid-vagina.

PREOPERATIVE ■⌀ Patient Evaluation In most instances, graft placement is anticipated for those with prior radiation or with fistula recurrence. Thus, preoperative planning includes assessment of tissue vascularity, connective tissue strength, and ability to adequately mobilize vaginal tissues to create a multilayered repair closure. For this procedure, a woman must have adequate labial fat, which is also assessed prior to surgery.

FIGURE 45-11.1╇ Labial incision.

During consenting, women are informed of the potential for postoperative vulvar numbness, pain, paresthesias, or hematoma. Because one of the labia majora is repositioned as the graft, patients are counseled regarding the cosmetic consequences.

■⌀ Patient Preparation Because of the risk of poor wound healing in these complicated repairs, antibiotic prophylaxis listed in Table 39-6 (p. 835) is warranted. Thromboprophylaxis is given as outlined in Table 39-8 (p. 836. The necessity of bowel preparation for this procedure is unclear, and administration is individualized based on concomitant procedures.

INTRAOPERATIVE ■⌀ Surgical Steps ➊╇ Anesthesia and Patient Positioning In most cases, a Martius flap graft and fistula repair can be performed with general or regional anesthesia, and the need for postoperative hospitalization is individualized. The patient is positioned in standard lithotomy position, the vagina is surgically prepared, and a Foley catheter is inserted.

and graft size needed. In many cases, a 6- to 8-cm incision is made beginning below the level of the clitoris and is extended inferiorly.

➍╇ Mobilization of the Fat Pad.╇ The vulvar incision edges are retracted laterally, and sharp dissection is used to free the labial fat pad (Fig. 45-11.2). This tissue is vascular, and vessels ideally are ligated or coagulated prior to transection. For rectovaginal fistulas, a broad base is left inferiorly, and the fat pad is detached superiorly. For vesicovaginal and urethrovaginal fistulas or urethral diverticula, the broad base of the pad is maintained superiorly, while the fat pad is detached inferiorly. In each instance, releasing the pad with this specific polarity anatomically permits the largest possible graft to cover the repair site. Occasionally, bilateral fat pads are needed. ➎╇ Graft Placement.╇ After the pad is freed,

a tunnel is created by bluntly dissecting with a hemostat that travels from the vulvar incision, underneath the vaginal epithelium, and to the vaginal incision at the repair site. The tunnel must be sufficiently broad to avoid vascular compression and graft necrosis. A suture is placed at the graft tip and used to pass the graft through the tunnel and into the vagina (Fig. 45-11.3).

➏╇ Graft Fixation.╇The graft is secured

specific defect is repaired as outlined in its respective section of this chapter.

to the vaginal muscularis overlying the repair site with several interrupted stitches using 3-0 gauge delayed-absorbable suture (Fig. 45-11.4).

➌╇ Labial Incision.╇After repair comple-

❼╇ Incision Closure.╇With hemostasis

➋╇ Fistula or Diverticulum Repair.╇ The

tion, the lateral margin of one labium majus is incised (Fig. 45-11.1). The length of the incision is tailored to specific labial anatomy

established, the vulvar incision is closed along its length using continuous or interrupted stitches of 3-0 gauge delayed-absorbable

FIGURE 45-11.2╇ Mobilization of the fat pad.

CHAPTER 45

Martius Bulbocavernosus Fat Pad Flap

■⌀ Consent

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SECTION 6 FIGURE 45-11.3╇ Graft placement.

sutures. For a deep cavity at the harvest site, fatty tissue may be reapproximated in layers to close this space with several interrupted 2-0 or 3-0 gauge delayed-absorbable sutures. Alternatively, a drain may be placed in the cavity. The vaginal epithelium overlying the defect repair is closed in a continuous running

FIGURE 45-11.4╇ Graft fixation.

fashion using 3-0 gauge delayed-absorbable suture.

POSTOPERATIVE Care after surgery is predominantly dictated by the associated defect repair. Ideally, the

vaginal and perineal sites are kept dry rather than wet, and baths are avoided during the first 6 weeks. After each void or stool, patients rinse with a water-filled squirt bottle and gently pat dry.

Surgeries for Pelvic Floor Disorders

PREOPERATIVE

Sacral Neuromodulation

■⌀ Patient Evaluation

Sacral neuromodulation or sacral nerve stimulation (SNS) electrically stimulates the sacral nerves to modulate reflexes that influence the bladder, sphincters, and pelvic floor (Noblett, 2014). Currently, the InterStim System is the only implantable SNS device that is Food and Drug Administration (FDA)-approved for the following primary indications: urgency-frequency, urgency urinary incontinence, nonobstructive urinary retention, and fecal incontinence. Although not FDA-approved for chronic pelvic pain, interstitial cystitis/painful bladder syndrome, or chronic idiopathic constipation, it may sometimes be used if these symptoms coexist with the previously listed primary indications. This surgery is typically offered to women who have failed to adequately improve with multiple other conservative therapies. The mechanism of action is unclear, but one explanation describes modulation of reflex neural pathways involved with bladder storage and emptying and with innervation of the pelvic floor. Of these, pudendal afferent somatic fibers are thought to play an important role (deGroat, 1981; Gourcerol, 2011). SNS is generally completed in two phases. First, during a test phase, a slender, 30-cm long permanent lead that conducts electrical impulses to its tip is placed into one posterior sacral foramen and adjacent to a sacral nerve root, most commonly S3. This lead is connected to a temporary external pulse generator to permit an efficacy trial lasting 1 to 2 weeks. If symptoms are decreased by at least 50 percent, then the patient is deemed a suitable candidate for permanent generator implantation. During the second or implantation phase, the lead is connected a permanent implantable pulse generator (IPG), and the IPG is tucked within a subcutaneous pocket created in the buttock. This staged approach is illustrated in these atlas pages. A variation of these classic steps, termed percutaneous nerve evaluation (PNE), in� serts a temporary lead through the S3 foramen in the office, under local anesthesia, and generally without fluoroscopic guidance. However, despite these advantages, the trial period with PNE is brief (3 to 7 days), and the less securely anchored temporary lead more easily migrates away from the target nerve.

Preoperative testing will vary depending on the indication. For urinary symptoms, women undergo full evaluation including urodynamic testing, voiding diary, cystoscopy, and other selected tests described in Chapter 23 (p. 523). For fecal incontinence, colonoscopy, endoanal sonography, manometry, and possibly pudendal nerve testing, described in Chapter 25 (p. 564), are completed during evaluation.

■⌀ Consent Failure to significantly improve symptoms may follow either SNS phase. However, approximately 70 percent of those who undergo permanent IPG implantation achieve a greater than 50-percent symptom improvement (Van Kerrebroeck, 2012). Pain at the IPG site and superficial wound infection may also complicate either phase. Long-term adverse changes include altered bowel or bladder function, undesirable sensations, neurostimulator site numbness, lead migration, and surgical device revision, replacement, or required removal. The IPG device is a relative contraindication for MR imaging, although certain IPG models permit head imaging.

■⌀ Patient Preparation A single prophylactic antibiotic dose may or may not be administered according to surgeon preference. Although not rigorously studied, prophylaxis is recommended by some due to needle passage from skin

FIGURE 45-12.1╇ Foramen needle insertion.

to perineural tissue in the presacral space. Thromboprophylaxis is typically not required given the procedure’s short duration.

INTRAOPERATIVE ■⌀ Surgical Steps ➊╇ Anesthesia and Patient Positioning.╇ Although the procedure can be performed using local anesthesia and intravenous sedation, we prefer general anesthesia for the test phase. Importantly, neuromuscular blockade prohibits adequate motor response evaluation and is contraindicated. The patient is positioned prone on a Wilson frame or with a pillow under the lower abdomen to flex the hip 30 degrees for easier access to the sacrum. Pillows are also placed under the shins to allow the toes to move freely during test stimulation. The drape is positioned to permit inspection of the pelvic floor and soles for muscle responses. The area from the lower back to the perineum is surgically prepared. A Foley catheter is typically not required due to the surgery’s brevity.

➋╇ Identification of S3 Foramina.╇ These

landmarks for lead placement are located approximately 9 cm above the coccyx and 1 to 2 cm lateral to the midline (Fig. 45-12.1). Fluoroscopy is currently the most common method of identifying the necessary bony landmarks intraoperatively. The fluoroscopic C-arm is draped and moved into the anteroposterior (AP) position to allow mapping of the sacral region including foramina. With this, the skin overlying the S3 foramina is outlined with a surgical marker.

CHAPTER 45

45-12

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SECTION 6 FIGURE 45-12.2╇ Correct lead positioning.

➌╇ Foramina Needle Insertion.╇ An insu-

lated foramen needle is inserted through the skin at a site approximately 2 cm lateral to the midline, 2 cm superior to the sciatic notch, and cephalad to the inked outline of the foramen. The needle is guided at a 60-degree angle caudally until the S3 foramen is penetrated. Optimally, the needle is placed into the medial and superior aspect of the S3 foramen. The needle penetrance depth, which is usually 2.5 to 4.0 cm, is confirmed and adjusted with fluoroscopic guidance by a laterally positioned C-arm. Once in place, the needle is used to conduct electrical test impulses to the S3 nerve. This nerve contracts the levator ani muscles to create an inward retraction or “bellows” movement. S3 stimulation also causes the great toe to flex downward, that is, plantar flexion. In anesthetized patients, a sensory response cannot be elicited, but evidence suggests that motor responses may be more or at least as predictive of success (Cohen, 2006; Govaert, 2009; Peters, 2011). The typical patient sensation with S3 stimulation is a tapping or vibration in the vagina, rectum, or perineum. Once the desired S3 motor reflexes are obtained (“bellows and toe”), lead placement is initiated. If these are absent, needle depth or angle is adjusted to achieve the desired responses. Also, a needle in the contralateral foramen or in a foramen up or down one vertebral space may be tried.

Next, using fluoroscopy, the long, flexible lead is passed down the introducer sheath into the S3 foramen. To aid threading, the lead contains a temporary stiff inner stylet. A recently introduced curved stylet better follows anatomic contours to position the lead close to the nerve root (Jacobs, 2014). The lead also contains four circumferential electrode bands arranged in series at its tip, and proximal to these lie four plastic barbs or tines to ultimately anchor the lead within soft tissues (Fig. 45-12.2). With correct lead positioning as shown, the most proximal of the four electrode bands are fluoroscopically visible just anterior to the sacrum. All four electrodes on the lead should conduct pulses and elicit S3 motor responses. If necessary, the lead can be repositioned within the foramen. Once correctly positioned, the introducer sheath and

then the curved lead stylet are removed. As the introducer sheath is removed, the four tines or barbs lock into place. Thus, the lead cannot be retracted after this point. All four electrodes are again tested to confirm the previously observed responses. If lead advancement is needed, its stylet is replaced and the lead advanced. Retraction is more problematic. The lead is removed using gentle traction, and Steps 3 and 4 are repeated. The desired range of stimulation amplitude to achieve desired motor responses is 1 to 2 milliamps. Responses at lower amplitudes may indicate that the lead lies too close to the nerve, whereas requisite higher amplitudes can decrease battery longevity.

➎╇ Pulse Generator Incision and Lead

Passage.╇ Several centimeters below the iliac crest, a 4-cm transverse incision is made over the lateral portion of the buttock that is ipsilateral to the selected foramen. Sharp and blunt dissection is used to create a deep pocket that can house the extension device for the temporary external pulse generator and eventually, the permanent IPG. The pocket should remain above the gluteal muscle fascia but is made sufficiently deep to accommodate the final IPG. After the pocket is created, a pointed passing device is used to create a narrow tunnel between the lead and the pocket (Fig. 45-12.3). The core of the passing device is removed, leaving a hollow straw within the tunnel (inset). The lead is then manually threaded laterally

➍╇ Lead Placement.╇ Once positioned, the

stylet present within the foramen needle is removed and replaced with a guide wire to the appropriate depth. The foramen needle is then removed while holding the guide wire in place. A small incision is made on either side of the guide wire, and a combined introducer sheath/hollow dilator tool is then slid over the guide wire to occupy the foramen needle’s former position. The hollow dilator is unscrewed from the introducer sheath, and the dilator and guide wire are removed together. This leaves only the introducer sheath in place.

FIGURE 45-12.3╇ Pulse generator incision and lead passage.

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through this straw and into the pocket. The straw is then removed laterally.

FIGURE 45-12.4╇ Within pocket, lead joins extension wire that extends to temporary pulse generator.

(First Phase).╇Within the subcutaneous pocket, the lead is next connected to an extension wire that serves to join the lead to the temporary pulse generator (Fig. 45-12.4). A stab incision is then created lateral to the pocket. The passing device is again used and, this time, guides the extension wire through a second tunnel between the pocket and stab incision. The subcutaneous tissue is then closed over the connector in the pocket with 2-0 gauge delayed-absorbable suture in an interrupted or running fashion. The skin is closed with a subcuticular stitch using 4-0 gauge delayed-absorbable suture or with other suitable skin closure methods. Similarly, the stab incision is closed. Last, the extender wire is joined to a temporary external pulse generator, which is used for 1 to 2 weeks (see Fig. 45-12.4).

❼╇ Implantable Pulse Generator PlaceÂ�

ment (Second Phase).╇ If significant symptom relief is obtained, the permanent IPG is placed 1 to 2 weeks after initial surgery. The procedure is performed with the patient prone and usually with general anesthesia for airway control. The buttock incision is opened down to the connector. The connector and extension wire are removed. The permanent IPG is connected to the lead, and then placed into the subcutaneous pocket (Fig. 45-12.5). The incision is closed again as in Step 6.

POSTOPERATIVE

FIGURE 45-12.5╇ Final implanted pulse generator.

Pain or erythema at the incision site suggests cellulitis, abscess, or seroma. These symptoms are evaluated as soon as possible, and antibiotics are instituted if needed. Unusual pain is also evaluated immediately as this could suggest lead malfunction. A woman can turn the device off by herself if necessary. Primary symptoms are continually assessed postoperatively, and the IPG is reprogrammed as needed. Reprogramming the device or changing leads will often lead to symptom improvement.

CHAPTER 45

➏╇ Placement of the Extension Device

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45-13

PREOPERATIVE

INTRAOPERATIVE

Anterior Colporrhaphy

■⌀ Patient Evaluation

■⌀ Surgical Steps

The anterior vaginal wall is the most frequent site of clinically recognized prolapse (Brincat, 2010). One method to correct this is anterior colporrhaphy, which reapproximates attenuated fibromuscular tissue between the vagina and bladder to elevate the bladder to a more anterior and anatomically normal position. Anatomic success rates following this surgery are modest at 1 year (Altman, 2011; Weber, 2001). Thus, strategies to improve these colporrhaphy rates include: (1) concurrent vaginal paravaginal defect repair (PVDR), (2) concurrent apical support surgeries, or (3) synthetic or biologic mesh placement instead of or in addition to colporrhaphy. Of these, PVDR attempts to provide lateral support to the anterior vaginal wall. However, the vaginal PVDR is less favored as its required dissection creates a large defect within tissue that carries significant nerves and vessels. Also, efficacy data are lacking. Synthetic mesh placement is associated with improved anterior prolapse anatomic outcomes (61 versus 35 percent) (Altman, 2011). But this disparity in anatomic success does not always reflect symptom success rates (Chmielweski, 2011). Symptom improvement rates for mesh range from 75 to 96 percent compared with ranges of 62 to 100 percent for native tissue (Lee, 2012). Moreover, mesh use significantly increases risks of mesh erosion, vaginal lumen narrowing, and pelvic abscess (Maher, 2013). These may be associated with dyspareunia, urinary complaints, and chronic pelvic pain (Food and Drug Administration, 2011). Currently, few data guide patient selection for mesh placement, which may be best reserved for those with recurrent prolapse or those with medical comorbidities that preclude alternative procedures (American College of Obstetricians and Gynecologists, 2011). Moreover, surgeons using mesh need adequate training and experience, and patients are educated regarding risks and benefits. Alternatively, cadaveric fascia has been similarly used, but surgical success using this tissue is not significantly improved compared with colporrhaphy alone (Gandhi, 2005). Last, increasing data suggest that vaginal apex support plays a critical role in anterior vaginal wall suspension (Lowder, 2008; Summers, 2006). Thus, anterior colporrhaphy is now often complemented by apical support procedures.

As stated, women with anterior wall prolapse often have other compartment defects, and a complete POP-Q examination, described in Chapter 24 (p. 540), aids surgical planning. In addition, anterior vaginal wall prolapse is frequently associated with stress urinary incontinence (SUI) (Borstad, 1989). Even those who are continent, however, may have occult SUI unmasked following prolapse correction. Thus, preoperative urodynamic evaluation is often recommended. During this evaluation, the prolapse is reduced to its anticipated postoperative position to mimic pelvic floor anatomy and dynamics following surgery (Chaikin, 2000; Yamada, 2001). The decision to perform a concurrent prophylactic antiincontinence procedure is then dictated by individual urodynamic findings and adequate patient counseling.

■⌀ Consent For most women, anterior colporrhaphy has low complication rates. Of these, recurrence of the anterior vaginal wall defect is one of the most frequent. De novo SUI described earlier, prolonged catheter use for urinary retention, and voiding dysfunction are also discussion points. Although infrequent, postoperative dyspareunia is another cited complication. However, preoperative symptoms related to sexual function in general improve with anterior colporrhaphy (Weber, 2001). Uncommonly, serious hemorrhage, cystotomy, or ureteral injury may occur intraoperatively. If mesh is used, these latter risks may be increased, and bowel or ureteral injury is possible. Accordingly, intraoperative cystoscopy is recommended. Less common short-term postoperative mesh complications include wound infection or hematoma. Long-term data from randomized trials show mesh erosion rates that range from 5 to 19 percent; chronic pain, up to 10 percent; and dyspareunia, 8 to 28 percent (American College of Obstetricians and Gynecologists, 2011).

➊╇ Anesthesia and Patient Positioning.╇ After adequate general or regional anesthesia is administered, a patient is placed in standard lithotomy position, the vagina is surgically prepared, and a Foley catheter inserted. A short Auvard weighted speculum may be positioned to retract the posterior vaginal wall.

➋╇ Concurrent Surgery.╇Anterior colporrhaphy can be performed with the uterus in situ or alternatively, following hysterectomy. If other reconstructive surgeries are required, they may precede or follow anterior colporrhaphy.

➌╇ Vaginal Incision.╇ In those with prior

hysterectomy and adequate apical support, two Allis clamps are placed on each side of the midline, 1 to 2 cm distal to the vaginal apex or at the upper extent of the anterior vaginal wall prolapse (Fig. 45-13.1) Clamps are gently pulled laterally to create tension, and the vaginal wall between them is incised transversely. If hysterectomy precedes the repair, the two Allis clamps are placed at the opened cuff edge on either side of midline. A third clamp is placed in the midline vaginal wall, 3 to 4 cm distal to the apical transverse incision. All three clamps are held, creating gentle outward tension. Metzenbaum scissors tips are insinuated beneath the epithelium in the midline of the previously made transverse incision and directed away from the vaginal apex. Scissor blades are opened and closed, while the surgeon exerts gentle

■⌀ Patient Preparation Bowel preparation is generally not indicated for isolated anterior colporrhaphy but may be recommended at the surgeon’s discretion if other compartmental repairs are planned. Antibiotic prophylaxis with a first- or second-generation cephalosporin is recommended immediately prior to surgery as cystoscopy is also performed. Thromboprophylaxis is given as outlined in Table 39-8 (p. 836).

FIGURE 45-13.1╇ Tissue plane dissection.

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CHAPTER 45

FIGURE 45-13.2╇ Vaginal wall incision. forward pressure that is parallel to and within the plane beneath the vaginal epithelium. This technique allows separation of the epithelium from the fibromuscular layer. This dissection continues caudad to reach the distal, midline Allis clamp. The undermined vaginal wall is then incised in the midline longitudinally. The midline Allis clamp is then replaced more distally, and the process continues until the vaginal epithelium has been divided to within 2 to 3 cm of the external urethral opening (Fig. 45-13.2). This ending spot corresponds to a midpoint along the length of the urethra. If the anterior wall prolapse does not extend distally beyond the bladder neck, then the distal epithelial incision terminates at the neck. In addition, if a concurrent midurethral sling is planned, the colporrhaphy incision terminates just proximal to the bladder neck to allow a separate incision for sling placement.

FIGURE 45-13.3╇ Separation of epithelium from fibromuscular layer. line plication. The steps are then repeated on the contralateral side.

span of attenuated tissue. However, excessive tension is avoided to prevent sutures from pulling through the fibromuscular tissue or from ➎╇ Traditional Anterior Colporrhaphy.╇ significantly narrowing the vagina. As sutures Plication of the fibromuscular layer to the midare tied, the midline bladder bulge is elevated line is then begun. For this, an interrupted stitch by the surgeon gently upward and away from of 2-0 gauge delayed-absorbable suture is placed the incision line. Such plication creates a firm on one side of the midline beginning nearest the fibromuscular wall layer to support the bladder apex. This same needle and suture are carried to and if indicated, the urethra (Fig. 45-13.4). the other side of the midline, and a mirror stitch is placed the same distance from the apex. To ➏╇ Vaginal Paravaginal Defect Repair.╇ plicate tissue, the bites of each stitch are generIf vaginal PVDR is to be performed, the vagously spaced to bring together the wide lateral inal dissection described above is extended

➍╇ Lateral Dissection.╇Along the freed

epithelial edges, additional Allis or Allis-Adair clamps are placed to create gentle outward tension, while the vaginal epithelium is dissected laterally off the vagina’s fibromuscular wall (Fig. 45-13.3). This is accomplished with one finger placed behind the epithelium to accentuate the dissection plane, while scissors are held parallel to the vagina and cut connective tissue fibers between the epithelium and fibromuscular layer. Once the desired tissue plane is entered, a combination of sharp and blunt dissection readily separates the layers. Simultaneous countertraction on the fibromuscular layer by an assistant using tissue forceps or a gauze-covered finger can aid dissection. This separation is extended laterally toward the pelvic walls until substantial fibromuscular tissue is exposed to permit mid-

FIGURE 45-13.4╇ Midline plication completed.

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➑╇ Mesh Placement.╇Various marketed mesh kits are available, and full descriptions for placement are provided by individual manufacturers. In general, a broad mesh sling supports the proximal anterior vaginal wall and has mesh arms that extend and anchor to the sacrospinous ligaments (SSLs) to provide apical support. Concurrently, the distal extent of the mesh ends at the level of the bladder neck. For placement of anterior and apical mesh repair kits, the paravesical space is entered by lateral dissection similar to the steps for vaginal PVDR (Step 6). The ATFP and the ischial spines are palpated. A finger also slides medially over the SSL. The recommended fixation point on this ligament is 2 to 3 cm medial to the ischial spine, which is similar to the fixation point for the traditional SSL fixation procedure (p. 1112). ➒╇ Cystoscopy.╇ Kwon and coworkers (2002)

FIGURE 45-13.5╇ Vaginal paravaginal defect repair.

laterally to the pelvic side walls at the level of the arcus tendineus fascia pelvis (ATFP) (Chap. 38, p. 808). Dissection also generally extends from the dorsal surface of the pubic bones to the ischial spines. Blunt dissection is typically used to enter the space of Retzius. If a paravaginal defect is present, the space is easily entered. Visualization of the pelvic sidewall is aided by Breisky-Navratil and lighted retractors. If present, the ATFP appears as a white line running from pubic bone’s dorsal surface to the ischial spine. In some cases, the ATFP is attenuated and indistinct, and stitches are instead anchored to the obturator internus muscle’s investing

fascia. For repair, a series of four to six 2-0 gauge permanent sutures are placed in the ATFP or obturator fascia and attached to the paravaginal connective tissue (Fig. 45-13.5).

❼╇ Incision Closure.╇Depending on the size of the original anterior wall defect, some redundant vaginal wall will likely be present and require trimming (see Fig. 45-13.4). Liberal trimming, however, can place the vaginal wall incision on excessive tension, affect wound healing, and narrow the vagina. The vaginal epithelium is reapproximated in a running fashion with a 2-0 gauge delayedabsorbable suture.

performed cystoscopy following 346 anterior colporrhaphy procedures and found unexpected injury in 2 percent of cases. These each required suture removal and replacement. Accordingly, cystoscopy is warranted to document integrity of the ureteral orifices, bladder, and urethral lumen.

POSTOPERATIVE For most women, recovery following anterior colporrhaphy is rapid and associated with few complications. Urinary retention or UTI, however, is common. Prior to discharge, an active voiding trial is performed. If a Foley catheter remains, a second voiding trial can be repeated in a few days or at the surgeon’s discretion. As with other vaginal surgery, diet and activity can be advanced as tolerated. Women, however, abstain from intercourse until wound healing is complete, typically at 6 to 8 weeks following repair.

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45-14

Paravaginal defect repair (PVDR) is a prolapse procedure that aims to correct lateral defects in the anterior vaginal wall. The procedure involves attachment of the lateral vaginal wall to the arcus tendineus fascia pelvis (ATFP) (Fig. 38-24, p. 817). This procedure is rarely performed alone and is more often combined with other prolapse procedures, especially abdominal sacrocolpopexy. PVDR is ineffective treatment for stress urinary incontinence (SUI). That said, abdominal PVDR may be performed in conjunction with the antiincontinence Burch colposuspension if a lateral anterior wall defect and prolapse complaints coexist with SUI. PVDR can also be performed laparoscopically or robotically by those with advanced skills. If sutures can be placed the same as in the abdominal approach, the results are expected to be equivalent, but data are limited.

PREOPERATIVE ■⌀ Patient Evaluation Demonstration of lateral vaginal wall defects on physical examination is required prior to surgery. If significant anterior wall prolapse is identified, evaluation for SUI or occult SUI is pursued. In women who have a paravaginal defect, other pelvic support defects such as apical or posterior vaginal prolapse commonly coexist. Thus, attempts to identify these defects precede surgery.

■⌀ Consent Paravaginal defect repair provides support to the lateral vaginal walls, but as with other prolapse procedures, long-term success rates may diminish with time. The procedure involves surgery in the space of Retzius, which has the potential for significant blood loss. In particular, risks of bleeding and bladder injury are generally greater in patients with prior space of Retzius surgery as dense adhesions between bladder and pubic bone are common. Inaccurate suture placement can result in injury to the bladder and/or ureters, although this is infrequent.

■⌀ Patient Preparation As with most abdominal urogynecologic surgeries, antibiotic prophylaxis is given to pre-

CHAPTER 45

Abdominal Paravaginal Defect Repair

FIGURE 45-14.1╇ Dissection in the space of Retzius.

vent wound infection (Table 39-6, p. 835). Bowel preparation may be implemented at the surgeon’s discretion if additional procedures are planned. Thromboprophylaxis is given as outlined in Table 39-8 (p. 836).

INTRAOPERATIVE ■⌀ Surgical Steps ➊╇ Anesthesia and Patient Positioning.╇ When performed in conjunction with apical or other repairs, this surgery is typically performed as an inpatient procedure under general anesthesia. Following administration of anesthesia, the patient is placed in low lithotomy position in booted support stirrups. Adequate exposure to the vagina is vital because a vaginal hand is used to elevate and dissect the paravaginal/paravesical space. The abdomen and vagina are surgically prepared, and a Foley catheter with a 10-mL balloon is inserted.

➋╇ Abdominal Incision.╇ A low transverse incision placed 1 to 2 cm cephalad to the symphysis pubis affords the best exposure to the space of Retzius. This procedure is typically done in conjunction with abdominal sacrocolpopexy, and the abdominal cavity is entered (Section 43-2, p. 929). If performed in isolation or with a Burch colposuspension, entry into the peritoneal cavity is not necessary to open the space of Retzius. ➌╇ Entering the Space of Retzius.╇ After

incision of the fascia, the rectus muscles are separated in the midline and retractors are used to hold them apart. To open the space of Retzius, the correct dissection plane lies directly behind the pubic bone, deep to the transversalis fascia but superficial to the perito-

neum. Loose areolar tissue is gently dissected in a lateral-to-medial fashion with atraumatic forceps or scissors beginning immediately behind the pubic bone (Fig. 45-14.1). If the correct plane is entered, this avascular potential space opens easily and without significant hemorrhage. Small bleeding vessels within the loose areolar tissue are coagulated as encountered. If significant bleeding does occur, the wrong tissue plane has likely been entered. From prior surgery in this space, the bladder often adheres to the pubic bone and anterior abdominal wall and thus sharp dissection is indicated. After the medial portion of the space of Retzius is opened, the obturator canal is identified bilaterally so that its associated vessels and nerve can be avoided. The canal is generally found 5 to 6 cm lateral from the pubic symphysis midline and 1 to 2 cm below the iliopectineal line. The ischial spine is then palpated 4 to 6 cm below and posterior to the obturator canal. The remainder of the paravaginal space is opened with gentle blunt dissection using a gauze sponge. This dissection is generally directed lateromedially, that is, from obturator fascia to lateral bladder border, to expose the ATFP and paravaginal tissue. To assist, a vaginal hand pushing up into the space creates a firm surface to dissect against. In addition, a malleable retractor gently displaces the bladder to the contralateral side. Large paravaginal blood vessels are often noted along the lateral vaginal wall. Bleeding from these vessels can be controlled by upward pressure of the vaginal hand while hemostatic sutures are placed.

➍╇ Identification of the Arcus Tendineus Fascia Pelvis.╇ The ATFP runs along the pelvic sidewall between the pubic bone and

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SECTION 6 FIGURE 45-14.2╇ Placement of paravaginal sutures.

the ischial spine as a white connective tissue condensation. In those with defects, it may be attenuated, torn in the middle, or completely avulsed from the sidewall. Even in these cases, the distal third of the ATFP is generally preserved and easily identified.

➎╇ Placement of Paravaginal Sutures.╇ One or two fingers of the surgeon’s nondominant hand are placed in the vagina to elevate the lateral vaginal wall on the planned side of defect repair. At the same time, a medium-sized malleable retractor is used to reflect the bladder medially and protect it and the ureter from inadvertent suture placement or entrapment. Usually four to six interrupted 2-0 gauge permanent sutures placed approximately 1 cm apart are needed to obliterate the paravaginal defect. The ultimate suture line extends from the level of the ischial spine to the level of the bladder neck or proximal

FIGURE 45-14.3╇ Final suture placement.

urethra (Fig. 45-14.2). Each suture passes through the paravaginal tissue just lateral to the bladder wall and through the ATFP or obturator internus fascia and tied. A vaginal finger covered by a thimble for protection presses upward against the lateral vaginal wall to help isolate the paravaginal tissue and assess suture penetration. If a suture punctures the vaginal lumen, it is removed, discarded, and replaced by a more superficial stitch. If bleeding follows, the suture may be tied to constrict involved vessels. Prior to suture placement, the obturator canal and neurovascular bundle are identified and avoided. After all sutures are placed, the procedure is repeated on the other side of the vagina (Fig. 45-14.3).

➏╇ Cystoscopy.╇ This is performed to note efflux from both ureteral orifices and to exclude bladder-perforating sutures. A

misplaced suture might be seen as a dimple in the bladder wall. If found, sutures entering the bladder are removed abdominally and properly placed.

❼╇ Incision Closure.╇ After vigorous irriga-

tion of the space of Retzius, the abdomen is closed in a standard fashion (Section 43-2, p. 930). If the peritoneum was opened, closure is recommended to prevent small bowel adhesions in the space of Retzius.

POSTOPERATIVE In general, recovery follows that associated with laparotomy or endoscopy and varies depending on concurrent surgeries and incision size. A voiding trial as described in Chapter 42 (p. 917 is performed prior to hospital discharge.

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Posterior colporrhaphy, also colloquially termed posterior repair, is traditionally used to repair prolapse of the posterior vaginal compartment. Specifically, posterior colporrhaphy techniques attempt to reinforce the fibromuscular tissue layer between the vagina and rectum to prevent prolapse of the rectum into the vaginal lumen. The tissue plicated in the midline is often reapproximated distally to the level of the hymen and here includes reapproximation of the perineal body tissue. This is especially important for women who display “perineal descent” during preoperative evaluation. Women with such poor perineal strength may often reinforce (or splint) the perineal body to aid defecation. For these women, perineorrhaphy is often carried out concurrently. Often, the posterior vaginal wall apex must also be suspended to obtain successful repair and prevent recurrence. The apex may be suspended vaginally to the uterosacral or sacrospinous ligament or abdominally to the anterior longitudinal ligament of the sacrum. Thus, a careful preoperative evaluation is essential to restore anatomy. There are three current transvaginal repairs of posterior wall prolapse. First, traditional midline plication of levator ani muscles, also known as levator myorrhaphy or levatorplasty, plicates the puborectalis muscle in the midline (Francis, 1961). Second, midline vaginal wall plication without levator myorrhaphy brings together the vaginal wall muscularis and adventitial layers in the midline. Tissue previously referred to as “rectovaginal fascia” is in fact these muscularis and adventitial layers, as histologic studies of normal anatomy illustrate a lack of true fascia between the vagina and rectum. Last, defectdirected, also called site-specific, repair reapproximates attenuated vaginal wall at specific bulge sites rather than rotely in the midline. Among these, evidence suggests that midline plication without levator myorrhaphy has superior objective outcomes compared with site-specific repair and has lower dyspareunia rates than levator myorrhaphy (Karram, 2013). For these reasons, midline plication without levator myorrhaphy is the procedure of choice for posterior compartment prolapse except perhaps in select cases, such as women with large genital hiatus undergoing colpocleisis. Importantly, compared with these methods, a biologic or synthetic graft in the posterior compartment does not improve anatomic

PREOPERATIVE ■⌀ Patient Evaluation A detailed discussion of symptoms begins every patient evaluation prior to colporrhaphy. Often, patients may associate all of their bowel symptoms to a posterior wall bulge, but the two may not be related. Specifically, if constipation is a major complaint, further evaluation and trial of nonsurgical treatment is typically indicated (Chap. 25, p. 569). Symptoms most likely to be cured or improved by posterior repair include the sensation of vaginal bulge and the need to digitally compress the rectal vault for defecation. Also termed vaginal splinting, compression involves placing fingers in the vagina and pushing downward over the defect or sweeping forward to help empty bowel. As another compensatory action, a digit may be inserted in the rectum to scoop out stool. Posterior wall prolapse commonly accompanies other support defects, and patients undergo a complete pelvic organ prolapse examination. If concurrent anterior vaginal wall or vaginal apex prolapse is present, these are also repaired.

■⌀ Consent In addition to standard surgical risks, this procedure may be associated with failure to correct symptoms or anatomy. Accordingly, a patient and surgeon identify treatment goals and clarify expectations. In the few completed randomized studies, current techniques give a less than optimal anatomic repair, and success rates approximate 70 percent. Another frequent postoperative risk is dyspareunia, which is more common following the levator ani muscle plication discussed earlier. Accordingly, levator plication is not recommended in women who desire to preserve coital function. Injury to the rectum or rectovaginal fistula is another rare but potential complication.

■⌀ Patient Preparation Depending on surgeon preference, patients may be instructed to take in only clear liquids the day prior to surgery and complete one or two enemas that night or the morning of surgery. Ballard and associates (2014), however, noted no distinct advantage to

this. Antibiotics and thromboprophylaxis are given as outlined in Tables 39-6 and 39-8 (p. 835).

INTRAOPERATIVE ■⌀ Surgical Steps ➊╇ Anesthesia and Patient Positioning.╇ If done in isolation, posterior colporrhaphy is typically a day-surgery procedure for healthy women and performed under general or regional anesthesia. A patient is placed in standard lithotomy position in candy-cane or booted support stirrups. The vagina is surgically prepared, and a Foley catheter inserted.

➋╇ Concurrent Surgery.╇ Posterior colpor-

rhaphy can be performed with the uterus in situ or alternatively, following hysterectomy. If other reconstructive surgeries are required, they may precede or follow posterior colporrhaphy. Notably, completion of the posterior repair prior to vaginal apex suspension permits the plicated and thus more substantial tissue to be anchored to selected ligaments during apical suspension.

➌╇ Vaginal Incision and Dissection.╇ Two Allis clamps are placed on the posterolateral wall of the distal vagina on either side of the midline. Clamps are gently pulled laterally to create tension, and the vaginal wall between them is incised transversely at or just proximal to the level of the hymen and superficial to the perineal body. A third Allis clamp is placed in midline and 3 to 4 cm proximal to the introitus. All three clamps are held, creating gentle outward tension. Metzenbaum scissors tips are insinuated beneath the epithelium in the midline of the previously made transverse incision and directed cephalad (Fig. 45-15.1). Scissor blades are opened and closed, while the surgeon exerts gentle forward pressure that is parallel to and within the plane beneath the vaginal epithelium. This technique allows separation of the epithelium from the fibromuscular layer. This dissection continues cephalad to reach the proximal midline Allis clamp. The undermined vaginal epithelium is then incised in the midline longitudinally. The midline Allis clamp is then replaced further cephalad, and the process continues until the vaginal epithelium has been divided to the level of the vaginal apex. If a concurrent hysterectomy has been performed, the colporrhaphy incision generally extends to the cuff incision. In either case, if only a simple discrete distal to mid-vagina defect is present, then the midline colporrhaphy incision stops just cephalad to that defect’s proximal border.

CHAPTER 45

Posterior Colporrhaphy

or functional outcomes (Maher, 2013; Paraiso, 2006; Sung, 2012). Well-designed studies that demonstrate efficacy and safety of newly developed grafts are needed before surgeons incorporate these materials into their practices.

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SECTION 6 FIGURE 45-15.1╇ Vaginal incision and dissection.

➍╇ Lateral Dissection.╇Along the freed epithelial edges, additional Allis or Allis-Adair clamps are placed to create gentle outward tension, while the vaginal epithelium is dissected laterally off the vagina’s fibromuscular wall. This is accomplished with one finger placed behind the epithelium to accentuate the dissection plane. Scissors are held parallel to the vagina and cut connective tissue fibers between the epithelium and fibromuscular layer.

FIGURE 45-15.3╇ Midline defect.

FIGURE 45-15.2╇ Rectal examination.

During this early lateral dissection, the perineal body is fused with the vaginal wall fibromuscular layer, and scarring may be present from prior episiotomy. Thus, clear tissue planes are not typically present, and sharp dissection is required. Cephalad to the perineal body, once the desired tissue plane is entered, a combination of sharp and blunt dissection readily separates the layers. Simultaneous countertraction on the fibro-

muscular tissue by an assistant using tissue forceps or a gauze-covered finger can aid dissection. Separation in the correct tissue plane is essential. Deep dissection can enter rectum, whereas superficial dissection can create holes in the vaginal epithelium, often called “button holes.” This tissue separation is extended laterally toward the pelvic walls until substantial fibromuscular tissue is exposed to permit

FIGURE 45-15.4╇ Midline plication.

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FIGURE 45-15.5╇ Distal defect. midline plication. The steps are then repeated on the contralateral side.

➎╇ Rectal Examination.╇Rectal examination is performed to exclude rectal injury and to help identify the edges of the fibromuscular wall to be plicated (Fig. 45-15.2).

➏╇ Midline Plication.╇A series of inter-

rupted 2-0 gauge delayed-absorbable sutures are used to plicate the vaginal muscularis and perineal body tissue along the length of the posterior vaginal wall (Figs. 45-15.3 and 45-15.4). As noted, levator plication is avoided in patients who desire to preserve coital function as the risks of vaginal lumen narrowing and dyspareunia may be higher. To plicate tissue, an interrupted stitch of 2-0 gauge delayed-absorbable suture is placed on one side of the midline beginning nearest the apex. This same needle and suture are carried to the other side of the midline, and a mirror stitch is placed the same distance from the apex. The the bites of each stitch are generously spaced to bring together the wide lateral span of attenuated tissue. Such plication creates a firm fibromuscular wall layer to support the rectum and if indicated, the perineal body. However, excessive tension is avoided to prevent sutures from pulling through the

FIGURE 45-15.6╇ Defect-directed repair. fibromuscular tissue or from significantly narrowing the vagina. As sutures are tied, the midline rectal bulge is gently pushed downward by the surgeon and away from the incision line. Rectal examination is again performed after all sutures are placed to exclude inadvertent suture placement into the rectum. If identified, these are removed and correct suture placement completed.

❼╇ Defect Assessment.╇ In some instances, a discrete defect is identified in the posterior fibromuscular layer after the initial dissection. Defects may be lateral, midline, apical, or perineal (Figs. 45-15.5 and 45-15.6). Repair focuses solely on the defect, which is closed by interrupted stitches of 2-0 gauge delayed-absorbable sutures. This is generally a one-layer closure. This repair may be complemented by a midline plication if significant tissue attenuation is still noted. ➑╇ Indicated Apical Suspension.╇ If indi-

cated, apical suspension is performed after vaginal wall plication. The proximal posterior vagina is affixed to either the uterosacral or sacrospinous ligament, as described on page 1107. If perineorrhaphy is planned, it is also completed prior to incision closure.

9 Incision Closure.╇ Following plication, redundant vaginal wall often remains and requires trimming. Liberal trimming, however, can narrow the vagina and can place the vaginal wall incision on excessive tension that impairs wound healing. The vaginal mucosa is reapproximated in a running fashion using a 2-0 gauge delayed-absorbable suture. Widely positioned sutures are avoided as they can create accordion-type bunching of the vaginal epithelium and subsequent vaginal shortening when the final suture is tied.

POSTOPERATIVE Patients are instructed on perineal hygiene. Constipation and straining are avoided, and stool softeners are usually prescribed. As with other vaginal surgery, diet and activity can be advanced as tolerated. Women, however, abstain from intercourse until wound healing is complete, typically at 6 to 8 weeks following repair. Some women have urinary retention after posterior repairs, even without an antiincontinence procedure. If unable to void spontaneously by the time of discharge, a patient can go home with a catheter and be seen again within a week for removal.

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Perineorrhaphy The perineal body serves as core support of the distal vagina, rectum, and pelvic floor. Therefore, a damaged or weakened perineal body may contribute to distal prolapse. Reinforcement of this structure, that is, perineorrhaphy, is often performed in conjunction with other reconstructive procedures, such as posterior colporrhaphy. To reestablish distal support, perineorrhaphy lengthens the anteroposterior dimension of a shortened perineal body, while the genital hiatus is concurrently narrowed.

PREOPERATIVE ■⌀ Patient Evaluation During assessment, the length of the genital hiatus is measured in centimeters both at rest and with Valsalva maneuver from the external urethral opening at 12 o’clock to the posterior aspect of the hymeneal ring at 6 o’clock. The perineal body is measured from the hymeneal ring at 6 o’clock to the mid-anus. With perineorrhaphy planning, the degree to which the perineal body is lengthened can be tailored according patient symptoms, surgical goals, and clinical findings. With typical perineorrhaphy, the degree of perineal body lengthening is minimized to create or maintain a genital hiatus wide enough to preserve comfortable intercourse. Moreover, in sexually active postmenopausal women whose partners have decreased erectile tone, entry into the vagina may be difficult if the introitus is too narrow. Thus, following perineorrhaphy, 2 to 3 fingers ideally comfortably pass through the introitus. For women with “perineal descent” who have to splint to defecate or in those with distal defects and attenuated perineal body tissue, perineorrhaphy may be coupled with posterior colporrhaphy. As described on page 1093, the distal extent of the plicated rectovaginal wall can be reattached to the perineal body. This reestablishes continuity of connective tissue support in the posterior vaginal compartment. In some women, pelvic support takes precedence, and coital function is also not desired. With “high” perineorrhaphy, the superior-toinferior extent of the perineal body is lengthened and generally accompanied by plication of the levator ani muscle fascia at the superior aspect of the perineal body. The result of this extensive perineorrhaphy is a shorter genital hiatus length and narrower introitus and vaginal lumen. This may be an advanta-

geous adjunct to colpocleisis. However, data showing improved colpocleisis outcomes by adding levator myorrhaphy are limited (Gutman, 2009).

■⌀ Consent A patient preparing for perineorrhaphy is counseled regarding risks of postoperative dyspareunia, prolapse recurrence, or wound complications, such as a stitch abscess. Bleeding from perineal skin tearing during intercourse may also result and require minor surgical revision.

■⌀ Patient Preparation Because of the surgical site’s close proximity to the anus and also because bowel injury is possible, antibiotic prophylaxis is administered prior to surgery to minimize wound infection risks (Table 39-6, p. 835). Bowel preparation, which may employ clear liquid diet and enemas, mirrors that for posterior repair (p. 1093). Thromboprophylaxis is given as outlined in Table 39-8 (p. 836).

INTRAOPERATIVE ■⌀ Surgical Steps ➊╇ Anesthesia and Patient Positioning Perineorrhaphy is typically performed under general or regional anesthesia, and this choice is often dictated by concurrent surgeries planned. The patient is placed in standard lithotomy position in candy-cane or booted support stirrups. A vaginal and rectal examination under anesthesia is again performed to assess the size of the perineal body and defects of the posterior vaginal wall, which may also require repair. The vagina is surgically prepared, and a Foley catheter inserted. ➋╇ Concurrent Surgery.╇If concurrent surgeries have been included, perineorrhaphy is the final procedure in most cases.

➌╇ Incision.╇ To determine the approximate

appearance of the final repair, Allis clamps are placed on the posterolateral walls of the vagina at or just proximal to the hymen. These are brought together in the midline and 2 or 3 fingers should easily pass through the intended genital hiatus. If the resulting opening is too narrow, both Allis clamps are moved closer to the midline, and the above steps are repeated. With this technique, a surgeon can judge the final size of the introitus and perineal body. Because scarring and retraction can develop, it is prudent to err on the side of leaving the genital hiatus larger rather than smaller. To begin, a diamond-shape incision

is made with its cephalad tip extending 2 to 3 cm into the vagina and the caudal tip extending to a point approximately 2 cm above the anus.

➍╇ Removal of Skin and Mucosa.╇For traction, Allis clamps are placed at each corner of the diamond. Metzenbaum scissors are used to excise the perineal skin and vaginal epithelium within the diamond away from the underlying tissue. During dissection, the scissor tips are held parallel to the perineal and vaginal tissues, respectively. Sharp dissection must be performed over the perineal body. This area contains a normal condensation of tissue, and scarring may also be present. As a result, development of good tissue planes is often not possible. A dilute vasopressin solution may be injected to decrease bleeding from extensive venous sinuses that are typically encountered in this region from obstetric or vaginal delivery scars. Frequent rectal examination during dissection may be required to assess the amount of tissue present between the anal and vaginal epithelium to prevent entry into the rectum.

➎╇ Suture Placement.╇ One centimeter cau-

dal to the hymeneal ring, a 0-gauge delayedabsorbable suture on a CT-1 needle is used to approximate the connective tissue surrounding the perineal muscles (bulbospongiosus and superficial transverse perineal muscles) in the midline. In suturing this tissue, a wide lateral bite is taken, and suture is directed first in an inward-to-outward and then outward-to-inward sequence (Fig. 45-16.1). This suture technique ultimately buries knots below the plicated muscles. However, initially, the first suture is held and not tied. Downward traction is placed, and a second suture is placed approximately 1 cm cephalad. This suture ideally reapproximates the separated ends of the perineal membrane. As with the first, this suture is not tied. A third suture can be placed 1 cm further cephalad to this, if necessary. In a similar fashion, one to two stitches are placed 1 cm apart and caudad to the primary suture. These lower stitches plicate the connective tissue surrounding the superficial transverse perineal muscles and upper extent of the external anal sphincter muscle in the midline. The sutures are then progressively tied beginning with the lowermost. In some cases, a second, more superficial layer is placed in the perineal body for additional support.

➏╇ Vaginal

and Perineal Closure.╇ Starting at the vaginal apex, the vaginal epithelium is closed in a running fashion using 2-0 gauge delayed-absorbable suture (Fig. 45-16.2). When creating a running suture line in the

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FIGURE 45-16.1╇ Suture placement.

vagina, stitches are placed close together. If suture bites are placed far apart during epithelial closure, the vagina can be shortened. The running suture reapproximates the hymeneal ring and then is brought into the perineal area. The same suture may be used in a running mattress method to reapproximate the subcutaneous tissue to the end of the incision, near the anus. The skin is then reapproxi-

FIGURE 45-16.2╇ Wound closure.

mated in an interrupted or running fashion using 3-0 gauge delayed-absorbable suture.

POSTOPERATIVE Patients are instructed on perineal hygiene. Constipation is avoided and stool softeners are usually prescribed. As with other vaginal surgery, diet and activity can be advanced as

tolerated. Women, however, abstain from intercourse until wound healing is complete, typically at 6 to 8 weeks following repair. Some women have urinary retention after perineorrhaphy, even without an antiincontinence procedure. If unable to void spontaneously by the time of discharge, a patient can go home with a catheter and be seen again within a week for removal.

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Abdominal Sacrocolpopexy Abdominal sacrocolpopexy (ASC) using graft material is a widely accepted transabdominal prolapse operation, and many consider it the preferred procedure to correct advanced apical prolapse. Grafts of autologous, cadaveric, or synthetic materials may be used, but permanent (synthetic) mesh has the best success rate and is selected unless otherwise contraindicated (Culligan, 2005). The graft augments native tissue and suspends the upper third of the vagina to the anterior longitudinal ligament of the sacrum. In addition to correcting apical prolapse, the graft also covers proximal portions of the anterior and posterior vaginal walls. As such, ASC also corrects apical segment prolapse of the anterior vagina wall (“apical” or “transverse” cystoceles) and of the posterior vaginal wall (enteroceles and “high” rectoceles). A modification of the procedure, sacrocolpoperineopexy, is used if concomitant perineal descent is present and believed to contribute to patient symptoms (Cundiff, 1997). One advantage to ASC is its durability, and long-term success rates for apical suspension approximate 90 percent. It may be used as a primary procedure or alternatively as a repeat surgery for patients with recurrences after other prolapse repair failures. In addition, ASC is often chosen for women believed to be at high risk for recurrence and for whom mesh would augment their own tissue. Examples include those with connective tissue disease, history of recurrent hernia, obesity, or chronically increased intraabdominal pressure such as chronic obstructive pulmonary disease or chronic constipation. Abdominal synthetic mesh aids durability, but its use is balanced against the potential for complications, as discussed later. Although the vaginal apex can also be successfully suspended with vaginal approach procedures such as sacrospinous ligament fixation (p. 1112) and uterosacral ligament suspension (p. 1107), ASC offers distinct advantages. First, ASC maintains or lengthens the vagina, in contrast to vaginal approaches, which may shorten it. Second, the use of synthetic “permanent” mesh with multiple attachment sites to the vagina has a very low risk of apical failure. Finally, unlike vaginal approaches, in which the vaginal apex is directly affixed to a structure such as the uterosacral or sacrospinous ligament, ASC repositions the vaginal apex to its nearly normal anatomic position using intervening graft material. Thus, the apex typically

remains mobile, which possibly lowers dyspareunia rates. Sacrocolpopexy can be performed by laparotomy, by conventional laparoscopy, and with robotic assistance. If minimally invasive surgery (MIS) is performed in the same manner as the open operation, similar results can be expected (p. 1103). However, only limited data are currently available on longterm success rates with these MIS approaches (Freeman, 2013; Maher, 2013; Paraiso, 2011).

PREOPERATIVE ■⌀ Patient Evaluation Prolapse of the vaginal apex often coexists with other prolapse sites along the vagina. Accordingly, a careful preoperative search is performed for other prolapse sites. If necessary, ASC can be completed concurrently with paravaginal defect repair, posterior repair, or other prolapse surgeries. Beer and Kuhn (2005) found that approximately 70 percent of ASC procedures were performed with other pelvic reconstructive operations. With the technique we describe, a concurrent enterocele will be repaired by the colpopexy, and other enterocele repairs are thus unnecessary. Prior to ASC, patients with symptoms of urinary incontinence undergo simple or complex urodynamic testing to clarify the type of incontinence and determine if an antiincontinence procedure will be beneficial. For those with SUI, a concurrent antiincontinence operation is generally performed. Because prolapse correction can unmask occult SUI in some women, clinicians also test those without incontinence while manually reducing the prolapse. Last, apical suspension can predispose to later development of anterior vaginal wall prolapse and SUI. Thus, stresscontinent women undergoing ASC may elect a prophylactic SUI procedure. To evaluate this practice, the CARE (Colpopexy After Reduction Efforts) trial found that continent women undergoing ASC plus a prophylactic urethropexy had a 2-year postoperative SUI incidence of 32 percent. Without preventive urethropexy, SUI rates following ASC were 45 percent (Brubaker, 2006, 2008). Importantly, adding an antiincontinence procedure decreases, but does not eliminate, the risk of later de novo SUI. At this time, it is unclear how best to extrapolate these findings to women who elect to have sacrocolpopexy and midurethral sling procedures.

■⌀ Consent Recurrent prolapse is common following any corrective surgery. Thus, a surgeon should be aware of recurrence rates quoted in the literature and his or her own personal

rates. Although apical prolapse recurrence is infrequent, later prolapse of the anterior and posterior vaginal walls is more common. An extension of the CARE trial used a clinically based definition of anatomic failure. It showed that by 5 years, nearly one third of women met the composite definition of failure (Nygaard, 2013). However, 95 percent had no retreatment for their prolapse. Mesh erosion develops in 2 to 10 percent of cases. It is generally found at the apex and occurs more often if hysterectomy is performed concurrent with ASC. Erosion may arise soon after surgery or years later (Beer, 2005; Nygaard, 2004, 2013). Many technical points described in the following steps aim to prevent this complication.

■⌀ Patient Preparation Bowel preparation will vary depending on surgeon preference. Patients can be instructed to take only clear liquids the day prior to surgery and complete one or two enemas that night or the morning of surgery. Alternatively, a mechanical bowel preparation using agents listed in Chapter 39 (p. 835) may be preferred. Ballard and associates (2014), however, noted no distinct advantage to this for urogynecologic operations. Antibiotics and thromboprophylaxis are given as outlined in Tables 39-6 and 39-8 (p. 835). For postmenopausal women, vaginal estrogen cream use during the 6 to 8 weeks prior to surgery has been routinely recommended. Estrogen treatment is thought to enhance vascularity and thereby increase tissue strength and promote healing. Although this is logical and commonly practiced, no data suggest that preoperative vaginal estrogen cream decreases mesh erosion or prolapse recurrence rates.

INTRAOPERATIVE ■⌀ Instruments and Materials The upper vagina must be elevated and distended by a vaginal manipulator to allow adequate dissection and delineation of the vaginal wall fibromuscular layers for mesh placement. The manipulator may be a cylindrical Lucite rod or a large EEA (end-toend anastomosis) sizer, which is present in most operating rooms and shown in Figure 46-21.4 (p. 1202). The ideal bridging material for this procedure is permanent, nonantigenic, easily cut or customized, and readily available. The ideal mesh has a large pore size to allow host tissue ingrowth, is monofilament to decrease bacterial adherence, and is flexible. Currently, polypropylene mesh is the most common synthetic graft used (American Urogynecologic Society, 2013, 2014b).

Surgeries for Pelvic Floor Disorders

■⌀ Surgical Steps Following administration of general anesthesia, the patient is positioned in a modified supine position with thighs parallel to the ground and legs in booted support stirrups. Correct positioning prevents nerve injury and allows access to the vagina for manipulation and examination, to the bladder for cystoscopy, and to the abdomen for proper selfretaining retractor placement. The buttocks are positioned at the table edge or slightly distal to allow full range of vaginal manipulator motion. The vagina and abdomen are surgically prepared, and a Foley catheter is inserted.

➋╇ Incision.╇ A vertical or transverse abdomi-

nal incision may be used, and selection is directed by a woman’s body habitus and by planned concurrent procedures. A Pfannenstiel incision generally provides adequate access to the sacrum and deep pelvis. If a Burch colposuspension, paravaginal defect repair, or other surgery in the space of Retzius is planned, then a low transverse incision that is positioned closer to the symphysis may be preferred.

➌╇ Bowel Packing.╇ A self-retaining retrac-

tor, preferably a Balfour type, is placed, and the bowel is packed up and out of the pelvis with moist laparotomy sponges. Bowel packing attempts to shift the sigmoid colon farther to the patient’s left, thereby permitting access to the midline and right aspects of the sacrum.

➍╇ Concomitant Hysterectomy.╇Some

data suggest that hysterectomy at the time of ASC leads to higher mesh erosion rates (Culligan, 2002; Griffis, 2006). To reduce erosion risks at the cuff, some surgeons advocate supracervical hysterectomy, theorizing that the cervical stump may act as a barrier to prevent ascending infection and erosion (McDermott, 2009). If a total abdominal hysterectomy is performed, the vaginal apex is closed with absorbable suture such as 0-gauge polyglactin 910 (Vicryl) in a running or interrupted fashion. A second imbricating layer using the same suture may be placed to reduce potential mesh erosion. Another preventive measure is avoiding mesh fixation near the cuff suture line. Specifically, a 1-cm margin from this suture line may avert early mesh erosion during the cuff’s healing phase.

➎╇ Identification of Pelvic Anatomy.╇ Important boundaries during presacral space dissection are identified beneath the peritoneum prior to the posterior peritoneal incision. These include the aortic bifurcation, iliac vessels, right ureter, right uterosacral ligament, medial border of the rectosigmoid

➏╇ Peritoneal Incision.╇ The rectosigmoid

colon is gently retracted to the left with a malleable ribbon or similar retractor. The peritoneum overlying the sacral promontory, between the rectosigmoid colon’s medial border and the right ureter, is elevated with tissue forceps and incised sharply. The incision is extended caudally into the posterior culde-sac of Douglas. As the incision approaches the deeper portion of the cul-de-sac, it is kept between the medial border of the rectum and the right uterosacral ligament. A vaginal manipulator directed ventrally to create tension aids dissection. The incision may then be continued to the posterior vaginal wall and toward the vaginal apex. Maintaining proper orientation is critical during this step as inadvertent deviation can cause ureteral or iliac vessel injury on the right, or colon injury on the left. Similarly, if the initial peritoneal incision is extended above the sacral promontory, the left common iliac vein should be identified and avoided. This vessel can lie less than 1 cm from the promontory and is generally difficult to visualize or palpate due to its absent pulsatility and decreased tone. Final closure of this peritoneal incision allows the mesh to lie retroperitoneally. This may lower the risk of bowel-to-mesh adhesions and of bowel obstruction from small-bowel loops entrapped below the bridging mesh strip.

❼╇ Identification of Anterior Longitudinal

Ligament.╇ Following peritoneal incision, the loose connective tissue between the peritoneum and the sacrum is sharply and bluntly dissected to expose the anterior longitudinal ligament lying along the sacrum’s vertical midsection. Generally, this presacral space dissection is started at the promontory and continued 3 to 4 cm inferiorly to the upper extent of the S2 vertebra. Within the connective tissue of the presacral space, fibers of the superior hypogastric nerve plexus, right and left hypogastric nerves, and the inferior mesenteric and superior rectal artery and vein are embedded (Fig. 38-23, p. 816). Of these, the right hypogastric nerve is the most common structure identified during dissection. Below the aortic bifurcation, this midline cordlike nerve courses laterally and at the lower sacral levels,

reaches the right pelvic sidewall. Transection of this nerve is ideally avoided. Also of seminal importance, the middle sacral vessels typically adhere to the anterior surface of the ligament. Once found in the area exposed for mesh attachment, middle sacral vessels can be avoided, ligated, or coagulated depending on surgeon’s preference and operative findings. The middle sacral vein also forms anastomoses with the lateral sacral veins that contribute to the sacral venous plexus. Vessels of this plexus can be extensive, especially in the lower part of the sacrum.

➑╇ Presacral Space Hemorrhage.╇Careful exposure of the anterior longitudinal ligament and overlying vessels helps prevent bleeding during suture placement. Despite these efforts, laceration of the sacral venous plexus can lead to rapid and substantial blood loss, and several steps are critical to its control. First, pressure is applied immediately and held for several minutes. This may be particularly effective for venous bleeding. Sutures and clips may be useful, but tearing of small veins frequently worsens with suturing. Additionally, as vessels retract into the bone, isolation and ligation becomes difficult. Sterile thumbtacks directed through lacerated vessels and pushed into the sacrum can effectively compress such vessels. Unfortunately, these tacks are not routinely found in many operating rooms. Alternatively, various topical hemostatic agents have been used to control bleeding refractory to these initial steps (Table 40-5, p. 861). Of these, the fibrin sealant family allows conformation to irregular wounds, which is a distinct advantage for presacral space hemorrhage. In refractory cases, vascular surgery consultation may be prudent. Also, injury to the iliac vessels or aorta necessitates immediate consultation.

➒╇ Sacral Suture Site Selection.╇ To anchor

the suspending mesh strips proximally, a surgeon must decide whether to place sutures through the anterior longitudinal ligament at higher or lower sacral levels. Suture placement at the S3 or S4 vertebral bodies increases the risk of sacral venous plexus laceration, and this practice has largely been abandoned. Suture placement above the sacral promontory risks left common iliac vein injury and penetration of the L5-S1 disc, which may lead to painful discitis or osteomyelitis (Good, 2013a; Wieslander, 2006). However, this disc is the most protuberant structure in the presacral space, and mesh is commonly affixed here, especially during the learning phase of ASC (Abernathy, 2012). For correct sacral promontory identification, the steep angle of descent between L5 and S1 can be used. That said, even correct suture placement at S1 and the sacral

CHAPTER 45

➊╇ Anesthesia and Patient Positioning.╇

colon, and sacral promontory, which is the upper anterior surface of the S1 vertebra. An understanding that the right ureter, right common iliac artery, and left common iliac vein all lie within 3 cm of the sacral promontory’s midline may lower rates of their injury during surgery in the presacral space (Good, 2013b; Wieslander, 2006). Moreover, both ureters are threatened during dissection of the bladder off the anterior vaginal wall and during suturing of the anterior mesh strip.

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SECTION 6 FIGURE 45-17.1╇ Placement of sacral sutures. promontory still risks middle sacral vessel laceration. However, at S1, the middle sacral vessels are visible and can be easily isolated and avoided or when necessary, clipped or coagulated. Additionally at S1, the anterior longitudinal ligament is thicker and stronger than at lower sacral levels (White, 2009). Affixing sutures here minimizes suture avulsion risks. Finally, attachment of the mesh at S1 may result in a more anatomic suspension of the vaginal apex (Balgobin, 2013). For these reasons, we prefer to affix mesh to the anterior surface of S1, with the most cephalad suture placed at or just below the sacral promontory. If safe suture placement over the S1 vertebra is prohibited, then the level of the L5-S1 disc is an alternative. Shallow tissue “bites” are needed here to avoid the disc as the anterior longitudinal ligament is only 1 to 2 mm thick.

➓╇ Sacral Suture Placement.╇Typically, three or four serial permanent sutures are used to affix the sacral portion of mesh to the anterior longitudinal ligament. These stitches can be placed first, as described here, or later after vaginal mesh attachment. Needle passage moves from right to left with each stitch, and sutures are aligned vertically. Starting with the lowest suture, they are spaced approximately 0.5 to 1 cm apart. With suturing, 2-0 gauge permanent material, each double-armed with SH needles, is passed through the full thickness of the anterior longitudinal ligament (Fig. 45-17.1). During this, based on findings, suture “bites” either encompass or avoid vessels. Once completed, sutures are held by a hemostat

FIGURE 45-17.2╇ Dissection of the anterior vaginal wall. and not tied. Their needles are covered with a surgical towel to avoid stick injuries. ╇ Anterior Vaginal Wall Dissection.╇ Prior to mesh attachment, the peritoneum and bladder must be dissected off the proximal vagina. Dissection of the bladder from the upper third of the anterior vaginal wall is aided by the vaginal manipulator. The cervical stump or vaginal apex is displaced cephalad and dorsally, and its covering peritoneum is incised transversely and proximal to the bladder’s cephalad margin. With prior hysterectomy, careful identification of the vaginal apex and superior extent of bladder is critical to avoid cystotomy. This is especially important in women with short vaginal lengths or vesicovaginal adhesions. In these cases, retrograde bladder filling and Foley bulb identification may help delineate the upper bladder margin. With cystotomy, several options are possible. If the cystotomy is small and close to the bladder dome, then a two- to threelayered bladder closure, followed by an interposition flap (omental or peritoneal), may be considered. However, if the cystotomy is large or nears the trigone, an alternative approach to vault suspension using native tissue may be considered to minimize mesh erosion into the bladder or fistula formation. Alternatively, the cystotomy can be repaired, and ASC deferred for a later time. Once the correct vesicovaginal space is entered, the bladder is sharply dissected from the anterior vaginal wall for a distance of approximately 4 to 6 cm caudad to create an extensive surface for mesh fixation. However, the extent of this dissection varies depending

on intraoperative anatomy. Sharp rather than blunt dissection is preferred in the vesicovaginal space (Fig. 45-17.2). Electrosurgical energy use is minimized to reduce risks of delayed thermal bladder injury. Dissection progresses at a depth above the fibromuscular layer of the vaginal wall. Entry into this proper plane lowers the rate of incidental entry into the vagina, which may increase future mesh erosion risks. If the vaginal lumen is entered, the opening is irrigated copiously and closed in two imbricated layers using 2-0 or 3-0 gauge delayed-absorbable suture. ╇ Posterior Vaginal Wall Dissection.╇ To expose an area of adequate size for mesh fixation, the rectovaginal space is entered, and the rectum is separated from the posterior vagina. For this, the vaginal manipulator now displaces the vaginal apex ventrally. The reflection of the rectum against the posterior vaginal wall is identified, and the peritoneum is incised transversely 2 to 3 cm proximal to this reflection line. The right and left uterosacral ligaments are used as lateral dissection boundaries. With gentle outward traction on the peritoneum, the rectovaginal space is developed with a combination of sharp and blunt dissection. In the absence of adhesions or fibrosis, the rectovaginal space easily opens inferiorly to the superior margin of the perineal body, which lies 3 to 4 cm above the hymen. Identification of loose gauzy connective tissue fibers usually indicates dissection in the correct plane. Also, the white, glistening posterior vaginal wall provides another visual clue, and dissection is kept close to this tissue to avoid inadvertent rectal entry.

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FIGURE 45-17.3╇ Posterior mesh secured and draped forward. Initially placed sacral sutures are seen in the background. In contrast, fatty tissue or excessive bleeding generally indicates incorrect plane dissection and potential proximity to the rectum. ╇ Graft Principles.╇ Whether two separate strips of self-cut mesh or a commercially preformed Y-shaped mesh is used, several surgical principles are generally followed. First, depending on the extent of dissections, six to 12 sutures on the anterior and a similar number on the posterior vaginal wall are placed through the mesh and the vaginal wall muscularis. Sutures ideally do not enter the vaginal lumen because epithelial healing over the stitches may be incomplete, especially with braided suture. However, if the fibromuscular layer is thin, this may not be possible. In this setting, many select monofilament, delayedabsorbable suture, which has a greater propensity for epithelialization postoperatively. Second, sutures are tied down loosely to avoid tissue strangulation and vaginal wall necrosis, which may lead to mesh or suture erosion. Third, the lower extent of the mesh does not abut the bladder or rectal reflections to minimize potential risks of pelvic organ dysfunction or mesh erosion of into these organs. Last, mesh is positioned symmetrically across the width of both the anterior and posterior vaginal walls. At our institution, we fashion the two mesh strips only after vaginal dissection is completed. The broader area of each strip will cover the dissected anterior vaginal surface and posterior vaginal surface, respectively. Each strip also has a narrowed portion that will extend to the sacrum and be affixed to the anterior longitudinal ligament. This

FIGURE 45-17.4╇ Anterior and posterior mesh in place.

narrowed portion reduces mesh bulk, especially near the rectum on the left and the iliac vessels and ureter on the right, to lower mesh erosion rates. However, excessive narrowing may compromise overall repair strength (Balgobin, 2011). Generally, the narrow portion of mesh measures approximately 2 cm. Lengthwise, the proximal end of mesh is initially left long to allow correct positioning to the sacrum and later is trimmed. ╇ Mesh Placement.╇ To begin, the vaginal manipulator is pushed cephalad and ventrally to fully expose the dissected posterior vaginal wall and stabilize the vagina for suturing. The mesh is commonly attached to the posterior vaginal wall with two to four rows of 2-0 gauge permanent or delayed-absorbable sutures, and rows are placed approximately 1.5 cm apart (Fig. 45-17.3). Depending on the vaginal width and the lateral extent of dissection, each row consists of two to three sutures spaced 1 to 1.5 cm apart. The inferior and lateral extents of the dissected vagina are adequately exposed prior to suture placement to avoid incorporation of rectum into a stitch. For the anterior vaginal wall, mesh is sutured in exactly the same fashion as was performed on the posterior wall (Fig. 45-17.4). ╇ Mesh Sizing and Sacral Attachment.╇ For this step, the prior sacral dissection is again exposed, and the two proximal portions of each mesh strip are held together by a right-angle clamp for maneuvering. The vaginal manipulator is removed and replaced by surgeon fingers. Then, by digital pressure directed cephalad, the cuff is gently elevated,

and the proximal portions of mesh are extended to the earlier placed sacral sutures. Alternatively, the cuff can be gently elevated by the vaginal manipulator. With correct positioning, apical suspension reduces prolapse of the apex and the apical segments of the anterior and posterior vaginal walls. Moreover, the mesh segment between the vagina and sacrum should be tension free. Once the desired mesh position and length are determined, the excess mesh above the most cephalad sacral suture is trimmed off. This avoids mesh contact with the right ureter, iliac vein, and other vascular structures that all lie within 1 to 2 cm of the fixation site (Kohli, 1998; Nygaard, 2004). The six needles of the three double-armed sacral sutures are then passed through the proximal portions of both mesh strips (Fig. 45-17.5). Each of the three sutures is then tied to secure the proximal mesh to the anterior longitudinal ligament (Fig. 45-17.6). To prevent air knots while the lowest sacral suture is secured, the surgeon gently pushes the vaginal apex against the lower part of the sacrum with the vaginal manipulator. ╇ Peritoneal Closure.╇Reapproximation of the peritoneum over the mesh can be accomplished in a running or interrupted fashion using 3-0 or 2-0 gauge absorbable suture (Fig. 45-17.7). Placing this mesh retroperitoneally theoretically may lower the risk of bowel obstruction, but this complication has been reported despite peritoneal reapproximation (Pilsgaard, 1999). During closure, the right ureter is kept in constant view to avoid kinking or direct injury.

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SECTION 6 FIGURE 45-17.5╇ Mesh attachment to the sacrum. ╇ Cystoscopy.╇ Cystoscopy is routinely performed prior to laparotomy closure to document ureteral integrity and absence of bladder sutures or injury. Urethral examination is important if an antiincontinence procedure is also performed. ╇ Abdominal Closure.╇ The abdomen is closed in a standard fashion (Section 43-1 or 43-2, p. 928).

POSTOPERATIVE ■⌀ Patient Care Postoperative in-hospital management is similar to that for other intraabdominal surgeries.

FIGURE 45-17.6╇ Final mesh placement.

Specific to ASC, a passive or active voiding trial can be performed on postoperative day 1 or 2, depending on the patient’s condition and extent of dissection. Some women have urinary retention after apical suspension, even without an antiincontinence procedure. If unable to void spontaneously by the time of discharge, a patient can go home with a catheter and be seen again within a week for removal. A stool softener is prescribed when regular diet is tolerated, and constipation and straining are ideally avoided. At routine postoperative visits, the patient is evaluated for prolapse recurrence and mesh or suture erosion. Symptoms of pelvic floor dysfunction are also elicited. Anatomic suc-

FIGURE 45-17.7╇ Peritoneal closure.

cess does not always correlate with functional success, and vice versa. Thus, continual evaluation of surgical results is based on anatomy and on symptoms such as urinary incontinence, defecatory dysfunction, pelvic pain, and sexual dysfunction.

■⌀ Complications Following ASC, the graft material or its attaching sutures can erode through the vaginal epithelium. On average, symptoms develop 14 months following surgery, and vaginal bleeding and discharge are classic symptoms (Kohli, 1998). The diagnosis is generally straightforward, as mesh or sutures can be seen directly during speculum examination. Mesh erosion through the vaginal mucosa may initially be treated with a 6-week or longer course of intravaginal estrogen cream. For those with exposed mesh and symptoms, surgical removal in an operating suite may be performed vaginally. Epithelium around the erosion site is sharply dissected from the mesh and undermined. The mesh is grasped, placed on gentle tension, dissected off the overlying tissue, and as much mesh as can be identified is resected. The vaginal epithelial edges are then trimmed to freshen edges and reapproximated in a running or interrupted fashion using 2-0 gauge delayed-absorbable suture. Failure of these wounds to heal is interpreted as a sign of graft or tissue infection, and more extensive or complete removal of the graft is considered. Sutures that are eroding into the vagina may be cut and removed in the office. Fortunately, removal of sutures or portions of eroding mesh does not generally compromise prolapse correction.

Surgeries for Pelvic Floor Disorders

INTRAOPERATIVE

Minimally Invasive Sacrocolpopexy

■⌀ Surgical Steps

Sacrocolpopexy (SC) is increasingly being performed with a minimally invasive approach using conventional laparoscopy or robotassisted laparoscopy. The basic procedural steps are the same as for laparotomic ASC and differ mainly by abdominal entry method and instruments used. Steps are outlined here, but a fuller discussion is found in Section 45-17. Although not as extensively studied as abdominal sacrocolpopexy (ASC), limited data suggest that minimally invasive SC has similar short-term functional and anatomic results, shorter hospitalization, but longer operating times and greater cost (Judd, 2010; Siddiqui, 2012). Several randomized trials have compared outcomes and costs of laparoscopic sacrocolpopexy (LSC) with robotic sacrocolpopexy (RSC) (Anger, 2014; Paraiso, 2011). Compared with LSC, RSC carries increased cost, operative time, and higher pain scores, but short-term anatomic and functional outcomes and complications are similar. Data also show a longer robotic learning curve to achieve proficiency. That said, as robotic technology and training continues to develop, operative time, costs, and complications will likely decline.

PREOPERATIVE ■⌀ Patient Evaluation Candidates for minimally invasive SC undergo the same prolapse and incontinence evaluation as for ASC (p. 1098). As discussed in Chapter 41 (p. 874), factors influencing approach include patient overall health, restrictions to prolonged anesthesia, body habitus, intraabdominal adhesions, and surgeon skill.

➊╇ Anesthesia and Patient Positioning.╇ Following administration of general anesthesia, the patient is positioned for laparoscopy in booted support stirrups as fully described in Chapter 41 (p. 879). The buttocks are positioned slightly distal to the table edge to compensate for mild upward patient migration that often occurs in the steep Trendelenburg position needed for laparoscopy. Correct positioning decreases nerve injury rates, provides access to the vagina, and allows full rotation of vaginal manipulator and laparoscopic instruments. The vagina and abdomen are surgically prepared, and a Foley catheter is inserted.

➋╇ Incision and Trocar Placement.╇A full description of minimally invasive entry is found in Chapter 41 (p. 889). For LSC, four ports are generally used (Fig. 45-18.1). A 10-mm umbilical port houses the laparoscope; one 5-mm port is placed subcostally and lateral to the rectus abdominis muscle on either side for tissue manipulation; and two 10-mm ports, one in each lower quadrant, allow needle-bearing sutures to be threaded into the abdomen. Knots are tied using an extracorporeal technique, illustrated in Chapter 41 (p. 899). For RSC, five ports are placed in a shallow “W” formation. One 12-mm umbilical port houses the laparoscope; one 8- or 10-mm assistant port is placed subcostally lateral to the rectus abdominis muscle on the right; and three 8-mm robotic ports are positioned in bilateral lower quadrants, with two on the left and one on the right. We dock the robotic cart on the patient’s left to permit manipulation of the vagina. Knots are tied using intracorporeal knot-tying techniques.

■⌀ Consent Consent considerations mirror those for ASC. Additionally, with the minimally invasive approach, patients are counseled and consented for laparotomy if surgery cannot be completed by MIS. In addition, complications more common to laparoscopy are discussed (Chap. 41, p. 877). These include puncture injury to organs and vessels during abdominal entry, positioning neuropathies, and delayed thermal injury to intraabdominal organs from electrosurgical tools.

Hysterectomy.╇ The same considerations described for ASC apply to minimally invasive SC. An additional concern with minimally invasive total hysterectomy is the use of electrosurgery to amputate the uterus and its potential for greater cuff dehiscence and mesh erosion rates (Chap. 44, p. 1036). Moreover, limited data currently suggest that total hysterectomy at the time of minimally invasive sacrocolpopexy significantly increases the mesh erosion risk (Tan-Kim, 2011). Accordingly, in appropriately selected patients, supracervical hysterectomy (SCH) is preferred. During the final steps of SCH, to prepare for subsequent sacrocolpopexy, the serosal edges of the cervix may be reapproximated over the exposed endocervical canal using three to five interrupted 2-0 or 0-gauge polyglactin 910 (Vicryl) sutures.

➍╇ Pelvic Anatomy Delineation.╇To

begin sacrocolpopexy, the bowel is gently swept out of the pelvis and above the pelvic brim. With LSC, the rectosigmoid epiploicae may be sutured to the left pelvic sidewall to aid presacral space visualization. With RSC, to accomplish the same goal, an atraumatic grasper used through the third robotic port gently displaces the rectosigmoid laterally. Next, the aortic bifurcation and iliac vessels are identified, and the sacral promontory is visualized and probed in the midline. With RSC, promontory palpation using conventional laparoscopic instruments prior to robot docking is important. This provides tactile anatomic information that is not obtainable robotically. Last, other structures and boundaries are identified as described for ASC.

➎╇ Peritoneal Incision.╇The peritoneum

overlying the sacral promontory in the midline is elevated with tissue forceps and incised sharply with endoscopic scissors (Fig. 45-18.2). The incision is extended caudally into the posterior cul-de-sac of Douglas and then to the vaginal apex (Fig. 45-18.3). Upward and outward traction on the right and left peritoneal edges aids with dissection. Monopolar energy delivered through the scissors is intermittently used for peritoneal dissection and to control small-vessel bleeding.

➏╇ Anterior

■⌀ Patient Preparation This mirrors preparation for ASC and covers antibiotics and thromboembolism prophylaxis and bowel preparation options (p. 1098).

➌╇ Concomitant

FIGURE 45-18.1╇ Port placement.

Longitudinal Ligament Identification.╇ Following peritoneal incision, the loose connective tissue between the peritoneum and the sacrum is sharply and bluntly dissected to expose presacral space anatomy similar to that for ASC. Gentle dissection with scissors or atraumatic tissue forceps removes fat and areolar tissue from the sacrum. Beneath these tissues, the shiny white anterior longitudinal ligament is seen overlying the bone in the midline. A gauze sponge introduced through the assistant port

CHAPTER 45

45-18

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SECTION 6 FIGURE 45-18.2╇ Peritoneal incision overlying the sacrum. or a laparoscopic Kittner can assist this dissection. During dissection, significant hemorrhage can occur. To apply bleeding site pressure, a gauze sponge and atraumatic forceps can be introduced through an assistant port. Bleeding management otherwise follows that during ASC (Step 8, p. 1099).

❼╇ Sacral Suture Site Selection.╇This

FIGURE 45-18.3╇ Peritoneal incision extended caudad.

traction on the peritoneum, the rectovaginal space is entered and developed with a combination of sharp and blunt dissection similar to that with ASC. During minimally invasive procedures, with patients positioned in steep Trendelenburg, angling a straight vaginal manipulator may be difficult and thus may limit posterior wall exposure. Access can be

improved by instead using a medium-sized Deaver retractor in the vagina with its tip directed anteriorly.

➓╇ Mesh Placement.╇Affixing mesh to the posterior proximal vagina mirrors that in ASC. One strip of mesh is threaded into the peritoneal cavity through one of the 8or 10-mm assistant cannulas. With graspers

is completed in a similar manner to that described for ASC. The anterior surface of S1 may be poorly seen with a 0-degree laparoscope due to this vertebral surface’s steep angle of descent. In these cases, switching from a 0-degree to a 30-degree scope and directing it downward improves viewing.

➑╇ Anterior Vaginal Wall Dissection.╇ A

vaginal manipulator is placed to elevate the vaginal apex, and the peritoneum covering it is incised transversely. Sharp and blunt dissection is used to separate the peritoneum and bladder from the anterior vaginal wall (Fig. 45-18.4). The use of electrosurgery during dissection is limited in an effort to minimize delayed thermal injury to the bladder or ureters.

➒╇ Posterior Vaginal Wall Dissection.╇ The cervical stump or vaginal apex is next directed cephalad and ventrally. The peritoneum covering the posterior vaginal wall is incised transversely at a level proximal to the reflection of the rectum against the posterior vaginal wall (Fig. 45-18.5). The right and left uterosacral ligaments are used as lateral dissection boundaries. With gentle outward

FIGURE 45-18.4╇ Dissection of the anterior vaginal wall.

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CHAPTER 45

FIGURE 45-18.5╇ Dissection of the posterior vaginal wall. placed through a contralateral operating port, the mesh is guided into place and held against the dissected portion of posterior vaginal wall. The same sutures and suturing principles used for ASC are used for minimally invasive sacrocolpopexy (Fig. 45-18.6). Sutures are placed through the mesh and the vaginal wall using laparoscopic or robotic needle drivers. However, with LSC, the knots are secured using the extracorporeal knot tying technique, but with RSC, the intracorporeal technique is used. Accordingly, long sutures, usually 30 to 36 inches, are used for LSC,

FIGURE 45-18.7╇ Anterior mesh placement.

FIGURE 45-18.6╇ Posterior mesh placement.

but short sutures, approximately 6 inches, are used for RSC. With the vaginal manipulator serving as a support, a second strip of mesh is sutured to the anterior vaginal wall in the same manner as on the posterior vaginal wall (Figs. 45-18.7 and 45-18.8). ╇ Mesh Sizing and Sacral Attachment.╇ For this step, the prior sacral dissection is again exposed, and the two proximal portions of mesh are held together by an atraumatic tissue forceps for maneuvering.

Using the vaginal manipulator, the cuff is gently elevated, and the proximal portions of mesh are extended to the earlier exposed ligament over the S1 vertebra. With correct positioning, apical suspension reduces prolapse of the apex and the apical segments of the anterior and posterior vaginal walls. Moreover, the mesh segment between the vagina and sacrum should be tension free. ╇ Sacral Suture Placement.╇ Once desired mesh position and length are determined,

FIGURE 45-18.8╇ Anterior mesh sutured.

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SECTION 6 FIGURE 45-18.9╇ Mesh attachment to the sacrum.

excess fabric above the planned most cephalad sacral suture is trimmed off. The sacral portion of the mesh is then secured to the anterior longitudinal ligament with three to four stitches that ultimately are aligned vertically along the S1 vertebra. For this, the proximal portions of both mesh strips are held against the ligament, and each stitch travels from right to left. The lowest stitch is placed first, and the needle enters the right side of the mesh, drives through the longitudinal ligament under direct visualization, and exits on the mesh’s left side. To prevent air knots as the lowest sacral suture is secured, the surgeon elevates the vaginal manipulator to gently push the vaginal apex closer to and against the lower part of the sacrum. Two or three additional sutures are next placed in the same fashion, each at a

FIGURE 45-18.10╇ Peritoneal closure.

more cephalad level. Ideally, each suture lies approximately ½ cm from the previous one, and the most cephalad suture is at or just below the level of the promontory (Fig. 45-18.9).

╇ Cystoscopy.╇ This is routinely performed prior to port closure to document ureteral integrity and exclude bladder sutures or injury. Urethral examination is important if an antiincontinence procedure is also performed.

╇ Peritoneal Closure.╇ The peritoneum is closed over the intervening and sacral portions of the mesh with 2-0 delayed-absorbable suture in a running fashion (Fig. 45-18.10). If desired, the peritoneum over the vaginal apex is closed over the exposed mesh in a similar fashion.

╇ Wound Closure.╇Subsequent surgery completion steps follow those of laparoscopy (Chap. 41, p. 897).

╇ Return to Supine Position.╇With RSC, the robot is undocked at this point. With both RSC and LSC, the patient is returned to a supine position, and the abdomen deflated prior to cystoscopy.

POSTOPERATIVE Patients are usually discharged from the hospital on postoperative day 1. As with other minimally invasive surgery, diet is advanced as tolerated and early ambulation is encouraged. Other postoperative management specific to sacrocolpopexy mirrors that for ASC.

Surgeries for Pelvic Floor Disorders

45-19

The vaginal apex can be effectively suspended with various vaginal or abdominal surgeries. Of these, suturing the apex to the high (proximal) portion of each uterosacral ligaments (USL), that is, uterosacral ligament suspension (USLS), is more commonly performed vaginally, although abdominal and laparoscopic approaches are suitable. Although often modified, the ultimate USLS goal is vaginal apex support restoration by affixing the anterior and posterior vaginal walls to the uterosacral ligaments at and above the level of the ischial spines. The steps described here outline our preferred approach, which is a modification of the USLS procedure described by Shull and associates (2000). Another vaginal apical suspension procedure, sacrospinous ligament fixation (SSLF), also strives to correct apical prolapse. However, if USLS and SSLF are compared, USLS maintains the normal vaginal axis orientation and was thought to lower rates of dyspareunia and anterior vaginal wall prolapse. However, authors of the Operations and Pelvic Muscle Training in the Management of Apical Support Loss (OPTIMAL) trial compared outcomes of these two and found that after 2 years, both showed equal composite success scores nearing 60 percent (Barber, 2014). These rates are lower than the 70- to 90-percent success rates generally reported for these apical suspension procedures, but retreatment rates remained low at 5 percent (Margulies, 2010). Of complications in the OPTIMAL trial, neurologic pain persisted in 4 percent of SSLF cases, but ureteral obstruction was more frequent after USLS and approximated 3 percent. In addition to apical prolapse correction, vaginal USLS effectively repairs apical enteroceles, and thus other enterocele repairs are unnecessary. However, apical prolapse commonly develops in conjunction with anterior and posterior compartment prolapse. Thus, vaginal USLS is often performed with other surgeries such as colporrhaphy and perineorrhaphy to correct these defects.

PREOPERATIVE ■⌀ Patient Evaluation As just noted, apical prolapse often coexists with other sites of prolapse, and a careful preoperative assessment is performed. Also prior to vaginal USLS, patients with urinary incontinence symptoms undergo

■⌀ Consent Recurrent prolapse is common following any corrective surgery. Thus, a surgeon should be aware of recurrence rates quoted in the literature and his or her own personal rates. As noted in the prior section, urinary incontinence or voiding or defecatory dysfunction may follow USLS. Also, USLS fixes the upper vagina to the USL and has a potential to shorten the vaginal canal. Accordingly, dyspareunia is another postoperative risk. Moreover, sacral plexus nerve injury with subsequent neuropathy ensues in up to 7 percent of women following vaginal USLS (Barber, 2014; Montoya, 2012). Thus, women are counseled regarding the possible need for suture release if severe buttock pain that radiates to the posterior thigh develops postoperatively. Mild buttock pain without associated radiation and without motor deficits generally resolves during several weeks of expectant management that incorporates analgesics. Last, apical suspension suture erosion and vaginal granulation tissue are frequently reported complications (Barber, 2014).

■⌀ Patient Preparation Bowel preparation will vary depending on surgeon preference. Patients can be instructed to take only clear liquids the day prior to surgery and complete one or two enemas the night prior to or the morning of surgery. Alternatively, a mechanical bowel preparation, listed in Chapter 39 (p. 835), may be preferred. Ballard and associates (2014), however, noted no distinct advantage to this for urogynecologic operations. Antibiotics and thromboprophylaxis are given as outlined in Tables 39-6 and 39-8 (p. 835).

➊╇ Anesthesia and Patient Positioning.╇ Vaginal USLS is typically performed under general anesthesia. The patient is placed in standard lithotomy position using candycane or booted support stirrups. Examination under anesthesia assesses the degree of prolapse and confirms the need for planned surgeries. The vagina and abdomen are surgically prepared, and a Foley catheter is inserted.

➋╇ Vaginal Apex Incision.╇The initial

incision can be made in various ways. If complementing vaginal hysterectomy, the vaginal cuff is already open, and each USL transfixing suture is already held by a hemostat. However, if the patient has previously undergone hysterectomy, the vaginal apex is grasped with Allis clamps, and the overlying epithelium is incised vertically or horizontally depending on circumstances. For example, for concurrent colporrhaphy, a midline vertical apical incision that extends distally along the anterior and/or posterior vaginal wall is preferred. Alternatively, in patients with large apical enteroceles and redundant apical tissue, a diamond-shaped portion of epithelium can be excised and a new apex created. However, excessive tissue excision that may result in vaginal shortening is avoided. Stitches may then be placed at the lateral boundaries of the intended new apex for later identification. With enterocele, epithelial dissection at the apex typically reveals a peritoneal sac, which is incised to allow peritoneal cavity entry. Last, if a clear dissection plane is not identified, USLS can be performed by an extraperitoneal approach, or SSLF may be performed instead.

➌╇ Packing, Retraction, and IdentiÂ�

fication.╇ Bowel must be adequately packed away for proper USL visualization to avoid bowel injury when high uterosacral sutures are placed. First, a Deaver retractor displaces the bladder upward. Then, a right-angle retractor or two fingers in the posterior cul-de-sac gently displace the posterior peritoneum and underlying rectum downward to avoid

CHAPTER 45

Vaginal Uterosacral Ligament Suspension

simple or complex urodynamic testing to clarify the type of incontinence. For those with SUI, a concurrent antiincontinence operation is generally performed. Because prolapse correction can unmask occult incontinence, clinicians also test continent women while manually reducing the prolapse with a moderately full bladder. Women with such occult SUI are carefully counseled and may also elect to also undergo antiincontinence surgery. Last, fully continent women undergoing vaginal prolapse surgery are also at risk for later development of postoperative SUI. To evaluate whether a prophylactic midurethral sling (MUS) placed during apical and anterior vaginal prolapse surgery reduces this risk in stress-continent women, the OPUS (Outcomes Following Vaginal Prolapse Repair and Midurethral Sling) trial was conducted. Investigators concluded that prophylactic MUS in these asymptomatic women leads to a 27-percent postoperative SUI incidence at 1 year compared with a 43-percent rate without concomitant prophylactic MUS (Wei, 2012). These results support earlier findings of the CARE trial (p. 1098). Importantly, adding an antiincontinence procedure decreases, but does not eliminate, the risk of de novo SUI. As another preoperative step, some suggest that estrogen may increase the vaginal wall thickness for easier dissection and suture placement. However, randomized controlled trials analyzing this treatment for reducing suture erosion or prolapse recurrence risks are lacking.

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SECTION 6

tion, gentle traction on each suture should confirm correct placement and incorporation of adequate USL tissue. Excess laxity during such USL traction usually indicates insufficient tissue to provide adequate apical support, and the suture is replaced. Hematomas form occasionally following inadvertent laceration of pelvic sidewall veins. Application of pressure with a sponge stick will typically control bleeding.

➎╇ Other Procedures.╇ Once all the sus-

pensory sutures are placed through each USL, colporrhaphy is completed if indicated. If a perineorrhaphy or midurethral sling procedure is planned, we defer these until the USLS operation is completed.

➏╇ Vaginal Wall Suture Placement.╇

FIGURE 45-19.1╇ Vaginal view of sutures placed into uterosacral ligaments and vaginal walls. peritoneum tearing, which creates bleeding and difficult USL identification. Two moist laparotomy sponges tied together are then gently threaded into the posterior cul-desac to pack bowel into the upper pelvis. The Deaver retractor is then repositioned to cover the laparotomy sponges. Gentle upward retractor traction exposes the mid and proximal USL portions and the deep posterior culde-sac close to the sacrum. Two Allis clamps are next placed at approximately 5 and 7 o’clock positions on the posterior vaginal wall and incorporate the posterior peritoneum. Gentle downward Allis clamp traction tenses the USLs, which are then traced with the contralateral index finger. The strong ligament fibers can be traced from their distal attachments in the vagina to their proximal sacral attachment. Concurrently, the ischial spines, which protrude from the lateral pelvic walls and lie anterolateral to the USLs, are palpated. Ureters are usually indistinct to touch, but they course anterolateral to the USLs. A lighted Breisky-Navratil retractor is useful for retracting the rectum medially to further expose the USLs. A second similar retractor is often positioned on the opposite side for improved visualization of the proximal USL.

➍╇ Suture Placement into the UteroÂ�

sacral Ligament.╇ Following adequate exposure, two to three sutures are placed through one USL. Sutures are equally spaced along

the mid to proximal length of each ligament. Long, straight needle drivers are useful for this. The sutures are individually tagged as they are placed, preferably with labeled clamps numbered 1 through 3 for one side and 4 through 6 for the other. Sutures are then loosely secured to the ipsilateral surgical drape. For the most distal stitch, we use a 2-0 gauge delayed-absorbable suture (black) with a swaged on SH needle. For the more proximal stitch(es), a similar gauge permanent material (blue) is selected instead (Fig. 45-19.1). To begin, the distal absorbable suture perforates the USL at its midlength, which lies at approximately the level of the ischial spine. The subsequent, more proximal sutures are placed approximately 0.5 cm to 1 cm cephalad from each prior suture. Two or three sutures are placed on each side, and this number is guided by surgeon preference, the extent of USL exposed, and vaginal cuff width. With each stitch placement, the needle tip ideally passes through the most medial portion of the ligament in a lateral-to-medial direction. These specifics attempt to minimize ureteral entrapment or kinking risks. Moreover, to lower rectal injury rates, an assistant retracts the rectum to the contralateral side, and suture purchases do not extend too medial, that is, beyond the ligament width. Similarly, suture bites that are too deep risk injury to internal iliac vessels or sacral nerves (Wieslander, 2007). At comple-

Vaginal packing is first removed, and ultimately, four to six sutures (two or three from each USL) are placed along the vaginal cuff width. If one begins on the patient’s left side, the free end of the left distal absorbable USLS suture (suture 1) is threaded into a Mayo needle. The needle and suture then pierce the left lateral anterior vaginal wall at the apex. The other needle-bearing suture end similarly penetrates the posterior wall (see Fig. 45-19.1). Each suture strand traverses the full vaginal wall thickness, including the epithelium. Next, the proximal (permanent) USLS suture(s) are similarly passed through the anterior and posterior vaginal walls, each medial to the previous suture. To lower suture erosion rates, permanent sutures traverse the full thickness of the fibromuscular layer but not the epithelium. However, a substantial thickness of fibromuscular wall is incorporated to prevent tissue tearing, which can create suture bridges that are bowel obstruction risks. The same steps are then repeated on the right. Ultimately, on each side, the most cephalad USLS sutures (sutures 3 and 6) are placed most medially on the vaginal cuff. The most distal USLS sutures (sutures 1 and 4) are placed most laterally on the vaginal cuff. For organization, all completed sutures are held within numbered clamps on their respective sides. At this point, indigo carmine or methylene blue dye is given intravenously in preparation for cystoscopy that follows knot tying. Knots are secured starting with most medial cuff sutures (sutures 3 and 6) and ending with the most lateral (sutures 1 and 4) (Fig. 45-19.2). The vaginal wall is confirmed to approximate the ULSs. Both this approximation and the order in which sutures are tied may prevent suture bridges. All sutures are held with their corresponding numbered clamps after tying until cystoscopy is completed.

❼╇ Cystoscopy.╇ This is performed to document ureteral patency and exclude bladder

Surgeries for Pelvic Floor Disorders

POSTOPERATIVE

FIGURE 45-19.2╇ Lateral view of sutures placed into the left uterosacral ligament. sutures or cystotomy. The ureter lies closest to the lower portion of the USL. Thus, if ureteral obstruction is suspected, the most distal USLS suture on the ipsilateral side is released first, and cystoscopy is repeated. If no flow is noted, the next most proximal suture is released, and this is continued cephalad in a stepwise fashion until efflux is seen.

➑╇ Rectal Examination.╇The rectum is digitally explored to confirm approximation of the cuff against the USLs and exclude sutures entering the rectum. ➒╇ Closure of the Vaginal Cuff.╇The suspension suture ends are now cut, and the vaginal cuff is reapproximated in a running

Following vaginal USLS, postoperative care mirrors that for vaginal surgery. Postoperative activity in general can be individualized, although intercourse is usually delayed until after 6 weeks following surgery. A voiding trial can be completed on postoperative day 1, depending on the patient’s condition and general progress. Some patients have urinary retention after apical suspension, even without an antiincontinence procedure. If unable to void spontaneously by the time of discharge, the patient can be discharged with a catheter and followed up within a week for removal. Patients are screened for lower extremity neuropathy prior to discharge. Suture erosion with granulation tissue can be a short- or long-term complication and is managed as described on page 1102.

CHAPTER 45

fashion with 2-0 gauge delayed-absorbable suture. Alternatively, four interrupted 2-0 absorbable sutures are placed through the full thickness of the anterior and posterior vaginal cuff prior to tying of the USL sutures and held for later cuff closure. This practice aids cuff closure with high suspensions, in which vaginal edges may be inaccessible without pulling that in turn disrupts the repair.

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45-20 SECTION 6

Abdominal Uterosacral Ligament Suspension Uterosacral ligament suspension (USLS) is more commonly performed vaginally (p. 1107). But for some situations, an abdominal approach, either via laparotomy or laparoscopy, offers advantages. For example, with advanced apical prolapse, many consider abdominal sacrocolpopexy (ASC) the preferred procedure. However, limited data suggest that total hysterectomy concurrent with ASC leads to higher mesh erosion rates. Thus, with total abdominal hysterectomy, abdominal USLS represents an ASC alternative to reduce graft erosion. A second possible indication is the setting of iatrogenic cystotomy during ASC. In this case, to minimize mesh erosion into the bladder or fistula formation, ASC can be aborted and USLS performed instead (p. 1102). Last, although not evidence-based, for women with concurrent pelvic cancer, mesh placement may not be ideal, and thus, USLS may be preferred. During abdominal USLS, the mid to proximal span of both USLs is sutured to the anterior and posterior vaginal walls at the vaginal apex. Because of this suspension, enteroceles are effectively closed. Abdominal USLS is effective, and limited data show that success rates for the apical suspension approximate 90 percent (Lowenstein, 2009; Rardin, 2009). However, as with other apical procedures, subsequent anterior or posterior compartment defects are later risks.

this treatment’s ability to improve dissection or reduce suture erosion or prolapse recurrence risks. Consenting mirrors that for vaginal USLS (p. 1107). Antibiotics and thromboprophylaxis are given as outlined in Tables 39-6 and 39-8 (p. 835). Bowel preparation is selected according to surgeon preference as for vaginal USLS.

INTRAOPERATIVE ■⌀ Surgical Steps ➊╇ Anesthesia and Patient Positioning.╇ Following administration of general anesthesia, the patient is positioned in a low lithotomy position with thighs parallel to the ground and legs in booted support stirrups. The vagina and abdomen are surgically prepared, and a Foley catheter is inserted.

➋╇ Incision.╇ A midline vertical or low trans-

verse abdominal incision is suitable, and a self-retaining retractor and bowel packing clears the operative field. With a laparoscopic approach, port placement is similar to that described for laparoscopic sacrocolpopexy (p. 1103).

➌╇ Ureter Identification.╇ The ureters are identified early, as these can be trapped during suture placement through the USL and can be kinked with suture tying. Thus, frequent confirmation of ureter location and cystoscopy after the suspension sutures are tied are essential steps.

➍╇ Identification of Uterosacral LigaÂ�

ments.╇ Prior to hysterectomy, a surgeon identifies each USL by applying contralateral and upward uterine traction. With this technique, the USLs are stretched and more easily seen or palpated. In women with prior hysterectomy, the vaginal cuff is similarly elevated and deviated by a vaginal manipulator. The USLs run medial and posterior to the ureters, and their proximity explains the significant ureteral injury rate, which can reach 11 percent with vaginal USLS (Barber, 2000). The USL midpoint generally lies at the level of the ischial spines, which are located anterolateral to the USLs. In women with normal support, the cervix and upper vagina are located roughly at the level of these spines. Thus, this bony landmark is generally chosen as the site for the most distal USL suture. However, this site may be modified according to vaginal length and intraoperative findings.

➎╇ Uterosacral Ligament Suture PlaceÂ�

ment.╇ Following adequate exposure, two to three sutures are placed through one USL. Sutures are equally spaced along the mid to proximal length of each ligament. During suture placement, the vaginal cuff is elevated to accentuate the USLs. For the most distal stitch, we use a 2-0 gauge delayed-absorbable suture (black) with a swaged-on SH needle. For the more proximal stitch(es), a similar gauge permanent material (blue) is selected instead (Fig. 45-20.1). To begin, the distal absorbable suture perforates the USL at its midlength, which lies approximately at the level of the ischial spine.

PREOPERATIVE Before surgery, patients are examined to identify other prolapsed sites, which could be concurrently repaired. Similarly, overt or occult SUI is excluded. In addition, consenting includes a discussion regarding prophylactic antiincontinence surgery. As with other apical suspension procedures, and as described fully on page 1098, even stresscontinent women may benefit in many cases from a prophylactic antiincontinence procedure performed concurrently. However, for abdominal USLS, data on this prophylactic practice are lacking and must be extrapolated from ASC and vaginal USLS studies. Last, as another preoperative step, some suggest that estrogen aids dissection and suture placement, as the vaginal wall thickness is increased (Rahn, 2014, 2015). However, no randomized controlled trials have analyzed

FIGURE 45-20.1╇ Uterosacral ligament suture placement.

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FIGURE 45-20.2╇ Vaginal cuff suture placement.

The subsequent, more proximal sutures are placed approximately 0.5 to 1 cm cephalad from each prior suture. Two or three sutures may be placed on each side, and this number is guided by surgeon preference, the extent of USL exposed, and vaginal cuff width. With stitch placement, each needle tip ideally passes through the most medial portion of the ligament in a lateral-to-medial direction. Moreover, the assistant retracts the rectum to the contralateral side, and suture purchases do not extend too medial, that is, beyond the ligament width. Similarly, suture bites that are too deep risk injury to internal iliac vessels or sacral nerves (Wieslander, 2007). At completion, gentle traction on each suture should confirm correct placement and incorporation of adequate USL tissue. If not, the suture is replaced. Following each placement, sutures with needles still attached are then individually tagged, preferably with labeled clamps, and are loosely secured to the ipsilateral drape. This series is repeated on the other side.

➏╇ Hysterectomy.╇ These suspensory sutures may be placed through the USL before or after hysterectomy based on surgeon preference and intraoperative findings (Fig. 45-20.2). If sutures are placed prior to hysterectomy, they are held by numbered hemostats and not tied. Their needles are covered with a surgical towel to avoid stick injuries. Hysterectomy is then completed, and the cuff is closed. ❼╇ Vaginal Wall Suture Placement.╇ Ultimately, four to six sutures (two or three

FIGURE 45-20.3╇ All sutures secured.

from each USL) are placed along the vaginal cuff width. An EEA sizer or similar blunt manipulator is placed in the vagina for cuff movement. If one begins on the patient’s left side, the free end of the left distal absorbable USLS suture (suture 1) is threaded into a Mayo needle. The needle and suture then pierce the left lateral anterior vaginal wall at the apex. The other needle-bearing suture end similarly penetrates the posterior wall (see Fig. 45-20.1). Each suture strand may traverse the full vaginal wall thickness, including the epithelium. Next, the proximal (permanent) USLS sutures are passed through the anterior and posterior vaginal walls, each medial to the previous suture on the cuff. To lower suture erosion rates, permanent sutures traverse the full thickness of the fibromuscular walls but not the epithelium. However, a substantial thickness of fibromuscular wall should be incorporated to prevent tissue tearing, which can create suture bridges that are bowel obstruction risks. The same steps are repeated on the right side of the cuff. Ultimately on each side, the most cephalad USLS suture (suture 3 or 6) is placed most medially along the vaginal cuff width. The most distal USLS suture (suture 1 or 4) is placed most laterally on the vaginal cuff. For organization, all completed sutures are held within numbered clamps on their respective sides. At this point, knots are secured starting with the most medial sutures (sutures 3 and 6) and ending with the most lateral (sutures 1 and 4). The vaginal wall is confirmed to

approximate the ULSs (Fig. 45-20.3). Both this approximation and the order in which sutures are tied may prevent suture bridges. All sutures are held with their corresponding numbered clamps after tying until cystoscopy is completed.

➑╇ Cystoscopy.╇ To document ureteral

patency and exclude bladder sutures or cystotomy, cystoscopy is performed after all suspension sutures are tied. The ureter lies closest to the lower portion of the USL. Thus, if ureteral obstruction is suspected, the most distal USLS suture on the ipsilateral side is released first, and cystoscopy is repeated. If no flow is noted, the next most proximal suture is released, and this is continued cephalad in a stepwise fashion until efflux is seen.

➒╇ Rectal Examination.╇ This is performed to confirm approximation of the cuff to the USLs and exclude sutures entering the rectum. ➓╇ Incision Closure.╇ The abdomen is closed in a standard fashion (Chap. 43, p. 928).

╇ Concurrent Procedures.╇ If necessary, a paravaginal defect repair or other abdominal antiincontinence procedure may be performed prior to incision closure. If posterior repair or vaginal antiincontinence surgery is required, these will follow incision closure.

POSTOPERATIVE Following abdominal USLS, postoperative care mirrors that for abdominal sacrocolpopexy (p. 1102).

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45-21 SECTION 6

Sacrospinous Ligament Fixation Extending between the ischial spine and lower sacrum, the sacrospinous ligament (SSL) lies deep to the coccygeus muscle and adds significant stability to the bony pelvis. Fixation of the vaginal apex to this coccygeus-sacrospinous ligament (C-SSL) complex—namely, sacrospinous ligament fixation (SSLF)—is often selected for apical prolapse repair. Although there are many SSLF modifications, apex fixation to the right ligament is most often described, likely due to the leftsided location of the rectosigmoid (Goldberg, 2001; Kearney, 2003). Gaining access to the SSL also varies. In a more traditional approach, the pararectal space and SSL are accessed through a posterior colporrhaphy incision, and only the right aspect of the apical posterior vaginal wall is attached to the ligament. Alternatively, in the Michigan four-wall modification, the SSL is accessed through an apical incision, dissection to the SSL remains extraperitoneal, and both anterior and posterior vaginal walls are directly affixed to the SSL by four points that span the vaginal apex width. Advantageously, this technique may avoid anterior enterocele, contralateral vaginal wall descent, and the need for bilateral suspension (Larson, 2013). A modification of the original Michigan approach is described here (Morley, 1988). Success rates are comparable to those for other vaginal approaches for vault suspension (Barber, 2014; Maher, 2013). However, SSLF compares less favorably with abdominal sacrocolpopexy. But, SSLF averts abdominal surgery and is associated with shorter operating times and quicker recovery. For these reasons, it is often preferred for women with comorbidities. Additionally, this approach allows other concurrent support defects to be repaired vaginally as well.

PREOPERATIVE ■⌀ Patient Evaluation Before surgery, patients are examined to identify other prolapsed sites, which could be concurrently repaired. Similarly, overt or occult SUI is excluded. In addition, consenting includes a discussion regarding prophylactic antiincontinence surgery. As with other apical suspension procedures, and as described fully on page 1098, even stress-continent women may benefit in many cases from a prophylactic antiincontinence procedure performed

concurrently. Last, as another preoperative step, some suggest that estrogen aids dissection and suture placement, as the vaginal wall thickness is increased (Rahn, 2014, 2015). However, no randomized controlled trials have analyzed this treatment’s ability to improve dissection or reduce suture erosion or prolapse recurrence risks.

■⌀ Consent Because the vagina is fixed and laterally deviated with SSLF, dyspareunia is one postoperative risk. Also, recurrent prolapse is common following any corrective surgery. Although the apical prolapse rate following SSLF is below 10 percent, anterior vaginal wall prolapse rates can approach 30 percent (Barber, 2009). This anterior prolapse is attributed to the exaggerated posterior deflection of the vaginal axis, which exposes the anterior vaginal wall to greater intraabdominal stresses than other apical suspensions (Weber, 2005). Despite this theoretical vulnerability, the OPTIMAL trial cited earlier (p. 1107) compared SSLF and vaginal USLS 2-year outcomes and found equal composite success scores nearing 60 percent (Barber, 2014). These percentages are lower than the 70- to 90-percent success rates generally reported for these procedures. That said, actual retreatment rates remained low at 5 percent (Margulies, 2010). For most women, SSLF has low associated risks for serious complications, but neurovascular injury can occur. First, low-pressure vessel bleeding encountered during dissection and exposure of the pararectal space is generally attributed to retractor or needle injury of the extensive venous plexus that drains the rectum and vagina. This bleeding can usually be controlled with sustained pressure from pararectal space packing. Second, arterial bleeding may follow aggressive retraction and subsequent middle rectal artery avulsion or laceration. The internal pudendal and inferior gluteal arteries are also at risk if a needle inadvertently extends past the proximal SSL border. Arterial bleeding is best controlled by vessel ligation or clipping. An internal iliac ligation for such bleeding is ineffective due to extensive collateral circulation in the pelvis. The pudendal nerve and lower sacral nerves such as S3 and S4 can also be damaged if the needle exits or enters past the ligament’s proximal (upper) margin. Sutures that are placed too close to the sacrum risk injury to S4 or the nerve to the levator ani muscles (Roshanravan, 2007). Even sutures that are placed in the recommended mid and lower aspect of the SSL can entrap or lacerate the nerve to the levator ani muscles. Pelvic floor muscle spasms, buttock pain, and dyspareunia may be manifestations.

Moreover, sacral plexus nerve injury with subsequent neuropathy has followed vaginal SSLF. As described on page 1107, persistent neurologic pain was noted in 4 percent of SSLF cases in the OPTIMAL trial. Accordingly, women are counseled that additional surgery for suture release may be needed if severe buttock pain that radiates to the posterior thigh persists postoperatively. Mild buttock pain without associated radiation or without motor deficits is common and generally resolves within several weeks and with expectant management that incorporates analgesics. This buttock pain is generally attributed to entrapment of the nerve to the levator ani muscle. Of other complications, ureteral and rectal injuries and ileus are rare, mainly because this procedure is extraperitoneal. In addition, as with any apical suspension procedure, voiding and defecatory dysfunction can develop.

■⌀ Patient Preparation Bowel preparation will vary depending on surgeon preference. Patients can be instructed to take only clear liquids the day prior to surgery and complete one or two enemas that night or the morning of surgery. Alternatively, a mechanical bowel preparation using agents listed in Chapter 39 (p. 835) may be preferred. Ballard and associates (2014), however, noted no distinct advantage to this for urogynecologic operations. As with most vaginal surgery, because of the risk posed by the normal vaginal flora for postoperative wound cellulitis and abscess, preoperative antibiotics are warranted. Typical agents are found in Table 39-6 (p. 835). Additionally, thromboprophylaxis is provided as outlined in Table 39-8 (p. 836).

INTRAOPERATIVE ■⌀ Surgical Instruments Suture placement into the SSL can be performed with various ligature carriers and include the Deschamps ligature carrier, Miya hook, Capio ligature carrier, and Endo Stitch. Alternatively, a Mayo needle and long, straight needle driver can be used. Using the Deschamps ligature carrier, a surgeon threads the suture through an eye at the needle-shaped carrier tip. Arcs and curves constructed into the instrument aid ease of suture placement. Once the tip of the Deschamps carrier passes through the ligament, the suture is retrieved with a nerve hook, as shown in atlas Step 4. Disadvantages to this device, however, include the relative thickness of the needle tip, which may be difficult to drive through the ligament. Alternatively, disposable devices have become popular, in particular the Capio ligature carrier. This device is easier to manipulate

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FIGURE 45-21.1╇ Coccygeus-sacrospinous ligament complex and surrounding pelvic anatomy. Vaginal apex diamond or “T” incisions. than the Miya hook. Also, its design aids placement of sutures using ligament palpation and thus obviates the need for extensive dissection. To expose the ligament, Deaver and Breisky-Navratil retractors are commonly used.

■⌀ Surgical Steps ➊╇ Anesthesia and Patient Positioning.╇ After general anesthesia has been administered, a woman is placed in standard lithotomy position. The vagina is surgically prepared, and a Foley catheter is inserted. Initially, vaginal vault prolapse is reduced to place the vagina in a normal anatomic position.

➋╇ Vaginal Wall Incision.╇In the setting

of vaginal cuff prolapse, the apex is grasped and brought to the level of the ligament to confirm adequate vaginal length or need for redundant tissue excision. With advanced prolapse, a new apex site is required and most often lies posterior to the former hysterectomy scar (Kearney, 2003). When indicated, excess vaginal tissue will be excised. At the planned apex, four points in a diamond configuration are grasped with Allis clamps, are directed inward, and individually brought to lie against the SSL. This ensures fixation off tension and correction of any anterior and posterior vaginal wall redundancy. These points include one midline anterior, one midline posterior, and two lateral ones. Once determined, the diamond-shaped redundant vaginal wall within these four Allis clamps is incised to a depth reaching the underlying loose preperitoneal connective tissue (Fig 45-21.1). If this diamond lies posterior to the prior cuff scar, the peritoneum is generally easily identified and the enterocele sac may be entered intentionally or inadvertently. If this diamond lies anterior to the prior cuff, then

FIGURE 45-21.2╇ Entry into right pararectal space through rectal pillar.

dissection proceeds more superficially to avoid bladder entry. If vaginal shortening is a concern, then a transverse incision is made at the new apex site and no tissue is excised. Next, a vertical incision that extends several centimeters posteriorly from this transverse incision’s midpoint creates a “T” incision that aids access into the pararectal space (Fig. 43-21.1, dotted line). With either incision configuration, the intended apex site is marked with sutures or clamps to maintain proper orientation during fixation. In the setting of concomitant vaginal hysterectomy, after hysterectomy completion, the lateral edges of the anterior and posterior vaginal walls are grasped with Allis clamps and brought into direct contact with the SSL to similarly assess for excess tension or redundancy. A vertical incision is then made through the midline posterior vaginal wall at the open cuff and extended 2 to 3 cm distally. The extraperitoneal space between the vaginal wall and the peritoneum is entered. Then, the pararectal space is entered as described next.

➌╇ Access to the Right Sacrospinous

Ligament.╇ Whether the SSL is accessed through the apex (Michigan modification) or through the posterior vaginal wall (traditional approach), the same retroperitoneal spaces are entered. Namely, the rectovaginal space and then the pararectal space are entered sequentially to reach the SSL (Fig. 45-21.2). Following entry into the rectovaginal space, traction on the vaginal epithelium with an Allis clamp and countertraction on peritoneum with tissue forceps are applied, while sharp or blunt dissection is directed toward the right ischial spine. Important anatomic structures during entry into the right pararectal space include the rectum, which lies medially and is retracted leftward to avoid injury; blood vessels and peritoneum, which lie ventrally and superiorly; and the levator ani muscles, which

are found dorsal and laterally. To enter the pararectal space, the rectal pillars, also known as deep uterosacral ligament fibers, are perforated as shown by the arrow in Figure 45-21.2. This tissue is typically attenuated in women with advanced prolapse and thus easier to perforate. In some cases, perforation with a hemostat or similar instrument is needed. Once in the pararectal space, the ischial spine tip is palpated, and the index finger moves gently medially toward the lower, lateral border of the sacrum to delineate the C-SSL complex (Fig. 45-21.3). This step also allows blunt digital dissection of loose connective tissue from the ligament’s midportion.

➍╇ Retractor Positioning.╇ Two to three retractors are positioned to adequately expose the C-SSL complex (Fig. 45-21.4). We prefer a small Deaver to displace the peritoneum and blood vessels superiorly, a Breisky-Navratil retractor to displace the rectum medially, and a second Breisky-Navratil retractor to displace the levator muscles inferiorly and further expose the ligament’s lower portion. Retraction is gentle to avoid vessel or rectal injury. A rectal examination at this point aims to exclude rectal laceration. During dissection and retractor positioning, vessels in the area may be lacerated, and hemostasis is obtained with direct pressure, electrosurgical coagulation, or ligatures. ➎╇ SSL Suture Placement.╇Once the

C-SSL complex is delineated, sutures are placed approximately two fingerbreadths or 2 to 3 cm medial to the ischial spine, which roughly corresponds to the SSL midportion (Roshanravan, 2007; Walters, 2007). Sutures placed too close to the spine risk injury to the pudendal nerves or vessels. Needle entry or exit points ideally remain within the mid to lower portion of the ligament. This lowers injury risk to the inferior gluteal vessels and pudendal

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Atlas of Gynecologic Surgery

SECTION 6 FIGURE 45-21.3╇ Anatomy delineated. or sacral nerves, which course in close proximity to the upper SSL margin. We use the Deschamps ligature carrier or a tapered Mayo needle with a half-circle radius to ultimately pass four sutures (two absorbable and two permanent) through the ligament (see Fig. 45-21.4). To begin, two long sutures, one delayed-absorbable (black) and one permanent (blue) are threaded through the carrier eye. For the absorbable sutures, we select either 2-0 or 0-gauge polydioxanone (PDS II), and for the permanent sutures, we use similar-gauge polypropylene (Prolene). Thus, with a single ligament penetration, four sutures ends are available Alternatively, four delayed-absorbable sutures using 0-gauge polydioxanone can be used.

When the Deschamps ligature carrier is used, sutures are retrieved using a nerve hook, as shown. Once the suture ends are retrieved, suture traction is applied to test their anchorage. Firm resistance during traction confirms proper placement. Laxity indicates superficial placement through the coccygeus muscle or overlying fascia, and the sutures are replaced deeper into C-SSL. At this point, the four suture ends are paired by color, tagged by individually numbered hemostats, and loosely secured to the surgical drape. The second carrier pass is then completed approximately 1 cm medial to the first. Based on intraoperative findings, the order of the carrier passes may be reversed, that is, the lateral suture is placed second. Adequate anchorage

is similarly confirmed, and these sutures are then paired and tagged. Ultimately, these two carrier passes result in four suture pairs that will later be sutured to the anterior, posterior, and lateral vaginal walls. Adequate suture labeling (1 through 4) avoids suture tangling and later suture bridging at the fixation site. The delayed-absorbable suture (black), which is placed most laterally on the ligament is labeled “1” and will be placed through the right lateral aspect of the vaginal cuff. The delayed-absorbable suture (black) placed most medial on the ligament is labeled “4” and will be placed through the left lateral aspect of the vaginal cuff. Sutures 3 and 4 correspond to the permanent sutures (blue). These ultimately will be placed through the medial portion of the cuff. If indicated, anterior colporrhaphy is performed at this time. If performed, the anterior vaginal wall is reapproximated with 2-0 or 3-0 gauge absorbable suture to the level of the cuff. Rectoceles are often corrected with SSLF, and posterior colporrhaphy is not frequently required. If a posterior midline plication, perineorrhaphy, or midurethral sling is planned, we prefer to complete this after apical suspension.

➏╇ Vaginal Apex Suturing.╇The SSL

sutures are then sequentially anchored to the anterior and posterior fibromuscular walls of the vagina apex along the vaginal cuff width. To begin, the two ends of suture 1 are grasped. The end that is most cephalad on the ligament is threaded through the Mayo needle eye. This is then driven through the full thickness of the lateral right anterior vaginal wall including the epithelium, at the site of the initial intendedapex marking suture. The other end of suture 1 is then driven through the lateral right posterior wall. Similar steps are subsequently repeated on the cuff’s left side with delayedabsorbable suture 4 (Fig. 45-21.5). Suture ends are not tied but instead held on their respective sides by a hemostat. Attention is then directed to the permanent sutures (2 and 3). First and medial to those of suture 1, the ends of suture 2 are driven through the anterior and posterior fibromuscular vaginal walls at a point right of the cuff midline. To lower suture erosion rates, permanent sutures traverse the full thickness of the fibromuscular walls but not the epithelium. However, a substantial fibromuscular wall thickness is incorporated to prevent tissue tearing, which can create suture bridges and incomplete healing of the vaginal wall to the ligament. Second and medial to those of suture 4, the ends of suture 3 are driven through the anterior and posterior fibromuscular vaginal walls at a point left of the cuff midline.

❼╇ Suspension of the Vaginal Vault.╇ At FIGURE 45-21.4╇ Retractor exposure and ligature placement.

this point, knots are secured starting with suture 4 and ending with suture 1. A pulley

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FIGURE 45-21.5╇ Lateral apex suturing. stitch may be used for the permanent sutures. With this stitch, a knot is secured on the vaginal wall (posterior wall in this case) (Fig. 45-21.6). As shown in Figure 45-21.7, traction on the other suture end (anterior dashed strand) pulls the tied wall (posterior) to the SSL. However, with the four-wall modification, this type of stitch is not necessary. Each suture is tied down to ensure direct apposition of the vaginal walls to the SSL (Fig. 45-21.8). Both this snug approximation and the order in which sutures are tied may prevent suture bridges. All sutures are held with their corresponding numbered clamps after tying until cystoscopy is completed. Rectal examination confirms apposition of the vaginal cuff to the SSL and excludes rectal injury.

FIGURE 45-21.7╇ Pulley stitch.

FIGURE 45-21.6╇ Permanent suture placement (blue strands).

➑╇ Cuff closure.╇ If needed, the remainder of the vaginal cuff may be closed in a running fashion using 2-0 gauge delayed-absorbable suture.

POSTOPERATIVE Following SSLF, postoperative care mirrors that for vaginal surgery. Postoperative activity in general can be individualized, although intercourse is usually delayed until after 6 weeks following surgery. A voiding trial can be completed on postoperative day 1, depending on the patient’s condition and general progress. Some patients have urinary retention after apical suspension, even without an antiincontinence procedure. If unable to void spontaneously by the time of discharge, the

patient can be discharged with a catheter and followed up within a week for removal. Patients are screened for lower extremity neuropathy prior to discharge. Mild gluteal pain is common and typically resolves within several weeks. Severe gluteal pain that radiates down the posterior thigh and leg is a sign of sacral nerve entrapment and is generally treated by prompt suture release. Dyspareunia is commonly attributed to the posterolateral deflection of the vaginal axis. However, given the anatomic position of the nerves to the coccygeus and levator ani muscles, entrapment of these nerves may possibly lead to transient or sustained muscle spasm and dysfunction (Roshanravan, 2007). If levator muscle tenderness is identified, physical therapy may be helpful.

FIGURE 45-21.8╇ Vaginal apex approximated to ligament.

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Atlas of Gynecologic Surgery

45-22 SECTION 6

McCall Culdoplasty Culdoplasty techniques are used to obliterate the posterior cul-de-sac of Douglas and prevent herniation of small bowel into the vaginal wall, that is, enterocele. Thus, culdoplasty usually complements procedures that further expose the posterior cul-de-sac to enterocele, such as retropubic urethropexy procedures. However, evidence-based studies have not borne out these benefits, and current concepts of specific pelvic-support defect repair have decreased the popularity of culdoplasty. Nevertheless, this procedure is still performed and may have value when completed in conjunction with other prolapse procedures. Of these, McCall culdoplasty is most commonly performed during vaginal hysterectomy to close the cul-de-sac, add support to the posterior vaginal apex, and possibly prevent enterocele formation. With traditional McCall culdoplasty, two to three horizontal internal rows using permanent sutures are placed from one uterosacral ligament (USL) to the other to obliterate the posterior cul-de-sac (McCall, 1957). The term internal denotes that these sutures remain totally intraabdominal and do not penetrate into the vaginal lumen. In addition, one to two rows of absorbable external sutures are similarly placed through the USLs, but these pass through the posterior vaginal cuff. Several modifications aim to provide better vaginal apex support. These include the Mayo/McCall culdoplasty and the modified McCall culdoplasty. The steps described next outline our approach. Importantly, if significant vaginal apex prolapse or enterocele is already present, then we prefer an apical suspension procedure such as sacrocolpopexy, sacrospinous ligament fixation, or vaginal uterosacral ligament suspension, as more data support their efficacy.

PREOPERATIVE ■⌀ Patient Evaluation McCall culdoplasty is generally performed following vaginal hysterectomy in patients with enterocele or preventively in those without. Because the degree of pelvic organ prolapse will dictate reconstructive surgeries planned, a thorough prolapse evaluation is performed.

■⌀ Consent As with any pelvic reconstructive surgery to correct prolapse, the risk of enterocele

formation or recurrence is discussed. In addition, because this procedure involves placement of sutures through the uterosacral ligaments, risks similar to uterosacral ligament suspension procedures are addressed and include dyspareunia, ureteral or bowel injury, and sacral plexus nerve damage (p. 1107). Suture erosion risks are low.

■⌀ Patient Preparation Bowel preparation will vary depending on surgeon preference and is typically dictated by concurrent surgery planned. Antibiotics and thromboprophylaxis are given as outlined in Tables 39-6 and 39-8 (p. 835).

INTRAOPERATIVE ■⌀ Surgical Steps ➊╇ Anesthesia and Patient Positioning.╇ McCall culdoplasty is typically performed under general anesthesia, although epidural or spinal regional methods may also be appropriate in select cases. The patient is placed in standard lithotomy position using candy-cane or booted support stirrups. The vagina is surgically prepared, and a Foley catheter is inserted. Vaginal hysterectomy is completed as described in Section 43-13 (p. 957), but the vaginal cuff is left open for culdoplasty completion. Excess peritoneum or vaginal wall may be excised at this time if indicated.

➋╇ Packing.╇ After vaginal hysterectomy, a moist pack is placed into the posterior cul-desac to prevent descent of bowel or omentum. ➌╇ Identification of Uterosacral LigaÂ�

ments and Ureters.╇This mirrors that described for the vaginal uterosacral ligament suspension procedure (p. 1107). Briefly, a Deaver retractor displaces the bladder upward, and gentle upward retractor traction exposes the distal to mid-USL portions. Two Allis clamps are next placed at approximately 5 and 7 o’clock positions on the posterior vaginal wall and incorporate the posterior peritoneum. Gentle downward Allis clamp traction tenses the USLs, which are then traced with the contralateral index finger from their distal attachments in the vagina toward the sacrum. Ureters are typically indistinct to touch, but they course anterolateral to the USLs. Lighted Breisky-Navratil retractors are useful on either side to further expose the USLs.

➍╇ Suture Placement.╇For the internal McCall sutures, we use 2-0 gauge permanent

suture with a swaged-on SH needle. For the external McCall sutures, a similar-gauge delayed-absorbable material is selected. The number of suture rows placed is guided by cul-de-sac depth, vaginal cuff width, and surgeon preference. Generally, two to three internal and one to two external rows are placed. Of the internal sutures, the first suture row is the most distal of these, and each subsequent row is placed progressively cephalad across the posterior cul-de-sac. Each row begins with a stitch into one USL. The needle tip pierces the most medial portion of the left USL and travels in a lateral-to-medial direction. As with other USL suspension procedures, these specifics attempt to minimize ureteral entrapment risks. Moreover, to reduce rectal injury rates, the rectum is retracted to the contralateral side, and suture purchases do not extend too medial, that is, beyond the ligament width. The needle then travels through the cul-de-sac peritoneum or rectal serosa with intervening suture bites and exits through the opposite USL. Each row is spaced approximately 0.5 cm to 1 cm cephalad from the previous one. The internal McCall sutures are tagged, held, and tied only after placement of the external McCall sutures. Following these internal rows, the first external suture is placed through the full thickness of the posterior vaginal wall and incorporates the posterior peritoneum and USL (Fig. 45-22.1). Progressive left-to-right bites are then taken serially through the rectal serosa to reach the opposite uterosacral ligament (Fig. 45-22.2). Finally, the suture enters the opposite uterosacral ligament, passed through the posterior peritoneum, and exits through the full vaginal wall thickness to reenter the vagina.

➎╇ Suture Tying.╇ The internal sutures are tied first. These sutures are sequentially tied beginning with the most proximal sutures and progressing caudad. The external sutures are then tied, and again the most cephalad of these is tied first. ➏╇ Rectal Examination.╇The rectum is digitally explored to exclude sutures entering the rectum. ➐╇ Cystoscopy.╇ This is performed after all

McCall culdoplasty sutures are tied to document ureteral patency and exclude bladder sutures or cystotomy.

➑╇ Vaginal Cuff Closure.╇ Upon completion of McCall culdoplasty, the remaining steps of vaginal hysterectomy will follow as described in Section 43-13 (p. 961).

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FIGURE 45-22.1╇ Uterosacral ligament suture placement.

POSTOPERATIVE Following vaginal hysterectomy and McCall culdoplasty, postoperative care mirrors that for vaginal surgery. Activity in general is

FIGURE 45-22.2╇ Suture reenters the vagina prior to securing.

individualized, although intercourse is usually delayed until 6 weeks. As with other uterosacral ligament suspension procedures, patients are screened for lower extremity neuropathy prior to discharge. Suture ero-

sion with granulation tissue can be a shortor long-term complication and is managed as described on page 1102.

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45-23 SECTION 6

Abdominal Culdoplasty Procedures

preparation, listed in Chapter 39 (p. 835), may be selected. Antibiotics and thromboprophylaxis are given as outlined in Tables 39-6 and 39-8 (p. 835)

INTRAOPERATIVE ■⌀ Surgical Steps

Included in this group are the Moschcowitz and Halban operations. As with other culdoplasty techniques, the goal is posterior cul-de-sac obliteration to prevent enterocele. However, evidence-based studies have not borne out these benefits, and the popularity of culdoplasty has declined. Nevertheless, this procedure is still performed and may have value when completed with other prolapse procedures. Selection of either the Halban or Moschcowitz procedure is based on surgeon preference and concurrent abdominal or vaginal pathology. Permanent sutures are generally used to close the cul-de-sac, and procedures differ by the orientation of suture placement. No trials have compared these techniques’ efficacy head-to-head.

PREOPERATIVE ■⌀ Patient Evaluation Culdoplasty is typically performed with other prolapse surgeries. Thus, thorough pelvic organ prolapse evaluation is performed, and all prolapse sites are considered when planning surgical correction. As with other prolapse procedures, patients are evaluated for existing or occult urinary incontinence.

➊╇ Anesthesia and Patient Positioning.╇ Abdominal culdoplasty is typically performed under general anesthesia. Patient positioning mirrors that described more fully for ASC on page 1099. Thus, following administration of general anesthesia, the patient is positioned in a low lithotomy position with thighs parallel to the ground and legs in booted support stirrups. The vagina and abdomen are surgically prepared, and a Foley catheter is inserted.

➋╇ Surgical Incision.╇ Either transverse or

vertical incision may be used for culdoplasty. Incision choice is dependent on concurrent surgeries planned. A self-retaining abdominal retractor is placed and concurrent surgeries such as hysterectomy and vault suspension are performed.

➌╇ Special

Considerations.╇ Following completion of initial procedures, the culde-sac is exposed and evaluated for suture placement. Additionally, an end-to-end anastomosis (EEA) sizer may be placed within the vagina or rectum to identify borders of the

■⌀ Consent As with any pelvic reconstructive surgery to correct prolapse, the risk of enterocele recurrence following abdominal culdoplasty is discussed. Additionally, risks of ureteral and bowel injury are included in the consenting process. During Halban and Moschcowitz culdoplasty, the rectosigmoid is plicated to the posterior vaginal wall. Accordingly, defecatory dysfunction and technical difficulty in performing subsequent colonoscopy have been reported following these culdoplasty procedures. Adhesion formation and difficulty with dissection in this space during subsequent operation may also be encountered.

■⌀ Patient Preparation Bowel preparation will vary by surgeon preference. Patients can drink only clear liquids the day before surgery and complete one or two enemas the night prior to or the morning of surgery. Alternatively, mechanical bowel

FIGURE 45-23.1╇ Halban culdoplasty.

posterior cul-de-sac and allow correct suture placement. Prior to culdoplasty, both ureters are identified again. In the past, these procedures have focused on suturing peritoneal and serosal surfaces. However, it is currently believed that a more effective approach incorporates deep bites into the muscularis of the vagina and rectosigmoid but avoiding entry into bowel and vaginal lumens. Also, adjacent rectosigmoid veins are protected to avert hematomas from needle sticks. If bleeding develops, direct vascular compression provides effective control in most instances.

➍╇ Halban Culdoplasty.╇ Several rows of

2-0 gauge permanent sutures are placed longitudinally through the serosa and muscularis of the rectosigmoid (Fig. 45-23.1). Rows are placed approximately 1 cm apart. The same sutures are then advanced through the peritoneum of the deep cul-de-sac and up toward the apex of the posterior vaginal wall. As much of the cul-de-sac as possible is obliterated, but to avoid ureteral injury, sutures are not placed lateral to the uterosacral ligaments.

➎╇ Moschcowitz Culdoplasty.╇Concentric

2-0 gauge permanent sutures are placed in the cul-de-sac beginning at the base and are directed upward almost to the level of the vaginal apex (Fig. 45-23.2). During placement, sutures are placed through the posterior vaginal wall and then advanced through the right uterosacral ligament, the rectosigmoid colon muscularis, and finally the left uterosacral

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➏╇ Rectal Examination.╇ This is performed to exclude sutures entering the rectum.

after all culdoplasty sutures are tied to document ureteral patency.

➑╇ Incision Closure.╇ The abdominal incision is closed as described in Chapter 43 (p. 928).

POSTOPERATIVE Following culdoplasty, postoperative care follows that for any major abdominal surgery. Hospitalization typically varies from 1 to 3 days, and return of normal bowel function usually dictates this course. Postoperative activity in general can be individualized, although intercourse is usually delayed until 6 weeks. FIGURE 45-23.2╇ Moschcowitz culdoplasty. ligament. The number of concentric rings required depends on the cul-de-sac depth, and usually three to four rings are sufficient. Rings are positioned 1 to 2 cm apart. As with

the Halban procedure, to reduce ureteral kinking, the lateral extent of the each suture ring should incorporate only the medial width of the uterosacral ligament.

CHAPTER 45

❼╇ Cystoscopy.╇ Cystoscopy is performed

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45-24 SECTION 6

Colpocleisis Pelvic organ prolapse surgery can broadly be grouped as reconstructive or obliterative. Colpocleisis, also known as colpectomy, vaginal extirpation, and vaginectomy, is an obliterative surgery for advanced vaginal or uterovaginal eversion. To correct prolapse, all obliterative procedures close the vaginal canal and thus are only indicated in symptomatic women who do not desire to preserve vaginal anatomy or coital function or who are medically unsuitable for reconstructive surgery. Specifically, this operation may be performed quickly with general, regional, or local anesthesia. The two main obliterating surgeries are partial colpocleisis and complete colpocleisis. With the partial procedure, also called LeFort colpocleisis, central rectangular sections of vaginal epithelium are dissected from the anterior and posterior vaginal walls, and the denuded fibromuscular layers are apposed and sewn together. This elevates the prolapse back into the pelvic cavity effectively and closes the vagina. The remaining lateral epithelial strips are fashioned into drainage tracts on either side for genital tract fluid egress. Thus, this surgery is appropriate for women with or without a uterus (Fig. 45-24.1).

In contrast, with total or complete colpocleisis, the entire circumference of vaginal epithelium is resected before vaginal walls are approximated. Drainage tracts are lacking, thus, it is typically used for posthysterectomy vault prolapse. If the uterus is present, concurrent total vaginal hysterectomy and closure of the peritoneum and vaginal cuff are performed prior to complete colpocleisis. Obliterative procedures are effective, and success rates range from 91 to 100 percent (Abassy, 2010; Fitzgerald, 2006; Weber, 2005). However, these rates are interpreted in the context of patients’ shorter life expectancies, limited activity levels, and variable outcome definitions. Anatomic success following colpocleisis is likely due to the amount of vaginal tissue sutured together to create a shelf of support. Several studies evaluating symptom improvement have also found high rates of patient satisfaction and functional improvement yet low rates of regret for sexual function loss (Barber, 2007; Fitzgerald, 2008; Gutman, 2009; Hullfish, 2007). SUI following colpocleisis is common, thus prophylactic antiincontinence surgery is considered. Additionally, high perineorrhaphy (p. 1096) or levator myorrhaphy (p. 1093) is recommended to narrow the genital hiatus and potentially decrease the recurrent prolapse risk. Last, concurrent hysterectomy eliminates the risk of uterine or cervical cancer and of postoperative hemato- or pyometra.

FIGURE 45-24.1╇ Prolapse correction following placement of serial sutures.

However, patient morbidity, including greater blood loss, increased transfusion risk, and longer procedure time, is increased with hysterectomy. Also, support success rates following colpocleisis are similar whether or not the uterus is removed (Abassy, 2010; Fitzgerald, 2006; Weber, 2005). Thus, hysterectomy is selected based on a woman’s general health, surgical goals, and comorbid genital tract disease risks.

PREOPERATIVE ■⌀ Patient Evaluation Because access to the cervix and endometrial cavity is not possible following this procedure, preinvasive lesions should be excluded. Specifically, a normal cervical cancer screening result is documented prior to surgery, and evaluation of the endometrium with either endometrial biopsy or sonography is recommended. The full extent of prolapse should be defined prior to surgery. Importantly, colpocleisis is difficult in women with good distal support of either the anterior or posterior vaginal walls. Women with advanced prolapse often do not display SUI because the urethra is kinked by prolapsing organs. However, with replacement of the prolapse, many with occult SUI do manifest symptoms. Thus, cough stress test or urodynamic testing has traditionally been performed with the prolapse elevated and replaced to search for occult SUI. Urinalysis and a postvoid residual measurement are also evaluated. For those who demonstrate SUI or occult SUI, antiincontinence surgery is recommended. However, even without SUI, a prophylactic antiincontinence procedure is considered to prevent later de novo SUI. Still, benefits of an additional procedure are weighed against the potential risk of urinary retention. For SUI, midurethral slings or urethral bulking agents are suitable options. Last, women with global prolapse frequently have some degree of ureteral kinking and obstruction. Thus, preoperative pyelography, CT urography, or renal sonography may be elected to identify or exclude ureteral obstruction. Alternatively, preoperative or intraoperative cystoscopy prior to the colpocleisis can be used to document ureteral patency. Known preexisting obstruction will assist with interpretation of cystoscopy findings performed at the procedure’s end. Also, with known ureteral obstruction, preoperative stent placement is considered to potentially assist with ureter identification during surgery. Colpocleisis ideally will unkink the ureter, and this can be documented during intraoperative cystoscopy after prolapse correction.

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■⌀ Consent

■⌀ Patient Preparation Bowel preparation, if any, will vary depending on surgeon preference. Patients can be instructed to take only clear liquids the day before surgery and complete one or two enemas the night prior to or the morning of surgery. Alternatively, a mechanical bowel preparation, listed in Chapter 39 (p. 835), may be elected. Antibiotic and thromboprophylaxis are given as outlined in Tables 39-6 and 39-8 (p. 835).

INTRAOPERATIVE ■⌀ Anesthesia and Patient Positioning General or regional anesthesia is preferred, although colpocleisis can be performed under local anesthesia. A patient is placed in standard lithotomy position using candy-cane or booted support stirrups, the vagina is surgically prepared, and a Foley catheter is inserted.

■⌀ Surgical Steps—LeFort Partial Colpocleisis As noted, LeFort partial colpocleisis may be performed in women with or without a uterus, but the following description outlines steps in women without prior hysterectomy. Throughout the ➊╇ Vaginal Marking.╇ descriptions of both colpocleisis procedures, proximal and distal will describe prolapsed anatomy rather than final prolapse-corrected anatomy. To begin, the rectangular areas of vaginal mucosa on the anterior and poste-

CHAPTER 45

Women considering this procedure must be fully aware that future vaginal intercourse is not possible. Thus, a patient’s partner is ideally included in the decision and consenting process. Patients expressing hesitation or doubt are excluded as candidates. First, as with any prolapse surgery, prolapse recurrence risk is discussed, although this risk is low with colpocleisis. Of note, later de novo rectal prolapse is disproportionately prevalent, and this unique complication was reported in 4 percent of women in one study (Collins, 2007). Second, as discussed, urinary incontinence may develop postoperatively. In addition, ureteral injury has been described. Third, in the unlikely situation that cervical or uterine malignancy develops after LeFort partial colpocleisis, the diagnosis may be potentially delayed. Finally, postoperative morbidity and mortality are especially pertinent in the elderly, and risks for cardiac, thromboembolic, pulmonary, or cerebrovascular events approximate 5 percent (Fitzgerald, 2006). FIGURE 45-24.2╇ Anterior vaginal wall incision. rior vaginal walls are outlined with a surgical marker or electrosurgical blade. The size of these areas to be removed is determined by the length and width of vaginal walls. On the anterior wall, the proximal edge of the rectangle extends to within 1 to 2 cm of the bladder neck . On the posterior wall, the proximal rectangle edge extends to within 1 to 3 cm of the posterior hymenal ring. The distal rectangle edges reach to within 1 to 2 cm of the cervicovaginal junction both anteriorly and posteriorly. The lateral edges of each rectangle are drawn to leave approximately 2-cm wide lateral epithelial borders on either side. These will be fashioned into lateral channels of adequate caliber to conduct drainage.

➋╇ Vaginal Infiltration.╇The rectangular areas of the vaginal wall to be removed may be thoroughly infiltrated with 50 mL of a dilute hemostatic solution. One example is 20 units of synthetic vasopressin (Pitressin) in 60 mL of saline. This infiltration extends beyond the anticipated incision boundaries. Without infiltration, bleeding can be significant during epithelial excision. Needle aspiration prior to injection is imperative to avoid intravascular injection of this potent vasoconstrictor. The anesthesiologist is also informed of vasopressin administration, as patient blood pressure may suddenly rise following injection. Blanching at the injection site is common. Due to the vasoactive effects of vasoconstrictors, patients with certain comorbidities may not be suitable candidates for their

use. These can include a history of angina, myocardial infarction, cardiomyopathy, congestive heart failure, uncontrolled hypertension, migraine, asthma, and severe chronic obstructive pulmonary disease.

➌╇ Vaginal Dissection.╇Previously outlined areas are sharply incised down to the fibromuscular layer. If the anterior dissection is performed first, the vaginal wall epithelium within the previously marked anterior rectangle is dissected off the underlying vaginal wall fibromuscular layer using both sharp and blunt dissection (Fig. 45-24.2). Dissection in the correct plane will prevent inadvertent bladder or bowel entry. One effective technique places a finger behind the vaginal wall, while cephalad dissection with Metzenbaum scissors advances parallel to the vaginal wall epithelium. Bleeding during dissection can generally be controlled with pressure and electrosurgical coagulation. Occasionally, figure-of-eight stitches of 2-0 gauge absorbable suture are needed if large venous sinuses are cut. Next, the vaginal wall epithelium within the previously marked posterior rectangle is similarly dissected off the fibromuscular layer on the posterior vaginal wall (Fig. 45-24.3). Of note, some prefer to dissect posteriorly first to avoid obscuring blood from the anterior wall that may ooze into the surgical field. ➍╇ Apical and Lateral Channels.╇After these rectangles are removed, a row of interrupted stitches using 2-0 gauge delayedabsorbable suture are placed through the

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SECTION 6 FIGURE 45-24.3╇ Posterior vaginal wall incision. anterior and posterior distal transverse epi�the�lial edges (Fig. 45-24.4). These will effectively close the fibromuscular layer over the cervix and create the apical channel. Next, lateral channels on each side are formed and connect with this apical channel. For this, the lateral anterior and posterior epithelial edges are approximated along their full length (Fig. 45-24.5). This lateral row of

FIGURE 45-24.4╇ Initial suture placement.

sutures begins distally and progresses proximally to the original proximal transverse incision near the bladder neck. The lateral channels can be created in a stepwise fashion, alternating from one side to the other.

➎╇ Anterior-to-Posterior Vaginal Wall

Approximation.╇ With the lateral canals now fashioned, the uterus can be sequentially

elevated into the pelvic cavity. For this, a surgeon places progressive rows of interrupted 2-0 gauge permanent or delayed-absorbable sutures that approximate the anterior and posterior fibromuscular layers along the distal prolapsed-tube width (Fig. 45-24.6). Successive transverse tiers of sutures are placed approximately 1 cm apart until the proximal transverse incision is reached (Fig. 45-24.7). These rows create a tissue septum that elevates and supports the uterus (see Fig. 45-24.1).

➏╇ Cystoscopy.╇ With either colpoclei-

sis procedure, cystoscopy is performed to exclude urinary tract injury and document ureteral patency.

❼╇ Closure of the Vaginal Epithelium.╇ This layer is then reapproximated in a running fashion with 2-0 or 3-0 gauge delayedabsorbable suture (Fig. 45-24.8). Importantly, the ostia of the bilateral drainage tracts remain patent.

➑╇ Concurrent Surgery.╇ At this point, an antiincontinence procedure may be completed as needed. Perineorrhaphy may be performed before or after vaginal wall closure (p. 1096).

■⌀ Surgical Steps—Complete Colpocleisis

FIGURE 45-24.5╇ Creation of lateral drainage canals.

➊╇ Vaginal Infiltration.╇ The vaginal cuff is placed on traction, and a vasoconstrictive agent may be injected in a similar fashion

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CHAPTER 45

FIGURE 45-24.6╇ Second row of sutures. to that described for the LeFort partial colpocleisis.

➋╇ Vaginal Incision and Dissection.╇ To

begin, the borders of planned dissection are marked circumferentially with a pen or electrosurgical blade. When redundant tissue is present, marking three to four smaller rectangles over the entire prolapsed vaginal tube helps maintain orientation during dissection. First, the vaginal epithelium is incised anteriorly at a point 1 to 2 cm distal to the bladder neck. Ultimately, this will be a point that lies approximately 1 cm proximal to the neck. Incision placement here will prevent

FIGURE 45-24.8╇ Vaginal mucosa closure.

FIGURE 45-24.7╇ Subsequent row of sutures. downward displacement of the bladder neck and the proximal urethra during apposition of the anterior and posterior vaginal walls. Additionally, it will allow room for the midurethral sling if one is planned. As the incision is swept circumferentially around the prolapse tube, a 1- to 2-cm distance is maintained distal to the hymeneal ring. The vaginal epithelium is sharply and bluntly dissected off the underlying

FIGURE 45-24.9╇ Anterior vaginal wall incision.

fibromuscular layer (Figs. 45-24.9 and 45-24.10). Dissection is kept close to the epithelium to avoid inadvertent bladder or rectal entry. Once the desired plane is identified, sharp and blunt dissection can proceed quickly until the entire vaginal epithelium is removed. One technique for sharp dissection involves positioning a finger behind the vaginal wall and dissecting with Metzenbaum scissors parallel to the vaginal wall and close

FIGURE 45-24.10╇ Posterior vaginal wall incision.

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SECTION 6 A B

FIGURE 45-24.12╇ A. Cephalad pressure against telescoping vaginal tube as serial sutures are secured. B. Completely inverted vaginal tube.

to the epithelium. After entry into the correct plane, blunt dissection with a gauze-covered index finger may allow rapid and wide development of this avascular space. There are areas where dissection may be difficult. For example, upon reaching the prolapsed vaginal apex and uterosacral ligament remnants, extensive scarring may be present that requires sharp dissection. The entire vaginal epithelium is removed from the prolapsed vaginal tube.

fibromuscular layer but avoid deep penetration into the bladder, ureter, or rectum (Fig. 45-24.11). The first purse-string suture is placed approximately 1 cm from the cuff, and tied while the cuff is inverted with atraumatic forceps or a hemostat (Fig. 45-24.12). The cut suture tails are held with a clamp and the second suture is placed 1 cm proximally. The hemostat tip inverts the vagina while the second suture is tied, and used again to tag the second suture. Progressive purse-string sutures are placed similarly 1 cm apart until the proximal edge of cut vaginal epithelium is reached. These serial steps telescope the prolapsed vaginal tube cephalad and toward the pelvic cavity. Depending on the size of the prolapse, approximately six to eight suture rings are needed to completely invert the prolapsed vaginal tube.

➌╇ Suture Placement.╇To plicate the vaginal walls together and elevate the everted vagina, a surgeon places a series of circumferential purse-string sutures around the vaginal tube. With 2-0 gauge permanent or delayedabsorbable suture, stitches incorporate the

➍╇ Finishing Steps.╇ Final steps are similar with both colpocleisis procedures. First, cystoscopy is performed to exclude urinary tract injury and document ureteral patency. The vaginal epithelium is then reapproximated in a running fashion with 2-0 or 3-0 gauge

FIGURE 45-24.11╇ Circumferential suturing.

delayed-absorbable suture. At this point, an antiincontinence procedure may be performed. Perineorrhaphy may be performed before or after vaginal wall closure (p. 1096).

POSTOPERATIVE Hospital admission is often prudent given the usual older age and comorbidities of these patients. A normal diet can be given immediately. Oral analgesics are usually sufficient. A voiding trial is performed prior to discharge as all patients can experience urinary retention from a levator myorrhaphy or perineorrhaphy. Patients with urinary retention can return within a week for a subsequent voiding trial and catheter removal. In general, recovery with colpocleisis is quick and typically without complication. Postoperative bleeding is not anticipated, save for spotting from the surgical site. As with any prolapse procedure, constipation is avoided to protect repair strength during healing. Thus, stool softeners are recommended. Resumption of normal activities is encouraged with the exception of heavy lifting for several months.

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45-25

External anal sphincter (EAS) and/or internal anal sphincter (IAS) repair is most commonly performed in patients with acquired fecal incontinence (FI) and an anterior sphincter defect. One of two methods may be selected for sphincter repair and include an end-to-end technique or an overlapping method. The end-to-end technique is most often used by obstetricians at delivery to reapproximate torn anal sphincter ends. However, in women remote from delivery, the overlapping technique is often selected, and with this, disrupted ends are overlapped and then sutured. In cases remote from delivery, the overlapping method is preferred. However, the optimal technique or suture material for repair and the effects of pudendal neuropathy on treatment outcome are not well known (Madoff, 2004). With the overlapping method, short-term continence rates up to 85 percent were previously reported (Fleshman, 1991; Sitzler, 1996). However, newer reports show significant deterioration of FI during long-term postoperative surveillance (Bravo Gutierrez, 2004; Zutshi, 2009). In cases at delivery, no evidence shows that either method yields superior results (Fitzpatrick, 2000; Garcia, 2005). Moreover, overlapping repair requires increased technical skills and carries the potential for increased blood loss, operating time, and pudendal neuropathy. Accordingly, the endto-end technique is likely to remain the standard method for sphincter reapproximation at delivery until further data from randomized controlled trials are available.

PREOPERATIVE ■⌀ Patient Evaluation Because the etiology of FI in patients with documented sphincter defects may be multifactorial, careful preoperative evaluation attempts to distinguish underlying sources. Evaluation for structural gastrointestinal (GI) tract pathology typically involves colonoscopy and/or barium enema. Additionally, radiographic bowel transit studies can be used to diagnose slow transit time, which may be related to defecatory dysfunction. Specific to the anorectum, endoanal sonography can accurately define structural disruption of the EAS and IAS (Fig. 25-7, p. 568) and is generally performed prior to sphincter repair. Exceptions are cloacal-like defects or chronic fourth-degree lacerations.

a nonanatomic repair and do not perform it with sphincteroplasty.

■⌀ Patient Preparation Because of the high associated risk of wound complications, antibiotic prophylaxis is warranted to minimize wound infection following surgical contamination from vaginal and rectal flora. We use a combination of ciprofloxacin and metronidazole to obtain broad bacterial coverage. Additionally, we often continue this same antibiotic coverage orally for approximately 7 days postoperatively to help reduce wound complications (Maldonado, 2014). Although benefits from mechanical bowel preparation have not been demonstrated, some form of bowel preparation is typically administered the day or night before surgery. Options are listed in Chapter 39 (p. 835). Thromboprophylaxis is also provided as outlined in Table 39-8 (p. 835).

INTRAOPERATIVE ■⌀ Surgical Steps

■⌀ Consent Although many women may have improved FI immediately following anal sphincteroplasty, repair durability is poor. For example, 3 to 5 years following correction, only approximately 10 percent of women are fully continent of solid and liquid stool (Halverson, 2002; Malouf, 2000). Retrospective data show that no patients are continent 10 years following sphincteroplasty (Zutshi, 2009). However, despite FI based on validated questionnaires, the quality of life in these patients notably did not decline. Reasons for worsening continence following initial improvement remain unknown but may include aging, scarring, and progressive pudendal neuropathy either from initial injury or from the sphincter repair (Madoff, 2004). In addition, skeletal muscle repair is thought to have poor success because resting muscle tone places incision lines on constant tension. Thus, preoperative counseling informs that most individuals will improve after the procedure, but continence is rarely perfect and deteriorates over time. In addition to persistent FI, sphincteroplasty is associated with other surgical risks. More common serious complications are wound dehiscence and fistula formation. Ha and coworkers (2001) noted a wound complication in 12 percent and fistula formation in 4 percent. Dyspareunia is a risk, especially if levator myorrhaphy (p. 1093) is concomitantly performed in sexually active women. Moreover, we believe levator myorrhaphy is

➊╇ Anesthesia and Patient Positioning.╇ After administration of either general or regional anesthesia, a woman is placed in standard lithotomy position using candycane or booted support stirrups. The vagina and perineum are surgically prepared and draped, and a Foley catheter is inserted.

➋╇ Incision and Dissection.╇ A downward-

arching curvilinear incision is placed between the fourchette and anus, and this connects with a midline posterior vaginal wall incision (Fig. 45-25.1). The vaginal incision edges are placed on tension with Allis clamps. Along the distal 3 to 4 cm of the posterior vaginal wall, the vaginal epithelium is then sharply dissected off its underlying fibromuscular layer and off the perineal body. On the perineum, dissection continues distally and laterally with Metzenbaum scissors. Advancement is kept just deep to the perianal skin and progresses until the scarred and usually retracted edges of the EAS are identified within the ischioanal fossa. Dissection proceeds until the EAS muscle is sufficiently mobile to ensure a tension-free overlapping repair. As the inner arch of the EAS is sharply separated from the anal submucosa, care is taken to avoid anal lumen entry. To assist, a surgeon’s index finger within the anus can guide dissection depth, and concomitant upward traction by an assistant on the sphincter’s scarred ends helps accentuate the best dissection plane. Internal pudendal vessel branches

CHAPTER 45

Anal Sphincteroplasty

In these, the absent anterior portion of the sphincter(s) is easily identified clinically. Anal manometry and pudendal nerve conduction studies may identify physiologic dysfunction such as neuropathy. Although these tests provide additional information and can be used during counseling, they are not necessary in patients with FI and a documented sphincter defect. In fact, the relationship of pudendal nerve function, typically assessed by determining pudendal nerve terminal motor latency, to sphincteroplasty outcome remains controversial (Madoff, 2004). One study found no association between pudendal nerve status and long-term anal continence (Malouf, 2000). Clinicians have attempted to improve success rates by selecting only those women who may benefit most from surgery. Patient age, preoperative anal manometry readings, and pudendal nerve motor function have been evaluated as possible outcome predictors. However, research findings are conflicting, and none of these consistently predicts outcome (Bravo Gutierrez, 2004; Buie, 2001; El-Gazzaz, 2012; Gearhart, 2005).

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SECTION 6 FIGURE 45-25.1╇ Vaginal dissection.

can be lacerated or inferior rectal nerve injured, especially if lateral dissection extends beyond the 3 and 9 o’clock positions. Thus, if extensive lateral dissection is anticipated, the end-to-end method of repair is preferred. Scarring in the midline may be cut but is not excised. This fibrous tissue adds strength to the sphincter muscle approximation. However, with extensive scarring, sphincter muscle fibers may be difficult to isolate. A nerve stimulator or a needle tip electrosurgical blade can assist in delineating these fibers. Current will often contract them.

FIGURE 45-25.2╇ Internal anal sphincter identification.

With suturing, the disrupted IAS edges are approximated in a continuous or interrupted fashion using 3-0 or 2-0 gauge monofilament, delayed-absorbable sutures such as polydioxanone PDS II (Fig. 45-25.3). Sutures

are spaced approximately 0.5 cm apart. As the distal extent of the IAS is generally several millimeters cephalad to the distal extent of the EAS, reapproximation of the IAS ends above the anal verge. Suture placement and

➌╇ Suture Placement within the InterÂ�

nal Anal Sphincter.╇ The IAS contributes significantly to the anal canal resting tone, and its reapproximation is included in the repair. Grasped in Figure 45-25.2, the IAS is a smooth, rubbery, thickened white sheet lying deep to the EAS and superficial to the anal mucosa and submucosal layers. This muscle usually retracts laterally when severed. For suturing, we prefer monofilament, delayed-absorbable suture. First, because both the IAS and EAS muscles are under constant contraction, direct tissue reapproximation by these longer-acting sutures in theory allows adequate scar formation during the critical first 3 months of postoperative healing. Second, use of permanent suture for sphincteroplasty has been associated with high rates of suture erosion and wound dehiscence (Luck, 2005).

FIGURE 45-25.3╇ Following internal anal sphincter reapproximation, the external anal sphincter is identified and grasped.

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CHAPTER 45

FIGURE 45-25.4╇ Overlapping sphincteroplasty.

exposure of the IAS is aided by a finger in the rectum. In many cases when an IAS defect is diagnosed remote from delivery, both the IAS and the EAS are usually identified as a unit. This unit is repaired en-bloc as described next.

➍╇ Overlapping External Anal SphincteÂ�

roplasty.╇ The overlapping repair of the EAS or EAS/IAS muscle unit is accomplished by placing two rows of mattress stitches using 2-0 or 3-0 gauge monofilament, delayedabsorbable suture. Within each row, the first stitch is the most cephalad, and more caudal stitches are added sequentially. The first row of mattress sutures begins at a distance (1 to 1.5 cm) from the severed edge of the overlying muscle. These then travel through the distal end of the underlying muscle (Fig. 45-25.4). A final upward pass again through the overlying muscle completes the stitch. To aid viewing, the suture ends in this row are held until the second suture row is placed. The second row of stitches then traverses through and through to secure the free end of the overlying muscle to the underlying muscle. With the overlapping method, either the right or left dissected end of the muscle can be used as the overlying muscle based on intraoperative findings. If significant mobilization cannot be achieved due to scarring or missing sphincter, then an end-to-end repair is performed.

➎╇ End-to-End External Anal SphincteÂ�

roplasty.╇ When performed for FI remote from delivery, each end of the disrupted

FIGURE 45-25.5╇ End-to-end sphincteroplasty.

EAS and surrounding scar tissue is identified and grasped with an Allis clamp (see Fig. 45-25.3). The ends of the EAS and its surrounding fibrous tissue are brought to the midline and reapproximated using three to four interrupted stitches of delayed-absorbable, monofilament suture (Fig. 45-25.5).

➏╇ Perineal Body Reconstruction.╇ Patients

with anal sphincter defects often have a deficient perineal body. In these cases, perineal body reconstruction is performed following reapproximation of the IAS and EAS muscles. This mirrors Step 4 of perineorrhaphy in Section 45-16 (p. 1096). For this, the connective tissue surrounding the separated ends of the bulbospongiosus and superficial transverse perineal muscles are identified and reapproximated. A combination of 2-0 and 0-gauge absorbable sutures is used for this repair. Deep suture bites at the level of the hymen also reunite the perineal membrane, which attaches to both the vaginal walls and the perineal body at the level of the hymen.

➐╇ Incision Closure.╇Excision of excess perineal skin and/or vaginal epithelium may be required prior to closing the incision. Vaginal epithelium and then perineal skin is reapproximated in a running or interrupted

fashion using 2-0 or 3-0 gauge absorbable suture, again similar to perineorrhaphy.

POSTOPERATIVE Pain varies postoperatively, and some women can be discharged home on postoperative day 2, whereas others require longer hospitalization. The Foley catheter is removed on postoperative day 1 or 2. An active voiding trial is performed, and some women may have difficulty voiding due to pain, inflammation, and levator ani muscle spasm. To limit trauma to the healing repair, we try to delay defecation for several days. Although data are lacking, we encourage patients to forego food and drink on day 1. They are subsequently advanced to clear liquids for 3 or 4 days. Stool softeners are given when a solid diet is begun and are continued for at least 6 weeks. Diet or agents that add bulk to the stool are discouraged as this may increase the repair breakdown risk. Local wound care involves perineal cleansing with a plastic water bottle following urination or defecation. Ambulation is encouraged, but physical exercise and sexual intercourse are delayed for 8 weeks. The first postoperative visit is typically 4 weeks following surgery.

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45-26 SECTION 6

Rectovaginal Fistula Repair In general, rectovaginal fistulas (RVFs) encountered by gynecologists are those complicating obstetric events and develop in the distal third of the vagina just above the hymen. Surgical management of these “low” RVFs varies by the condition of the external anal sphincter (EAS) but is usually achieved by a transvaginal or transanal approach. Midlevel RVFs are found in the middle third of the vagina and are also usually due to obstetric trauma. These can often be repaired transvaginally or transanally by a tension-free layered closure. High RVFs may follow hysterectomy or radiation therapy and lie close to the cervix or the vaginal cuff, and these are most commonly repaired abdominally. Fistulas identified during or shortly after delivery are suitable for immediate repair. However, fistulas are not repaired in the setting of inflammation, induration, or infection. Moreover, fistulas that are associated with radiation therapy and recurrent fistula, due to poor tissue vascularity, often require interposition of a vascular flap. Outcomes vary depending on the underlying cause and repair method. Success rates following obstetric injury repair range from 78 to 100 percent (Khanduja, 1999; Tsang, 1998). However, in cases with episioproctotomy, the reported success rate is 74 percent, and in those repaired by rectal advancement flap, rates reach only 40 to 50 percent (Mizrahi, 2002; Sonoda, 2002). Fistulas from radiation, cancer, or active inflammatory bowel disease are more difficult to treat successfully. In general, success rates are highest with the first surgical attempt at repair (Lowry, 1988).

may require examination under anesthesia with lacrimal duct probing. Coexisting anal incontinence is assessed, as this may be related to sphincter damage or other etiologies and is likely to persist after fistula repair.

■⌀ Consent Specific risks following rectovaginal fistula repair include fistula recurrence, dyspareunia, and vaginal narrowing or shortening. Fecal incontinence can follow some repairs if the anal sphincter is disrupted during surgery, as with episioproctotomy, or if coexistent sphincter defects are not recognized and repaired.

■⌀ Patient Preparation A rigorous bowel preparation is preferred to clear all stool from the rectal vault. Accordingly, a mechanical bowel preparation is advised the day prior to surgery, and options are listed in Chapter 39 (p. 835). If stool is still present in the rectum at the beginning of surgery, then a povidone-iodine (Betadine) flush with a Malecot drain may be needed. Antibiotic prophylaxis is given concurrent with surgery, however, additional doses during the days before surgery are not indicated. We use a combination of ciprofloxacin and metronidazole to obtain broad bacterial coverage. Additionally, thromboprophylaxis is provided as outlined in Table 39-8 (p. 836).

INTRAOPERATIVE ■⌀ Surgical Steps ➊╇ Anesthesia and Patient Position.╇ Rectovaginal fistula repair is typically an inpatient procedure, performed under general or regional anesthesia. A patient is placed in standard lithotomy position in candy-cane or booted support stirrups. The vagina is surgically prepared, and a Foley catheter is inserted.

➋╇ Fistula Identification.╇The

fistula is identified and its course is traced with a probe or dilator. Small fistulas may be dilated to improve identification of the tract.

➌╇ Vaginal Incision.╇ For a midlevel or

low RVF not involving the external anal sphincter, a circular incision is made in the vaginal epithelium surrounding the fistula (Fig. 45-26.1). The incision is made sufficiently wide to permit tract excision and generous mobilization of surrounding tissues for closure without excess suture-line tension (Fig. 45-26.2). Remember that tenets of proper fistula repair emphasize tension-free, multilayered closure, and excellent hemostasis. The entire fistula tract is then excised (Fig. 45-26.3). This creates an anal or rectal opening that is often significantly larger than that found preoperatively.

➍╇ Closure of the Rectal Wall.╇ Using 3-0 gauge delayed-absorbable suture, the edges of the anal mucosal defect are reapproximated

PREOPERATIVE ■⌀ Patient Evaluation As outlined in Chapter 25 (p. 574), a thorough evaluation is necessary to assess the etiology and delineate the full extent of a fistula. Unless RVFs are obviously from a prior obstetric event, fistulous tract biopsy is indicated to exclude malignancy or inflammatory conditions. Proctoscopy or colonoscopy is warranted if inflammatory bowel disease, malignancy, or gastrointestinal infection is suspected. If there are questions regarding the etiology, complexity, or number of fistulas, then imaging may be needed. At times, pinpoint fistulas are difficult to identify and

FIGURE 45-26.1╇ Vaginal incision.

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FIGURE 45-26.2╇ Mobilization of surrounding vaginal mucosa. in a running or interrupted fashion. Each bite or suture is spaced no more than 5 mm apart (Fig. 45-26.4). Although absorbable sutures can be placed into the rectal lumen, we prefer to reapproximate the submucosal tissue without needle or suture entering the rectum. One or two additional layers of the same gauge suture are placed in the anal or rectal wall muscularis to reinforce the submucosal closure. If the internal anal sphincter (IAS) but not the EAS is involved, the above additional layers incorporate the torn IAS edges.

FIGURE 45-26.4╇ Closure of the rectal wall.

FIGURE 45-26.3╇ Fistulous tract excision.

This step ideally reduces the postoperative anal incontinence risk. Alternatively, with very small RVFs, a purse-string suture can be placed to encircle the anal defect, and its perimeter lies a few millimeters from the resected fistulous tract rim. This suture is tied and inverts the defect’s edges into the bowel lumen. Additional reinforcing layers are then placed as described above.

➎╇ Closure of the Vaginal Fibromuscular Layer.╇ The fibromuscular layer of the vagina

is next reapproximated with 2-0 gauge delayedabsorbable sutures in a running or interrupted fashion (Fig. 45-26.5). If possible, two layers are completed to minimize incision tension and reinforce the repair. With anovaginal fistulas, these additional layers also reapproximate perineal body tissue. If the fistula involves the EAS, an episioproctotomy—that is, conversion of the defect into a fourth-degree laceration—can be elected. Following excision of the fistulous tract and mobilization of surrounding tissue, repair of the episioproctotomy is similar to the layered repair of an obstetric fourth-degree laceration. Briefly, the anal submucosa is reapproximated with 3-0 gauge

FIGURE 45-26.5╇ Closure of the fibromuscular layer.

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absorbable suture in a running or interrupted fashion. Repair of the IAS, EAS, and perineal body reconstruction mirror that for anal sphincteroplasty (p. 1125).

➏╇ Martius Bulbocavernosus Fat Pad

Graft.╇ In cases in which avascular or fibrotic tissue is extensive, a Martius graft may be

placed between the fibromuscular layer and vaginal epithelium (p. 1083).

➐╇ Vaginal Wall Closure.╇ Excess vaginal

mucosa is trimmed, and the vaginal mucosa is closed in a continuous running fashion using 3-0 gauge absorbable or delayedabsorbable suture.

POSTOPERATIVE Normal activity can resume during the first postoperative days. Intercourse, however, is delayed at least 6 weeks or until the vaginal incision is healed. To limit trauma to the healing repair, dietary modifications are instituted similar to those for sphincteroplasty (p. 1127).

Surgeries for Pelvic Floor Disorders

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Lowry AC, Thorson AG, Rothenberger DA, et al: Repair of simple rectovaginal fistulas. Influence of previous repairs. Dis Colon Rectum 31(9):676, 1988 Luck AM, Galvin SL, Theofrastous JP: Suture erosion and wound dehiscence with permanent versus absorbable suture in reconstructive posterior vaginal surgery. Am J Obstet Gynecol 192:1626, 2005 Madoff RD: Surgical treatment options for fecal incontinence. Gastroenterology 126:S48, 2004 Maher C, Feiner B, Baessler K, et al: Surgical management of pelvic organ prolapse in women. Cochrane Database Syst Rev 4:CD004014, 2013 Maldonado PA, Good MM, McIntire DD, et al: Overlapping sphincteroplasty for cloacal defect following obstetrical injury: presenting characteristics and subjective long-term outcomes. Female Pelvic Med Reconstr Surg 20(4);Suppl:S111, 2014 Malouf AJ, Norton CS, Engel AF, et al: Long-term results of overlapping anterior anal-sphincter repair for obstetric trauma. Lancet 355:260, 2000 Margulies RU, Rogers MA, Morgan DM: Outcomes of transvaginal uterosacral ligament suspension: systematic review and metaanalysis. Am J Obstet Gynecol 202(2):124, 2010 McCall ML: Posterior culdeplasty; surgical correction of enterocele during vaginal hysterectomy; a preliminary report. Obstet Gynecol 10(6):595, 1957 McDermott CD, Hale DS: Abdominal, laparoscopic, and robotic surgery for pelvic organ prolapse. Obstet Gynecol Clin North Am 36: 585, 2009 Meltomaa SS, Haarala MA, Taalikka MO, et al: Outcome of Burch retropubic urethropexy and the effect of concomitant abdominal hysterectomy: a prospective long-term follow-up study. Int Urogynecol J 12:3, 2001 Miklos JR, Moore RD: Laparoscopic extravesical vesicovaginal fistula repair: our technique and 15-year experience. Int Urogynecol J 26(3): 441, 2015 Mizrahi N, Wexner SD, Zmora O, et al: Endorectal advancement flap: are there predictors of failure? Dis Colon Rectum 45(12):1616, 2002 Mohr S, Brandner S, Mueller MD, et al: Sexual function after vaginal and abdominal fistula repair. Am J Obstet Gynecol 211:74.e1, 2014 Monga AK, Robinson D, Stanton SL: Periurethral collagen injections for genuine stress incontinence: a 2-year follow-up. Br J Urol 76:156, 1995 Monga AK, Stanton SL: Urodynamics: prediction, outcome and analysis of mechanism for cure of stress incontinence by periurethral collagen. BJOG 104:158, 1997 Montoya TI, Luebbehusen HI, Schaffer JI, et al: Sensory neuropathy following suspension of the vaginal apex to the proximal uterosacral ligaments. Int Urogynecol J 23(12):1735, 2012 Morley GW, DeLancey JO: Sacrospinous ligament fixation for eversion of the vagina. Am J Obstet Gynecol 158:872, 1988 Nguyen JN, Jakus-Waldman SM, Walter AJ, et al: Perioperative complications and reoperations after incontinence and prolapse surgeries using prosthetic implants. Obstet Gynecol 119(3):539, 2012 Nilsson CG, Palva K, Aarnio R, et al: Seventeen years’ follow-up of the tension-free vaginal tape procedure for female stress urinary incontinence. Int Urogynecol J 24(8):1265, 2013

Surgeries for Pelvic Floor Disorders transobturator (IVS-04) midurethral slings: randomized trial. Eur Urol 56:24, 2009 Rehman H, Bezerra CCB, Bruschini H, et al: Traditional suburethral sling operations for urinary incontinence in women. Cochrane Database Syst Rev 1:CD001754, 2011 Richter HE, Albo ME, Zyczynski HM, et al: Retropubic versus transobturator midurethral slings for stress incontinence. N Engl J Med 362(22):2066, 2010 Roshanravan SM, Wieslander CK, Schaffer JI, et al: Neurovascular anatomy of the greater sciatic foramen and sacrospinous ligament region in female cadavers: implications in sacrospinous ligament and iliococcygeal fascia vaginal vault suspension. Am J Obstet Gynecol 197(6):660.e1, 2007 Rovner ES: Urinary tract fistulae. In Kavoussi LR, Novick AC, Partin AW, et al (eds): Wein: Campbell-Walsh Urology, 10th ed. Philadelphia, Saunders, 2012 Schimpf MO, Rahn DD, Wheeler TL, et al: Sling surgery for stress urinary incontinence in women: a systematic review and metaanalysis. Am J Obstet Gynecol 211(1):71.e1, 2014 Schulz JA, Stanton SL, Baessler K, et al: Bulking agents for stress urinary incontinence: short-term results and complications in a randomized comparison of periurethral and transurethral injections. Int Urogynecol J Pelvic Floor Dysfunct 15:261, 2004 Shah SM, Gaunay GS: Treatment options for intrinsic sphincter deficiency. Nat Rev Urol 9(11):638, 2012 Shull BL, Bachofen C, Coates KW, et al: A transvaginal approach to repair of apical and other associated sites of pelvic organ prolapse with uterosacral ligaments. Am J Obstet Gynecol 183(6):1365, 2000 Siddiqui NY, Geller EJ, Visco AG: Symptomatic and anatomic 1-year outcomes after robotic and abdominal sacrocolpopexy. Am J Obstet Gynecol 206:435.e1, 2012 Sitzler PJ, Thomson JP: Overlap repair of damaged anal sphincter. A single surgeon’s series. Dis Colon Rectum 39(12):1356, 1996 Song PH, Kim YD, Kim HT, et al: The 7-year outcome of the tension-free vaginal tape procedure for treating female stress urinary incontinence. BJU Int 104(8):1113, 2009 Sonoda T, Hull T, Piedmonte MR, et al: Outcomes of primary repair of anorectal and rectovaginal fistulas using the endorectal advancement flap. Dis Colon Rectum 45(12):1622, 2002 Steele AC, Kohli N, Karram MM: Periurethral collagen injection for stress incontinence with and without urethral hypermobility. Obstet Gynecol 95:327, 2000 Summers A, Winkel LA, Hussain HK, et al: The relationship between anterior and apical compartment support. Am J Obstet Gynecol 194:1438, 2006

Sung VW, Rardin CR, Raker CA, et al: Porcine subintestinal submucosal graft augmentation for rectocele repair: a randomized controlled trial. Obstet Gynecol 119(1):125, 2012 Tan-Kim J, Menefee SA, Luber KM, et al: Prevalence and risk factors for mesh erosion after laparoscopic-assisted sacrocolpopexy. Int Urogynecol J 22(2):205, 2011 Theofrastous, Cobb DL, Van Dyke AH, et al: A randomized trial of suprapubic versus transurethral bladder drainage after open Burch urethropexy. J Pelvic Surg 872, 2002 Tsang CB, Madoff RD, Wong WD, et al: Anal sphincter integrity and function influences outcome in rectovaginal fistula repair. Dis Colon Rectum 41(9):1141, 1998 Van Kerrebroeck PE, Marcelissen TA: Sacral neuromodulation for lower urinary tract dysfunction. World J Urol 30(4):445, 2012 Walters MD, Karram MM (eds): Surgical treatment of vaginal vault prolapse and enterocele. In Urogynecology and Reconstructive Pelvic Surgery, 3rd ed. Philadelphia, Mosby, 2007, p 262 Weber AM, Richter HE: Pelvic organ prolapse. Obstet Gynecol 106: 615, 2005 Weber AM, Walters MD, Piedmonte MR, et al: Anterior colporrhaphy: a randomized trial of three surgical techniques. Am J Obstet Gynecol 185:1299, 2001 Wei JT, Nygaard I, Richter HE, et al: A midurethral sling to reduce incontinence after vaginal prolapse repair. N Engl J Med 366:2358, 2012 White AB, Carrick KS, Corton MM, et al: Optimal location and orientation of suture placement in abdominal sacrocolpopexy. Obstet Gynecol 113(5):1098, 2009 Wieslander CK, Rahn DD, McIntire DD, et al: Vascular anatomy of the presacral space in unembalmed female cadavers. Am J Obstet Gynecol 195:1736, 2006 Wieslander CK, Roshanravan SM, Schaffer JI, et al: Uterosacral ligament suspension sutures: anatomic relationships in unembalmed female cadavers. Am J Obstet Gynecol 197(6):672.e1, 2007 Yamada T, Ichiyanagi N, Kamata S, et al: Need for sling surgery in patients with large cystoceles and masked stress urinary incontinence. Int J Urol 8:599, 2001 Zoorob D, Karram M: Bulking agents: a urogynecology perspective. Urol Clin North Am 39(3):273, 2012 Zullo F, Palomba S, Russo T, et al: Laparoscopic colposuspension using sutures or Prolene meshes: a 3-year follow-up. Eur J Obstet Gynaecol Reprod Biol 117:201, 2004 Zutshi M, Hull T, Bast J, et al: Ten-year outcome after anal sphincter repair for fecal incontinence. Dis Colon Rectum 52:6, 2009 Zyczynski HM, Sirls LT, Greer WJ, et al: Findings of universal cystoscopy at incontinence surgery and their sequelae. Am J Obstet Gynecol 210(5):480.e1, 2014

CHAPTER 45

Noblett KL, Cadish LA: Sacral nerve stimulation for the treatment of refractory voiding and bowel dysfunction. Am J Obstet Gynecol 210(2):99, 2014 Norton P, Brubaker L: Urinary incontinence in women. Lancet 367:57, 2006 Nygaard I, Brubaker L, Zyczynski HM, et al: Longterm outcomes following abdominal sacrocolpopexy for pelvic organ prolapse. JAMA 309(19): 2016, 2013 Nygaard IE, McCreery R, Brubaker L, et al: Abdominal sacrocolpopexy: a comprehensive review. Obstet Gynecol 104:805, 2004 Ockrim JL, Allen DJ, Shah PJ, et al: A tertiary experience of urethral diverticulectomy: diagnosis, imaging and surgical outcomes. BJU Int 103(11):1550, 2009 Paraiso M, Barber M, Muir T, et al: Rectocele repair: a randomized trial of three surgical techniques including graft augmentation. Am J Obstet Gynecol 195:1762, 2006 Paraiso MF, Jelovsek JE, Frick A, et al: Laparoscopic compared with robotic sacral colpopexy for vaginal prolapse. A randomised controlled trial. Obstet Gynecol 118(5):1005, 2011 Pathi SD, Rahn DD, Sailors JL, et al: Utility of clinical parameters, cystourethroscopy, and magnetic resonance imaging in the preoperative diagnosis of urethral diverticula. Int Urogynecol J 24(2):319, 2013 Peters KM, Killinger KA, Boura JA: Is sensory testing during lead placement crucial for achieving positive outcomes after sacral neuromodulation? Neurourol Urodynam 30:1489, 2011 Pilsgaard K, Mouritsen L: Follow up after repair of vaginal vault prolapse with abdominal colposacropexy. Acta Obstet Gynecol Scand 78: 66, 1999 Pshak T, Nikolavsky D, Terlecki R, et al: Is tissue interposition always necessary in transvaginal repair of benign, recurrent vesicovaginal fistulae? Urology 82(3):707, 2013 Rahn DD, Good MM, Roshanravan SM, et al: Effects of preoperative local estrogen in postmenopausal women with prolapse: a randomized trial. J Clin Endocrinol Metab 99(10): 3728, 2014 Rahn DD, Marinis SI, Schaffer JI: Anatomical path of the tension-free vaginal tape: reassessing current teachings. Am J Obstet Gynecol 195(6):1809, 2006 Rahn DD, Ward RM, Sanses TV, et al: Vaginal estrogen use in postmenopausal women with pelvic floor disorders: systematic review and practice guidelines. Int Urogynecol J 26(1):3, 2015 Rardin CR, Erekson EA, Sung VW, et al: Uterosacral colpopexy at the time of vaginal hysterectomy: comparison of laparoscopic and vaginal approaches. J Reprod Med 54(5):273, 2009 Rechberger T, Futyma K, Jankiewicz K, et al: The clinical effectiveness of retropubic (IVS-02) and

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Surgeries for Gynecologic Malignancies

46-1: Radical Abdominal Hysterectomy (Type III). .

1134

46-10: Pelvic Lymphadenectomy..

. . . . . . . . .

1169

46-20: Small Bowel Resection. . . . . . . . . .

. . . . . . . . .

1198

46-2: Modified Radical Abdominal Hysterectomy (Type II). . . . . . . . 1140

46-11: Paraaortic Lymphadenectomy..

. . . . . . . . .

1172

46-21: Low Anterior Resection. . . . . . . . . .

. . . . . . . . .

1200

46-3: Minimally Invasive Radical Hysterectomy.. . .

46-12: Minimally Invasive Staging for Gynecologic Malignancies. . . . . . . . . . . .

46-4: Total Pelvic Exenteration. . . . .

. . . . .

. . . . . . . . . . .

46-5: Anterior Pelvic Exenteration. . . . . . . . 46-6: Posterior Pelvic Exenteration. . . . . . . . 46-7: Incontinent Urinary Conduit.. .

. . . . .

. . . . . . . .

1142 1149 1155

46-13: En Bloc Pelvic Resection. . . . . . . . . . .

. . . . . . . .

. . . . . . . . . . .

46-8: Continent Urinary Conduit. . . . . . . . . . . . . . .

. . . . .

46-9: Vaginal Reconstruction. .

. .

1156

1186

. . . . . . . . .

1188

1204

. . . . . .

1206

. . . . . . . . . . . .

1208

46-23: Appendectomy. . 46-24: Skinning Vulvectomy. . . . .

46-25: Radical Partial Vulvectomy. . . . . . . . .

. . . . . . . .

46-26: Radical Complete Vulvectomy. . . . . . . . . . . .

1213

. . . . . .

1216

. . . . . . .

1219

. . . . . . . . . . . . . . . .

1221

. . . . . . . . . . .

1192

46-27: Inguinofemoral Lymphadenectomy.. . . .

. . . . . . . . .

1195

46-28: Reconstructive Grafts and Flaps. . . . . .

. . . . . . . . . . .

1197

References. .

46-18: Large Bowel Resection. . . . . . . . . .

1165

46-19: Ileostomy. .

hysterectomy differs from simple hysterectomy in that the parametrium, paravaginal tissue, and their lymphatics are widely resected to achieve negative tumor margins. Described in this section, type III (radical) hysterectomy is chiefly indicated for stage IB1 to IIA cervical cancer or small central recurrences following radiation therapy, or for clinical stage II endometrial cancer when tumor has extended to the cervix (Koh, 2015).

1210

. . . . .

1190

1161

The five “types” of hysterectomy are defined in Chapter 30 (p. 669). Of these, radical

1182

. . . . .

. . . . . . .

46-17: Colostomy.

Radical Abdominal Hysterectomy (Type III)

1176

. . . . . . .

46-16: Diaphragmatic Surgery. . . . . . . . . . . . . .

1157

46-1

. . . .

. . . . . . . .

46-14: Omentectomy. . 46-15: Splenectomy.

46-22: Intestinal Bypass. .

Type III radical hysterectomy is increasingly being performed by minimally invasive approaches (p. 1142). With these techniques, the principles of the abdominal operation are still applied. Namely, radical hysterectomy is a dynamic operation that requires a focused, consistent surgical approach but also significant intraoperative decision making. Familiarity with its concepts continues to be critically important in developing expertise in complex pelvic surgery.

Surgeries for Gynecologic Malignancies

PREOPERATIVE Radical hysterectomy is not appropriate for women with higher-stage cancers. Thus, accurate clinical staging is critical prior to selection of this surgery. Pelvic examination under anesthesia with cystoscopy and proctoscopy is not mandatory for smaller cervical cancer lesions, but the clinical staging described in Chapter 30 (p. 663) should be completed before proceeding surgically. To refine patient selection, for most patients with grossly visible cervical tumors, abdominopelvic computedtomography (CT) or magnetic resonance (MR) imaging is also performed to identify nodal metastases or undetected local tumor extension. That said, there are limitations on what can be reliably detected preoperatively (Chou, 2006).

■⌀ Consent Women undergoing hysterectomy are specifically counseled regarding the loss of fertility. In those considering bilateral salpingo-oophorectomy (BSO), a discussion of menopause and hormone replacement is included and detailed in Chapter 43 (p. 951). The tone of the consenting process should reflect the extent of the operation required to hopefully cure or at least begin treatment of the malignancy. Moreover, a patient must be advised that the procedure may be aborted if metastatic disease or pelvic tumor extension is found (Leath, 2004). Radical abdominal hysterectomy can result in significant morbidity from shortand long-term complications. These complications may develop more frequently in women with obesity, prior pelvic infections, and previous abdominal surgery, in whom surgery may be more difficult (Cohn, 2000). Of potential intraoperative complications, the most common is acute hemorrhage. Blood loss may reach 500 to 1000 mL, and transfusion rates are variable, but high (Estape, 2009; Naik, 2010). Subacute postoperative complications may include significant postoperative bladder or bowel dysfunction from surgical denervation (20 percent), symptomatic lymphocyst formation (3 to 5 percent), and ureterovaginal or vesicovaginal fistula (1 to 2 percent) (Franchi, 2007; Hazewinkel, 2010; Likic, 2008). With any cancer surgery, risk for venous thromboembolism (VTE) is also increased. Additionally, long-term effects on sexual function and other body functions are candidly reviewed and are detailed on page 1139 (Jensen, 2004; Serati, 2009).

For this, a blood sample is typed and crossmatched for potential transfusion. Pneumatic compression devices or subcutaneous heparin or both is planned because of the typically longer surgery and postoperative recovery times and the increased VTE risk associated with cancer (Table 39-8, p. 836) (Martino, 2006). Bowel preparation with a polyethylene glycol-electrolyte solution (GoLYTELY) is no longer commonly used. Inadvertent bowel injury is rare unless extenuating circumstances are identified. However, it may be helpful to empty the colon to limit fecal spill if extensive pelvic adhesions are anticipated due to prior infection, endometriosis, or radiation therapy. Suitable perioperative antibiotic prophylaxis to prevent most surgical site infection is found in Table 39-6 (p. 835). Typically, a third-generation cephalosporin is given intravenously at spaced intervals. Compared with simple hysterectomy, the high-volume blood loss during radical hysterectomy clears antibiotics more rapidly from the operative site, and longer surgery may extend past the antibiotic half-life. Both necessitate the additional doses (Bouma, 1993; Sevin, 1991).

■⌀ Concurrent Surgery Early-stage cervical cancer most frequently spreads via the lymphatics. Thus, adjunctive lymph node removal seeks to identify occult metastases. Pelvic lymphadenectomy is typically completed just before or immediately after radical hysterectomy, and paraaortic lymphadenectomy may also be indicated in some circumstances (p. 1169) (Angioli, 1999). Spread to the adnexa is much less common than via the lymphatics. Thus, the decision for BSO depends on a woman’s age and potential for metastases (Shimada, 2006). If ovaries are preserved, then salpingectomy alone is recommended to reduce future risk of some epithelial ovarian cancers (Society of Gynecologic Oncology, 2013). In candidates for ovarian preservation, transposition of ovaries out of the pelvis may be considered in young women if postoperative radiation is anticipated. However, ovarian function may be shortlived. Also, in transposed ovaries, symptomatic periadnexal cysts are commonplace (Buekers, 2001). Oocyte and ovarian cryopreservation techniques have advanced and may soon be a more widespread option (Chap. 20, p. 466).

INTRAOPERATIVE ■⌀ Surgical Steps ➊╇ Anesthesia and Patient Positioning.╇ General anesthesia is mandatory, but epidural

placement may be considered for postoperative pain control (Leon-Casasola, 1996). Bimanual examination is performed in the operating room before scrubbing to reorient a surgeon to the patient’s individual anatomy. The patient is positioned supine. After anesthesia administration, hair in the path of the planned incision is clipped if needed; a Foley catheter is placed; and abdominal preparation is completed.

➋╇ Abdominal Entry.╇A midline vertical abdominal incision provides excellent exposure, but typically prolongs hospital stays and increases postoperative pain. Alternatively, Cherney or Maylard incisions offer postoperative advantages found with transverse incisions and allow access to the lateral pelvis (Chap. 43, p. 931). However, upper paraaortic nodes are not readily accessible through these transverse incisions. A Pfannenstiel incision offers limited exposure and is reserved only for selected patients (Orr, 1995). ➌╇ Exploration.╇ After abdominal entry, a surgeon first thoroughly explores the abdomen for obvious metastatic disease. Firm, enlarged lymph nodes and any other suspect lesions are removed or biopsied. Confirmation of metastases or pelvic tumor extension leads to a decision on whether to proceed or abort an operation based on overall intraoperative findings and clinical situation (Leath, 2004). ➍╇ Entering the Retroperitoneal Space.╇ The uterus is placed on traction with curved Kelly clamps at the cornua. The round ligament is sutured with 0-gauge delayed-absorbable suture as laterally as possible, and the tie is held on tension to aid entry into the retroperitoneal space. Lateral round ligament transection later aids excision of the parametrium out to the pelvic sidewall. Once the round ligament is divided, the broad ligament beneath separates into thin anterior and posterior leaves that contain loose areolar connective tissue between. Similar to simple hysterectomy, the anterior leaf of the broad ligament is placed on traction and is sharply dissected to the vesicouterine fold. The posterior leaf of the broad ligament is then placed on traction and sharply dissected along the pelvic sidewall parallel to the infundibulopelvic (IP) ligament.

➎╇ Ureter Isolation.╇Loose areolar connective tissue of the retroperitoneal space is bluntly dissected in the area lateral to the IP until the external iliac artery is palpated just medial to the psoas major muscle. The index and middle fingers are placed on either side of the artery, and the areolar connective tissue is bluntly finger dissected toward the patient’s head using a backward “walking” motion (Fig. 46-1.1).

CHAPTER 46

■⌀ Patient Evaluation

■⌀ Patient Preparation

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Atlas of Gynecologic Surgery

Uterine a. Superior vesical a.

SECTION 6

External iliac a.

FIGURE 46-1.1╇ Finding the ureter. To permit further cephalad inspection, the medial portion of the broad ligament’s posterior leaf is elevated. This permits direct identification of the common iliac artery bifurcation and origins of the external and internal iliac arteries. Here, the ureter crosses over the bifurcation. To isolate the ureter at this site, the surgeon bluntly dissects with a finger or suction tip in a sweeping motion from top to bottom along the medial peritoneal leaf to identify and sufficiently mobilize the lateral surface of the ureter. To free the medial surface, a Babcock clamp grasps the ureter, and Mixter rightangle clamp tips are opened and closed parallel to the ureter to develop an avascular space between it and its medial peritoneal attachment. Through this space, clamp tips are then passed beneath the ureter to grasp a quarterinch-wide Penrose drain. The drain is then pulled through this space to surround and isolate the ureter. This assists in identifying its location throughout the remainder of surgery.

➏╇ Creating Spaces.╇The parametrium

that will be removed with the hysterectomy specimen lies between the paravesical and pararectal spaces. Thus, creation of these spaces is needed to isolate the parametrium for transection. The pararectal space is developed by gently placing the right index finger lateral to the IP and between the internal iliac artery and ureter. The finger tracks in a gentle swirling motion at a 45-degree angle downward toward the midline and aiming for the coccyx (Fig. 46-1.2). Once formed, this space is bordered by the rectum and ureter medially, internal iliac artery laterally, cardinal ligament anteriorly, and the sacrum posteriorly.

FIGURE 46-1.2╇ Opening the pararectal space. In contrast, the paravesical space is formed by holding the lateral tie of the round ligament and bluntly following the external iliac artery caudally to the pubic ramus. The index and middle finger of the right hand then sweep intervening avascular areolar tissue deeply and medially toward the midline. The developed paravesical space is bounded by the bladder and superior vesical artery medially, the external iliac vessels laterally, the pubic symphysis anteriorly, and the cardinal ligament posteriorly. Once paravesical and pararectal spaces are created, the parametrium is now isolated between these two openings.

❼╇ Adnexa.╇ With hysterectomy, ovaries may

be retained or removed. If uninvolved with cancer, indications are similar to those for benign hysterectomy (Chap. 43, p. 951). If ovarian preservation is planned, the surgeon performs salpingectomy by serially clamping, cutting, and ligating the mesosalpinx (Section 43-6, p. 939). The uteroovarian ligament is then clamped, cut, and ligated close to the uterus. The ovary is tucked laterally during hysterectomy completion. Alternatively, if BSO is planned, the IP ligament is doubly clamped, cut, and ligated. The uteroovarian ligament is left intact and the adnexa are ultimately removed with the uterine specimen.

➑╇ Uterine Artery Ligation.╇ For this step,

lateral reflection of the broad ligament’s lateral leaf just distal to the round ligament will reveal the superior vesical artery. This vessel is bluntly dissected to better define its location and is grasped with a Babcock clamp and placed on lateral traction. A right-angle clamp is used to develop an avascular space beneath the vessel that should accommodate a

narrow curved Deaver retractor. Lateral traction on the superior vesical artery prevents its inadvertent ligation and aids in identification of the uterine artery (Fig. 46-1.3). Next, a surgeon’s left hand is inserted into the pelvis with the middle finger placed in the paravesical space, the index finger in the pararectal space, and the uterus with attached Kelly clamps cupped in the palm. The uterus is held on firm medial traction to expose the lateral pelvic sidewall. To visualize the uterine artery, a surgeon sharply dissects parametrial attachments and intervening areolar connective tissue beginning at the internal iliac artery and continuing caudad to the superior vesical artery. The origin of the uterine artery is found during this caudal dissection. Tissues surrounding the uterine artery are bluntly dissected, and a right-angle clamp is placed beneath this artery to retrieve a 2-0 gauge silk suture. The uterine artery tie is placed as close as possible to its origin from the internal iliac artery. The process is repeated to place a separate silk suture far enough medial to enable vessel transection. Black silk ties help identify the proximal and distal portions of the uterine artery throughout the remainder of the operation. A small vascular clip (Hemoclip) can also be placed lateral to the silk tie on the proximal uterine artery for additional security of hemostasis. The uterine artery is then cut. The underlying uterine vein may also then be isolated, clipped or tied, and cut.

➒╇ Uniting Paravesical and Pararectal

Spaces.╇ The parametrial tissues have been pressed together by development of the paravesical and pararectal spaces. Parametrial resection to unite the upper (ventral) portion

Surgeries for Gynecologic Malignancies

1137

CHAPTER 46

FIGURE 46-1.3╇ Ligating the uterine artery. of these spaces begins near the sidewall, moves medially, and can be performed by several methods. These include: (1) clamping, cutting, and suturing, (2) stapling with gastrointestinal anastomosis (GIA) stapler, (3) electrosurgical blade dissection in which a right-angle clamp elevates and isolates parametrial tissue, or (4) use of an electrothermal bipolar coagulator (LigaSure) (Fig. 46-1.4). Dissection is continued until the parametrium overlying the ureter is mobile.

➓╇ Ureter Mobilization.╇ In this same area of the pelvis, tips of a right-angle clamp are positioned between the ureter and peritoneal leaf. As previously described, opening and closing the tips downward and parallel to the ureter develops an avascular plane to

FIGURE 46-1.5╇ Mobilizing the ureter.

FIGURE 46-1.4╇ Uniting the spaces by parametrial resection. bluntly dissect the ureter from the medial peritoneal leaf. The ureter is placed on gentle lateral traction by grasping the previously placed Penrose drain with the left hand. The right index finger carefully sweeps the ureter downward and laterally until a “tunnel” through the paracervical tissue can be palpated ventromedially as the ureter enters this tissue (Fig. 46-1.5). Additional parametrial dissection is often required to ensure that the uterine artery and surrounding soft tissue has been lifted medially and off the ureter. ╇ Bladder Dissection.╇ Electrosurgical dissection is performed to free the bladder distally from the cervix and onto the upper vagina. This may need to be repeated several times as the tunnel is progressively unroofed and the

ureter is more directly visible. To allow adequate vaginal margins, the bladder will eventually need to be dissected so that it lies several centimeters distal to the cervical portio and onto the upper vagina. ╇ Unroofing the Ureteral Tunnel.╇ The uterus is placed on lateral traction, and the proximal ureter is held on traction to straighten it by gently pulling on the Penrose drain. The previously created tunnel opening is palpated. Concurrently, a right-angle clamp is inserted with its tips directed upward, while direct visualization of the underlying ureter is confirmed. The tips are then directed medially toward the cervix, “pop” through the paracervical tissue, and create a new distal opening (Fig. 46-1.6). One tip of a second

FIGURE 46-1.6╇ Unroofing the ureteral tunnel.

1138

Atlas of Gynecologic Surgery

SECTION 6 FIGURE 46-1.7╇ Uterosacral ligament transection. clamp is placed through the tunnel and then through the new distal opening. The clamp then closes around the paracervical tissue that lies above and lateral to the ureter. Within the tunnel, the ureter is bluntly dissected and pushed posteriorly toward the tunnel floor. It should be visible below before cutting the overlying paracervical tissue. Delayed-absorbable 3–0 suture ties are used to secure the paracervical tissue pedicles that are held by the right-angle clamps, but significant bleeding is commonplace during these steps. The same procedure may be repeated several times caudally to completely unroof the tunnel and expose the ureter. The dissection proceeds in a proximal to distal fashion with direct visualization of the ureter at all times to prevent injury. After being unroofed, the ureter is retracted upward, and filmy attachments between the it and tunnel bed are sharply divided. ╇ Uterosacral Resection.╇ Posterior radical dissection is often best performed near the operation’s end because exposed retroperitoneal tissues typically ooze until the vaginal cuff is closed. The cervical external os is palpated, and at this level, the electrosurgical blade is used to superficially incise or “score” the peritoneum between the uterosacral ligaments. This score line joins the incision line of the previously cut posterior broad ligament peritoneum. Between the uterosacral ligaments, a plane is developed by gently pressing a finger toward the vaginal wall without poking through and into the vaginal vault. This

FIGURE 46-1.8╇ Vaginal transection.

rectovaginal plane is developed by gentle pressure toward the sacrum and enlarged laterally until three fingers can be comfortably inserted. This maneuver frees the rectosigmoid from the uterosacral ligaments and prevents inadvertent bowel injury. Remaining peritoneal attachments are sharply dissected to fully expose the rectovaginal space. The exposed uterosacral ligaments can be visualized, palpated, clamped at the pelvic sidewall, then cut, and ligated with 0-gauge delayedabsorbable suture (Fig. 46-1.7). This procedure may need to be repeated to complete transection of the uterosacral ligament and adjacent supportive tissues. ╇ Vaginal Resection.╇ At this point in the operation, the radical hysterectomy specimen is held in place only by the paracolpium and vagina. The bladder and ureters are further bluntly and sharply dissected free until at least 3 cm of upper vagina will be included with the resected specimen. Curved clamps are placed on the lateral paracolpium. The ureter should be lateral and directly visible. Tissue is then cut and suture ligated with 0-gauge delayed-absorbable suture. The upper vagina can then be: (1) clamped, cut, and suture ligated, (2) stapled, or (3) sharply transected with electrosurgical blade and suture ligated (Fig. 46-1.8). The specimen is carefully examined to ensure an adequate upper vaginal segment and grossly negative margins. ╇ Suprapubic Catheter Placement.╇ This catheter may aid postoperative voiding

trials in carefully selected, motivated patients (Pikaart, 2007). ╇ Ovarian Transposition.╇For those in whom ovarian function preservation is desired, transposing adnexa out of the anticipated pelvic radiation field is an option. A distal portion of the ovary is grasped with a Babcock clamp. Using traction, dissection is performed to mobilize the IP ligament so that the ovary can be lifted into the upper abdomen. For future radiography or CT interpretation, a large vascular clip is placed on the residual uteroovarian ligament stump to serve as an ovarian location marker. For transposition, a 0-gauge silk suture is placed at this stump site and tied. Its needle is covered but remains attached to the suture. A handheld abdominal retractor is then used to expose an area of the lateral posterior peritoneum as high as possible in the abdomen. The silk suture needle is then uncovered and placed through the peritoneum, and the ovary is elevated by this “pulleystitch” and tied. The lateral pelvic defect is closed with a continuous running stitch using 0-gauge delayed-absorbable suture to prevent internal herniation, that is, entrapment of bowel within the peritoneal defect. Ovaries are inspected before abdominal closure to exclude vascular compromise by transposition. ╇ Final Steps.╇ Active bleeding should be immediately controlled when the radical hysterectomy specimen has been removed. A dry laparotomy sponge may be held firmly deep

Surgeries for Gynecologic Malignancies

POSTOPERATIVE Immediate postoperative care following radical hysterectomy in general follows that for laparotomy. Early ambulation after radical hysterectomy is especially important to prevent thromboembolic complications (Stentella, 1997). Moreover, following laparotomy for cancer, anticoagulants are continued for 2 to 4 weeks postoperatively (American College of Obstetricians and Gynecologists, 2013). Early feeding, including rapid initiation of a clear liquid diet, may also shorten the hospital stay (Kraus, 2000). Bladder tone returns slowly, and a major cause is thought to be partial sympathetic and

parasympathetic denervation during radical dissection (Chen, 2002). Thus, Foley catheter drainage is commonly continued until a patient is passing flatus because improving bowel function typically accompanies resolving bladder hypotonia. Removal of the catheter or clamping of the suprapubic tube should be followed by a successful voiding trial (Chap. 42, p. 917). A voiding trial may be attempted prior to hospital discharge or at the first postoperative visit. Patients with adequate function are instructed to press gently on the suprapubic area for several days afterward to help completely empty the bladder during voiding and prevent retention. Successful voiding may take several weeks to achieve. In addition to urinary retention, tenesmus and constipation are frequent immediate symptoms that should improve significantly over months or years (ButlerManuel, 1999; Sood, 2002). Postoperative stool softeners are often prescribed. Nerve-sparing radical hysterectomy is a method demonstrating improved postoperative bladder function (Raspagliesi, 2006). However, many patients have preexisting abnormal urodynamic findings that are simply exacerbated by radical hysterectomy (Lin, 1998, 2004). In the 3 percent of women

who develop long-term bladder hypotonia or atony, intermittent self-catheterization is preferred to indwelling urinary catheterization (Chamberlain, 1991; Naik, 2005). For cervical cancer patients undergoing BSO, estrogen replacement therapy is not contraindicated and may be initiated in the hospital at the discretion of the treating oncologist. Cervical cancer survivors treated with radical hysterectomy have much better sexual functioning than those who receive radiation therapy. Despite this, more than half of surgical patients postoperatively report a worse sex life (Butler-Manuel, 1999). Severe orgasmic problems, uncomfortable intercourse due to reduced vaginal length, and severe dyspareunia may develop but often resolve within 6 to 12 months. However, persistent lack of sexual interest and poor lubrication may be longterm or permanent changes (Jensen, 2004). Disturbed vaginal blood flow response during sexual arousal may account for much of the reported constellation of symptoms (Maas, 2004). Eventually, patients treated by surgery alone can expect a quality of life and overall sexual function similar to peers without a history of cancer (Frumovitz, 2005).

CHAPTER 46

in the pelvis for several minutes to tamponade raw surfaces. Topical hemostatic agents may be employed (Table 40-5, p. 861). With bleeding controlled, a surgeon then assesses the vascular support to the ureter and other sidewall structures. To structures that appear particularly devascularized, an omental J-flap may provide additional blood supply (Section 46-14, p. 1186) (Fujiwara, 2003; Patsner, 1997). Routine pelvic suction drainage and closure of the peritoneum are not necessary (Charoenkwan, 2014; Franchi, 2007).

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Atlas of Gynecologic Surgery

46-2 SECTION 6

Modified Radical Abdominal Hysterectomy (Type II) Four procedural differences distinguish a modified radical hysterectomy (type II) hysterectomy from the more radical type III procedure (Section 46-1, p. 1134). First, the uterine artery is transected where it crosses the ureter (rather than at its origin from the internal iliac artery). Second, only the medial half of the cardinal ligament is resected (instead of division at the sidewall). Additionally, the uterosacral ligament is divided halfway between the uterus and sacrum (rather than at the sacrum). And last, a smaller margin of upper vagina is removed. These modifications serve to reduce surgical time and associated morbidity, while still enabling complete resection of smaller cervical tumors (Cai, 2009; Landoni, 2001). Clear indications for modified radical hysterectomy are few and controversial (Rose, 2001). Stage IA1 (with lymphovascular space invasion) or IA2 cervical cancer are the most common diagnoses (Koh, 2015). Type II hysterectomy is also performed on occasion for: (1) preinvasive or microinvasive disease when a more invasive lesion cannot be excluded, (2) selected stage IB1 disease with 3 times that of serum amylase. If a drain has been placed, fluid may be sent to the laboratory if this complication is suspected. Pancreatic leak usually presents early in the postoperative period and can be managed conservatively with percutaneous drainage (Kehoe, 2009). Patients undergoing splenectomy will be at lifelong risk for episodes of overwhelming sepsis. Accordingly, the pneumococcal and meningococcal vaccines are recommended and the Haemophilus influenzae type b is considered postoperatively (Kim, 2015). Importantly, these vaccines may be given together but are not administered earlier than 14 days following splenectomy. In addition, patients are instructed to seek immediate medical attention for fevers, which may rapidly progress to serious illness.

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Diaphragmatic Surgery Patients with advanced ovarian cancer will often have tumor implants or confluent plaques involving the diaphragm. The right hemidiaphragm is most frequently affected. Implants are typically superficial, but invasive disease can extend through the peritoneum to the underlying muscle. Accordingly, gynecologic oncologists are prepared to perform diaphragmatic ablation, stripping (peritonectomy), or full-thickness resection. These surgical procedures increase the rate of optimal tumor debulking and correlate with improved survival (Aletti, 2006a; Tsolakidis, 2010).

PREOPERATIVE ■⌀ Patient Evaluation Imaging studies may suggest diaphragmatic nodularity, but the extent is difficult to ascertain until exploration in the operating room.

■⌀ Consent Patients with presumed advanced ovarian cancer are informed of the possible need for extensive upper abdominal surgery to achieve optimal cytoreduction. Pulmonary complications after diaphragmatic surgical techniques most commonly include atelectasis and/or pleural effusion. However, empyema, subphrenic abscess, and pneumothorax are also possible (Chereau, 2011; Cliby, 2004).

INTRAOPERATIVE ■⌀ Instruments It is generally advisable to have a cavitational ultrasonic surgical aspiration (CUSA) system and/or argon beam coagulator (ABC) available for ovarian cancer debulking procedures, since one or both can be useful in eradicating diaphragmatic disease. These tools are discussed further in Chapter 40 (p. 859).

■⌀ Surgical Steps ➊╇ Anesthesia and Patient Positioning.╇ As with other major intraabdominal surgeries, diaphragmatic surgery requires general anesthesia. The patient is positioned supine, the abdomen is surgically prepared to accommodate an incision to the sternum, and a Foley catheter is inserted.

FIGURE 46-16.1╇ Diaphragm stripping.

➋╇ Abdominal Entry.╇Diaphragmatic surÂ�

gery requires a vertical midline incision that has been extended to the sternum, passing to the right side of xiphoid process, for maximum exposure. Following abdominal entry, a surgeon carefully assesses the entire abdomen and pelvis to confirm the ability to resect all gross disease. Ideally, diaphragmatic surgery is performed only if optimal tumor debulking can thereby be achieved.

➌╇ Diaphragmatic Ablation.╇ A few scattered, small tumor implants on the surface of the right or left hemidiaphragm can usually be easily ablated with the CUSA or ABC. This simple technique may be all that is required. ➍╇ Diaphragmatic Stripping.╇ Confluent plaques of tumor or extensive implants indicate the need for resection of the peritoneum. For this, the right side of the anterior rib cage is retracted sharply upward. The liver is manually retracted downward and medially to aid division of the falciform ligament, right coronary ligament, and right triangular ligament of the liver with sharp dissection using an electrosurgical blade. This maneuver significantly mobilizes the liver and allows it to be held medially away from the diaphragm. Dissection begins on the right side of the diaphragm, where the diaphragmatic peritoneum meets the anterior abdominal wall. Allis clamps are used to grasp the peritoneum above the tumor plaque and place it on tension. The peritoneal incision is created transversely above the tumor with an electrosurgical blade, and a plane is developed with blunt dissection to separate the peritoneum from the underlying muscle fibers of the

Â� diaphragm. The free peritoneal edge is placed on tension with Allis clamps to maintain traction. The incision is then extended medially and laterally to encompass the implants (Fig. 46-16.1). The specimen eventually becomes large enough to grasp with a left hand to aid in “stripping” the peritoneum off the diaphragm. Electrosurgical blade dissection proceeds dorsally until all implants are contained within the peritoneal specimen. At this point, it can be detached.

➎╇ Diaphragmatic Resection.╇ OccasionÂ�

ally, tumor has penetrated through the peritoneum, and a plane cannot be developed to strip the diaphragm. In these circumstances, fullthickness diaphragmatic resection is required. A self-retaining retractor is placed, and the liver mobilized. A transverse peritoneal incision is made above the tumor plaque, and at this point, the inadequacy of stripping is determined. The ventilator is temporarily turned off to avoid lung parenchymal injury, and an electrosurgical blade is used to cut through the diaphragmatic muscle into the pleural cavity above the tumor. Ventilation may then be resumed while Allis clamps are placed to retract the specimen into the peritoneal cavity. Both pleural and peritoneal surfaces should be visible to aid in complete resection of the disease. After resection, primary mass closure of the diaphragmatic defect is then performed with a running stitch using 0-gauge polydioxanone monofilament (PDS) suture or interrupted stitches of silk suture. To evacuate the pneumothorax, a red rubber catheter is placed through the defect into the pleural space prior to securing the final

Surgeries for Gynecologic Malignancies

➏╇ Final Steps.╇The patient is placed in Trendelenburg position at the completion of stripping or resection to check the integrity of the diaphragmatic closure. The upper abdomen is filled with saline and observed

for air leaks as the patient is ventilated. The presence of air bubbles indicates the need to reintroduce the red rubber catheter through the hole, resuture the defect, and retest the closure. Chest tubes are not routinely required.

POSTOPERATIVE Atelectasis is common with any diaphragmatic surgery, and routine postoperative respiratory expansion techniques are appropriate

(Chap. 39, p. 827). Diaphragmatic stripping is associated with an increased incidence of pleural effusion, especially when the pleural space is entered. Fortunately, most will self-resolve, and only a few will require postoperative thoracentesis (Dowdy, 2008). Patients having full-thickness diaphragmatic resection are carefully monitored with chest radiographs for evidence of a pneumo- or hemothorax. Those few who do not resolve with supportive care measures may require chest tube drainage to aid lung reexpansion (Bashir, 2010).

CHAPTER 46

knot. The ventilator is turned off at the end of inspiration to maximally inflate the lungs while the catheter is placed on suction. The catheter is removed concomitantly with tying the knot, and mechanical ventilation is resumed (Bashir, 2010). Grafts are not typically needed, even for large defects (Silver, 2004).

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Colostomy A colostomy is a surgical anastomosis between created openings in the colon and anterior abdominal wall to divert bowel contents into an external collection bag. Colostomies serve several purposes and may be used: (1) to protect distal bowel repair from disruption or contamination by feces, (2) to decompress an obstructed colon, and (3) to evacuate feces if the distal colon or rectum is excised. In gynecologic oncology, specific indications for performing a colostomy are innumerable. Some of the more common ones include rectovaginal fistula, severe radiation proctosigmoiditis, bowel perforation, and rectosigmoid resection in which reanastomosis is not feasible. A colostomy may be temporary or permanent, and its duration is dictated by clinical circumstances. For instance, recurrent endstage cervical cancer with obstruction may warrant a permanent colostomy. In contrast, only temporary diversion is needed to allow healing of an intraoperative bowel injury that occurred during benign gynecologic surgery. In addition, the location of the stoma and the decision to perform an end or loop colostomy are also clinically based. A loop colostomy is constructed by creating an opening in a loop of colon and bringing both ends through the stoma. Alternatively, an end colostomy stoma contains only the proximal end of the transected colon. The distal end is stapled and left intraabdominally. Regardless of the clinical circumstances, the same surgical principles apply during colostomy: adequate bowel mobilization, sufficient blood supply, and a tension-free tunnel through the abdominal wall without bowel constriction. Strict attention to these seemingly straightforward steps ensures the best possible outcome. In some circumstances, a laparoscopic colostomy may be possible (Jandial, 2008).

PREOPERATIVE ■⌀ Patient Evaluation The colostomy site, typically on the patient’s left, is ideally marked preoperatively by an enterostomal therapist to ensure that the postoperative stoma will be located in an easily accessible area when sitting and standing.

■⌀ Consent Concerns regarding postoperative quality of life changes are common with this procedure.

Accordingly, a surgeon carefully describes a colostomy’s medical purpose and its expected temporary or permanent duration. Much of the fear regarding “wearing a bag” can be assuaged with compassionate preoperative counseling and education. Many times, postoperative results are actually superior to a patient’s current symptoms and quality of life. Perioperative complications may include fecal leakage into the abdomen or retraction of the stoma. Long-term complications involve parastomal hernia, stricture, and the potential need for surgical revision.

■⌀ Patient Preparation To minimize fecal contamination during bowel incision, aggressive bowel preparation such as with a polyethylene glycol with electrolyte solution (GoLYTELY) may be considered the day prior to surgery unless contraindicated, such as with bowel obstruction or perforation. Additionally, broad-spectrum antibiotics are given preoperatively due to the possibility of stool contamination of the operative site. With stool spill, postoperative antibiotic doses for 24 to 48 hours and a drain near the anastomosis are reasonable.

INTRAOPERATIVE ■⌀ Surgical Steps ➊╇ Anesthesia and Patient Positioning.╇ Colostomy is performed under general anesthesia with the patient positioned supine. Prior to surgery, the abdomen is surgically prepared, and a Foley catheter is inserted.

➋╇ Abdominal Entry and ExploÂ�ration.╇ Although concurrent surgery may dictate the approach, a midline vertical incision, due to its superior exposure, is generally preferred when colostomy is a possibility. The bowel segment is selected as distally as possible to preserve normal bowel. Dissection and adhesiolysis are performed as necessary to mobilize the bowel to obtain sufficient length before creating the abdominal wall stoma opening. The colon is elevated to ensure that it will reach the selected stoma site without tension. If the bowel fails to reach the selected site without tension despite maximal mobilization, then the proposed stoma site is moved to accommodate the available bowel length.

➌╇ End Colostomy.╇ This type of diversion is commonly used for rectovaginal fistulas and severe proctosigmoiditis after radiation. Ideally, a more distal colon site is used since bowel content becomes progressively more solid and less voluminous as it moves from

the cecum to the rectum. As a result, the ostomy bag does not need to be changed as often, and the risk of dehydration or electrolyte abnormalities is reduced. If performing an end sigmoid colostomy, the distal bowel may simply be stapled closed and left in the pelvis (Hartmann pouch). In contrast, a more proximal end colostomy performed for a distal colonic obstruction will require that the distal bowel also be brought to the abdominal wall and opened, either at the same site or as a second ostomy. This distal-bowel-loop ostomy serves as a “mucus fistula” to prevent a closed loop obstruction and subsequent colonic perforation from mucus or gas accumulation. The stoma site for a sigmoid colostomy is selected based on an imaginary line drawn from the umbilicus to the left-sided anterior superior iliac spine. The site is sufficiently lateral from the midline to allow application of the ostomy appliance. But, it is located sufficiently medial because stoma support from the rectus muscle lowers stoma-site hernia risks. To begin, a Kocher clamp is used to elevate the skin and an electrosurgical blade, set to a cutting mode, is used to remove a 3-cm circle of skin. The fascia is exposed by blunt dissection. In obese patients, a cone through the subcutaneous fat with its tip at the fascia may need to be removed to prevent bowel constriction. A cruciate incision is made on the anterior sheath. The fibers of the rectus abdominis muscle are bluntly separated, and another cruciate incision is cut on the posterior sheath. The opening is bluntly expanded to accommodate two or three fingers. After the colon is divided as described in Section 46-21, Step 5 (p. 1201), the proximal bowel is mobilized by incising the peritoneum toward the splenic flexure along the white line of Toldt, which is the reflection of posterior abdominal parietal peritoneum over the mesentery of the descending colon. A Babcock clamp is then placed through the skin opening to grasp the stapled end of bowel and lift it through the abdominal opening (Fig. 46-17.1). The bowel should appear pink, and its mesentery must not be twisted. The primary vertical abdominal incision is then closed. The stoma is not ordinarily “matured” until the abdominal wall and skin are closed, with a dressing in place. First, the table is tilted to the left to minimize bowel spillage and fecal contamination of the incision site, and then the intestinal staple line is excised. Circumferential interrupted 3–0 and 4–0 gauge delayed-absorbable sutures are placed through the bowel mucosa and skin dermis (Fig. 46-17.2). The ostomy bag appliance may then be attached.

Surgeries for Gynecologic Malignancies

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CHAPTER 46

FIGURE 46-17.1╇ End-sigmoid colostomy: bowel pulled through abdominal wall incision.

➍╇ Loop Colostomy Principles.╇ The typiÂ�

cal indications for this type of procedure include protection of a distal anastomosis, relief of colonic obstruction, and colonic perforation. Accordingly, loop colostomy can be performed at any site along the colon where indicated. A loop colostomy in general is intended to be a temporary or palliative procedure. It is easier to take down, often simpler

FIGURE 46-17.2╇ End-sigmoid colostomy: bowel mucosa sutured to skin.

to perform, and does not necessarily require designation of loops as distal or proximal. However, fecal matter will eventually pass through to the distal segment. As a result, this type of colostomy is not a permanent solution to a fistula or proctosigmoiditis.

➎╇ Transverse Loop Colostomy.╇As a stand-alone procedure, a transverse loop

FIGURE 46-17.3╇ Transverse loop colostomy: bowel segment elevated.

colostomy is most often performed to relieve a distal obstruction and can be used in an emergent or palliative setting. This colostomy is performed in the left upper quadrant by creating a 5-cm transverse incision over the rectus abdominis muscle midway between the costal margin and the umbilicus. The anterior and posterior fascia, rectus abdominis muscle, and peritoneum are opened longitudinally by sharp and blunt dissection. The omentum is separated from the underlying transverse colon along enough length to allow the bowel segment to be pulled up through the incision without it. Next, a one-quarter inch Penrose drain is placed through the mesocolon for traction, and the bowel loop is brought through the incision (Fig. 46-17.3). A Hollister

FIGURE 46-17.4╇ Transverse loop colostomy: bowel opened.

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Atlas of Gynecologic Surgery

SECTION 6

bridge or similar device is passed through the mesenterotomy in place of the Penrose drain. The skin incision is then closed around the bowel loop without constricting it. The bowel is then “matured” by opening the antimesenteric half of the bowel along the tenia with an electrosurgical blade and leaving a 1-cm margin on each end (Fig. 46-17.4). The colostomy edges are sutured to the skin with interrupted stitches of 3–0 gauge delayed-absorbable suture.

➏╇ Final Steps.╇ The stoma is carefully inspected and ideally is pink and comfortably positioned. A dusky color may indicate

bowel ischemia, which can lead to sloughing, necrosis, and retraction. Tension on the bowel may be improved with a� dditional colon mobilization. Constriction of a loop colostomy within the abdominal wall opening can be improved by broadening the fascial incision or removing additional subcutaneous fat. With end colostomy, on occasion, the tip may need to be transected further distally to reach a viable bowel segment. All of these steps are cumbersome but are much easier to perform during the operation rather than postoperatively after complications become obvious.

POSTOPERATIVE Morbidity is comparable for end and loop colostomies (Segreti, 1996a). Complications may be immediate or not evident for several months. Common complications specific to a colostomy may include wound infection, necrosis, bowel obstruction, hematoma, retraction, fistula, fecal leakage, sepsis, stricture, and parastomal herniation (Hoffman, 1992). Many of these complications are manageable with supportive care and local measures. Dramatic symptoms are infrequent but may require operative revision. Careful attention during initial surgery will prevent most of these morbidities.

Surgeries for Gynecologic Malignancies

46-18

Partial colectomy is most often performed as part of cytoreductive surgery for ovarian cancer, although other indications include radiation injury and colonic fistula. Surgical principles are similar, whether a bowel segment to be removed is from the ascending, transverse, or descending colon. Rectosigmoid (low anterior) resection is somewhat more complex and is reviewed in Section 46-21 (p. 1200). Ideally during colectomy, a surgeon will achieve meticulous hemostasis, remove the smallest required length of colon, avoid fecal spill, and confirm bowel continuity by excluding possible sites of proximal or distal intestinal obstruction. In addition, bowel must be sufficiently mobilized to create a tension-free anastomosis that is watertight, large caliber, and supported by adequate blood supply. During surgery planning, insufficient bowel length for reanastomosis, a malnourished patient, questionable vascular supply, or undue anastomosis tension may instead require a permanent or temporary diverting colostomy. A general familiarity with colonic blood supply is important for partial colectomy. The ascending and transverse colon are supplied by the superior mesenteric artery via the ileocolic, right colic, and middle colic branches. The descending and sigmoid colon are supplied by the left colic and sigmoid branches of the inferior mesenteric artery. As a result, these vessels form an effective anastomotic vascular network that allows large bowel resection at virtually any segment of the colon.

To minimize fecal contamination during bowel incision, most surgeons still recommend aggressive bowel preparation. One choice, a polyethylene glycol with electrolyte solution (GoLYTELY), may be considered the day prior to surgery unless contraindicated, such as with bowel obstruction or perforation. However, there is no evidence that patients benefit from this practice, and bowel preparation may not lower the risk of postoperative complications (Guenaga, 2009; Zhu, 2010). If a bowel obstruction is present, then cleansing only the distal colon with enemas is a secondary option. The patient is also marked for a colostomy if that is a possibility. Moreover, if a complicated resection or prolonged recovery is anticipated, postoperative TPN administration is considered. Preoperative antibiotics and perioperative VTE prophylaxis are warranted, and options are listed in Tables 39-6 and 39-8 (p. 835).

INTRAOPERATIVE ■⌀ Instruments To prepare for complicated resections, a surgeon should have access to all types and sizes of bowel staplers. These include end-to-end anastomosis (EEA), gastrointestinal anastomosis (GIA), and transverse anastomosis (TA) staplers. Additionally, a ligate-divide-staple (LDS) device or electrothermal bipolar coagulator (LigaSure) may aid in vessel ligation.

■⌀ Surgical Steps ➊╇ Anesthesia and Patient Positioning.╇ Rectovaginal examination under anesthesia

is mandatory before positioning any patient for abdominal gynecologic cancer surgery. A palpable mass with compression of the rectum or rectovaginal septum indicates the need for low lithotomy with legs comfortably positioned in booted support stirrups to prepare for possible low anterior resection and anastomosis. Supine positioning is otherwise appropriate. Sterile preparation of the abdomen, perineum, and vagina is completed, and a Foley catheter is inserted.

➋╇ Abdominal Entry.╇A midline vertical

incision is preferable if partial colectomy is anticipated as this incision provides access to the entire abdomen. Required dissection, adhesiolysis, or other unanticipated findings may render exposure from a transverse incision inadequate.

➌╇ Exploration.╇ A surgeon first explores the entire abdomen to lyse adhesions, to “run” the bowel and evaluate its appearance from duodenum to rectum, to exclude other potential sites of obstruction proximally or distally, and to determine the extent of the bowel resection. Colonic blood supply at the splenic flexure, hepatic flexure, and ileocecal valve can be tenuous. As a result, resection boundaries ideally lie beyond these areas if possible. For example, in Figure 46-18.1, because of the known tenuous blood supply at the hepatic flexure, the proximal line of transection includes several centimeters of transverse colon. Similarly, the distal line of transection includes 8 to 10 cm of the terminal ileum because the ileocecal artery is sacrificed. Leaving this terminal ileum would render it vulnerable to necrosis from insufficient remaining vascular support.

PREOPERATIVE ■⌀ Patient Evaluation The need for partial colectomy during ovarian cancer cytoreductive surgery is usually decided intraoperatively and is based on clinical circumstances. For example, although preoperative CT images may suggest tumor at multiple sites near the colon, these lesions are often superficial and may be removed without colectomy. Typically, the need for colectomy is more obvious preoperatively for those with radiation damage or fistula. However, the extent of resection will still generally be unclear until the operation is underway.

■⌀ Consent Patients are fully informed of the potential for colostomy, anastomotic leak, and abscess formation. A postoperative ileus should also be anticipated.

FIGURE 46-18.1╇ Area of resection encompasses tumor.

CHAPTER 46

Large Bowel Resection

■⌀ Patient Preparation

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SECTION 6

Once the segment is selected, a window is made in the mesocolon proximal and distal to the lesion. A one-quarter inch Penrose drain is pulled through each location’s opening to provide traction.

➍╇ Mobilization of the Colon.╇The

bowel is next mobilized by incising peritoneum along the white line of Toldt and/ or along the hepatic or splenic flexures— depending on the resection site. For the case shown in Figure 46-18.1, the right retroperitoneal space is entered at the mid-ascending colon, continued along the white line of Toldt, and extended toward and around the cecum to a site beyond the distal Penrose drain. The entry opening is created with an electrosurgical blade just lateral to the colon. This space is bluntly expanded, and electrosurgical dissection is next guided cephalad past the proximal Penrose drain while providing countertraction on the colon. The bowel segment may be bluntly mobilized medially as necessary. Partial infracolic omentectomy may be required for resections involving the transverse colon.

➎╇ Resection.╇ A GIA stapler is inserted to

replace one Penrose drain, is positioned around the entire colon diameter, and is fired. This stapler lays two rows of staples and transects interposed bowel. A second stapling and transection is then repeated at the other Penrose drain site. Staying close to the bowel segment’s wall, the bowel segment may then be detached from its underlying mesentery, using an LDS device, electrothermal bipolar coagulator, or individual clamps and 0-gauge delayed-absorbable suture ligation. During this process, as much of the mesentery as possible is preserved to provide adequate blood supply to the anastomosis. The specimen is then removed.

➏╇ Side-to-Side Anastomosis.╇ The proximal and distal bowel ends are held parallel against each other to estimate their position following anastomosis. Typically, additional mobilization of the bowel by incising adhesions and peritoneum is required using a combination of electrosurgical blade and blunt dissection. The two segments must comfortably approximate antimesenteric borders without tension. For larger resections, the mesentery of each segment may also need to be dissected to achieve sufficient mobility. The proximal and distal stapled bowel ends are skeletonized of fatty tissue to create an anastomosis with maximal mucosa-to-mucosa contact. To accomplish this, the proximal staple line is elevated with two Allis clamps at its lateral edges. DeBakey forceps grasp surrounding fatty tissue and place it on traction, while an electrosurgical blade is used to dissect this tissue away from the bowel serosa. The dissection is then performed on the distal rectal segment in similar fashion.

FIGURE 46-18.2╇ GIA stapler creates a side-to-side anastomosis of the ileum (left) and transverse colon (right). Inset: TA stapler line closes the distal end of the anastomosis. The antimesenteric tip of each staple line is excised with scissors, and the bowel is held vertically by Allis clamps to prevent fecal spill. One or two seromuscular silk stay sutures may be placed distally on each bowel end to help align the correct position and prevent slippage. One fork of the GIA stapler is then inserted as deeply as possible into each of the bowel lumens (Fig. 46-18.2). The bowel segments are evenly positioned, and the device is then fired along the antimesenteric surfaces and removed. This stapler places two staggered rows of titanium staples and simultaneously transects tissue between these rows. The bowel interior should be examined for bleeding sites, which may be electrosurgically coagulated. The remaining opening may then be stapled across with a TA stapler, and residual bowel tissue above the TA staple line is excised. The mesenteric defect is reapproximated with interrupted or running 0-gauge delayed-absorbable suture to prevent an internal hernia.

❼╇ Final Steps.╇ The abdomen is irrigated

with copious warmed saline at the conclusion of any bowel resection, especially if feces have spilled during the procedure. Drains are not routinely required and may impair healing.

POSTOPERATIVE Morbidity after large bowel resection is significantly increased by various factors,

but especially by preexisting obstruction, malignancy, obesity, radiation damage, or sepsis. Moreover, patients undergoing multiple bowel resections have greater blood loss and longer hospital stay (Salani, 2007). Anastomotic leaks are the most specific complication and typically present as an abscess or fistula, or as peritonitis within days or weeks of surgery. Some localized leaks can be managed with initiation of TPN, CT-guided drainage, antibiotic administration, and bowel rest for a couple of weeks. However, urgent reoperation is indicated for nonlocalized intraperitoneal perforation and its resulting peritonitis. This will usually require temporary colostomy (Kingham, 2009). Pelvic abscesses may also result from intraÂ�operative fecal spillage or hematoma superÂ�infection. Usually these will resolve with CT-guided drainage and antibiotics. Gastrointestinal hemorrhage should be rare with stapled procedures. In addition, symptomatic anastomotic strictures are infrequent and often present as colonic obstruction. Some strictures can be managed with endoscopic stents, but often they require reoperation. Small or large bowel may also become obstructed by postoperative adhesions or tumor progression. Last, a prolonged ileus can develop and be slow to resolve. Most of these complications will depend primarily on the patient’s underlying nutrition and the clinical circumstances prompting the primary surgery.

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46-19

Relatively few patients will require ileostomy for management of a gynecologic malignancy. For those who do, loop ileostomy is usually a temporary procedure that is performed to protect a distal anastomosis (Nunoo-Mensah, 2004). Palliation of a large-bowel obstruction or diversion of a colonic fistula may be other indications (Tsai, 2006). On occasion, ovarian cancer will involve the entire colon, requiring colectomy with a permanent end ileostomy and formation of a Hartmann pouch (Song, 2009).

CHAPTER 46

Ileostomy

FIGURE 46-19.1╇ Ileal loop opened with cautery.

PREOPERATIVE ■⌀ Patient Evaluation Stoma placement is particularly important for an ileostomy since the effluent will be more corrosive than that of a colostomy. Ideally, the site is marked preoperatively by an enterostomal therapist.

■⌀ Consent In general, many of the complications from this procedure mirror those of colostomy: retraction, stricture, obstruction, and herniation. Patients are informed that temporary loop ileostomies can be taken down later without a laparotomy.

■⌀ Patient Preparation Bowel preparation is preferred whenever there is a potential for more extensive bowel resection. However, ileostomy can safely be performed in virtually all circumstances without cleansing. Antibiotics and VTE prophylaxis are warranted, and options are listed in Tables 39-6 and 39-8 (p. 835).

INTRAOPERATIVE ■⌀ Surgical Steps ➊╇ Anesthesia and Patient Positioning.╇ Ileostomy is performed under general anesthesia. Patients are generally supine, but low lithotomy is acceptable.

➋╇ Abdominal Entry.╇A midline vertical

incision is preferable for most situations in which an ileostomy is considered.

➌╇ Exploration.╇ After abdominal entry, a surgeon first explores the abdomen, lyses

adhesions, “runs” the bowel length to identify obstructive sites, and determines the need for ileostomy. An ileum loop is selected that will reach several centimeters above the skin. Additionally, to reduce the effluent volume, the selected loop is located as distally along the bowel length as possible. On occasion, tethering of small bowel by carcinomatosis or radiation injury will significantly reduce mobility and will require a more proximal diversion.

➍╇ Loop Ileostomy.╇A one-quarter inch Penrose drain is placed through a mesenterotomy at the selected loop’s apex. The loop can then be approximated to the stoma site, which is created to accommodate two fingers as described for an ileal conduit (Section 46-7, p. 1159). The loop is pulled through the abdominal wall opening so that several centimeters protrude above the skin surface. The Penrose drain is removed and replaced with either the cut end of a red rubber catheter or another device that can be sewn to the skin to elevate the loop. The loop should be tensionfree and patent. The proximal end of the loop is placed in the lower position to reduce fecal flow into the distal bowel. The skin of the abdominal wall is then closed around the stoma. The ileostomy is “matured” by longitudinally incising the bowel loop and everting its walls with Allis clamps. Circumferential interrupted stitches of 3–0 and 4–0 gauge delayed-absorbable sutures are placed through the dermis and bowel mucosa (Fig. 46-19.1). An ostomy bag may then be applied. ➎╇ End Ileostomy.╇ If a total colectomy is

performed or if the bowel is too tethered or the patient too obese for a loop to reach the abdominal wall, the distal ileum may need to be divided instead of brought out as a loop.

The segment is selected, a mesenterotomy is made, and the GIA stapler is fired. An appropriate stoma site is identified, and with a few modifications, the end ileostomy is matured as in colostomy (Section 46-17, p. 1192). Typically, the abdominal wall opening will be smaller in diameter. Unless there is a distal colon obstruction necessitating creation of a mucus fistula, the distal bowel segment can be left in the peritoneal cavity. An attempt is made to evert the single stoma by turning the bowel wall over on itself using Allis clamps. In each quadrant of the stoma, stitches of 3–0 gauge delayed absorbable suture are placed through the dermis, the seromuscular layer of the bowel at the skin level, and a full-thickness bite at the cut edge of the everted bowel.

POSTOPERATIVE The stoma is carefully examined postoperatively for its appearance and function. The loop supporting rod may be removed in 1 to 2 weeks, but potentially earlier if the stoma becomes dusky or the loops seem constricted or are obstructed. Ileostomy may be associated with significant postoperative complications. Highoutput effluent may result in electrolyte abnormalities that are difficult to correct. In addition, approximately 10 percent of patients will require early reoperation for small-bowel obstruction or intraabdominal abscess (Hallbook, 2002). Specifically, if loop ileostomy is indicated to protect a low anterior anastomosis, it is more commonly associated with bowel obstruction and ileus than is loop colostomy (Law, 2002). Longterm complications such as a peristomal hernia or retraction are also possible.

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Atlas of Gynecologic Surgery

46-20 SECTION 6

Small Bowel Resection Indications for small bowel resection in gynecologic oncology are numerous and include ob�struction, tumor invasion, perforation, intra� operative injury, fistulas, or radiation damage. Unlike the large bowel, where greater attention is required to ensure an adequate blood supply to the anastomotic site, the small intestine has a consistent cascade of vessels that all arise from the superior mesenteric artery. However, unique situations such as radiation damage, obstructive dilatation, and edema can compromise this vasculature dramatically. In these situations, meticulous dissection is especially crucial to prevent inadvertent removal of the bowel serosa, enterotomy, and bowel damage that will impair anastomotic healing. In general, surgical principles with this procedure are much the same as those for large bowel resection (Section 46-18, p. 1195).

PREOPERATIVE ■⌀ Patient Evaluation Small bowel obstructions (SBOs) that do not resolve with nasogastric suction decompression and bowel rest may result from postoperative adhesions or tumor progression. Patients with recurrent gynecologic malignancy, particularly those with ovarian cancer, are preoperatively imaged by abdominopelvic CT with oral contrast. Numerous sites of obstruction may be suspected that would indicate a woman with end-stage disease who might be better served by placement of a palliative percutaneous draining gastrostomy tube. Patients with an SBO following pelvic radiation often have stenosis at the terminal ileum. This vulnerability stems from its proximity to the radiation field of many gynecologic cancers and its limited mobility compared with other small-bowel segments.

obstruction. Antibiotics and VTE prophylaxis are provided (Chap. 39, p. 835). If a complex fistula is present or an extensive resection for radiation damage is anticipated, then postoperative TPN may be advisable.

INTRAOPERATIVE ■⌀ Instruments The surgeon should have access to all types and sizes of bowel staplers, such as end-to-end anastomotic (EEA), gastrointestinal anastomotic (GIA), and transverse anastomotic (TA) staplers, to prepare for complicated resections.

■⌀ Surgical Steps ➊╇ Anesthesia and Patient Positioning.╇ Small bowel resection is performed under general anesthesia. Patients are generally supine, but low lithotomy or other positioning with access to the anterior abdominal wall is acceptable.

➋╇ Abdominal Entry.╇A midline vertical incision is preferable for most situations in which a small-bowel resection is considered.

➌╇ Exploration.╇ The surgeon explores the entire abdomen first to identify the obstruction. Infrequently, an adhesion may be located and lysed to quickly relieve an obstruction, thereby avoiding small bowel resection. More often, an area is discovered that warrants removal. Importantly, the remainder of the bowel must be examined to exclude other obstructive sites.

Peritoneum and adhesions attached to the involved portion of small bowel are dissected to mobilize the bowel. The small intestine can be damaged easily by rough handling and extensive blunt dissection—particularly if the bowel is edematous, densely adhered, or previously irradiated. Trauma is minimized to reduce spillage of intestinal contents by inadvertent enterotomy. Ideally, healthy-appearing serosa for anastomosis is identified at sites both proximal and distal to the lesion while preserving a maximum amount of intestine.

➍╇ Dividing Small Bowel.╇The involved bowel is brought through the abdominal incision. A one-quarter inch Penrose drain is pulled through a mesenterotomy at the proximal and distal sites to be approximated. A GIA stapler is inserted to replace the Penrose drain and is fired. This is repeated at the other bowel site (Fig. 46-20.1). These staple lines minimize contamination of the abdomen with bowel contents. A wedge of mesentery then is “scored” by superficially creating a V shape with an electrosurgical blade. The mesentery is divided by a ligate-divide-staple (LDS) device, electrothermal bipolar coagulator (LigaSure), or clamps and 0-gauge delayed-absorbable suture ligatures. Achieving hemostasis will be more difficult with edematous or inflamed tissue, and thus smaller mesentery pedicles should be sequentially divided. The bowel specimen is then removed. ➎╇ Performing Side-to-Side Anastomosis.╇ The proximal and distal bowel segments are elevated with Allis clamps and matched parallel along their antimesenteric borders.

■⌀ Consent Depending on circumstances, patients are counseled regarding the intraoperative decision-making process to decide on anastomosis, bypass, or ileostomy. Leaking, obstruction, and/or fistula formation are possible complications. Less common outcomes include shortbowel syndrome and vitamin B12 deficiency, both described later.

■⌀ Patient Preparation Aggressive bowel preparation is often contraindicated, particularly in patients with

FIGURE 46-20.1╇ Identifying proximal and distal sites.

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CHAPTER 46

FIGURE 46-20.2╇ Side-to-side anastomosis.

To help alignment, one or two silk stay sutures are placed through the antimesenteric border of each segment beyond the tip of where the GIA stapler fork will reach. The antimesenteric corner of each segment is excised at the staple line just deeply enough to enter the lumen and sufficiently widely to permit passage of one GIA stapler fork. Massively distended bowel from an obstruction may be decompressed by inserting a pool suction tip into the proximal bowel end. Allis clamps are replaced on the bowel at the edge of each opening. These clamps and silk stay sutures assist insertion of one fork of the GIA stapler into each segment and aid in bowel positioning (Fig. 46-20.2). The bowel is rotated to bring the antimesenteric borders together, Allis clamps are removed, and the GIA stapler is closed and fired. The remaining enterotomy is regrasped with three Allis clamps to approximate for closure. The TA stapler is placed around the bowel beneath the Allis clamps and is closed (Fig. 46-20.3). The Allis clamps elevate the enterotomy and assist with correct positioning of the TA stapler. The stapler is fired, excess tissue above the stapler is trimmed sharply, and the stapler is opened and removed. The mesenteric defect may be closed next with running 0-gauge delayed-

FIGURE 46-20.3╇ Closing the enterotomy.

absorbable suture to prevent internal herniation—that is, herniation of bowel or omentum through the mesenteric defect.

➏╇ Final Steps.╇The abdomen is copiously irrigated with warmed saline. This is performed at the conclusion of any bowel resection, but particularly if bowel contents spill during the procedure. Drains are not required routinely and may impair healing. In general, it is prudent to place a nasogastric tube to decompress the stomach postoperatively until bowel function has resumed. Palpation of the stomach will confirm correct placement, or else the anesthesiologist can be directed to advance or pull back the tube as needed. If this is overlooked, correct location can only be reliably confirmed postoperatively by chest radiography.

POSTOPERATIVE The underlying health of the patient, diagnosis, and indications for small bowel resection will dictate much of the potential postoperative morbidity. Ileus is common. Fistula formation, anastomotic leakage, and obstruction are more serious problems that may require reoperation. Two specific complications are unique to extensive small bowel surgery.

First, short-bowel syndrome may develop. More than half the small intestine can be removed without impairing nutritional absorption as long as the remaining bowel is functional. Accordingly, this syndrome is more likely to develop from extensive radiation damage than from surgical resection. Symptoms include diarrhea and dehydration. Maldigestion, malabsorption, nutritional deficiencies, and electrolyte imbalance are often noted. As a result, home TPN may be required in some patients (King, 1993). A second complication, vitamin B12 deficiency, results from inadequate absorption and depletion of available stores. The ileum measures on average 300 cm in length, and vitamin B12 and bile salts are only absorbed in the ileum’s distal 100 cm. Malabsorption in this segment may result from radiotherapy or extensive intestinal resection (Bandy, 1984). If vitamin B12 deficiency is suspected, a complete blood count (CBC), peripheral blood smear, and serum cobalamin (B12) level are collected as part of an initial laboratory assessment. Accepted lower limits of serum vitamin B12 levels in adults range between 170 and 250 ng/L. One option for replacement is 1 mg intramuscularly weekly for 8 weeks, followed by longterm monthly injections (Centers for Disease Control and Prevention, 2011).

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Atlas of Gynecologic Surgery

46-21 SECTION 6

Low Anterior Resection Rectosigmoid resection, also known as low anterior resection, is mainly used in gynecologic oncology to achieve optimal cytoreduction of primary or recurrent ovarian cancer (Mourton, 2005). This procedure is distinguished from other types of large bowel resection in that it requires mobilization and transection of the rectum distally, below the peritoneal reflection. Following resection of the involved rectosigmoid segment, proximal and distal bowel ends are usually anastomosed. Low anterior resection is the most common bowel operation for primary tumor debulking (Hoffman, 2005). For example, en bloc pelvic resection combines low anterior resection with hysterectomy, bilateral salpingooophorectomy, and removal of surrounding peritoneum (Section 46-13, p. 1182) (Aletti, 2006b). In addition, total and posterior pelvic exenterations incorporate many of the same principles of tissue dissection to remove centrally recurrent cervical cancer and achieve widely negative soft tissue margins. Other less common indications for low anterior resection are radiation proctosigmoiditis and intestinal endometriosis (Urbach, 1998). Occasionally, additional large or small bowel resections will be performed concomitantly with low anterior resection (Salani, 2007).

PREOPERATIVE ■⌀ Patient Evaluation Bowel symptoms may or may not be present in women with rectosigmoid involvement of ovarian cancer. However, a surgeon should have greater suspicion if patients describe rectal bleeding or progressive constipation. A rectovaginal examination may help predict a need for low anterior resection. Additionally, CT images may suggest rectosigmoid invasion of tumor. However, prediction prior to surgery is difficult. Many ovarian cancers intraoperatively may be easily lifted away from the bowel, or surface tumors may be removed without resection.

In general, progressively higher complication rates and poorer long-term bowel function follow anastomoses that are more distal and approach the anal verge. However, the operation is designed to encompass the tumor. Thus, an end sigmoid colostomy with Hartmann pouch is another, albeit less attractive, option for very low resections. In general, a protective loop colostomy or ileostomy is not required, but patients are counseled for that possibility in the event of poor nutrition, tenuous bowel blood supply, or anastomosis tension. Anastomotic leaks develop in fewer than 5 percent of procedures (Mourton, 2005).

■⌀ Patient Preparation To minimize fecal contamination during resection, bowel preparation such as with a polyethylene glycol with electrolyte solution (GoLYTELY) is generally considered prior to surgery. Antibiotics and VTE prophylaxis are warranted, and suitable options are found in Tables 39-6 and 39-8 (p. 835).

INTRAOPERATIVE ■⌀ Instruments All types and sizes of bowel staplers such as end-to-end anastomosis (EEA), gastrointestinal anastomosis (GIA), and transverse anastomosis (TA) staplers should be available. Additionally, a ligate-divide-staple (LDS) device or electrothermal bipolar coagulator (LigaSure) may be used for vessel ligation.

■⌀ Surgical Steps ➊╇ Anesthesia and Patient Positioning.╇ Low anterior resection via laparotomy requires general anesthesia. Rectovaginal

examination under anesthesia is performed before positioning any patient for abdominal gynecologic cancer surgery. A palpable mass with compression of the rectum or rectovaginal septum prompts patient positioning in low lithotomy with legs safely placed in boot support stirrups. This allows access to the rectum in cases requiring EEA stapler insertion for anastomosis. Alternatively, supine positioning may be appropriate if no mass is palpable by rectovaginal examination. In such cases, if a mass is more proximally located, low rectal anastomosis can be performed entirely within the pelvis.

➋╇ Abdominal Entry.╇A midline vertical

incision provides generous operating space and upper abdominal access. This is preferable if low rectal anastomosis is anticipated because the descending colon may need to be mobilized around and beyond the splenic flexure of the colon. Transverse incisions often fail to provide sufficient exposure.

➌╇ Exploration.╇ A surgeon first explores the entire abdomen to determine if disease is resectable. If not, then the procedure’s benefit is reevaluated. On occasion, imminent bowel obstruction, infection, or other clinical circumstances may dictate resection regardless of residual tumor. The pelvis and rectosigmoid are palpated to mentally plan for the resection and determine whether en bloc pelvic resection or an exenterative procedure is indicated. ➍╇ Visualization.╇ The bowel is packed into the upper abdomen, and retractor blades are positioned to allow access to the deep pelvis and the entire rectosigmoid colon. Ureters are identified at the pelvic brim and are held laterally on Penrose drains to expose the peritoneum and mesentery that can next be safely dissected.

■⌀ Consent Patients should be prepared for the possibility of low anterior resection any time ovarian cytoreductive surgery is discussed. The survival benefit of achieving minimal residual disease warrants the risks of this procedure. However, low anterior resection significantly extends operative time, and hemorrhage may contribute to a need for blood transfusion (Tebes, 2006).

FIGURE 46-21.1╇ Dividing the proximal end.

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➎╇ Dividing the Proximal Sigmoid Colon.╇

➏╇ Dividing the Mesentery.╇OccasionÂ�

ally, the tumor is small and superficially located, requiring only a wedge resection of underlying mesentery to remove it with the bowel segment. More frequently, the entire mesentery needs to be divided to provide access to the avascular plane between the rectosigmoid and the sacrum (retrorectal space). For this, a right-angle clamp is placed through sections of the mesentery, and an LDS device or electrothermal bipolar coagulator divides this tissue. Dissection is continued caudally to divide the mesentery (Fig. 46-21.2). Typically, one or more pedicles will have a blood vessel that slips out and requires clamping with a right-angle clamp and ligation with 0-gauge delayed-absorbable suture. Blunt dissection is performed in the pelvic midline to identify the large superior rectal vessels, which are branches of the inferior mesenteric artery. This artery and vein are large and are separately doubly clamped, cut, and ligated with 0-gauge delayed-absorbable suture. From this midline, dissection then progresses laterally on both sides until no tissue is visible between the ureters. The common iliac artery bifurcation and sacrum are entirely visible.

❼╇ Dividing the Rectum.╇The proximal sigmoid colon and attached mesentery are repacked into the upper abdomen to improve pelvic exposure. The rectosigmoid is held superiorly, and blunt dissection is performed caudally in the retrorectal space to mobilize the distal bowel beyond the tumor to define the location of planned resection. The ureters are traced along the pelvic sidewall. Lateral blunt dissection is performed to further mobilize the rectosigmoid. Lateral mesenteric attachÂ�ments are isolated and divided with an LDS device or electrothermal bipolar coagulator or are grasped between Pean clamps, cut, and ligated. Selfretaining retractor blades may require repositioning as dissection proceeds more distally. The anterior bowel serosa is generally visible throughout its course beyond the peritoneal

CHAPTER 46

The sigmoid colon is held on traction proximal to the tumor and in the approximate area where it will be divided. The ureter is located, and a right-angle clamp is used to guide superficial electrosurgical blade dissection of the peritoneum and mesentery up to the bowel serosa. A similar dissection is repeated on the other side. Blunt dissection may then be performed to define the entire circumference of the sigmoid colon. Epiploica and adjacent fatty tissue are held with DeBakey forceps and dissected away with an electrosurgical blade from the proposed area of transection. The GIA stapler is placed across the sigmoid colon, fired, and removed (Fig. 46-21.1). FIGURE 46-21.2╇ Dividing the distal end. reflection and into the levator muscles. Lateral and posterior bowel margins are surrounded by fatty tissue, mesentery, and rectal pillars. The distal rectum beyond the tumor is grasped and rotated to aid exposure of these attachments. Attachments are divided using alternating electrosurgical blade dissection and vascular pedicle division and/or right-angle clamping and transection. Division continues circumferentially until the rectal serosa is entirely visible. The curved cutter stapler (Contour) is a good choice for the limited space of the deep pelvis. The rectosigmoid is held on traction, while the stapler is gently inserted into the pel-

vis around the rectal segment. The ureters and any lateral tissue are pushed safely away, the stapler is fired, and the low anterior resection specimen is removed (see Fig. 46-21.2). The pelvis is irrigated, and a laparotomy sponge is left in place to tamponade any surface oozing.

➑╇ Mobilization.╇ The final decision is now

made to perform an anastomosis instead of an end sigmoid colostomy. The upper abdominal retractors are removed, and the proximal sigmoid colon is mobilized by incising peritoneum along the white line of Toldt toward and/or around the splenic flexure (Fig. 46-21.3). A combination of electrosurgical

FIGURE 46-21.3╇ Mobilizing the descending colon.

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Atlas of Gynecologic Surgery

SECTION 6 Sigmoid colon

Anvil

Rectum

Shaft Stapler

FIGURE 46-21.4╇ Performing end-to-end anastomosis. Inset: The EEA stapler device head.

blade and blunt dissection is typically used. The proximal sigmoid colon is intermittently placed into the deep pelvis to assess the extent of further dissection needed to achieve a tension-free anastomosis. Ideally, the proximal sigmoid colon sits comfortably on top of the distal rectum. To achieve this, mobilization may encompass the entire splenic flexure of the colon. Occasionally, the hepatic flexure may also need to be mobilized. Sufficient mobility is critical to ensure a tension-free anastomosis.

➒╇ Preparing the Anastomotic Sites.╇ The proximal and distal stapled bowel ends now must be cleared of fatty tissue or epiploica to allow sufficient mucosa-to-mucosa contact during anastomosis. The staple line of the proximal sigmoid colon is grasped with two Allis clamps at the lateral edges and elevated. Adson forceps are used to delicately place any surrounding fatty tissue on traction, and an electrosurgical blade is used to dissect these away from the bowel serosa. This can be particularly difficult in patients with prominent diverticulosis. A similar dissection may also be required on the distal rectal segment.

➓╇ Placing the Anvil.╇ The largest possible EEA circular stapler that will fit the bowel segments, typically the 31-mm size, is used. This provides a commodious anastomosis that will lessen the chances of symptomatic rectal stenosis. The proximal sigmoid colon is again held with Allis clamps, and scissors are used to remove the entire staple line. The Allis clamps are replaced to grasp the mucosa/serosa and hold open the proximal sigmoid colon. Sizing instruments may be used if necessary to decide which EEA instrument is best. The EEA device contains

an anvil that will be placed in the proximal bowel and a stapler that is placed in the distal bowel. Articulation of the anvil and stapler head allows firing of a staple ring at this articulation site to form the anastomosis. First, the anvil is detached from the stapler, lubricated, and gently inserted by rotating it into the proximal sigmoid colon. Its concave surface faces proximally, away from the anticipated anastomotic site (Fig. 46-21.4 inset). Sequential stitches that pierce through bowel serosa, muscularis, and mucosa create a purse string around the anvil. These “through-andthrough” stitches using 2–0 Prolene suture are placed 5 to 7 mm from the mucosal edge. The purse string begins and ends on the outside of the bowel serosa around the anvil spike and is then tied securely. Allis clamps are removed. A quicker alternative is to use a stapler purse-string suture device. Irrigation may be performed if bowel contents have spilled. ╇ Placing the Stapler.╇The distal rectal stump is reexamined to ensure that all Â�surrounding fatty tissue has been dissected free. The surgical team then reviews the details of using an EEA instrument. A phantom application is helpful. After this, the shaft of the stapler is extended and its spike is attached. The shaft and spike are then retracted into the instrument. The EEA is lubricated and gently inserted into the anus until the circular outline is visible and seen to be gently pressing on the rectal staple line. A wing nut located on the device handle is gently rotated, and this extends the shaft and its spike. This is guided by the abdominal surgeon so that the spike is brought out just posterior to the staple midline. In the abdomen, gentle countertraction against the rectum may be helpful as the sharp

spike tip pops through the entire bowel wall thickness. The shaft subsequently becomes visible and the spike is removed. ╇ Stapling.╇ The abdominal surgeon lowers the proximal sigmoid colon to the distal rectum and connects the hollow tip of the anvil into the metal shaft of the EEA. An audible “click” should be heard to confirm articulation. The tip of the EEA is held perfectly still, while the wing nut is again rotated to retract the shaft back into the EEA until the handle indicator is in the correct Â�position. This draws the anvil into apposition with the stapler head. The safety is released, and the instrument is fired by squeezing and depressing the handles completely. Incomplete squeezing can result in partial stapling. The wing nut is then turned to the specified position to release the staple line. The EEA with its attached anvil is then gently rotated and slowly removed from the rectum. The anastomosis is visualized by the abdominal surgeon throughout the process. Distal retraction of the anastomosis or inability to remove the EEA suggests that the stapler was not completely fired. This situation may be salvaged by gently pulling the EEA through the anus and cutting inside the staple line to release the anastomosis. The anvil is removed from the EEA instrument and inspected to confirm that two completely intact circular “donuts” of rectal tissue are present. ╇ Rectal Insufflation.╇ Warmed saline is irrigated into the pelvis. The integrity of the anastomosis may now be checked by gently inserting a proctoscope or red rubber catheter into the anus, but distal to the anastomosis. Air is then insufflated into the bowel. The abdominal surgeon gently palpates the sigmoid colon to make certain that air is

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POSTOPERATIVE

entering the sigmoid colon proximal to the anastomotic site. No air bubbles are visible if the connection is watertight (Fig. 46-21.5). The appearance of bubbles suggests a leak, but this should be double-checked for authenticity. Occasionally, air is being erroneously pumped into the vagina rather than the rectum due to incorrect placement of the red rubber catheter. If there is any valid suspicion for a leak, the distal rectum should be divided again and the anastomosis redone. Reinforcing interrupted suture to close the

air leak may be attempted in select situations, but this is riskier. Diverting colostomy may also be considered if the problem cannot otherwise be managed. ╇ Final Steps.╇All pedicles sites are rechecked for hemostasis, and the pelvis is irrigated. Nasogastric suction is not routinely required. In addition, prophylactic suction drainage of the pelvis does not improve outcome or influence the severity of complications (Merad, 1999).

CHAPTER 46

FIGURE 46-21.5╇ Testing the anastomosis.

The most common early postoperative complications are similar to those for other major abdominal operations and include fever, self-limiting ileus, wound separation, and anemia requiring transfusion. Serious events such as bowel obstruction and fistula develop infrequently (Gillette-Cloven, 2001). Long-term, some patients will have a poor functional result, including fecal incontinence or chronic constipation (Rasmussen, 2003). Low rectal anastomoses have much higher intraperitoneal leakage rates than large bowel anastomoses. Leakage of stool leads to fever, leukocytosis, lower abdominal pain, and ileus. These should prompt abdominopelvic CT imaging with oral contrast. If a leak is present, it may appear as a pelvic abscess, or at times, contrast extravasation can be demonstrated into the fluid collection. Occasionally, this complication can be successfully managed with percutaneous drainage of the abscess, bowel rest, and broad-spectrum antibiotics. Otherwise, a temporary diverting loop ileostomy or colostomy may be required (Mourton, 2005). Risk factors for postoperative leakage include previous pelvic irradiation, diabetes mellitus, low preoperative serum albumin, long surgical duration, and a low anastomosis (≤6 cm from the anal verge) (Matthiessen, 2004; Mirhashemi, 2000; Richardson, 2006).

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Atlas of Gynecologic Surgery

46-22 SECTION 6

Intestinal Bypass This bowel anastomotic procedure typically connects a section of the ileum to the ascending or transverse colon and thereby “bypasses” a portion of diseased bowel. Following anastomosis, the closed, bypassed small-bowel segment remains. There are relatively few indications for intestinal bypass in gynecologic oncology, and this procedure accounts for less than 5 percent of all bowel operations performed for these cancers (Barnhill, 1991; Winter, 2003). In all circumstances, removal of diseased bowel and end-to-end anastomosis is preferable. However, some patients will have unresectable tumor, dense adhesions, extensive radiation injury, or other prohibitive factors. In these cases, a poor decision to proceed with an aggressive dissection can result in numerous enterotomies, hemorrhage, or other intraoperative catastrophes with major postoperative sequelae. Instead, an intestinal bypass can often quickly be performed with minimal morbidity. Many times a bypass is selected because it is the easiest palliative maneuver for a terminally ill patient. The main purpose is to relieve an obstruction, reestablish an adequate bowel communication, and restore the patient’s ability to take oral nourishment.

FIGURE 46-22.1╇ Aligning the bowel. later, is one long-term complication that is specific to the bypass procedure.

■⌀ Patient Preparation Aggressive bowel preparation with oral agents is usually contraindicated due to bowel obstruction or other dire circumstances. Broad-spectrum antibiotics are given perioperatively due to the possibility of stool contamination, and VTE prophylaxis is provided. If a prolonged recovery is anticipated, postoperative TPN is considered.

PREOPERATIVE

INTRAOPERATIVE

■⌀ Patient Evaluation

■⌀ Instruments

The intestinal tract is evaluated by CT scanning. Invariably, pelvic radiation injuries are located at the terminal ileum, but there may be complex fistulas or multiple sites of obstruction to be addressed. In most circumstances in which a bypass is considered, a surgeon should anticipate limitations in adequately exploring the abdomen intraoperatively. Careful analysis of preoperative findings will help ensure that bypass encompasses the entire lesion and does not leave a distal obstruction.

■⌀ Consent Patients usually have a miserable quality of life when bypass is considered, and the operation’s goal is mainly to improve patient symptoms. The counseling process should emphasize that intraoperative judgment will dictate whether a small bowel resection, ileostomy, large bowel resection, colostomy, or bypass is indicated. Many risks are similar to those of other intestinal surgical procedures and include anastomotic leaks, obstruction, abscess formation, and fistula. Blind loop syndrome, discussed

To prepare for complicated resections, bowel staplers such as an end-to-end anastomosis (EEA), gastrointestinal anastomosis (GIA), and transverse anastomosis (TA) staplers should be available.

■⌀ Surgical Steps ➊╇ Anesthesia and Patient Positioning.╇ Bypass is performed under general anesthesia with the patient positioned supine. Prior to surgery, the abdomen is surgically prepared, and a Foley catheter is inserted.

➋╇ Abdominal Entry and Exploration.╇ Colostomy generally requires a midline vertical incision for adequate exposure. A surgeon first explores the entire abdomen to identify bowel lesions. In addition, the remaining bowel is examined to exclude other obstructive sites. Healthy-appearing bowel proximal and distal to the lesion is selected with the intent of preserving the maximal amount of intestine. Typically, the bypass will entail

connecting a section of the ileum to the ascending or transverse colon.

➌╇ Aligning the Bowel.╇The two bowel

segments selected for the anastomosis are aligned side-to-side without tension or twisting. The hepatic or splenic flexure of the transverse colon may require mobilization from its peritoneal attachments to achieve a tensionfree connection. The antimesenteric borders of the bowel segments are held in position by 2–0 silk stay sutures that are placed approximately 6 cm apart along the length of the aligned bowel segments. Two Adson forceps are used to hold up the small-bowel serosa laterally and transversely on traction. An electrosurgical blade is used to enter the small bowel lumen on its antimesenteric surface (Fig. 46-22.1). The same maneuver is performed on the teniae coli to enter the colon.

➍╇ Performing the Side-to-Side AnastoÂ�

mosis.╇ One fork of the GIA stapler is inserted into each bowel segment lumen. The bowel is adjusted, if necessary, to position the antimesenteric surfaces between the stapler forks. The stapler is then closed and fired (Fig. 46-22.2). With stapling, the initial small bowel openings that were cut to admit the stapler forks are fused into one open defect. This opening can be closed with the TA stapler and the excess bowel trimmed. As a result this TA staple line, the diseased bowel loop is also simultaneously sealed.

➎╇ Final Steps.╇ Occasionally, small bleeding sites on the staple line will need spot electrosurgical coagulation. The anastomosis is also palpated to verify an adequate lumen. The bowel is reexamined to make certain that the connection is watertight and that there is no tension on the anastomosis.

Surgeries for Gynecologic Malignancies

POSTOPERATIVE Recovery after bypass surgery should be rapid compared with that following a large resection with anastomosis. In general, postoperative ileus will resolve in several days,

and patients may begin oral alimentation. The underlying clinical situation prompting the need for bypass surgery will dictate most of the clinical course. Relatively minor complications such as febrile morbidity and wound infection or wound separation occur

CHAPTER 46

FIGURE 46-22.2╇ Performing side-to-side anastomosis.

� commonly. Fistulas, obstruction, anastomotic leaks, abscesses, peritonitis, and perforation are more difficult to manage and often lead to a prolonged postoperative course or death. Blind loop syndrome is a condition of vitamin B12 malabsorption, steatorrhea, and bacterial overgrowth of the small intestine. The usual scenario is a bypass procedure that leaves a segment of nonfunctional, severely irradiated bowel behind. Stasis of the intestinal contents leads to dilatation and mucosal inflammation. Symptoms resemble a partial small bowel obstruction and include nausea, vomiting, diarrhea, abdominal distention, and pain. Bowel perforation is possible. Antibiotics will often alleviate the condition, but recolonization and resumption of the blind loop syndrome is common (Swan, 1974). The only definitive therapy for recurrent episodes is exploration with resection of the bypassed segment. To avoid this syndrome, a surgeon may still perform the sideto-side anastomosis. But, the closed loop can be relieved by creation of a mucus fistula at the abdominal wall.

1205

1206

Atlas of Gynecologic Surgery

46-23 SECTION 6

Appendectomy Removal of the appendix may be indicated during gynecologic surgery for various reasons. The need, however, is commonly not recognized until an operation is already underway, as signs and symptoms of benign gynecologic conditions can mimic appendicitis (Bowling, 2006; Fayez, 1995; Stefanidis, 1999). In addition, malignancies may involve the appendix. Ovarian cancer frequently metastasizes to the appendix, which thereby often warrants removal (Ayhan, 2005). Primary tumors of the appendix are rare but commonly metastasize to the ovaries. Thus, the initial surgical intervention is often performed by a gynecologic oncologist (Dietrich, 2007). Pseudomyxoma peritonei is the classic type of mucinous tumor of appendiceal origin that spreads to the ovaries and may implant throughout the abdomen (Prayson, 1994). Elective coincidental appendectomy is defined as the removal of an appendix at the time of another surgical procedure unrelated to appreciable appendiceal pathology. Possible benefits include preventing a future emergency appendectomy and excluding appendicitis in patients with chronic pelvic pain or endometriosis. Other groups that may benefit include women in whom pelvic or abdominal radiation or chemotherapy is anticipated, women undergoing extensive pelvic or abdominal surgery in which major adhesions are anticipated postoperatively, and patients such as the developmentally disabled in whom making the diagnosis of appendicitis may be difficult because of diminished ability to perceive or communicate symptoms (American College of Obstetricians and Gynecologists, 2014).

FIGURE 46-23.1╇ Clamping the mesoappendix.

PREOPERATIVE Specific preoperative tests or preparations are not required prior to appendectomy. In general, the consenting process for gynecologic surgery includes a discussion of possible “other indicated procedures” such as appendectomy when anticipated intraoperative findings and the potential for performing an appendectomy are uncertain. Most studies suggest that there is, at most, a small increased risk of nonfatal complications associated with elective coincidental appendectomy at the time of gynecologic surgery, whether performed during laparotomy or during laparoscopy (Salom, 2003). Hematoma formation at the mesoappendix may cause an ileus or partial small bowel obstruction. Perforation of the stump is rare and typically follows insecure suture placement.

INTRAOPERATIVE ■⌀ Surgical Steps ➊╇ Anesthesia and Patient Positioning.╇ Appendectomy is performed under general anesthesia in a supine position. Postoperative hospitalization is individualized and is dependent on concurrent surgeries and associated clinical symptoms.

➋╇ Abdominal Entry.╇ Appendectomy can

be performed through almost any incision. A laparoscopic approach or an oblique McBurney incision in the right lower quadrant of the abdomen is traditionally selected for appendectomy. However, in gynecologic cases, the needs of planned concurrent procedures will commonly dictate incision choice.

➌╇ Locating the Appendix.╇ The appendix is located by first grasping the cecum and gently elevating it upward into the incision. Insertion of the terminal ileum should be visible, and the appendix is typically obvious at this point. Infrequently, an appendix is retrocecal or otherÂ� wise difficult to identify. In this situation, the convergence of the three teniae coli can be followed to locate the appendiceal base. ➍╇ Mesoappendix Division.╇The appen-

dix tip is elevated with a Babcock clamp, and the cecum is held laterally to place the mesoappendix on gentle traction. The appendiceal artery is usually very difficult to distinguish reliably due to abundant surrounding fatty tissue. Thus, curved hemostats are used to successively clamp the mesoappendix and its vessels to reach the appendiceal base (Fig. 46-23.1). The first hemostat is placed horizontally—aiming directly toward the base of the appendix. The second hemostat is placed at a 30-degree angle so that the tips meet, but Metzenbaum scissors have room to cut between the two clamps. The mesoappendix pedicle is ligated with 3–0 gauge delayedabsorbable suture. This step is typically repeated once or twice to comfortably reach the base of the appendix. An alternative is to use an electrothermal bipolar coagulator (LigaSure) to divide the mesoappendix.

➎╇ Appendix Ligation.╇ At this point, the

appendix has been completely isolated from the mesoappendix and is still held vertically by a Babcock clamp. A first hemostat is placed at the appendiceal base, and a second is positioned directly above (Fig. 46-23.2). A third hemostat is closed with a few millimeters of intervening tissue to allow for passage of a knife blade. The knife then cuts between

FIGURE 46-23.2╇ Ligation of the appendix.

Surgeries for Gynecologic Malignancies coagulation at the stump surface may also be performed.

➏╇ Final Steps.╇ There is no need to invert

the stump or to place a purse-string suture around it. The cecum may be returned to the abdomen, and remaining concurrent surgeries completed.

POSTOPERATIVE Patient care postoperatively is dictated by other surgeries performed. Delayed initiation of oral intake or administration of additional antibiotics is not required for appendectomy alone.

CHAPTER 46

the second and third clamps, and the appendix is removed. The contaminated knife and appendix are then handed off the field. A 2–0 silk suture is tied beneath the first hemostat as that clamp is slowly removed. A separate suture is then tied underneath the second hemostat for added security of the appendiceal stump. Gentle electrosurgical

1207

1208

Atlas of Gynecologic Surgery

46-24 SECTION 6

Skinning Vulvectomy The term skinning vulvectomy implies a wide, superficial resection that encompasses both sides of the vulva, that is, a complete simple vulvectomy. The surgical procedure is straightforward and removes the entire lesion. It is distinguished from a radical complete vulvectomy in that skinning vulvectomy removes only the squamous epithelium and dermis and preserves the subcutaneous fat and deeper tissues. A less extensive, unilateral procedure is better referred to as a wide local excision or partial simple vulvectomy (Section 43-28, p. 995). The usual indication for skinning vulvectomy is a woman with confluent, bilateral vulvar intraepithelial neoplasia (VIN) 2 to 3 who is not a candidate for directed ablation with carbon dioxide (CO2) laser or cavitational ultrasonic surgical aspirator (CUSA) (Section 43-28, p. 996). Fortunately, individuals with such extensive VIN are infrequently encountered. Paget disease without underlying adenocarcinoma and vulvar dystrophies refractory to standard therapy are other rare indications (Ayhan, 1998; Curtin, 1990; Rettenmaier, 1985). Despite its less radical resection, skinning vulvectomy can still be disfiguring and psychologically devastating. In addition, the defect is often large and cannot be closed primarily without a split-thickness skin graft (STSG) or other type of flap (Section 46-28, p. 1219).

PREOPERATIVE ■⌀ Patient Evaluation Colposcopy with directed diagnostic biopsy is required to exclude a squamous lesion with invasion, which would warrant a more radical procedure. Familiarity with an array of possible STSGs or flaps is crucial to planning the operation in the event primary closure is not possible.

■⌀ Consent Patients are informed that other more limited treatment options either have been exhausted or are inappropriate. The surgery may result in significant sexual changes, which may be permanent. Accordingly, surgeons emphasize that all efforts will be made to restore a functional, normal-appearing vulva. Fortunately, most physical complications are minor and include cellulitis or partial wound dehiscence.

FIGURE 46-24.1╇ Marking the incisions.

■⌀ Patient Preparation Complete bowel preparation is influenced by surgeon preference and only indicated if perianal skin is to be excised. In these cases, bowel preparation may minimize fecal soiling and permit initial wound healing prior to the first stool. Otherwise, enemas are sufficient. Antibiotics and VTE prophylaxis are typically given. Grafts are typically taken from the upper thigh, and donor site selection for STSG is described in Section 46-28 (p. 1219).

INTRAOPERATIVE ■⌀ Surgical Steps ➊╇ Anesthesia and Patient Positioning.╇ Regional or general anesthesia is generally required. The patient is placed in standard lithotomy position, and adjustments provide access to the entire lesion. Vulvar hair should be clipped. Intraoperative colposcopy may be needed to better delineate VIN lesion margins.

➋╇ Skin Incision.╇ The inner and outer inci-

sion lines are drawn to encompass the disease with margins of at least a few millimeters (Fig. 46-24.1). As an overview, once final markings are placed, the skin is dissected off one side of the vulva. The skin on the opposite side of the vulva is then removed, and the bridging skin overlying the perineal body is excised last. In performing this, the clitoris may be spared in many cases by making a horseshoe-shaped incision (as shown). To begin, if preserving the clitoris, the outer incision is started on one side of the

vulva at the anterolateral margin of the clitoris and is continued inferiorly along the length of the labium majus at least halfway to the perineal body. The inner incision on that same side of the vulva is then also taken through the full skin thickness to the same inferior halfway point. Incising the skin in stages reduces blood loss.

➌╇ Beginning the Dissection.╇ The speci-

men edge may then be reflected with an Allis clamp to provide traction as the avascular plane underneath the skin is dissected from the subcutaneous fatty tissue (Fig. 46-24.2). When the anterior skin edge is large enough, a hand is placed underneath to reflect the specimen more firmly and guide dissection inferiorly. The outer and inner skin incision is then extended on that same side downward toward the perineal body. Electrosurgical coagulation is used to achieve hemostasis before repeating the process on the contralateral side.

➍╇ Removal of the Specimen.╇The left and right outer skin incisions are joined in the midline superficial to the perineal body. The posterior vulvar tissue is held with an Allis clamp to provide traction for upward dissection toward the inner incision. The inner incision is made sufficiently proximal to encompass disease. This portion of the skinning vulvectomy is typically performed last because an avascular tissue plane superficial to the subcutaneous tissue is absent, and bleeding can be brisk. The specimen can be removed following detachment from the inner incision.

Surgeries for Gynecologic Malignancies

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CHAPTER 46

FIGURE 46-24.2╇ Performing the dissection.

The skinning vulvectomy specimen is carefully examined to grossly determine margins. A frozen section may be warranted if close VIN margins are suspected, to determine if more tissue requires excision. However, the margins of vulvar Paget disease cannot reliably be judged visually or by frozen-section analysis (Fishman, 1995). A stitch is placed on the specimen and noted on the pathology requisition form to orient the pathologist.

➎╇ Closure of the Defect.╇A dry lapa-

rotomy pad is held against the vulvar defect and slowly rolled downward to halt surface bleeding and aid meticulous electrosurgical

FIGURE 46-24.3╇ Primary closure.

coagulation of vessels. The operative site is irrigated and assessed. If the width of the defect is sufficiently narrow to permit primary closure, the surrounding tissue is mobilized. Lateral undermining may be particularly useful for a tension-free closure. Typically, 0 or 2–0 gauge delayed-absorbable vertical mattress sutures are then placed circumferentially with the knots laterally positioned (Fig. 46-24.3). However, if a split-thickness skin graft is required, the graft is now harvested and placed as described on page 1219.

➏╇ Final Steps.╇ A CO2 laser may be used to vaporize multifocal lesions outside the

operative field. This is described in Section 43-28 (p. 997).

POSTOPERATIVE If a primary closure is performed, postoperative care is essentially the same as described for patients undergoing radical partial vulvectomy (p. 1212). Long-term surveillance is mandatory regardless of margin status to identify recurrent or de novo sites of preinvasive disease. The Foley catheter can be removed without regard to urine spill unless a graft is placed or the patient is otherwise immobile.

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Atlas of Gynecologic Surgery

46-25 SECTION 6

Radical Partial Vulvectomy For vulvar cancer, to reduce the high morbidity associated with radical complete vulvectomy yet avoid sacrificing a cure, a less extensive resection may be used. Patients with well-localized, unifocal, clinical stage I invasive lesions are ideal candidates (Stehman, 1992). Radical partial vulvectomy is a somewhat ambiguously defined operation that generally refers to complete removal of the tumor-containing portion of the vulva, wherever it is located, with 1- to 2-cm skin margins and excision to the perineal membrane (Whitney, 2010). Radical hemivulvectomy refers to a larger resection that may be anterior, posterior, right, or left. Vulvectomy is typically performed concurrently with inguinofemoral lymphadenectomy to add prognostic information. However, in those with microinvasive disease undergoing wide local excision or skinning vulvectomy, lymphadenectomy is not required. The chief concern in performing a less extensive operation for vulvar cancer is the possibility of an increased risk of local recurrence due to multifocal disease. However, survival after partial or complete radical vulvectomy is comparable if negative margins are obtained (Chan, 2007; Landrum, 2007; Scheistroen, 2002; Tantipalakorn, 2009). Following radical partial vulvectomy, 10 percent of patients will develop a recurrence on the ipsilateral vulva, and this may be treated by reexcision (Desimone, 2007).

PREOPERATIVE ■⌀ Patient Evaluation Biopsy confirmation of invasive cancer is mandatory. An isolated squamous lesion

A

standard lithotomy position to provide full exposure to the vulva. The vulva is surgically prepared, and a Foley catheter is inserted.

with less than 1 mm of invasion, that is, microinvasion, may be adequately managed with only wide local excision (Section 43-28, p. 995). Multiple microinvasive lesions may require skinning vulvectomy (p. 1208). In general, patients undergoing radical partial vulvectomy do not require reconstructive grafts or flaps to cover operative defects.

➋ ╇ Radical Partial Vulvectomy: VariaÂ�

tions.╇ The area of tissue to be removed when radically excising a small cancer depends on the size and location of the tumor. In Figure 46-25.1, the dotted line indicates a planned skin incision for: (A) a 1-cm right labium majus tumor with 2-cm margins, (B) a 2.5-cm periclitoral tumor necessitating anterior hemivulvectomy, and (C) a 2.5-cm midline posterior fourchette tumor requiring posterior hemivulvectomy.

■⌀ Consent Morbidity after radical vulvar surgery is common. Wound separation or cellulitis develops frequently. Long-term changes may include displacement of the urine stream, dyspareunia, vulvar pain, and sexual dysfunction. Surgeons should be sensitive to these possible sequelae and counsel patients appropriately, emphasizing the curative intent and limited scope of the operation.

➌╇ Right Hemivulvectomy: Making the

Lateral Incision.╇ The planned excision is drawn on the vulva with a surgical marking pen to provide 2-cm margins (Fig. 46-25.2). Tapering the incision anteriorly and posteriorly will aid in a tension-free closure. The lateral skin incision is made with a knife (no. 15 blade) into the subcutaneous fat. Forceps are used to place the skin edges on traction and aid electrosurgical dissection downward until reaching the perineal membrane (Fig. 46-25.3). An index finger can then be used to develop the plane between the fat pad of the labium majus and the subcutaneous tissue of the lateral thigh.

■⌀ Patient Preparation Bowel preparation is influenced by surgeon preference and may be indicated with posteriorly located resections. In such instances, bowel preparation may minimize fecal soiling and permit initial wound healing prior to the first stool. Antibiotics and VTE prophylaxis are typically given prior to incision (Tables 39-6 and 39-8, p. 835).

➍╇ Right Hemivulvectomy: Completing

INTRAOPERATIVE

the Resection.╇ Tissue medial to this lateral resection border is next mobilized medially by blunt and electrosurgical dissection along the perineal membrane. The skin edge of the specimen is then placed on lateral traction, and the medial (vaginal mucosa) incision is incised from anterior to posterior. The labial fat pad is transected anteriorly, and the entire radical right hemivulvectomy specimen is placed on downward traction to aid final dissection along the mucosal incision in an anterior-to-posterior direction (Fig. 46-25.4). Notably, the vascular vestibular bulb is

■⌀ Surgical Steps ➊╇ Anesthesia and Patient Positioning.╇ Radical partial vulvectomy has been performed under local anesthesia combined with sedation in medically compromised patients (Manahan, 1997). However, regional or general anesthesia is typically required. Inguinal lymphadenectomy (p. 1216) is typically performed before vulvar resection. Patients may then be repositioned to

B

FIGURE 46-25.1╇ Radical partial vulvectomy: variations.

C

Surgeries for Gynecologic Malignancies

1211

CHAPTER 46

FIGURE 46-25.2╇ Right hemivulvectomy: outlining the skin incision.

typically encountered as the posterior resection is completed. Suture ligation of bleeding sites is often required. After completed resection, the specimen is examined to ensure adequate margins. It is marked at 12 o’clock with an orienting stitch, and this is noted on the pathology requisition form.

➎╇ Right Hemivulvectomy: Defect CloÂ�

sure.╇ A gauze sponge may be held firmly in the cavity and rolled downward to guide the electrosurgical blade in achieving hemostasis. The defect can then be irrigated and evaluated to determine requirement for a tension-free closure while minimizing anatomic distortion (Fig. 46-25.5). Several pedicles are visible, particularly at the

FIGURE 46-25.3╇ Right hemivulvectomy: lateral dissection to the fascia lata.

vaginal margin, where vessels were clamped and tied. In general, lateral undermining of the subcutaneous tissue will provide sufficient mobility to allow primary closure. Interrupted 0-gauge delayed-absorbable suture is used to create a layered reapproximation of deeper tissues. Interrupted vertical mattress sutures, often alternating 0 and 2–0 gauge suture, with knots placed laterally are used to close the skin (Fig. 46-25.6).

➏╇ Anterior Hemivulvectomy.╇ This vari-

ation requires removal of the clitoris and partial resection of the labia minora, labia majora, and mons pubis. The most anterior portion of the incision is first created on the mons and carried down to the pubic symphysis. The

FIGURE 46-25.4╇ Right hemivulvectomy: removal of the specimen.

specimen is reflected posteriorly to guide dissection. In the midline, the clitoral vessels are separately clamped, divided, and ligated with 0-gauge delayed-absorbable suture. The posterior incision is made above the urethral meatus, and careful attention to Foley catheter location helps avoid urethral injury. Layers of interrupted 0-gauge delayedabsorbable sutures are used to reapproximate deep tissue. Then, 3–0 gauge absorbable suture is used to close the defect in a direction that places the least tension on the suture line. Usually, the area surrounding the urethral meatus is left to granulate secondarily.

❼╇ Partial Urethral Resection (Optional).╇ If an anterior lesion encroaches on the urethral meatus, then a distal urethrectomy may be required to achieve a negative margin. Prior to this, the radical partial vulvectomy should otherwise be almost entirely completed. The

FIGURE 46-25.5╇ Right hemivulvectomy: evaluation of the surgical defect.

1212

Atlas of Gynecologic Surgery

POSTOPERATIVE SECTION 6 FIGURE 46-25.6╇ Right hemivulvectomy: closure of the surgical defect. urethra may be transected anywhere distal to the pubic arch. For this, the meatus is held with an Allis clamp, and the specimen placed on traction. The posterior urethra is incised with a knife, and the underlying uroepithelium and mucosa are sewn jointly to the adjacent vestibule skin at the 6 o’clock position with 4–0 gauge delayed-absorbable suture. The urethral incision is extended laterally, followed by additional sutures at 3 and 9 o’clock. The Foley balloon is deflated and removed from the bladder. Transection is completed, and a final stitch is placed at 12 o’clock. The Foley catheter is then replaced. Alternatively, the surgeon may forgo stitch placement altogether and allow the meatus to heal by secondary intent. Although urethral plication may be indicated in selected cases, resection of 1 to 1.5 cm of the distal urethra does not ordinarily result in a significant increase in urinary incontinence (de Mooij, 2007).

➑╇ Posterior Hemivulvectomy.╇ This variation entails removal of a portion of the labia majora, Bartholin glands, and upper perineal body. It is generally necessary to compromise the deep margin in this resection because of proximity to the anal sphincter and rectum.

The skin is first incised posteriorly, and a finger is placed into the rectum to guide proximal dissection. The specimen is gradually retracted upward off the sphincter. From the midline, dissection then proceeds laterally on each side until the anterior margin at the introitus can be incised to complete the resection. The perineal body is reinforced with interrupted sutures of 0-gauge delayed-absorbable material to provide bulk and to allow reapproximation of skin edges for a tension-free closure. Rectal examination is performed at the end of surgery to confirm the absence of palpable stitches or stenosis. Incontinence of flatus or stool may develop postoperatively despite efforts to preserve the sphincter.

➒╇ Final Steps.╇ Suction drains are not typi-

cally required but are at least considered in some circumstances. Copious irrigation is indicated at various times during closure of the defect to minimize postoperative infection. No formal dressing is applied. However, fluffed-out gauze may be placed at the perineum and held in place with mesh underwear to tamponade any subcutaneous bleeding and to promote a clean and dry operative site in the immediate postoperative period.

Meticulous care of the vulvar wound is mandatory to prevent morbidity. The vulva is kept dry by use of a blow dryer or fan. Within a few days, brief sitz baths or bedside irrigation followed by air drying will help keep the incision clean. Patients are instructed not to wear tight-fitting underwear upon discharge from the hospital. Moreover, instructions encourage loose-fitting gowns to aid healing and efforts to minimize wound tension. For posteriorly located defects near the anus, a low-residue diet and stool softeners will prevent straining and potential perineal incision disruption. Typically, the Foley catheter is removed postprocedure or at least on postoperative day 1. If a distal urethrectomy was performed or extensive periurethral dissection was required, then the catheter is removed within a few days. This permits tissue swelling and obstructive urinary retention concerns to abate. Early removal prevents ascending urinary infection. If immobility is encouraged to aid reconstructive graft or flap healing, then the timing of catheter removal is individualized. Notably, urine that comes in contact with the vulvar incision during normal voiding is of little clinical concern. Incision separation is the most common postoperative complication and often will involve only a portion of the incision (Burke, 1995). Stitches are removed as needed and affected portions of the wound are debrided. Efforts to keep the site clean and dry are continued. Granulation tissue will eventually allow healing by secondary intention, but recovery time will be significantly extended. Although negative-pressure wound therapy (wound vacuum-assisted closure) may be practical in rare instances, the location of most defects precludes effective device placement. Sexual dysfunction may stem from a sense of disfigurement. Scarring may also result in discomfort or altered sensation that lowers a woman’s sexual satisfaction. Clinician sensitivity to these concerns enables a dialogue to develop that can lead to possible management options (Janda, 2004).

Surgeries for Gynecologic Malignancies

1213

46-26

If cancers are so extensive that no meaningful portion of the vulva can be preserved, radical complete vulvectomy is indicated rather than the more limited radical partial vulvectomy (p. 1210). The operation is typically performed concurrently with bilateral inguinofemoral lymphadenectomy (p. 1216). With the radical complete vulvectomy technique currently used, intact skin bridges remain between the three incisions (vulvectomy incision and two lymphadenectomy incisions) to aid wound healing. Traditionally, the en bloc incision, colloquially termed the butterfly or longhorn incision, removed these skin bridges and the underlying lymphatic channels that potentially harbored tumor emboli “in transit” between the vulvar tumor and nodes (Gleeson, 1994c). However, such recurrences are rare, and the en bloc technique has been largely abandoned (Rose, 1999). Thus, the three-incision procedure is preferred because survival rates are equivalent and major morbidity is dramatically reduced (Helm, 1992). Removal of an extensive vulvar lesion with an adequate margin and with resection down to the perineal membrane usually creates a large surgical defect. In some cases, wound margins may be primarily closed without tension by undermining and mobilizing adjacent tissues. On other occasions, a split-thickness skin graft, lateral skin transposition, rhomboid flap, or other reconstructive procedure, described on page 1219, will be indicated to reduce the chances of wound separation.

PREOPERATIVE ■⌀ Patient Evaluation Biopsy confirmation of invasive cancer should precede surgery. Depending on the location of the tumor, the clitoris-sparing modification of radical complete vulvectomy is an option (Chan, 2004). Frequently, patients are elderly, obese, or have significant coexisting medical problems that must be considered.

■⌀ Consent Major morbidity is common soon after radical complete vulvectomy, and partial wound separation or cellulitis occurs frequently. Complete wound breakdown is more problematic, and weeks of aggressive hospital care may be required to promote secondary healing. Premature hospital discharge may result in

CHAPTER 46

Radical Complete Vulvectomy

FIGURE 46-26.1╇ Incisions. poor home wound care, and subsequent tissue necrosis often requires readmission and surgical debridement. Thus, meticulous attention to the wound is critical during patient admission and frequent office visits thereafter. Long-term changes may include displacement of the urine stream, dyspareunia, vulvodynia, and sexual dysfunction. Accordingly, surgeons counsel on these possible sequelae yet emphasize the curative intent of the operation and the need for adequate tumor-free margins to lessen local recurrence risks.

■⌀ Patient Preparation Bowel preparation is guided by surgeon preference and may be indicated with posteriorly located lesions. In addition, evaluation of potential graft donor sites is completed. Antibiotics and VTE prophylaxis are typically given prior to initial incision (Tables 39-6 and 39-8, p. 835).

INTRAOPERATIVE ■⌀ Surgical Steps ➊╇ Anesthesia and Patient Positioning.╇ Regional or general anesthesia is required, and inguinofemoral lymphadenectomy is performed first. The patient is then placed in standard lithotomy position. Exposure and surgical preparation of the operative field is planned to accommodate resection and reconstruction. Sites of potential donor graft harvest are also prepared as described on page 1219.

➋╇ Planning the Skin Incision.╇ The meÂ�dial

and lateral incisions are drawn to en�com� pass the tumor and provide a 1- to 2-cm margin around the tumor. The clitoris is included if necessary. Tapering the incision

anteriorly and posteriorly will also aid in a tension-free closure (Fig. 46-26.1).

➌╇ Anterior Dissection.╇The skin incision begins anteriorly with the knife (no. 15 blade) cutting into the subcutaneous fat. The incision is extended downward approximately three quarters of its length. The remainder of the posterior skin incision is completed later to decrease blood loss. Much of the anterior dissection is described in the preceding section on radical partial vulvectomy (Section 46-25, step 6, p. 1211). However, use of the Harmonic scalpel or bipolar electrocoagulation device (LigaSure) in this more extensive resection may decrease operative time and blood loss compared with use of a conventional electrosurgical blade (Pellegrino, 2008). Briefly, the incision is carried down to the pubic symphysis. The specimen is reflected downward on traction to guide dissection. The vascular base of the clitoris is clamped in the midline, transected, and suture ligated with 0-gauge delayed-absorbable suture (Fig. 46-26.2). Electrosurgical or Harmonic scalpel dissection then proceeds dorsally off the pubic bone until the inner incision line is reached anteriorly. This inner anterior incision is made above the urethral meatus to avoid injury to the urethra unless a distal urethrectomy is required (46-25, step 8, p. 1212). ➍╇ Lateral Dissection.╇Blunt finger dis-

section is performed to establish a plane lateral to the labial fat pads and at a depth to reach the perineal membrane. The vulvectomy specimen is placed on traction to guide dissection medially to reach the vaginal walls. Along the lower lateral sides of the vagina, the vascular vestibular bulb is encountered. Vessels are divided with the Harmonic scalpel or clamped, cut, and ligated with 0-gauge

1214

Atlas of Gynecologic Surgery

SECTION 6 FIGURE 46-26.2╇ Anterior dissection. delayed-absorbable suture to reduce bleeding (Fig. 46-26.3).

➎╇ Posterior Dissection.╇An outer skin incision is completed inferiorly with a knife as the vulvectomy proceeds posteriorly toward the perineal body. A finger is then placed into the rectum to prevent inadvertent injury, and the specimen is now held upward on traction (Fig. 46-26.4). Electrosurgical dissection along the deep fascia plane extends the outer incisions toward the midline. The dissection continues anteriorly away from the

FIGURE 46-26.4╇ Posterior dissection.

FIGURE 46-26.3╇ Medial dissection. anus until the inner incision can be made. With this, the entire complete radical vulvectomy specimen is detached.

➏╇ Evaluating the Specimen.╇A stitch

is placed at 12 o’clock on the specimen and noted on the laboratory requisition form to orient the pathologist. Skin retraction of the specimen will make it appear narrower and smaller than the defect. However, it is carefully inspected to assess its margins. Additional lateral or medial tissue margins can be separately sent if necessary.

Alternatively, a frozen section analysis can be requested to evaluate an equivocal margin.

➐╇ Closing the Defect.╇ The wound is copiously irrigated, and hemostasis is achieved with a combination of electrosurgical coagulation and clamping with suturing. The defect is then evaluated to determine the best method of closure (Fig. 46-26.5). Undermining lateral tissues will aid a tension-free primary closure. Deeper tissues are first reapproximated with 0-gauge delayed-absorbable suture and interrupted stitches. The vulvar skin is then

FIGURE 46-26.5╇ Surgical defect.

Surgeries for Gynecologic Malignancies

1215

sion, the graft is now harvested and placed as described on page 1219.

POSTOPERATIVE

FIGURE 46-26.6╇ Simple closure. closed with 0-gauge, or alternating with 2–0 gauge, delayed-absorbable vertical mattress sutures (Fig. 46-26.6). No stitches are placed between the skin and urethra if this

displaces the urethra or creates tension on it. Instead, this area can be allowed to heal secondarily by granulation. If a split-thickness skin graft or flap is required to close the inci-

If a primary closure is performed, postoperative care is essentially the same as described for patients undergoing radical partial vulvectomy (p. 1212). Because of a larger operative defect, the likelihood of morbidity is correspondingly increased. Management of reconstructive grafts and flaps is reviewed on page 1220.

CHAPTER 46

➑╇ Final Steps.╇ Suction drains do not prevent wound infection or breakdown but may be considered in some cases if the defect is large (Hopkins, 1993). If primary closure is performed, then fluffed-out gauze may be placed at the perineum and held in place with mesh underwear to keep the operative site clean and dry in the immediate postoperative period.

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46-27 SECTION 6

Inguinofemoral Lymphadenectomy Vulvar cancer staging is the primary indication for removal of groin nodes. Inguinal metastases are the most significant prognostic factor in vulvar squamous cancer, and their detection will necessitate additional therapy (Chap. 31, p. 682) (Homesley, 1991). Occasionally, in patients with ovarian or uterine cancer, suspicion of inguinal metastases will prompt removal. In general, lymphatic drainage from the vulva rarely bypasses the superficial nodes. Thus, a superficial node dissection is integral. These lymph nodes lie within the fatty tissue along the saphenous, superficial external pudendal, superficial circumflex iliac, and superficial epigastric veins. After superficial nodes are addressed, deep nodes may be removed. These nodes are consistently located just medial and parallel to the femoral vein within the fossa ovalis. To reach these, cribriform fascia preservation is recommended to avoid major morbidity (Bell, 2000). Generally, for patients with unilateral lesions distant from the midline, ipsilateral lymphadenectomy is usually sufficient (Gonzalez Bosquet, 2007). For bilateral lesions or those that encroach on the midline, bilateral lymphadenectomy is indicated. Sentinel lymph node mapping is a promising modality that has demonstrated great potential in reducing the radicality of detecting inguinal metastases (Van der Zee, 2008). This minimally invasive strategy is emerging as the future standard for vulvar cancer staging and is described in Chapter 31 (p. 686).

PREOPERATIVE

common and may include cellulitis, wound breakdown, chronic lymphedema, and lymphocyst formation. These events may develop within a few days, several months, or even years later. In contrast, intraoperative complications are less common, and hemorrhage from the femoral vessels is rarely encountered.

■⌀ Patient Preparation When both groins are dissected, a two-team approach is ideal to reduce operative time. Prophylactic antibiotics may be administered, but they have not been shown to prevent complications (Gould, 2001). VTE prophylaxis is also provided.

INTRAOPERATIVE ■⌀ Surgical Steps ➊╇ Anesthesia and Patient Positioning.╇ General or regional anesthesia may be used. Inguinal lymphadenectomy is performed prior to partial or complete radical vulvectomy. Legs are placed in booted support stirrups in low lithotomy position, are abducted approximately 30 degrees, and are flexed minimally at the hip to flatten the groin. Rotation of the thigh a few degrees outward will open the femoral triangle.

➋╇ Skin Incision.╇ The groin is incised 2 cm

below and parallel to the inguinal ligament starting 3 cm caudal and medial to the anterior superior iliac spine—aiming toward the adductor longus tendon (Fig. 46-27.1). The incision is 8 to 10 cm long and is taken through full skin thickness and 3 to 4 mm into the fat.

➌╇ Developing the Upper Flap.╇Adson forceps elevate and provide traction to the upper skin edge while a hemostat is opened underneath to begin cephalad dissection down

■⌀ Patient Evaluation Clinical palpation is not an accurate means of evaluating the groin nodes (Homesley, 1993). MR imaging and PET scanning are also relatively insensitive (Bipat, 2006; Cohn, 2002; Gaarenstroom, 2003). Fixed, large, clinically obvious groin metastases that appear unresectable are treated preoperatively with radiation before attempting removal.

■⌀ Consent Patients should understand the need for unilateral or bilateral groin dissection and its relationship to their cancer treatment. They should be prepared for a potentially several-week recovery in which postoperative complications areÂ�

FIGURE 46-27.1╇ Incisions.

through the subcutaneous fat and Scarpa fascia—aiming for a position in the midline of the incision and 3 cm above the inguinal ligament. Dissection proceeds downward until the glistening white aponeurosis of the external oblique muscle is identified. Adson forceps are then replaced with skin hooks to provide better traction. A semicircle of fatty tissue is rolled inferiorly and laterally along the aponeurosis using electrosurgical dissection and intermittent blunt dissection. During dissection, the superficial circumflex iliac vessels are divided with a Harmonic scalpel or clamped and ligated. Additionally, superficial epigastric and superficial external pudendal vessels are divided as they are encountered (Fig. 38-29, p. 823). Dissection proceeds until the lower margin of the inguinal ligament is exposed (Fig. 46-27.2).

➍╇ Developing the Lower Flap.╇The

posterior skin flap is now raised in a similar manner to the upper flap. Dissection progresses through the subcutaneous fat to the deep fascia of the thigh—aiming approximately 6 cm from the inguinal ligament toward the apex of the femoral triangle. As shown in Figure 46-27.1, the femoral triangle is bordered by the inguinal ligament superiorly, by the sartorius muscle laterally, and by the adductor longus muscle medially. Blunt finger dissection along the inner portion of the sartorius and adductor longus muscles aids development of the lower flap boundaries. The dissection progressively becomes deeper into the subcutaneous tissue of the thigh, but remains superficial to the fascia lata. The tissue exiting at the apex of the femoral triangle is divided. Dissection progresses toward the fossa ovalis in circumferential path (Fig. 38-29, p. 823). Nodebearing tissue is held on traction to aid its dissection. Venous tributaries are ligated as they are encountered.

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CHAPTER 46

FIGURE 46-27.2╇ Dissection of the upper flap.

➎╇ Removal of the Superficial Nodes.╇ The superficial lymph nodes lie within the fatty tissue just mobilized. The saphenous vein is encountered during the dissection of the medial side of the fat pad. The distal end this vein is individually transected and ligated with permanent suture for identification. If desired, saphenous vein transection can be avoided, and the vein can be salvaged by dissecting it from the fat pad. Circumferential dissection is next performed to isolate and remove the nodal bundle as it overlies the fossa ovalis (Fig. 46-27.3). The proximal end of the saphenous vein is separately ligated, unless the vessel has been preserved and can be dissected away from the nodal bundle. Remaining attachments are dissected from the cribriform fascia or clamped and cut to remove the specimen.

FIGURE 46-27.3╇ Dissection of the lower flap and removal of superficial nodes. a more orderly fashion than the superficial nodes. Fatty-lymphoid tissue is then dissected from the anterior and medial surfaces of the femoral vein. Following node removal, the femoral sheath edges may then be reapproximated using 3–0 gauge delayed-absorbable suture and/or covered with the sartorius muscle.

❼╇ Sartorius Muscle Transposition (OpÂ�tioÂ�

nal).╇ The fascia lata is incised to allow blunt dissection of the sartorius muscle (Fig. 46-27.5). The proximal sartorius muscle is then transected at its insertion to the anterior

superior iliac spine. A finger is wrapped around the upper part of the muscle to aid electrosurgical blade transection directly off the spine. Transection is as high as possible, with care taken to avoid the lateral femoral cutaneous nerve. The muscle is then further mobilized to cover the femoral vessels and sutured to the inguinal ligament with 2–0 gauge delayed-absorbable suture.

➑╇ Wound Closure.╇The surgical defect is carefully examined, made hemostatic, and irrigated. The groin is closed with layers of delayed-absorbable suture, and a

➏╇ Removal of the Deep Nodes.╇The femoral vein should be visible within the fossa ovalis. The deep groin nodes lie just medial and parallel to this vessel. Of these, Cloquet node is the uppermost. The residual deep femoral nodal tissue is excised by removing any fatty tissue along the anterior and medial surfaces of the femoral vein above the deep limit of the fossa ovalis. The femoral sheath and cribriform fascia remain intact if possible. If a clinically positive deep node cannot otherwise be reached, the cribriform fascia may be unroofed by making a longitudinal incision distally along the overlying femoral sheath (Fig. 46-27.4). Seven or eight underlying deep inguinal nodes are revealed, and these deep nodes are typically located in

FIGURE 46-27.4╇ Unroofing the cribriform fascia to remove deep nodes.

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SECTION 6 FIGURE 46-27.5╇ Sartorius muscle transposition.

Blake or Jackson-Pratt drain is brought out superolaterally and tied in place with permanent suture (Fig. 46-27.6). Staples are placed to reapproximate skin edges.

POSTOPERATIVE Suction drainage enables the incision to heal and the underlying space to be obliterated. Drain tubing is manually milked or stripped three times daily with index finger and thumb toward the suction device to prevent blockage. Drains may be removed when output declines to 20 to 25 mL per day. Typically,

FIGURE 46-27.6╇ Wound closure.

this requires approximately 2 weeks (Gould, 2001). Premature removal may result in a symptomatic lymphocyst that requires drain reinsertion or outpatient needle aspiration. The groin incision remains uncovered and is regularly examined. Postoperative complications are common, particularly wound cellulitis and breakdown. Preoperative radiation and removal of bulky, fixed nodes increase the risk of these. Unroofing the deep fascia can also unnecessarily expose the femoral vessels to erosion or sudden hemorrhage. A protective sartorius muscle transposition may be especially indicated in these selected

situations to prevent morbidity (Judson, 2004; Paley, 1997). Chronic lymphedema is another frequent complication of inguinal lymphadenectomy. In most reports, preservation of the saphenous vein has been shown to reduce the incidence (Dardarian, 2006; Gaarenstroom, 2003). Regardless, this condition is typically much more problematic with the addition of groin radiation. Supportive management is meant to minimize the edema and prevent symptomatic progression. Foot elevation, compression stockings, and, on occasion, diuretic therapy may be helpful.

Surgeries for Gynecologic Malignancies

46-28

Primary closure of a vulvar wound is typically not advised if closure of a large defect would create excessive incision tension or if other untoward factors are present. In these cases, a reconstructive skin graft or flap is preferable to a defect healing by secondary intent. In general, the simplest procedure that will achieve the best functional result should be selected. The decision to perform a split-thickness skin graft (STSG), lateral skin transposition, or rhomboid skin flap depends on clinical circumstances and surgeon experience. Variations of these techniques are occasionally used in gynecologic oncology (Burke, 1994; Dainty, 2005; Saito, 2009). Typical candidates for a skin graft or flap have undergone a large wide local excision, skinning vulvectomy, or partial or complete radical vulvectomy. Myocutaneous flaps, most commonly using the rectus abdominis and gracilis muscles, are used primarily in patients with prior radiation, very large defects, or a need for vaginal reconstruction (Section 46-9, p. 1167). However, a full description of the innumerable types of local flaps is beyond the scope of this section.

PREOPERATIVE ■⌀ Patient Evaluation Fortunately, a broad range of operative procedures are available—each with their advantages and disadvantages (Weikel, 2005). The size of the lesion and the anticipated postsurgical defect will largely dictate reconstructive

FIGURE 46-28.1╇ Large vulvar surgical defect.

■⌀ Consent A woman’s body image may be significantly altered following extensive vulvar surgery, and sexual dysfunction may be a problem (Green, 2000). When discussing these effects, patient responses vary widely. Some express minimal concern, whereas others are devastated by the thought of a disfiguring result. Accordingly, counseling is individualized, specifically addressing patient concerns. In addition, wound separation, infection, and wound healing by secondary intention are common. Moreover, patients are advised that recurrences of their underlying disease may recur within the graft or flap (DiSaia, 1995).

■⌀ Patient Preparation Prophylactic antibiotics are typically given, and bowel preparation is generally influenced by surgeon preference. Early ambulation may be detrimental to graft or flap healing. Therefore, to prevent VTE, use of pneumatic compression devices or subcutaneous heparin is especially warranted (Table 39-8, p. 836). For patients undergoing STSG, the hip, buttock, and inner thigh are carefully examined. The selected donor sites should contain healthy skin, should be hidden by a patient’s clothing postoperatively, and must be accessible in the operating room. Typically, a graft is taken from the upper thigh.

INTRAOPERATIVE ■⌀ Surgical Steps ➊╇ Anesthesia and Patient Positioning.╇ General or regional anesthesia is required.

The patient will need to be positioned in low lithotomy with complete access to the vulva, upper thighs, and mons pubis. Sterile preparation of the lower abdomen, perineum, thighs, and vagina is performed, and a Foley catheter is placed. Infrequently, the buttock or hip will be selected as the STSG donor site—this will require additional repositioning.

➋╇ Evaluating the Surgical Defect.╇ After

the vulvar resection has been completed and hemostasis is achieved, the wound is examined to confirm that primary closure is impossible (Fig. 46-28.1). The best graft or flap that will adequately cover a defect is determined.

➌╇ Split-thickness Skin Graft (STSG).╇ A

dermatome device is required to harvest the graft from the donor site when performing a STSG. At a setting of 18/1000ths to 22/1000ths, normal epithelium is harvested from the donor site (Fig. 43-25, p. 985). The STSG is placed in a basin and moistened with saline. The donor site is then sprayed with thrombin, covered with a transparent film dressing (Tegaderm), and wrapped firmly with gauze. The recipient site is irrigated with antibiotic solution, and hemostasis must be absolute. The graft is then held over the defect and cut to fit so that there is some overlap. Meticulous care is required to smooth graft wrinkles and avoid graft tension. Edges are then sutured to the skin with interrupted 3–0 gauge nylon suture (Fig. 46-28.2). Moistened gauze or cotton balls are placed over the graft and covered with opened and fluffed gauze squares to provide light pressure. To create a stable dressing, a few ties are usually placed through the covering dressing and lateral to the graft site. Alternatively, fibrin tissue adhesives and/or vacuum-assisted closure devices

FIGURE 46-28.2╇ Split-thickness skin graft.

CHAPTER 46

Reconstructive Grafts and Flaps

options. In some complicated cases, plastic surgery consultation may be indicated.

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SECTION 6

undermining to provide a reasonably smooth contour and is needed to aid closure of the remaining defects above and below the flap. Finally, a suction drain is placed at the donor site to prevent seromas caused by extensive tissue dissection and that could otherwise result in wound dehiscence.

POSTOPERATIVE

FIGURE 46-28.3╇ Lateral skin transposition. may further augment graft adherence and viability (Dainty, 2005).

➍╇ Lateral Skin Transposition.╇In some

cases, the skin lateral to the surgical defect is extensively undermined but still may not be able to cover a large defect and reach the medial skin margin. To perform a lateral skin transposition, a surgeon makes separate curvilinear relaxing upper thigh skin incisions bilaterally. As shown in Figure 46-28.3, the relaxing incisions are each undermined to the dotted line, which represents to lateral boarder of this dissection. The resulting mobility of the intervening vulvar skin bridge should allow for a tension-free primary closure using interrupted vertical mattress sutures. Last, the relaxing incisions are closed with interrupted 0-gauge delayed-absorbable suture.

➎╇ Rhomboid Flaps.╇A rhomboid is a

four-sided parallelogram with unequal angles

at its corners. When creating a rhomboid flap from adjacent tissue, a marking pen is used to draw all sides the same length as the short axis of the defect (A-C; Fig. 46-28.4). This minimizes wound tension and prevents necrosis. The diagonal A-C is continued in a straight line onto the adjacent vulvar skin lateral to the defect, and marked so that the length of AC = CE. The remaining rhomboid sides are drawn in parallel. Incisions are made through the skin and into the subcutaneous fat. A flap is developed to include underlying fatty tissue and is mobilized medially to cover the surgical defect. In repositioning the flap, (as shown by the arrow), line CE swings medially to appose line AB and is secured with stay sutures at the corners CA and EB. Flap edges are reapproximated with vertical mattress stitches using 0-gauge delayed-absorbable suture (Fig. 46-28.5). Typically, excess tissue folding at the corners requires significant trimming or

Patients are kept relatively immobile for the first 5 to 7 postoperative days to prevent tension on the reconstruction. Foley catheter drainage is also continued during these initial postoperative days. A low-residue diet, diphenoxylate hydrochloride (Lomotil), or loperamide hydrochloride (Imodium) tablets will aid healing by delaying defecation and preventing straining (Table 25-6, p. 570). Thromboembolic prophylaxis is continued until the patient is ambulatory. During the first few days postoperatively, the wound is examined frequently to identify signs of hematoma or infection. For STSGs, the transparent dressing may be removed from the donor site after approximately 7 days, and an antibiotic ointment applied. For skin flaps, positioning changes or release of some sutures may be helpful if ischemia is noted at the margins. Suction drains are discontinued when output is less than 30 mL per 24 hours. Women experience significant sexual dysfunction after vulvectomy. However, the extent of the surgery and need for reconstruction is less important than preexisting depression and hypoactive sexual dysfunction. Accordingly, postoperative psychologic counseling and treatment of depression may be particularly helpful (Green, 2000; Weijmar Schultz, 1990).

D A CA

C

E B

EB

FIGURE 46-28.5╇ Rhomboid flap: closure. FIGURE 46-28.4╇ Rhomboid flap: flap positioning.

Surgeries for Gynecologic Malignancies

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Naik R, Jackson KS, Lopes A, et al: Laparoscopic assisted radical vaginal hysterectomy versus radical abdominal hysterectomy—a randomized phase II trial: perioperative outcomes and surgicopathological measurements. BJOG 117:746, 2010 Naik R, Maughan K, Nordin A, et al: A prospective, randomised, controlled trial of intermittent self-catheterisation vs supra-pubic catheterisation for post-operative bladder care following radical hysterectomy. Gynecol Oncol 99:437, 2005 Negishi H, Takeda M, Fujimoto T, et al: Lymphatic mapping and sentinel node identification as related to the primary sites of lymph node metastasis in early stage ovarian cancer. Gynecol Oncol 94:161, 2004 Nick AM, Lange J, Frumovitz M, et al: Rate of vaginal cuff separation following laparoscopic or robotic hysterectomy. Gynecol Oncol 120(1):47, 2011 Nunoo-Mensah JW, Chatterjee A, Khanwalkar D, et al: Loop ileostomy: modification of technique. Surgeon 2:287, 2004 Orr JW Jr, Orr PJ, Bolen DD, et al: Radical hysterectomy: does the type of incision matter? Am J Obstet Gynecol 173:399, 1995 Paley PJ, Johnson PR, Adcock LL, et al: The effect of sartorius transposition on wound morbidity following inguinal-femoral lymphadenectomy. Gynecol Oncol 64:237, 1997 Park JY, Kim DY, Kim JH, et al: Laparoscopic compared with open radical hysterectomy in obese women with early-stage cervical cancer. Obstet Gynecol 119(6):1201, 2012 Park JY, Seo SS, Kang S, et al: The benefits of low anterior en bloc resection as part of cytoreductive surgery for advanced primary and recurrent epithelial ovarian cancer patients outweigh morbidity concerns. Gynecol Oncol 103(3):977, 2006 Patsner B, Hackett TE: Use of the omental J-flap for prevention of postoperative complications following radical abdominal hysterectomy: report of 140 cases and literature review. Gynecol Oncol 65:405, 1997 Pellegrino A, Fruscio R, Maneo A, et al: Harmonic scalpel versus conventional electrosurgery in the treatment of vulvar cancer. Int J Gynaecol Obstet 103:185, 2008 Penalver MA, Angioli R, Mirhashemi R, et al: Management of early and late complications of ileocolonic continent urinary reservoir (Miami pouch). Gynecol Oncol 69:185, 1998 Penalver MA, Bejany DE, Averette HE, et al: Continent urinary diversion in gynecologic oncology. Gynecol Oncol 34:274, 1989 Pikaart DP, Holloway RW, Ahmad S, et al: Clinical-pathologic and morbidity analyses of Types 2 and 3 abdominal radical hysterectomy for cervical cancer. Gynecol Oncol 107:205, 2007 Plante M, Roy M: Operative laparoscopy prior to a pelvic exenteration in patients with recurrent cervical cancer. Gynecol Oncol 69:94, 1998 Prayson RA, Hart WR, Petras RE: Pseudomyxoma peritonei: a clinicopathologic study of 19 cases with emphasis on site of origin and nature of associated ovarian tumors. Am J Surg Pathol 18:591, 1994 Puntambekar S, Kudchadkar RJ, Gurjar AM, et al: Laparoscopic pelvic exenteration for advanced pelvic cancers: a review of 16 cases. Gynecol Oncol 102(3):513, 2006 Pycha A, Comploj E, Martini T, et al: Comparison of complications in three incontinent urinary diversions. Eur Urol 54:825, 2008

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Kim DK, Bridges CB, Harriman HK, et al: Advisory Committee on Immunization Practices recommended immunization schedule for adults aged 19 years or older: United States, 2015. Ann Intern Med 162:214, 2015 King LA, Carson LF, Konstantinides N, et al: Outcome assessment of home parenteral nutrition in patients with gynecologic malignancies: what have we learned in a decade of experience? Gynecol Oncol 51:377, 1993 Kingham TP, Pachter HL: Colonic anastomotic leak: risk factors, diagnosis, and treatment. J Am Coll Surg 208:269, 2009 Koh WJ, Greer BE, Abu-Rustum NR, et al: Cervical cancer, version 2.2015. J Natl Compr Canc Netw 13(4):395, 2015 Koh WJ, Greer BE, Abu-Rustum NR, et al: Uterine neoplasms, version 1.2014. J Natl Compr Canc Netw 12(2):248, 2014 Kohler C, Tozzi R, Possover M, et al: Explorative laparoscopy prior to exenterative surgery. Gynecol Oncol 86:311, 2002 Kraus K, Fanning J: Prospective trial of early feeding and bowel stimulation after radical hysterectomy. Am J Obstet Gynecol 182:996, 2000 Kusiak JF, Rosenblum NG: Neovaginal reconstruction after exenteration using an omental flap and split-thickness skin graft. Plast Reconstr Surg 97:775, 1996 Lacey CG, Stern JL, Feigenbaum S, et al: Vaginal reconstruction after exenteration with use of gracilis myocutaneous flaps: the University of California, San Francisco, experience. Am J Obstet Gynecol 158:1278, 1988 Landoni F, Maneo A, Cormio G, et al: Class II versus class III radical hysterectomy in stage IBIIA cervical cancer: a prospective, randomized study. Gynecol Oncol 80:3, 2001 Landrum LM, Lanneau GS, Skaggs VJ, et al: Gynecologic Oncology Group risk groups for vulvar carcinoma: improvement in survival in the modern era. Gynecol Oncol 106:521, 2007 Larciprete G, Casalino B, Segatore MF, et al: Pelvic lymphadenectomy for cervical cancer: extraperitoneal versus laparoscopic approach. Eur J Obstet Gynaecol Reprod Biol 126:259, 2006 Law WL, Chu KW, Choi HK: Randomized clinical trial comparing loop ileostomy and loop transverse colostomy for faecal diversion following total mesorectal excision. Br J Surg 89:704, 2002 Leath CA III, Straughn JM Jr, Estes JM, et al: The impact of aborted radical hysterectomy in patients with cervical carcinoma. Gynecol Oncol 95:204, 2004 Lee CL, Wu KY, Huang KG, et al: Long-term survival outcomes of laparoscopically assisted radical hysterectomy in treating early-stage cervical cancer. Am J Obstet Gynecol 203(2):165.e1, 2010 Lee PK, Choi MS, Ahn ST, et al: Gluteal fold V-Y advancement flap for vulvar and vaginal reconstruction: a new flap. Plast Reconstr Surg 118:401, 2006 Leon-Casasola OA, Karabella D, Lema MJ: Bowel function recovery after radical hysterectomies: thoracic epidural bupivacaine-morphine versus intravenous patient-controlled analgesia with morphine: a pilot study. J Clin Anesth 8:87, 1996 Likic IS, Kadija S, Ladjevic NG, et al: Analysis of urologic complications after radical hysterectomy. Am J Obstet Gynecol 199:644.e1, 2008 Lin HH, Sheu BC, Lo MC, et al: Abnormal urodynamic findings after radical hysterectomy or pelvic irradiation for cervical cancer. Int J Gynaecol Obstet 63:169, 1998 Lin LY, Wu JH, Yang CW, et al: Impact of radical hysterectomy for cervical cancer on urody-

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Ramirez PT, Modesitt SC, Morris M, et al: Functional outcomes and complications of continent urinary diversions in patients with gynecologic malignancies. Gynecol Oncol 85:285, 2002 Rasmussen OO, Petersen IK, Christiansen J: Anorectal function following low anterior resection. Colorectal Dis 5:258, 2003 Raspagliesi F, Ditto A, Fontanelli R, et al: Type II versus type III nerve-sparing radical hysterectomy: comparison of lower urinary tract dysfunctions. Gynecol Oncol 102(2):256, 2006 Ratliff CR, Gershenson DM, Morris M, et al: Sexual adjustment of patients undergoing gracilis myocutaneous flap vaginal reconstruction in conjunction with pelvic exenteration. Cancer 78:2229, 1996 Rettenmaier MA, Braly PS, Roberts WS, et al: Treatment of cutaneous vulvar lesions with skinning vulvectomy. J Reprod Med 30:478, 1985 Rezk YA, Hurley KE, Carter J, et al: A prospective study of quality of life in patients undergoing pelvic exenteration: interim results. Gynecol Oncol 128(2):191, 2013 Richardson DL, Mariani A, Cliby WA: Risk factors for anastomotic leak after recto-sigmoid resection for ovarian cancer. Gynecol Oncol 103(2):667, 2006 Rose PG: Skin bridge recurrences in vulvar cancer: frequency and management. Int J Gynaecol Cancer 9:508, 1999 Rose PG: Type II radical hysterectomy: evaluating its role in cervical cancer. Gynecol Oncol 80:1, 2001 Saito A, Sawaizumi M, Matsumoto S, et al: Stepladder V-Y advancement medial thigh flap for the reconstruction of vulvoperineal region. J Plast Reconstr Aesthet Surg 62:e196, 2009 Salani R, Zahurak ML, Santillan A, et al: Survival impact of multiple bowel resections in patients undergoing primary cytoreductive surgery for advanced ovarian cancer: a case-control study. Gynecol Oncol 107:495, 2007 Salom EM, Mendez LE, Schey D, et al: Continent ileocolonic urinary reservoir (Miami pouch): the University of Miami experience over 15 years. Am J Obstet Gynecol 190:994, 2004 Salom EM, Schey D, Penalver M, et al: The safety of incidental appendectomy at the time of abdominal hysterectomy. Am J Obstet Gynecol 189:1563, 2003 Scambia G, Ferrandina G, Distefano M, et al: Is there a place for a less extensive radical surgery in locally advanced cervical cancer patients? Gynecol Oncol 83:319, 2001 Scheistroen M, Nesland JM, Trope C: Have patients with early squamous carcinoma of the vulva been overtreated in the past? The Norwegian experience 1977–1991. Eur J Gynaecol Oncol 23:93, 2002 Segreti EM, Levenback C, Morris M, et al: A comparison of end and loop colostomy for fecal diversion in gynecologic patients with colonic fistulas. Gynecol Oncol 60:49, 1996a Segreti EM, Morris M, Levenback C, et al: Transverse colon urinary diversion in gynecologic oncology. Gynecol Oncol 63:66, 1996b Serati M, Salvatore S, Uccella S, et al: Sexual function after radical hysterectomy for early-stage cervical cancer: is there a difference between laparoscopy and laparotomy? J Sex Med 6: 2516, 2009

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INDEX Note: Page numbers followed by f indicates figure and t for tables respectively. A ABCD system, for skin lesions, 10 Abdomen pain in. See Abdominal pain palpation of, 252 PID and peritonitis of, 67 radiography of, 37 rebound tenderness in, 252 Abdominal access/entry in abdominal hysterectomy, 952 in abdominal myomectomy, 945 in appendectomy, 1205 in Cherney incision, 931 in colostomy, 1191 in cornuostomy and cornual wedge resection, 941 in diaphragmatic surgery, 1189 in en bloc pelvic resection, 1181 in ileostomy, 1196 in intestinal bypass, 1203 in laparoscopic ovarian cystectomy, 1015 in laparoscopic salpingectomy, 1011 in laparoscopic salpingo-oophorectomy, 1019 in laparoscopic sterilization, 1006 in large bowel resection, 1194 in low anterior resection, 1199 in Maylard incision, 932 in midline vertical incision, 926, 927, 928 in modified radical abdominal hysterectomy (type II), 1140 in omentectomy, 1185 in ovarian cystectomy, 933 in ovarian drilling, 1021 in paraaortic lymphadenectomy, 1171 in pelvic lymphadenectomy, 1168 in Pfannenstiel incision, 929 in radical abdominal hysterectomy (type III), 1135 in salpingectomy and salpingostomy, 939 in salpingo-oophorectomy, 935 in small bowel resection, 1197 in splenectomy, 1187 in total pelvic exenteration, 1149 Abdominal culdoplasty procedures, 1118–1119, 1118f–1119f Abdominal hysterectomy, 950–956, 952f–956f. See also Hysterectomy abdominal incision infection following, 80 disadvantages of, 950 femoral nerve injury and, 844 intraoperative, 951–956

lower urinary tract injury during, 867 modified radical (type II), 1140–1141, 1140f–1141f obesity risk and, 75t for ovarian cancer, 751 and pelvic cellulitis, 78 pelvic infection following, 80, 80f postoperative, 956 postoperative infection, 76 preoperative, 950–951 consent, 951 decision-making for approach selection, 950–951 patient evaluation, 950 patient preparation, 951 radical (type III), 669t, 1134–1139, 1136f–1138f vesicocervical and vesicovaginal spaces during, 811 Abdominal incision infection, 80 Abdominal myomectomy, 945–947, 946f–947f for leiomyoma, 211–212 Abdominal pain acute, 251 conditions for, 164t etiologies of, 251t marked, 67 pelvic cellulitis and, 78 pelvic inflammatory disease and, 67 Abdominal paravaginal defect repair, 554–556, 1091–1092, 1091f–1092f anterior vaginal wall, 555 hysterectomy, 556 intraoperative, 1091–1092 surgical steps, 1091 perineal body, 556 posterior vaginal wall, 556 postoperative, 1092 preoperative, 1091 consent, 1091 patient evaluation, 1091 patient preparation, 1091 surgical plan, 555 for vaginal apex, 555–556 Abdominal peritonitis, 67 Abdominal sacrocolpopexy (ASC), 1098–1102, 1100f–1102f intraoperative, 1098–1102 instruments and materials, 1098 surgical steps, 1099–1102 postoperative, 1102 preoperative, 1098 for vaginal apex, 555 Abdominal wall

abdominal wall mass, 252, 265 anterior, 235 anatomy of, 796–798, 798f bimanual examination, 6f blood supply to, 798–799 endometriosis in, 235 innervation, 799 parietal peritoneum, 797–798 rectus sheath, 796–798, 797f skin, 796, 796f subcutaneous layer, 796, 796f supine and, 258 transversalis fascia, 796–797, 797f endometrial glands and stroma, 238f endometrioma, 235 hernia, 267–268, 267f Abnormal uterine bleeding (AUB), 180–201 definitions, 180 diagnosis, 181t, 182–188 algorithm to identify endometrial pathology, 183f b-hCG and hematologic testing, 184 cervical cytology/biopsy, 184 endometrial biopsy, 184–185, 185f history and physical examination, 182 hysteroscopy, 187 laboratory evaluation, 184–185 saline infusion sonography, 186–187 sonography, 185–187, 185f, 186f transvaginal sonography, 185–186, 187f “Wet Prep” examination and cervical cultures, 184 endometritis, 191–192 etiology classification, 188 external sources, 190–191 anticoagulants, 191 hormonal therapy, 191 intrauterine devices, 190–191 incidence, 180–181 irregular menstrual-type bleeding, 127 medical treatment of, 194t ovulatory disorders, 194–195 acute hemorrhage management, 194–195 chronic management, 194 pathophysiology, 181–182, 182f pictorial blood assessment chart, 181f primary endometrial dysfunction, 195–198 combination oral contraceptive pills, 196 iron therapy, 197 levonorgestrel-releasing intrauterine system, 195–196 medical treatment of, 195t nonsteroidal antiinflammatory drugs, 196–197

1225

1226

Index Abnormal uterine bleeding (Continuedâ•›) other hormonal agents, 197 tranexamic acid, 196, 196f uterine procedures, 197–198 structural abnormalities, 188–190 arteriovenous malformation, 190, 190f endocervical polyp, 189–190, 189f endometrial polyp, 188–189, 188f, 189f uterine enlargement, 188 surgical management, 197–198 abdominal myomectomy, 945–947, 946f–947f diagnostic hysteroscopy, 1037, 1037f endometrial ablation, 1043–1045, 1043f–1045f hysteroscopic myomectomy, 1040–1042 hysteroscopic polypectomy, 1038–1039, 1038f laparoscopic myomectomy, 1022–1025 sharp dilatation and curettage, 964–965, 964f–965f systemic causes of, 192–194 coagulopathy, 192–194 hyperthyroidism/hypothyroidism, 192 liver dysfunction, 192 renal dysfunction, 192 von Willebrand factor, 193–194 Abortifacient(s), 139 Abortion, 137–160 administration for, 154–155 aneuploid, 138, 138t consequences of, 155 early abortuses, chromosomal findings in, 138t hysteroscopic septoplasty and, 1048 induced, 150–152 classification, 151 counseling before elective abortion, 152 rates, 150 in the United States, 151–152 medical, 154–155 contraindications, 155 of early pregnancy, 154t postabortal contraception, 155 recurrent miscarriage, 144–150 alloimmune factors, 149 anatomic factors, 147–148 autoimmune factors, 148–149, 148t endocrinologic factors, 149–150 etiology, 145 evaluation and treatment, 150, 151t immunologic factors, 148–149 parental chromosomal abnormalities, 145–148 thrombophilias, 150 spontaneous, 137–144 clinical classification, 140–143 euploid abortion, 138–139 fetal factors, 138 incidence, 137–138 management, 143–144, 144t maternal factors, 139–140

suction D & C for, 966–968, 966f–968f surgical, 153–154 cervical preparation, 153 electric vacuum aspiration, 153 manual vacuum aspiration, 153–154 menstrual aspiration, 153 sharp D&C, 964–965, 964f–965f suction D&C, 966–968, 966f–968f techniques, 152–155, 152t training in, 152 terminology, 137 WHO definition of, 137 Abortion rate, 150, 421, 422 Abortion ratio, 150 Abscess bartholin gland duct, 82, 83f cystectomy, 975, 975f incision and drainage, 971–972, 971f–972f marsupialization, 973–974, 973f nonpuerperal breast, 282 ovarian, 78–79 pelvic, 79–80, 79f tuboovarian, 67–68, 68f vulvar, 82 incision and drainage of, 977–978, 977f–978f Absent breast development, 326 Absolute neutrophil count (ANC), 605 Acanthosis nigricans, 94, 391, 391f treatment for, 400 Accelerated radiotherapy with carbogen and nicotinamide (ARCON), 618 Accessory ovary, 423 Accommodation, rectal, 563 Accutane. See Isotretinoin Acessa system for myolysis, 885, 885f Acetabulum, 799, 800f Acetaminophen, 123t for chronic pelvic pain, 258 for genital ulcer infections, 56 Acetazolamide, and urinary incontinence, 525t Acetic acid in colposcopy, 638, 639f in vulvoscopy, 648 Acetowhite, 638, 639f, 641, 648 Acinetobacter species, 911 Acne vulgaris, 391 treatment of, 399–400 Acquired hypothalamic abnormalities, 376 Acquired uterine abnormalities, 147 Acrocordons (skin tags), vulvar, 96, 96f ACTH. See Adrenocorticotropic hormone (ACTH) Actinomyces infection, 83 Actinomyces israelii, 53, 83 Activated protein C resistance, 837 Acute bacterial cystitis, 73–75 diagnosis of, 73–74 treatment of, 74–75 Acute pyelonephritis, 75 Acute respiratory distress syndrome, 913

Acyclovir, 57t Adductor longus muscle, 823 Adenocarcinoma in situ (AIS), 624, 695f cervical conization for, 992–994, 992f–993f of cervix, 642 endocervical, 636t excision procedure for, 644 Pap testing for, 675 Adenocarcinomas, cervical, 661–662 clear cell, 662 diagnosis, 632–641, 662–663 invasive, 661f mesonephric, 662 minimal deviation, 661–662 mucinous, 661 prognosis of, 662 serous, 662 staging of, 667 surgical treatment, 672 Adenomatous polyps, test for, 10t Adenomyosis, 43–44, 44f, 213–214, 213f diagnosis, 213–214 diffuse, 213 focal, 213 management, 214 pathophysiology, 213 Adenosis, vaginal, 101, 423, 625 Adnexa, 669f adnexectomy in abdominal hysterectomy, 953, 953f in vaginal hysterectomy, 959–961, 960f anatomy of, 807f assessment of, 6, 6 bilateral, 744f detorsion of, 223 infection of, 78 laparoscopic salpingo-oophorectomy for, 1019–1020, 1020f in radical abdominal hysterectomy, 1136 in salpingectomy, 939 in salpingo-oophorectomy, 935, 936, 936f of tortuous and dilated pelvic vessels in, 261f in total laparoscopic hysterectomy, 1034 uterine, 809 Adnexal infection, 78, 78f Adnexal torsion, 222–223, 222f diagnosis, 222–223 management, 223 sonography, 252 vomiting associated with, 251 Adolescent sexuality, 330 Adrenal insufficiency, 832 Adrenarche, 329 a-Adrenergic agonists, and urinary incontinence, 525t a-Adrenergic blockers, and urinary incontinence, 525t Adrenocorticotropic hormone (ACTH), 342–343

Index Advanced-stage cervical cancer, treatment of, 672–673 chemoradiation, 672–673 pelvic exenteration, 673 radiation therapy, 672 stage IVB, 673 stages IIB through IVA, 672–673 AGC. See Atypical glandular cells (AGC) AIN. See Anal intraepithelial neoplasia (AIN) Alcock canal, 821 Alcohol abuse rates during gestation, 140 consumption and fertility, 429 dietary intake recommendations, 14t and risk of breast cancer, 287t substance use disorders, 301 and urinary incontinence, 525t Alendronate, for osteoporosis, 500t, 502 Alkylating agents, chemotherapeutic, 598–599, 598t cyclophosphamide, 598 ifosfamide (Ifex), 598–599, 599f Allergic and contact dermatitis, 323 Allergic reaction, 866 Alopecia, 391 Alprazolam, 304t Ambien CR, 18t Ambiguous genitalia, 409 Amenorrhea, 369–385 anatomic disorders, 370–373, 372f acquired disorders, 372–373 inherited disorders, 370–372 classification system, 370 diagnostic algorithm, 380f etiology of, 370t eugonadotropic, 378–379 nonclassic congenital adrenal hyperplasia, 379 ovarian tumor, 379 polycystic ovarian syndrome, 379 evaluation, 379–383 history, 379–380 physical examination, 381 testing, 381–383, 382t exercise-induced, 376 functional hypothalamic, pathophysiology of, 376–377 hypergonadotropic hypogonadism, 373–375 acquired abnormalities, 375 heritable disorders, 373–375 hypogonadotropic hypogonadism, 375–378 anterior pituitary gland disorders, 378 hypothalamic disorders, 375–377 model for development of, 377f normal menstrual cycle, 369–370 stress-induced, 376 treatment, 383–384 estrogen replacement, 383 infertility, 383–384 patient education, 384 polycystic ovarian syndrome, 383

American Association of Clinical Endocrinologists (AACE), 499 American College of Obstetricians and Gynecologists, 131, 305 American Psychiatric Association, 305 American Society for Colposcopy and Cervical Pathology (ASCCP), 634, 639 Aminoglycosides, 53–54 Aminoglycosides for acute pyelonephritis, 75 for gynecologic infection, 53–54 for hospital-acquired pneumonia, 911 for intrarenal oliguria, 911 Aminophylline, 123t Amitriptyline and chronic pelvic pain, 259, 259t for depression and anxiety, 304t and urinary incontinence, 525t, 570, 570t in vulvodynia, 100 Anal cytology, 650 Analgesics, 123t Anal incontinence, 269, 561–572 anal sphincteroplasty, 1125–1127, 1126f–1127f diagnosis, 564–569 anorectal manometry, 567–568 colonoscopy and barium enema, 569 electromyography, 569 endoanal ultrasonography, 568, 568f evacuation proctography, 568 magnetic resonance imaging, 568–569 medical history, 564–566 physical examination, 566–567 PNTML test, 569 epidemiology, 561 incontinence risks, 563–564 physiology, 561–563 anorectal sensation, 562–563 muscular contributions, 561–562, 562f, 563f rectal accommodation and compliance, 563 rectovaginal fistula, 573–575 classification, 573–574 definition of, 573–574 in distal wall of posterior vagina, 574f risk factors, 573t surgical repair of, 1128–1130, 1128f–1129f in woman underwent midline episiotomy, 574f sacral neuromodulation, 1085–1087 treatment, 569–572 minimally invasive procedures, 571–572 nonsurgical, 569–570 surgical, 570–571 Anal intraepithelial neoplasia (AIN), 650–651 anal cytology, 650 diagnosis, 650 high-resolution anoscopy, 650 histology, 650f management, 650–651

pathophysiology, 650 translucent acetowhite lesion of, 651f Anal sphincter complex, 815f Anal sphincteroplasty, 569, 571, 1125–1127, 1126f–1127f for anal incontinence, 571 intraoperative, 1125–1127 postoperative, 1127 preoperative, 1125 Anal triangle, 821 Anal wink reflex, 524, 548, 566 Anatomic abnormalities, associated with amenorrhea, 370–373, 372f acquired disorders, 372–373 cervical stenosis, 372, 901, 988, 992 intrauterine adhesions, 372–373, 372f, 428, 438, 462, 1052–1053, 1052f inherited disorders, 370–372 lower outflow tract obstruction, 370–371, 417, 417f müllerian defects, 371–372, 372t, 417–423, 418t, 419f, 983, 985 Anatomic stress incontinence, 522 ANC. See Absolute neutrophil count (ANC) Androgen excess, 413 Androgen insensitivity syndrome (AIS), 362, 370t, 380f, 413 complete, 413 Androgen production, abnormal, 412–413 Androgen receptors, 339 Anejaculation, 462 Anesthesia, 842 during abdominal hysterectomy, 951 during abdominal myomectomy, 945 during abdominal sacrocolpopexy, 1099 during abdominal uterosacral ligament suspension, 1110 during anal sphincteroplasty, 1125 during anterior colporrhaphy, 1088 during appendectomy, 1205 during bartholduring gland duct marsupialization, 973 during Burch colposuspension, 1061 during carbon dioxide laser cervical ablation, 991 during carbon dioxide laser vaporization of VIN, 997 during cervical intraepithelial neoplasia, 644, 644t during cold-knife conization, 992 during colostomy, 1191 during colpocleisis, 1121 during cornuostomy and cornual wedge resection, 941 during CUSA, 996 during diagnostic and operative cystoscopy and urethroscopy, 1058 during diagnostic hysteroscopy, 1037 during diagnostic laparoscopy, 1004 during diaphragmatic surgery, 1189 during en bloc pelvic resection, 1181 during endometrial ablation procedures, 1043

1227

1228

Index Anesthesia (Continuedâ•›) during Halban/Moschcowitz procedure, 1118 during hymenectomy, 969 during hysteroscopic myomectomy, 1040 during hysteroscopic polypectomy, 1038 during hysteroscopic septoplasty, 1048 during ileostomy, 1196 during inguinofemoral lymphadenectomy, 1215 during interval partial salpingectomy, 937 during intestinal bypass, 1203 intrauterine instillation, 843 during labia minora reduction, 981 laceration under, 101 during laparoscopic hysterectomy, 1026 during laparoscopic myomectomy, 1022–1023 during laparoscopic ovarian cystectomy, 1015 during laparoscopic salpingectomy, 1011 during laparoscopic salpingooophorectomy, 1019 during laparoscopic salpingostomy, 1013 during laparoscopic sterilization, 1006 during large bowel resection, 1194 during LEEP, 989 local, characteristics of, 842t during low anterior resection, 1199 during lysis of intrauterine adhesions, 1052 during martius bulbocavernosus fat pad flap, 1083 during McCall culdoplasty, 1116 during McIndoe procedure, 985 during midline vertical incision, 927 during midurethral sling release, 1074 during minimally invasive radical hysterectomy, 1142 during minimally invasive sacrocolpopexy, 1103 during minimally invasive surgery for gynecologic malignancies, 1175 during modified radical abdominal hysterectomy, 1140 during omentectomy, 1185 during ovarian cystectomy, 933 during ovarian drilling, 1021 during paraaortic lymphadenectomy, 1171 paracervical block, 841–843, 842f during paravaginal defect repair, 1091 during pelvic lymphadenectomy, 1168 during perineorrhaphy, 1096 during Pfannenstiel incision, 929 during posterior colporrhaphy, 1093 postoperative pain and, 843 during proximal fallopian tube cannulation, 1050 during pubovaginal sling, 1068 during radical abdominal hysterectomy, 1135 during radical complete vulvectomy, 1212 during radical partial vulvectomy, 1209

during reconstructive grafts and flaps, 1218 during rectovaginal fistula repair, 1128 during sacral neuromodulation, 1085 during sacrospinous ligament fixation, 1113 during salpingectomy and salpingostomy, 939 during salpingo-oophorectomy, 935 selection, 876–878 during sharp dilatation and curettage, 964 during skinning vulvectomy, 1207 during small bowel resection, 1197 during splenectomy, 1187 during suction dilatation and curettage, 966 during tension-free vaginal tape procedure, 1063 during total laparoscopic hysterectomy, 1033 during total pelvic exenteration, 1148 during trachelectomy, 962 during transcervical sterilization, 1046 during transobturator tape sling, 1066 transversus abdominis plane block, 843 during urethral bulking injections, 1070 during urethral diverticulum repair, 1075 during urethrolysis, 1072, 1073 during vaginal hysterectomy, 957 during vaginal myomectomy for prolapsed leiomyoma, 948 during vaginal reconstruction, 1164 during vaginal septum excision, 983 during vaginal uterosacral ligament suspension, 1107 during vesicovaginal fistula repair, 1078, 1079 during vestibulectomy, 979 during vulvar abscess incision and drainage, 977 during vulvoscopy, 649 during wide local excision, 995 Aneuploid abortion, 138, 138t Angelica sinensis, 498 Angiogenesis, 577 Angiotensin-converting enzyme inhibitors, and urinary incontinence, 525t Angular pregnancy, 173–174 Anococcygeal raphe, 803 Anocutaneous reflex, 257, 524, 528 Anorexia nervosa, 139 diagnosis of, 301t, 302 Anovulation abnormal uterine bleeding from, 181t, 192, 194 associated with PCOS, 379, 388–389 causes of, 194, 376, 378, 387, 393, 394t stress, 450 chronic, 370, 376, 379 consequences of, 379, 392, 471 erratic bleeding during MT, 474 evaluation for, 433–435 basal body temperature chart, 434, 434f clinical evaluation, 434

endometrial biopsy, 435 ovulation predictor kits, 435 serum progesterone, 435 sonography, 435 treatment of, 398 obesity and, 449 Antalgic gait, 256 Anterior abdominal wall, 235 anatomy of, 796–798, 798f bimanual examination, 6f blood supply to, 798–799 endometriosis in, 235 innervation, 799 parietal peritoneum, 797–798 rectus sheath, 796–798, 797f skin, 796, 796f subcutaneous layer, 796, 796f supine and, 258 transversalis fascia, 796–797, 797f Anterior abdominal wall nerve entrapment syndromes, 269–270, 270f Anterior colporrhaphy, 1088–1090, 1088f–1090f for anterior vaginal wall prolapse, 555 intraoperative, 1088–1090 surgical steps, 1088–1090 mesh or biomaterial with, 555 postoperative, 1090 preoperative, 1088 consent, 1088 patient evaluation, 1088 patient preparation, 1088 for vesicovaginal fistulas, 582 Anterior fornix, 810, 811f Anterior pelvic exenteration, 1154, 1154f for primary disease, 673 for secondary disease, 673–674 for vulvar recurrences, 688, 698 Anterior pituitary gland disorders, 378 Anterior pituitary hormones, 343–344 Antiangiogenesis agents, 604–605 bevacizumab, 604, 604f cediranib (Recentin), 604–605 mechanisms of action, 604f sunitinib, 604, 604f VEGF Trap, 604, 604f Antibiotic prophylaxis, 834 Antibiotics, for gynecologic infection, 52–55 aminoglycosides, 53–54 carbapenems, 54 cephalosporins, 53 clindamycin, 54 fluoroquinolones, 54–55 metronidazole, 54 monobactam, 54 penicillins, 52–53 tetracyclines, 55 vancomycin, 54 Anticholinergic agents, for urinary incontinence, 525t, 533–534, 533t Anticoagulant management, 830–832, 831t postoperative management, 832 preoperative management, 830–832, 831t

Index Anticoagulants, 123t Antidepressants, 123t, 281t Antihistamines, and urinary incontinence, 525t Antihypertensives, 123t Antiinflammatories, 123t Antimetabolites, 596–598, 597t 5-fluorouracil, 598 gemcitabine (Gemzar), 597–598 methotrexate, 596–597, 597f Antiphospholipid antibody idiotypes, 149 Antiphospholipid antibody syndrome (APS), 148 diagnostic criteria, 148t treatment of, 149 Antipsychotics, and urinary incontinence, 525t Antiretrovirals, 123t Antithrombin deficiency, 836 Antitumor antibiotics, 599–600, 599t bleomycin, 599–600 dactinomycin, 599 doxorubicin, 600 doxorubicin hydrochloride liposome, 600 Anxiety disorders, 298, 300t Aphthous ulcers, 94 Apixaban (Eliquis), 831t, 832 Appendectomy, 1205–1206, 1205f intraoperative, 1205–1206 postoperative, 1206 preoperative, 1205 Appendectomy appendicitis, 253 APS. See Antiphospholipid antibody syndrome (APS) ARCON. See Accelerated radiotherapy with carbogen and nicotinamide (ARCON) Arcuate line, 796, 797f Arcuate uterus, 35f, 423 Arcus tendineus fascia pelvis, 543, 802 in abdominal paravaginal defect repair, 1091–1092 in anterior colporrhaphy, 1090 in Burch procedure, 1062 Arcus tendineus levator ani, 802 Aripiprazole, 304t Aromatase inhibitors for breast cancer, 286, 291 effects of, 455f endometrial stromal tumors, 732 for endometriosis, 241 for leiomyomas, 203, 209 for ovulation induction, 453 Arrhythmias bipolar electrosurgery, 827 degree of heart failure and associated, 828 implantable cardioverter-defibrillators for, 827 pacemaker for, 827 Arrhythmias, 827 Arteriovenous malformation (AVM), 190, 190f Artery common iliac, 810f, 816, 817f external iliac, 798–799 femoral, 798

hypogastric, 808 inferior epigastric, 797–798, 797–799f, 888–889, 889f, 932, 932f internal iliac, 805t middle sacral, 817 obturator, 800f, 804, 805f, 805t, 818 ovarian, 806, 809 pelvic, 804–806, 805, 805f inferior gluteal arteries, 804 internal iliac, 804, 805t middle rectal arteries, 804 superior rectal artery, 804 superior vesical arteries, 804 pudendal, 822, 822f Sampson, 808 superficial epigastric, 798–799, 797–799f, 888-889, 889f superior vesical, 804, 805t, 805f, 813, 816, 818 uterine, 809, 810f vaginal, 805f, 805t, 809, 812–813 ASC. See Abdominal sacrocolpopexy (ASC) ASCCP. See American Society for Colposcopy and Cervical Pathology (ASCCP) ASC-US. See Atypical squamous cells of undetermined significance (ASC-US) Asherman syndrome, 147, 438, 460, 1052 hematometra, 212 hysterosalpingogram findings, 439f intrauterine adhesions with, 372–373, 372f, 437–438, 460 transvaginal saline infusion sonography, 34f Asherman syndrome, 460 Aspermia, 462 Aspirin, 123t Assisted reproductive technology (ART), 463–468 cervical pregnancy, 174 complications of, 466–468, 466–468 correction of male infertility, 461 ectopic pregnancy, 161–162, 163, 165 egg donation, 465 embryo, oocyte, or ovarian tissue cryopreservation, 466 gamete or zygote intrafallopian transfer, 465 gestational carrier surrogacy, 465 heterotopic pregnancy, 175 intracytoplasmic sperm injection, 465 ovarian hyperstimulation syndrome with, 456 preimplantation genetic diagnosis/ screening, 466 proximal tubal obstruction with, 458 smoking effects and, 429 for teratozoospermia, 463 in vitro fertilization, 464, 464f, 467t, 468t in vitro maturation, 466 Asthenospermia, 443, 463 Asthma, 826 counseling in, 18t Asymptomatic bacteriuria, 75 Atelectasis, 911 Atopic eczema, 91

Atypical ductal hyperplasia (ADH), 283 Atypical endometrial hyperplasia, 706–707 Atypical femur fractures (AFF), 502 Atypical glandular cells (AGC), 636 Atypical squamous cells of undetermined significance (ASC-US), 636 Autocrine communication, 334 Automatic stapling devices, 848 Autosomal trisomy, 138 Aviane, 120t AZF. See Azoospermia factor region (AZF) Azithromycin for chlamydial infection, 65t for granuloma inguinale, 59t for uncomplicated gonococcal infection, 65t Azoospermia, 462 Azoospermia factor region (AZF), 444 Aztreonam, 835t B Bacterial vaginosis, 51–52, 51f, 51t, 52t, 139 Bacteroides fragilis, 66 Baden-Walker halfway system, 542, 542t Barium enema (DCBE), 10t Bartholin gland carcinoma, 691 Bartholin gland duct abscess, 82, 83f, 97 cyst, 97, 97f cystectomy, 975–976, 975f incision and drainage, 971–972, 971f–972f marsupialization, 973–974, 973f Bartholin glands, 819f, 820 Basal cell carcinoma (BCC), of vulva, 690–691 Basivertebral veins, 817 Bazedoxifene for menopausal vasomotor symptoms, 497 for osteoporosis in mature woman, 501 Beaver blade, 992f Behçet disease, 95 Benign proliferative disease, 283 Benzamides, 281t Benzathine penicillin G, for syphilis, 58t Benzodiazepine-receptor agonists, 18t Benzodiazepines, 18t Benztropine mesylate, and urinary incontinence, 525t Bettochi hysteroscope, 902, 902 Bevacizumab, 604, 604f Beyaz, 120t Bicornuate uterus, 35f, 421–422, 422f Bidirectional suture, 898 Bioidentical hormones, for menopausal vasomotor symptoms, 497 Biological and targeted therapy, 603–605 antiangiogenesis agents, 604–605 bevacizumab, 604, 604f cediranib (Recentin), 604–605 mechanisms of action, 604f sunitinib, 604, 604f VEGF Trap, 604, 604f mammalian target of rapamycin inhibitors, 605 poly(ADP) ribose polymerase inhibitors, 605

1229

1230

Index Biopsy needles/markers, 41t Biphasic pills, 121 Bipolar disorders, 297, 877, 878 Bipolar electrosurgery, 859 BI-RADS. See Breast Imaging Reporting and Data System (BI-RADS) Bisphosphonates, for osteoporosis, 501–503 Black cohosh, 498–499 Bladder anatomy, 516, 517f, 518f anatomy of, 516, 517f, 813, 813f continence, 516 defects of, 414 dome, 518f evaluation of, 526–528, 528f, 1057–1060 overactive, 514, 514 pillars, 954 tissue response to, radiation therapy and, 620 Bladder emptying, 521–522, 521f Bladder exstrophy, 414 Bladder filling, 516–519, 517f–520f Bladder injury, 867 Bladder neck, 814 Bleomycin, 599–600 Blighted ovum, 137 Blood supply. See Arteries anterior abdominal wall, 798–799 external iliac branches, 798–799 femoral branches, 798 to ovary, 809 pelvic, 805–806, 805t to pelvis, 804–806, 805–806, 805f, 805t to uterus, 809 to vagina, 812 to vulva, 812–813 Blood vessels, 822 BMD. See Bone mineral density (BMD) Body mass index (BMI) abnormal weight, definitions of, 12t bariatric surgery in, 13 calculations of, 12 Bone mineral density (BMD), 240–241, 499–505 bazedoxifene for, 497 bone strength and, 478 densitometry, 39, 605 diagnosis, 479 prevention of, 479–483 treatment of, 499–505 hormonal therapy, 501 indications for, 499–501 nonhormonal antiresorptive agents for, 501–503, 502f nonpharmacologic therapy, 504–505 parathyroid hormone for, 503–504 Bone remodeling, 477f Bones, pelvic, 799–800 anatomy of, 800f coccyx, 799 innominate, 799 sacrum, 799

Botulinum toxin A, for urinary incontinence, 535 Bowel injury, 869–870 Bowel obstruction abdominal examination for, 252 imaging for, 253 infertility and, 428 large bowel resection, 1194–1195, 1194f–1195f palliative care for, 674, 754 small bowel resection, 1197–1198, 1197f–1198f Bowel obstruction, 915–916 Brachial plexus, 846 Brachytherapy, 616–617 for advanced-stage cervical cancers, 672 for endometrial cancer, 715 equipment for, 616–617, 616f–617f interstitial, 616 intracavitary, 616 low dose-rate vs. high dose-rate, 617 manual vs. remote afterloading, 617 for microinvasive carcinoma, 668 permanent, 616 radionuclides, 612t rectal toxicity of, 621 temporary, 616 vaginal, 619, 716, 731 for vaginal cancer, 697 Bravelle, for ovulation induction, 452t Breakthrough bleeding, 119, 180 Breast anatomy of, 275, 277f collagenous stroma and fat, 275 ductal systems, 275, 276f lymphatic drainage, 275, 277f terminal duct, 276f development of. See Breast development and disease diseases of. See Breast development and disease lobule, histology of, 276f physiology of, 275–276 Breast cancer BRCA1 mutation in, 288 BRCA2 mutation in, 288 hormone replacement therapy and, 286 inflammatory, 291–292, 292f invasive, 289–292 staging, 290, 290t tumor characteristics, 289–290 reproductive factors, 286 risk factor, 286, 287t risk stratification and management, 286–288 genetics, 287, 287t hereditary breast-ovarian cancer syndrome, 288 screening, 288–289 magnetic resonance imaging, 289 mammography, 288–289 other imaging modalities, 289 physical examination, 289

surveillance of, 291 treatment of, 290–291 chemotherapy, 291 hormonal therapy and targeted therapies, 291 radiation therapy, 291 surgery, 290–291 Breast development and disease, 275–276 absent breast development, 326 benign breast disease, 283–284 with atypia, 283–284 without atypia, 283 breast cancer, 286–292. See also Breast cancer invasive, 289–292 risk factor, 286 risk stratification and management, 286–288 screening, 288–289 breast lumps, 276–280, 279f diagnostic imaging, 277–278 evaluation of, 276–278 needle biopsy, 278 physical examination, 276, 278f triple test, 278 breast mass/infection, 326–327 breast shape, 326 cysts, 278, 279f ductal carcinoma in situ, 284–286 fibroadenomas, 278–279 fibroepithelial neoplasms, 278–280 infections, 281–282 nonpuerperal infections, 282 puerperal infections, 281–282 lobular carcinoma in situ, 284 mastalgia, 282, 283f nipple discharge, 280–281, 281f diagnostic algorithm, 280f galactorrhea, 280, 281t pathologic, 281, 281f normal vs. tuberous breast development, 326f phyllodes tumors, 279–280 polythelia, 325 premature thelarche, 326 tuberous breasts, 326 Breast examination, 2–4, 3f–4f clinical, 3 palpation technique, 2–3, 4f self, 2–3 Breast imaging, 37 Breast Imaging Reporting and Data System (BI-RADS), 278, 279t Breast infections nonpuerperal infections, 282 puerperal infections, 281–282 Breast masses, 276–280, 326–327 cysts, 278, 279f diagnostic imaging, 277–278 evaluation of, 276–278 fibroadenoma, 278–279 location of, 278f needle biopsy, 278

Index palpable, sonographic appearance of, 279f phyllodes tumors, 279–280 physical examination, 276, 278f triple test, 278 Breast shape, 326 Brenner tumor, malignant, 746 Brevicon, 120t Bristol Stool Scale, 566, 566f Brucella abortus, 139 Bulbocavernosus reflex, 524, 548 Bulbospongiosus muscle, 820 Bulimia nervosa, 139 diagnosis of, 302, 302t Bumetanide, and urinary incontinence, 525t Bupropion, for smoking cessation, 11t Bupropion SR, 304t Burch colposuspension, 1061–1062, 1061f–1062f for anatomic stress incontinence, 522 for anterior vaginal wall prolapse, 558 intraoperative, 1061–1062 surgical steps, 1061–1062 for intrinsic sphincteric defect, 522 postoperative, 1062 preoperative, 1061 consent, 1061 patient evaluation, 1061 patient preparation, 1061 for stress urinary incontinence, 532 Buspirone, 304t Butoconazole, for candidiasis, 62t Butyrophenones, 281t C CA125. See Cancer antigen 125 (CA125) Caffeine, 429t associated with abortion risk, 140 bone health and, 504 and impaired fertility, 429 polyuria or urinary frequency associated with, 524 premenstrual symptoms associated with, 305 Caffeine, and urinary incontinence, 525t CAIS. See Complete androgen-insensitivity syndrome (CAIS) Calcitonin, for osteoporosis in mature woman, 503 Calcium-channel blockers, 281t Calcium-channel blockers, and urinary incontinence, 525t Call-Exner body, 770, 770f Calymmatobacterium (Klebsiella) granulomatis, 59 Camper fascia, 796, 797f Campylobacter fetus, 139 Canal of Nuck, 819 Cancer antigen 19–9 (CA19–9), 216 Cancer antigen 125 (CA125), 214, 215 Cancer drug development, 607–608 Cancer growth, biology of, 592–593 cancer cell growth, 592 cell cycle, 592, 593f

cell kinetics, 592–593 doubling time, 592 gompertzian growth pattern, 592, 593f Cancer screening, 7–10 breast cancer, 288–289 MR imaging, 289 physical examination, 289 positron emission tomography (PET), 289 screening mammography controversy, 288–289 cervical cancer, 632–641, 657–658 Bethesda System, 635–637, 635t, 636t biopsy, 640–641, 641f, 663 cervical cytology, 632–633 colposcopy, 637–640, 638f–639f, 638t HPV testing, 633–634 Pap testing, 632–633, 637f, 663 screening guidelines, 634–635 colon cancer, 9–10, 10t HNPCC, 708, 736 endometrial cancer biopsy, 184–185, 185f, 397 endometrial sampling, 708 hysteroscopy, 187 laboratory testing, 709 Pap testing, 708 saline infusion sonography, 186–187 transvaginal sonography, 185–186 gestational trophoblastic neoplasia, 786–787 lung cancer, 10 ovarian cancer genetic screening, 737–737 genetic testing, 737 laboratory testing, 742 skin cancer, 10 vulvar cancer physical examination, 87 vulvar biopsy, 87–88, 88f vulvoscopy, 648–649 Cancer Therapy Evaluation Program (CTEP), 605 Candida albicans, 50 topical agents for treatment of, 62t vaginal infections, 60–63, 61f Candidiasis, 61–62, 324 topical agents for, 62t uncomplicated, 61–62 vulvovaginal, 61 Capacitation, 442 Caprini Risk Assessment Model, 836t Carbapenems, 54 Carbon dioxide laser cervical ablation, 643, 643t, 991, 991f Carbon dioxide laser vaporization, of VIN, 997–998 Carboplatin, 602 Carcinosarcoma, 722 diagnosis, 722–724 epidemiology, 722 generalist, role of, 723–724 imaging of, 723

pathology, 726–728, 727f prognosis, 732 staging of, 728–729, 729t treatment of, 732, 791 Cardiac complications hypertension, 914 myocardial infarction, 913–914 Cardiac evaluation diagnostic evaluation, 828 prevention strategies, 828–829 risk factors for, 827–828 Cardinal ligament, 808, 808f Cardiovascular disease (CVD), 13–14, 14t during menopausal transition, 483 CARE (Colpopexy and Urinary Reduction Efforts) trial, 558, 1098, 1107 Carnett sign, 256 Catapres. See Clonidine Cavitational ultrasonic surgical aspiration (CUSA), 649 for VIN, 996–997, 996f–997f CBAVD. See Congenital bilateral absence of the vas deferens (CBAVD) Cediranib, 604–605 CEE. See Conjugated equine estrogen (CEE) Cefazolin, 835t Cefixime, for uncomplicated gonococcal infection, 65t Ceftriaxone, 65t for chancroid, 59 for Neisseria gonorrhoeae, 64 for PID, 69t for pyelonephritis, 74t for surgical prophylaxis, 309t Celecoxib, and urinary incontinence, 525t Celiac disease, 265 Cell cycle-nonspecific agents, 593 Cell cycle-specific agents, 593 Cell generation time, 692 Centers for Disease Control and Prevention (CDC), 51, 58, 61, 64, 65, 66, 68, 69 Central precocious puberty (GnRHdependent), 327–328, 328t Cephalosporins, 53 first-generation, 53 for group A beta-hemolytic streptococcus, 324 for infectious vulvovaginitis, 324 for postgynecologic surgery infections, 79t second-generation, 53 third-generation, 53 for vulvar abscess, 82 Cervical abnormalities in infertility, correction of, 461, 461f Cervical adenocarcinomas, 661–662, 661f clear cell, 662 diagnosis, 632–641, 662–663 early-stage, 672 invasive, 661f mesonephric, 662 minimal deviation, 661–662 mucinous, 661

1231

1232

Index Cervical adenocarcinomas (Continuedâ•›) prognosis of, 662 serous, 662 staging of, 667 surgical treatment, 672 Cervical agenesis, 419–420 Cervical cancer, 126, 657–678 adenosquamous carcinomas, 662 advanced-stage primary disease treatment, 672–673 chemoradiation, 672–673 pelvic exenteration, 673 radiation therapy, 672 stage IVB, 673 stages IIB through IVA, 672–673 age-adjusted incidence and death rates of, 658t chemotherapy and response rates of, 674t diagnosis, 662–663 cervical biopsy, 663 Papanicolaou (Pap) test, 663, 663f physical examination, 662–663 symptoms, 662 E6 and E7 oncoproteins, effects of, 659f early-stage primary disease treatment, 667–672 adjuvant hysterectomy following primary radiation, 672 early-stage cervical adenocarcinoma, 672 hysterectomy, 668–670 positive pelvic lymph nodes, 671, 671t recurrence risk, 671–672 stage IA, 667–670 stage IB to IIA, 670–672, 670t surgical and radiotherapy complications, 671 glassy cell carcinoma, 662 histologic types, 660–662, 661t adenocarcinomas, 661–662, 661f squamous cell carcinoma, 660, 661f human papillomavirus and, 657–658 incidence, 657 local and distant tumor extension, 659–660 lymphatic drainage of cervix, 660f lymphatic spreading of, 659, 660f lymph node dissection, 666 lymphovascular space involvement, 659, 660f management during pregnancy, 675 neuroendocrine tumors, 662 palliative care, 674–675 pathophysiology, 658–660 tumorigenesis, 658 tumor spread, 659–660 prognosis, 666–667 radiologic imaging, 665–666 computed tomography, 666 magnetic resonance imaging, 666 positron emission tomography, 666 risks, 657–658 screening guidelines, 634–635 perspectives, 634

posthysterectomy, 635 screening discontinuation, 635 screening initiation, 634 screening interval and strategy, 634–635 secondary disease, 673–674 pelvic exenteration, 673–674 radiotherapy/chemotherapy for, 674 staging, 663–665, 664t, 665f surveillance, 673 survival rates according to stage, 667t treatment of, 667–673 advanced-stage treatment, 672–673 early-stage treatment, 667–672 Cervical cap, 129–130 Cervical conization, 663, 992–994, 992f–993f abnormalities in mucus production and, 441 in cervical stenosis, 372 cold-knife conization, 663, 992–993, 992f–993f gynecologic history and, 428 in hematometra, 212 laser conization, 993–994 LEEP conization, 993, 993f for microinvasive cervical cancer, 667, 668, 668t, 669 during pregnancy, 637, 637, 675 Cervical cryotherapy, 989–991, 990f for CIN, 651 Cervical cytology, for cervical neoplasia, 632–633 collection devices, 633f cytology collection, 633 Pap tests, 184, 632–633, 633f Cervical diverticula, 215 Cervical dysplasia, 126, 659f, 991 Cervical intraepithelial neoplasia (CIN), 630–632 management, 641–643 natural history of, 631–632, 631t risk factors, 630–631, 631t treatment of, 643–644 ablation, 643 cervical cryotherapy, 989–991, 990f CO2 laser cervical ablation, 991, 991f cold-knife conization, 644t, 664 cryosurgery, 643t excision, 643–644, 644t hysterectomy, 645 loop electrosurgical excision procedure, 988–989, 988f–989f surveillance following, 644 Cervical neoplasia, diagnosis of, 632–641 Bethesda system, 635–637, 635t, 636t epithelial cell abnormality management, 636–637 nonneoplastic findings, 637 specimen adequacy, 635–636 biopsy, 640–641 ectocervical, 640–641 endocervical sampling, 641 tools used for, 641f

cervical cancer screening guidelines, 634–635 perspectives on guidelines, 634 posthysterectomy, 635 screening discontinuation, 635 screening initiation, 634 screening interval and strategy, 634–635 cervical cytology, 632–633 collection devices, 633f cytology collection, 633 Pap tests, 632–633 colposcopy, 637–640 clinical considerations, 638t examination, 638–639 lesion grading, 639–640 preparation for, 637–640 Reid Colposcopic Index, 639, 640t solutions used for, 639f HPV testing, 633–634 cytology with, 633–634 primary, 634 Pap tests, 632–633 Cervical polyp. See Endocervical polyp Cervical pregnancy, 174–175, 175f Cervical stenosis, 102, 372, 901 Cervix, 624–627, 807, 807f ablation of, 643, 643t, 991, 991f abnormal bleeding from adenocarcinoma in situ of, 642 agenesis, 419–420 anatomy, 807, 807f atrophy, 25 cancer, 126, 657–678. See also Cervical cancer clear cell adenocarcinomas, 662 conization of, 663, 992–994, 992f–993f. See also Cervical conization dilatation and curettage, 964–968 dysplasia, 126, 659f, 991 ectopic pregnancy, 174–175, 175f endometriosis. See Endometriosis eversion, 102, 625 glandular cell abnormalities, 636–637 imaging of, 30, 665–666 incompetent, 147 infection, 60, 65t, 184, 441 infertility contribution, 441, 441f lymphatic drainage of, 660f mucus changes, 126–127, 441, 461 neuroendocrine tumors of, 662 Pap testing, 632–633, 637f, 663, 663f polyp. See Endocervical polyp preinvasive disease, 632, 988–991 prolapse of. See Pelvic organ prolapse (POP) stenosis, 102, 372, 901 supracervical hysterectomy and, 950–951, 950f trachelectomy, 670, 962–963, 962f–963f Cesarean scar defect, 215 Cesarean scar pregnancy, 175–176, 175f Chancroid, 59

Index Chemical tubal occlusion, 118 Chemotherapeutic drugs, 596–603 alkylating agents, 598–599, 598t cyclophosphamide, 598 ifosfamide (Ifex), 598–599, 599f antimetabolites, 596–598, 597t 5-fluorouracil, 598 gemcitabine (Gemzar), 597–598 methotrexate, 596–597, 597f antitumor antibiotics, 599–600, 599t bleomycin, 599–600 dactinomycin, 599 doxorubicin, 600 doxorubicin hydrochloride liposome, 600 carboplatin, 602 cisplatin, 602–603 hormonal agents, 603 plant-derived agents, 600–602, 601t taxanes, 600–601, 600f, 601t topoisomerase inhibitors, 602 vinca alkaloids, 600f, 601–602 Chemotherapy, principles of, 592–609 biological and targeted therapy, 603–605 antiangiogenesis agents, 604–605, 604f mammalian target of rapamycin inhibitors, 605 poly(ADP) ribose polymerase inhibitors, 605 cancer drug development, 607–608 cancer growth, biology of, 592–593 cancer cell growth, 592 cell cycle, 592, 593f cell kinetics, 592–593 doubling time, 592 gompertzian growth pattern, 592, 593f cell cycle-nonspecific agents, 593 cell cycle-specific agents, 593 chemosensitivity and resistance assays, 607 chemotherapeutic drugs, 596–603 alkylating agents, 598–599, 598t antimetabolites, 596–598, 597t antitumor antibiotics, 599–600, 599t carboplatin, 602 cisplatin, 602–603 hormonal agents, 603 plant-derived agents, 600–602, 601t clinical use of, 593–594 clinical setting, 593–594 directing care of patient, 594 drug regimens, 594 growth factors, 606–607 granulocyte colony-stimulating factors, 607 synthetic erythropoietins, 606–607 pharmacologic principles, 594–596 administration route and excretion, 595, 595t body surface area, 594–595 dosing and dose intensity, 594–595 drug interactions and allergic reaction, 595, 596t

drug resistance, 596 response to chemotherapy, evaluation of, 596, 596t side effects, 605–606 bone marrow toxicity, 605 dermatologic toxicity, 606 gastrointestinal toxicity, 605–606, 606t neurotoxicity, 606 Chemotherapy-induced emesis, drug regimens for prevention of, 606t Cherney incision, 931, 931f Child sexual abuse, 254t, 255, 310–311, 310t Chlamydia muridarum, 163 Chlamydia trachomatis, 324, 433, 441 bartholin gland duct abscess, 97 bleeding from, 183f cervicitis and cervical infection association with, 184 in child sexual abuse, 310–311, 310t ectopic pregnancy, 163 endometritis and, 191 infertility, 209 lymphogranuloma venereum, 59–60 pelvic inflammatory disease, 52, 176 prophylaxis against, 65t risks factors, 6t, 901 screening for, 5, 6t, 209, 901 spontaneous abortion and, 139 in suppurative cervicitis, 64–65 surgical abortion and, 153 symptoms, 52 in urethral diverticulum, 583 Chlorpromazine, and urinary incontinence, 525t Cholesterol chemical structure of, 336f interpretation of, 15t Choriocarcinoma, 764 Chromosomal structural abnormalities, 138 Chronic antithrombotic therapy, 831t for AUB, 295t Chronic hypertension, 14–15 Chronic obstructive pulmonary disease (COPD), 826 Chronic pelvic pain (CPP), 233–234, 253– 262, 254t concurrent lordosis and kyphosis in, 256f conscious pain mapping, 258 history, 253–255 musculoskeletal origins of, 256t ovarian remnant syndrome and, 261 ovarian retention syndrome and, 261 pelvic adhesions and, 260–261 pelvic congestion syndrome and, 261–262, 261f physical examination, 255–258 lithotomy, 257–258 pelvic floor muscle examination, 257f sitting and supine, 256–257 stance and gait, 255–256, 256f testing, 258

questions relevant to, 255t specific causes of, 260–262 surgery treatment, 259–260 testing, 258 treatment, 258–260 medical options, 258–259, 259t surgical, 259–260 Cimifuga racemosa, 498 CIN. See Cervical intraepithelial neoplasia (CIN) Ciprofloxacin, for granuloma inguinale, 59t Cisplatin, 595t, 602–603 for cervical cancer, 672–673, 672f, 674, 674t, 675 in endometrial cancer, 715 for GTN, 790 neurotoxicity of, 606 in ovarian cancer, 752, 752t for tumor hypoxia, 618 in vulvar cancer, 687 Citalopram, 304t for menopausal vasomotor symptoms, 498 Clean contaminated wounds, 75–76 Clean wounds, 75 Clear cell adenocarcinomas borderline, 739, 739f of cervix, 662 endometrial, 710, 712f of endometrium, 707t, 710, 712f epithelial, 746, 746f of ovary, 744t, 746, 746t of vagina, 423, 625, 698 Clindamycin, 52, 54, 835t, 865t, 912 Clinical breast examination (CBE), 3, 276, 278f Clinical target volume (CTV), 615 Clitoris, 819, 819f congenital abnormalities of, 414–415 vulvectomy radical complete, 1212 radical partial, 1210 skinning, 1207 Clitoromegaly, 415 Clomiphene citrate (CC) administration of, 451, 451f for ovulation induction, 451–452 Clonazepam, 304t Clonidine for menopausal vasomotor symptoms, 498 for smoking cessation, 11t Cloquet node, 823 Clostridium perfringens, 81 Clotrimazole with betamethasone, for candidiasis, 62t for candidiasis, 62t combination pack, for candidiasis, 62t Coccydynia, 269 Coccygeus-sacrospinous ligament (C-SSL) complex, 1112 Coccyx, 799 Coitarche, 330

1233

1234

Index CO2 laser ablation of vaginal preinvasive lesions, 646 of VIN, 649 CO2 laser conization, 993–994 for CIN, 644 Cold knife conization, 992–993, 992f–993f. See also Cervical conization in adenocarcinoma in situ, 642 in cervical stenosis, 102 for CIN, 643–644 clinical characteristics, 644t during pregnancy, 675 in primary invasive cervical carcinoma, 667, 668t Colicky pain, 251 Collaborative Review of Sterilization (CREST), 115, 116f Colles fascia, 818, 819 vulvectomy, 1210f, 1213 Colon cancer, 9–10, 10t, 265, 708 colonic obstruction and, 715 HNPCC and, 736 Colonic diverticular disease, 265 Colonography (CTC), 10t Colonoscopy, 10t Color Doppler mapping, 23–24 for acute lower abdominal pain, 252 for adnexal torsion, 222–223 for arteriovenous malformation, 190, 190f for AUB, 187, 188f, 189, 189f for color epithelial ovarian cancer, 742, 743f in ectopic pregnancy, 166–167, 167f for functional ovarian cysts, 218–219 for leiomyoma, 206 for pelvic congestion syndrome, 261–262, 261f Colostomy, 1191–1193, 1192f–1193f intraoperative, 1191–1193 postoperative, 1193 preoperative, 1191 Colpocleisis, 1120–1124, 1120f–1124f intraoperative, 1121–1124 anesthesia and patient positioning, 1121 surgical steps—complete colpocleisis, 1122–1124 surgical steps—lefort partial colpocleisis, 1121–1122 for pelvic organ prolapse, 554 postoperative, 1124 preoperative, 1120 consent, 1121 patient evaluation, 1120 patient preparation, 1121 Colporrhaphy anterior, 1088–1090, 1088f–1090f for anterior vaginal wall prolapse, 555 posterior, 1093–1095, 1094f–1095f Colposcopy acetic acid in, 638, 639f of cervical neoplasia, 637–640

clinical considerations, 638t examination, 638–639 lesion grading, 639–640 preparation for, 637–640 Reid Colposcopic Index, 639, 640t solutions used for, 639f Combined hormonal contraceptives, 118–126 administration of, 119–122 benefits of, 124t bleeding from, 191 and breast cancer, 126 during breastfeeding, 108t and cervical dysplasia, 126 combined oral contraceptive pills, 119–122, 119f administration of, 122 drugs influenced by, 123t formulations, 119–122, 120t–121t contraindications to, 119t drug interactions, 123–124 drugs reduces efficacy of, 124t for emergency, 131t extended cycle of, 123 formulations, 119, 120t–121t impact on sex hormone-binding globulin, 119 mean, 184, 830 and medical disorders, 124–126 cardiovascular disease, 124–125 cerebrovascular disorders, 125 diabetes mellitus, 124 HIV infections and antiretroviral therapy, 126 neoplastic diseases, 126 obese and overweight women, 124 seizure disorders, 125–126 systemic lupus erythematosus, 125 venous thromboembolism, 125 in migraine headaches, 125 pharmacology, 118–119 risk for VTE, 122 transdermal system, 122 transvaginal ring, 122, 122f von Willebrand disease and, 193 Combined oral contraceptive pills. See Combined hormonal contraceptives Commit, 11t Common iliac lymph nodes, 659 distal, 1170, 1178 lymphadenectomy, 666, 1168, 1178 sites of vaginal lymphatic drainage, 694 Common peroneal nerve anatomy, 845 avoiding compression of, patient positioning and, 879 Common Terminology Criteria for Adverse Events (CTCAE), 605, 620 Complete abortion, 142–143 Complete androgen-insensitivity syndrome (CAIS), 413 Complete hydatidiform mole, 780–781, 780f, 780t, 781f

Compression sonography, 36–37, 36f Compressor urethrae, 516, 814 Compton effect, 612 Computed tomography (CT), 39–40, 40f for acute abdominal pain, 252–253 for cervical cancer, 666, 670f chest, for phyllodes tumors, 280 of choriocarcinoma invading uterus, 786f for dermoid cyst, 325, 761 endometrial cancer, 709 epithelial ovarian cancer, 742 for GTN, 787 gynecologic malignancy, 40, 44–45 for hydronephrosis, 661f for hyperprolactinemia, 358 imaging following gynecologic surgery, 40 for low-malignant-potential tumors, 739 normal pelvic anatomy, 40 ovarian cancer, 742 PET-CT, 46f for PID, 67 quantitative, for bones, 39 for small bowel obstruction, 915 for vaginal cancer, 695, 696f in Veress needle entry, 890 Condom. See Female condom; Male condom Condyloma acuminata, 70, 70f, 96, 681 associated with vaginal bleeding in children, 327 CUSA for, 996 HPV infection, 629 surgical excision of, 325f Condylomata lata, 57–58 Conformal radiation therapy (CRT), 615–616 Congenital adrenal hyperplasia (CAH), 362 adult-onset, 363, 394t 17-alpha hydroxyprogesterone in, 394–395 CYP21A2 gene in, 380 diagnostic algorithm, 380f fetal, 414 nonclassic, 379, 382 382t, 383 simple virilizing, 362 Congenital anatomic anomalies, 43, 323, 456, 657 ART and risk of, 467 fallopian tube anomalies, 423 and infertility, 34–36 müllerian anomalies, 29, 417–423, 459. See also Müllerian anomalies developmental, 440 vaginal agenesis, 985 ovarian anomalies, 423 uterine anomalies, 437–438 developmental, 438–440 Congenital bilateral absence of vas deferens (CBAVD), 444, 462–463 Congenital vaginal cysts, 101, 417 Congestive heart failure (CHF), 827

Index Conjugated equine estrogens (CEE), 363, 493, 494, 497 for acute AUB, 194t BZA with, 501 for menopausal vasomotor symptoms, 496 for osteoporosis, 500t potency of, 365t Constitutional delay, 329 Contact dermatitis, 91, 91f, 91t Contaminated wounds, 76 Continent urinary conduit, 1160–1163, 1160f–1163f intraoperative, 1160–1162 postoperative, 1162–1163 preoperative, 1160 Continuous positive airway pressure (CPAP), 827 Contraception and sterilization, 330–331 contraceptive effectiveness chart, 106f emergency contraception, 131–132 fourth-tier contraceptive methods, 105, 130–131 medical eligibility criteria, 105–107 adolescence and perimenopause, 107 lactation, 106–107 second-tier contraceptive methods, 105, 118–128 combined hormonal contraceptives, 118–126 progestin-only contraceptives, 126–128 third-tier contraceptive methods, 105, 128–130 barrier methods, 128–130 cervical cap, 129–130 diaphragm plus spermicide, 128–129, 129f female condom, 128, 128f, 129f fertility awareness-based methods, 130 male condom, 128 top-tier contraceptive methods, 105, 107–118 contraceptive failure rates, 107t intrauterine contraception, 107–112 permanent contraception, 115–118 progestin implants, 112–115 Contraceptive effectiveness chart, 106f Contraceptive sponge, 101, 130, 131f Contrast-enhanced sonography, 29 Controlled ovarian hyperstimulation, 451 Copper-containing intrauterine devices, 132 Copper-T 380A, 109, 109f contraindications to, 109t efficacy of, 107t in emergency contraception, 131t positioning of, 28f pregnancy outcomes, 112t Cornua, 809 Cornuostomy and cornual wedge resection, 941–944, 941f–943f intraoperative, 941–944 postoperative, 944 preoperative, 941

Coronary artery disease (CAD), 827 Coronary heart disease (CHD), 492 hormone replacement therapy and risk of, 494 WHI study design for, 493–494 Corpus, uterine, 807, 807f Corpus albicans, 355 Corpus luteum, 36, 216, 347f, 354–355, 369 associated with lower abdominal pain, 164t bacterial invasion, 79 b-hCG in, 215 endometrial biopsy, 435 hemorrhage from, 218, 218f luteal phase, 354–355 management, 223 surgical removal of, 139, 149 Corticosteroids, 123t for aphthous ulcers, 94 for atopic dermatitis, 91 COCs affects efficacy of, 123t hypertension associated with, 15 for lichen sclerosus, 89–90 for lichen simplex chronicus, 88 for psoriasis, 91–92 for vaginal lichen planus, 93 for vulvar contact dermatitis, 91, 91t as vulvar irritants and allergens, 87t for vulvar lichen planus, 93 for vulvodynia, 100 Corticotropin-releasing hormone (CRH), 345–346 Cortisol-binding globulin (CBG), 365 Coumadin. See Warfarin CPAP. See Continuous positive airway pressure (CPAP) CREST. See Collaborative Review of Sterilization (CREST) CRH. See Corticotropin-releasing hormone (CRH) Crohn disease, 94, 94f, 573t, 869 CRT. See Conformal radiation therapy (CRT) Cryopreservation, of unfertilized eggs, 466 CTCAE. See Common Terminology Criteria for Adverse Events (CTCAE) CTEP. See Cancer Therapy Evaluation Program (CTEP) CTLA-4. See Cytotoxic T-lymphocyteassociated antigen 4 (CTLA-4) CTV. See Clinical target volume (CTV) Cul-de-sac of Douglas anatomy, 814 culdocentesis, 167, 167f entry into, 957, 957f, 986 uterine support and, 808 Culdocentesis, 167 Culdoplasty Halban, 1118, 1118f McCall, 1116–1117, 1117f procedures, 1118–1119, 1118f–1119f Current density, 858, 858f

CUSA. See Cavitational ultrasonic surgical aspiration (CUSA) Cushing syndrome, 396 CycleBeads, 130f Cyclessa, 120t Cyclobenzaprine, and urinary incontinence, 525t Cyclooxygenase-1 (COX-1), 196 Cyclooxygenase-2 (COX-2) inhibitors, and urinary incontinence, 525t Cyclopenthiazide, 123t Cyclophosphamide, 598 Cyclosporine, 123t CYP21A2 gene, 380 CYP11B1 mutation, 414 CYP21 mutation, 414 Cystectomy bartholin gland duct, 975–976, 975f laparoscopic ovarian intraoperative, 1015–1018 postoperative, 1018 preoperative, 1015 ovarian, 933–934, 933f–934f intraoperative, 933–934 postoperative, 934 preoperative, 933 Cystic vulvar tumors, 97, 97f Cystometrography, for urinary incontinence, 527 Cystoscopy, 1057–1060, 1058f–1060f intraoperative, 1058–1060 surgical steps, 1058–1060 postoperative, 1060 preoperative, 1058 Cystourethroscopy, 1064, 1067, 1069, 1075 for genitourinary fistulas, 580 for squamous cell carcinoma, 695 for urethral diverticulum, 585–586, 585f for vaginal cancer evaluation, 695t Cytotec, 153, 901, 964, 1040. See Misoprostol Cytotoxic T-lymphocyte-associated antigen 4 (CTLA-4), 690 D Dabigatran (Pradaxa), 832 Dactinomycin, 599 for GTN, 789–790 Dalteparin (Fragmin), 914t Da Vinci Surgical System, 887f DBE. See Deep-breathing exercises (DBE) Decidual cast, 168, 168f Deep-breathing exercises (DBE), 827 Deep infiltrating endometriosis (DIE), 231, 234–235, 236 Deep perineal space, 820, 821f Deep transverse perineal muscles, 814 Dehydroepiandrosterone (DHEA), 329, 338, 338f, 395 Delayed hemolytic transfusion, 866 Delayed hemolytic transfusion reactions, 866

1235

1236

Index Delayed puberty, 329, 329t Denosumab, for osteoporosis, 500t, 503 Depilation, 399 Depot medroxyprogesterone acetate (DMPA), 107t for abnormal uterine bleeding, 191, 195t for adenomyosis, 214 black box warning, 127, 239–240 during breastfeeding, 108t for endometrial hyperplasia for endometriosis, 239–240 formulations, 127 for leiomyoma, 207, 207t obesity, 14 for PCOS, 398 side effects, 127–128 Depression, 17–18, 297 chronic pelvic pain and, 255 Depth-dose curve, 612 Dermabond. See Octyl-2-cyanoacrylate Dermatitis allergic, 323 benign reactive, 286f contact, 91, 91f, 91t, 323 Dermatologic toxicity, of chemotherapy, 606 Dermatome maps, 250f Dermoid cyst. See Mature cystic teratoma Desipramine, 304t Desogen, 120t Desogestrel, 120t Desquamative inflammatory vaginitis, 101 Desvenlafaxine for depression, anxiety and premenstrual disorders, 304t for vasomotor symptoms, 497t, 498 Detrusor loops, 813 Detrusor muscle, 813 abdominal cavity and pressure generated by, 528f activity with voiding, 521–522 anatomy, 516, 517f anticholinergic medication impact on, 533 contraction, 514–515, 521, 521f in dysuria, 263 overactivity, 514 Detrusor sphincter dyssynergia, 522 DEXA. See Dual-energy x-ray absorptiometry (DEXA) DHEA. See Dehydroepiandrosterone (DHEA) DHEAS. See DHEA sulfate (DHEAS) DHEA sulfate (DHEAS), 394 adrenarche, 329 evaluation of, 382, 394t, 395f during menopause, 473–474 production by adrenal glands, 338f production by ovary, 338, 338f DHT. See Dihydrotestosterone (DHT) Diabetes mellitus, 16, 507t, 832 combined hormonal contraceptives and, 124

complications of, 832 counseling in, 19t diagnostic criteria for, 16t endocrine evaluation, 832 fecal incontinence and, 563t impaired glucose tolerance and, diagnosis of, 396t and obesity, 12, 12t PCOS and, 383, 387t perioperative management of, 833t, 834f pregnancy loss associated with, 139, 150 preventive care of, 16, 16t risk factors for, 16t type 2, 392 Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition (DSM-5), 297 Diaphragmatic surgery, 1189–1190, 1189f intraoperative, 1189–1190 postoperative, 1190 preoperative, 1189 Diarrhea, 916 associated fecal incontinence, 563t, 564, 569, 570 functional, 267t irritable bowel syndrome and, 265–267 Diazepam, 123t, 304t, 843 Dicumarol, 123t Dicyclomine, and urinary incontinence, 525t DIE. See Deep infiltrating endometriosis (DIE) Dienogest, 121t Dietary deficiency, 140 Diethylstilbestrol-induced reproductive tract abnormalities, 101, 423 Diffuse adenomyosis, 213 Dihydrotestosterone (DHT), 338 Dimenhydrinate, and urinary incontinence, 525t Diminished ovarian reserve, 373 correction of, 458 evaluation for, 435–437 antimüllerian hormone measurement, 436–437 antral follicle count, 437 follicle-stimulating hormone and estradiol measurement, 436 reproductive aging, 435–436, 435t Diphenhydramine, and urinary incontinence, 525t Diphenoxylate hydrochloride (Lomotil), for fecal incontinence, 570 Direct intraspinal neuronal reflexes, 249 Direct oral anticoagulants (DOACs), 832 Disopyramide, and urinary incontinence, 525t Disorders of sex development (DSD), 409–414 abnormal androgen production, 412 algorithm for, 414f chromosomal ovotesticular, 411 classification of, 409t

definitions, 409–411 gender assignment, 413 sex chromosome, 411 46,XX disorders, 412–413 46,XY disorders, 411–412 Disposable suturing devices, 898 Disseminated peritoneal adenomucinosis, 746 Disseminated peritoneal leiomyomatosis (DPL), 204 Distal tubal obstruction, 459 Distal tubal occlusion, 458 Distention media, 903–905, 903t carbon dioxide, 904 in cystoscopy and urethroscopy, 1058 fluid media, 904–905 Diuretics, and urinary incontinence, 525t Diverticulectomy, 1075–1076, 1075f–1076f for urethral diverticulum, 587 DMPA. See Depot medroxyprogesterone acetate (DMPA) Docetaxel (Taxotere), 601 Dong quai, 498 Dopamine, 345 Dopamine agonist for acquired pituitary dysfunction, 378 for amenorrhea, 383 for hyperprolactinemia, 150, 358–359, 361, 450 for pituitary adenomas, 359t, 360–361 in pregnancy loss, 151t for regulating anterior pituitary hormones, 345, 345t Dopamine depletors, 281t Dorsal lithotomy, 845–846, 845f–846f Dose volume histogram (DVH), 615–616 Dostinex, 361 Doxazosin, and urinary incontinence, 525t Doxepin, 304t and urinary incontinence, 525t Doxorubicin, 600 Doxorubicin hydrochloride liposome, 600 Doxycycline, 835t for bacterial infection, 55 in Bartholin gland duct incision and drainage, 972 for cervical abnormalities, 461 for chlamydial infection, 65t for granuloma inguinale, 59t for lymphogranuloma venereum, 60 in mechanical uterine distention, 1063 for Neisseria gonorrhoeae, 64 for PID, 68t, 69–70, 69t for post-HSG PID, 38–39 to reduce CHC efficacy, 124t in sharp dilatation and curettage, 964, 965 for SIS complications, 25 for syphilis, 58t for tuboovarian abscess, 68 for vulvar abscess, 82 Drospirenone, 120t DSD. See Disorders of sex development (DSD)

Index Dual-energy x-ray absorptiometry (DEXA), 39 Ductal carcinoma in situ (DCIS), 284–286, 285f Duloxetine, 304t DVH. See Dose volume histogram (DVH) Dysfunctional uterine bleeding, 194 Dysgenetic testis, 409 Dysgerminoma, 762–763, 763f Dyslipidemia, 15–16, 392 hypercholesterolemia, 15–16, 15t hypertriglyceridemia, 15t, 16 measurements of, 396–397 in PCOS, 392 Dysmenorrhea, 110, 214, 262 abnormal uterine bleeding and, 182 associated with anatomic abnormalities, 437 diagnosis of, 262 endometriosis and, 215 NSAIDs for, 196–197, 239, 239t ovulatory cycles associated with, 434 treatment of, 262 tubal sterilization and risk of, 117 uterine leiomyoma and, 207t Dyspareunia, 262–263 associated with pelvic organ prolapse, 545t diagnosis of, 263 endometriosis-associated, 234, 428 female sexual dysfunction with, 547 genitourinary syndrome of menopause and, 486t insertional, 263 in mature woman, treatment of, 505–506 menopausal transition and, 472t primary, 263 secondary, 263 and sexual dysfunction, 487 treatment of, 263 estrogen replacement, 505–506, 505t ospemifene for, 506 vaginal lubricants and moisturizers for, 506 and urethral diverticulum, 584 Dysplasia, cervical. See Cervical dysplasia Dysuria, 263–265 genital ulcer infections and, 55–56 genitourinary syndrome of menopause and, 486t in immunocompetent nonpregnant women, 73 lower abdominal pain and, 164t treatment of, 74 trichomoniasis associated with, 61t E Early pregnancy loss, 143, 144 Early-stage cervical cancer, treatment of, 667–672 adjuvant hysterectomy following primary radiation, 672 early-stage cervical adenocarcinoma, 672

hysterectomy, 668–670 positive pelvic lymph nodes, 671, 671t recurrence risk, 671–672 stage IA, 667–670 stage IB to IIA, 670–672, 670t surgical and radiotherapy complications, 671 EAS. See External anal sphincter (EAS) Eating disorders, 301–302, 376 anorexia nervosa, diagnosis of, 301t, 302 bulimia nervosa, diagnosis of, 302, 302t diagnosis, 302 treatment, 302 Econazole nitrate, for candidiasis, 62t Ectopic breast tissue, 96 Ectopic endometrium, 231 Ectopic pregnancy, 161–179 cervical pregnancy, 174–175, 175f cesarean scar pregnancy, 175–176, 175f clinical manifestations, 164 cornuostomy and cornual wedge resection for, 941–944, 941f–943f culdocentesis, 167 diagnosis, 164–165, 164f endometrial evidence, 167–168 epidemiology, 161 evaluation algorithm, 169f fallopian tube in, 161, 163, 163f, 166 heterotopic pregnancy, 175 interstitial pregnancy, 173–174, 174f laboratory findings, 165 serum b-hCG measurements, 165 serum progesterone levels, 165 laparoscopic photograph of, 168f laparoscopic salpingectomy for, 1011–1012, 1011f–1012f management, 168–173 expectant, 173 medical, 168–172, 170t methotrexate in, 170–171 other medical options, 171–172 surgical, 172 surveillance, 171–172 ovarian pregnancy, 173 pathophysiology, 162–164 persistent, 173 prevention of, 176 risk factors for, 161–162, 162f assisted reproductive technology, 161–162 contraception, 162 older reproductive-aged women, 162 smoking, 161 salpingectomy and salpingostomy in, 939–940, 939f serum b-hCG levels in, 163–164 sites and frequency of, 162f, 176 sonography, 165–167, 166f, 167f Edinburgh Postnatal Depression Scale (EPDS), 305 Eflornithine hydrochloride, 399 Egg donation, 465

EIN. See Endometrial intraepithelial neoplasia (EIN) Elective abortion, counseling before, 152 Elective single embryo transfer (eSET), 457 Electromagnetic radiation, 610 energy deposition, 611–612 Electrosurgery, 857–859 argon beam coagulation, 859 bipolar, 857f, 859 circuits in, 857f in hysteroscopy, 904–905 monopolar, 857–858, 857f, 884 patient grounding, 858–859 surgical effects of, 857–858, 858f Elemental iron, 830 EMB. See Endometrial biopsy (EMB) Embryo biopsy, 467 Embryology, 404–409, 404t, 405f, 406f ductal system development, 408–409, 408f external genitalia, 409, 410f gonadal determination, 406–408, 407f Embryonal carcinomas, 764 Embryonal rhabdomyosarcoma, 698–699, 699f Emergency contraception, 131–132 copper-containing intrauterine devices, 132 hormone-based options, 131–132 antiprogestins, 132 estrogen-progestin combinations, 132 mechanisms of action, 131–132 progestin-only regimens, 132 SPRM, 132 methods available for, 131t En bloc pelvic resection, 1181–1184, 1181f–1183f gastrointestinal bowel preparation, 834–835 intraoperative, 1181–1183 instruments, 1181 surgical steps, 1181–1183 postoperative, 1184 preoperative, 1181 Endocervical polyp, 102, 189–190, 189f associated with chronic pelvic pain, 254t bleeding from, 181t surgical ligation and excision, 190 Endometrial ablation procedures, 1043–1045, 1044f–1045f intraoperative, 1043–1045 postoperative, 1045 preoperative, 1043 for primary endometrial dysfunction, 197, 197t Endometrial biopsy (EMB), 835t for abnormal bleeding, 397 for abnormal uterine bleeding, 184–185 indications, 184 sampling methods, 184–185 for anovulation, 435 for endometrial polyp, 189 in nonatypical endometrial hyperplasia, 706

1237

1238

Index Endometrial biopsy (Continuedâ•›) for nonneoplastic endometrium, 474 in pelvic inflammatory disease, 67 with Pipelle catheter, 168, 185f steps of, 185f for vaginal cancer, 695t Endometrial cancer, 702–721 classification of, 709t clear cell carcinoma, 710–711, 712f diagnosis, 708–709 endometrial sampling, 708 imaging studies, 708–709 laboratory testing, 708 papanicolaou test, 708 signs and symptoms, 708 endometrial hyperplasia, 703–707 classification, 703–705, 705t clinical features of, 705–706 diagnosis of, 705–706, 705f, 706f treatment, 706–707 endometrial stroma and exophytic expansion, invasion of, 712, 712t endometrioid adenocarcinoma, 710, 710f epidemiology of, 702–703 generalist, role of, 709 hematogenous dissemination, 713 lymphatic channel invasion in, 712–713 mucinous carcinoma, 711–712, 712f pathogenesis, 707 pathology, 709–713 histologic grade, 709–710, 710t histologic type, 710–712 patterns of spread, 712–713 port-site metastasis in, 713 prevention, 707–708 prognostic factors, 717, 717t recurrent disease, 717–718 retrograde transtubal transport, 713 risk factors for, 702–703, 703t coexisting medical conditions, 703 environment, 702 family history, 703 menstrual and reproductive influences, 702 obesity, 702 older age, 702–703 smokers, 703 tamoxifen and, 703 unopposed estrogen therapy, 702 serous carcinoma, 710, 711f squamous cell carcinoma, 712 transitional cell carcinoma, 712 treatment, 713–717 chemotherapy, 715 estrogen replacement therapy, 716 fertility-sparing management, 717 FIGO staging system, 713t, 714f, 714t hormonal therapy, 716 radiation therapy, 715–716 surgical management, 713–715 surveillance, 715 targeted therapy, 715 type I and II, 707t

undifferentiated carcinoma, 712 unopposed estrogen therapy and, 702 UPSC management, 716–717 Endometrial hyperplasia, 703–707 atypical, 707 classification, 703–705, 705t clinical features of, 705–706 diagnosis of, 705–706, 705f, 706f nonatypical, 706–707 PCOS and, 392–393 risk factors for, 702–703, 703t, 705 treatment, 706–707 Endometrial intraepithelial neoplasia (EIN), 704–705 Endometrial polyps, 188–189, 188f, 437–438 appearance of, 439f associated with chronic pelvic pain, 254t bleeding from, 181, 181t hysteroscopic polypectomy, 147, 460, 1038–1039, 1038f MR imaging, 44 sampling for, 185 transvaginal color Doppler sonography of, 189f TVS for, 189 Endometrial receptivity, 357 Endometrial resection or ablation. See Endometrial ablation Endometrial stromal nodule, 725 Endometrial stromal sarcoma (ESS) diagnosis, 723 epidemiology, 722 FIGO staging of, 729t, 730f generalist, role of, 723–724 imaging of, 723 pathology, 725–726, 725–726, 726f, 726f prognosis, 732 treatment, 730–732 Endometrial stromal tumors, 722, 725–726 endometrial stromal nodule, 725 endometrial stromal sarcoma, 725–726, 726f FIGO staging of, 730f high-grade undifferentiated sarcoma, 726 treatment of, 732 Endometrioid adenocarcinomas, 709f, 710, 710f, 745, 745f Endometriosis, 230–248, 238f, 460–461 in anterior abdominal wall, 235 classification, 233, 233f diagnostic and treatment algorithm of, 238f diagnostic evaluation, 236–237 diagnostic imaging, 236–237, 236f, 237f laboratory testing, 236 laparoscopy, 237, 237f pathologic analysis, 237 physical examination, 236 dyspareunia, 234 endometrioma resection, 242 estrogen and progesterone, role of, 231–232

genome-wide association studies, 233 hysterectomy in, 243 incidence, 230 laparoscopic uterine nerve ablation in, 243 lesion removal and adhesiolysis in, 242 mendelian genetic inheritance pattern for, 232–233 pathophysiology, 230–233 anatomic sites, 231, 231f molecular mechanisms, 231–233 pathogenesis, 230–231 Pfannenstiel incision scar, 235f presacral neurectomy in, 242–243 rectosigmoid lesions and, 234–235 symptoms, 233–235 infertility, 234 pain, 233–234 from specific sites, 234–235 thoracic, 235 treatment, 237–244 add-back therapy, 240–241 androgens for, 241–242 aromatase inhibitors for, 241 combination hormonal contraceptives pills, 239 endometriosis-related infertility, 243–244 GnRH agonists for, 240–241 GnRH antagonists for, 241 medical treatment of pain, 239–242 NSAIDs, 239, 239t progestational agents, 239–240 SPRMs for, 241 surgical treatment of endometriosisrelated pain, 242–243 Endometritis, 191–192 Endometrium, 355–357, 807 endometrial function, regulation of, 355–357 estrogen and progesterone receptors in, 357 growth factors and cell adhesion molecules in, 357 histology across menstrual cycle, 355, 356f implantation window, 357 layers of, 355 myometrial contractility, 355–357 tissue degradation and hemorrhage, 355 vasoconstriction, 355–357 Endopelvic fascia, 802 Endoscopic retrieval pouches, 883 Enoxaparin (Lovenox), 830–831, 831t, 914t Enterobius vermicularis, 324 Enterocele, 540f posterior vaginal wall prolapse and, 556 small bowel peristalsis and, 549, 550f Enterococcus faecalis, 66 EPDS. See Edinburgh Postnatal Depression Scale (EPDS)

Index Epidermal and dermal lesions, vulvar, 96, 96f Epidermal inclusion cysts, 97, 98f Epididymal fullness, 433 Epilation, 399 Epithelial ovarian cancer, 740–755 clear cell adenocarcinoma, 746, 746f diagnosis, 741–742 CA125 level, 742 genetic testing, 736t, 742 imaging of, 742 OVA1, 742 paracentesis, 742 Risk of Ovarian Malignancy Algorithm, 742 symptoms and physical findings, 741–742 endometrioid adenocarcinomas, 745, 745f epidemiology, 735–737 fallopian tube carcinoma, 747, 747f generalist, role of, 742–743 Krukenberg tumor, 747, 748f mixed carcinoma, 746 mucinous adenocarcinomas, 745, 746f pathogenesis, 740–741, 741f pathology, 743–747 patterns of spread, 747–748 prevention of, 737–379 primary peritoneal carcinoma, 747, 747t prognostic factors, 753 prophylactic surgery for, 738–7339 risk factors for, 735–737, 736t secondary tumors, 747 serous tumors, 744, 745f small cell carcinomas, 746–747 surgical staging of, 748–749, 750t symptoms of, 741–742, 741f transitional cell carcinoma, 746 treatment of, 748–755 chemotherapy, 751–752, 752t cytoreductive surgery, 750–752, 754 intraperitoneal chemotherapy, 752, 752t intravenous chemotherapy, 752 salvage chemotherapy, 854 undifferentiated carcinomas, 746 Epithelioid trophoblastic tumor, 786 Epoophoron, 423 Erythromycin for chlamydial infection, 65t for granuloma inguinale, 59t Erythromycin ethyl succinate, for chlamydial infection, 65t Escherichia coli, 66, 97, 282, 911 Escitalopram, 304t eSET. See Elective single embryo transfer (eSET) Essure Permanent Birth Control System, 26, 28, 29, 41t, 117, 117f microinsert used in, 117f in transcervical sterilization, 117, 1046–1047, 1046f–1047f

Estazolam, 18t Estrogen- and progestin-releasing vaginal contraceptive ring, 122f Estrogen cream during abdominal sacrocolpopexy, 1098 for cervical stenosis, 102 in labial adhesion, 322 for lichen sclerosus, 90 in pelvic organ prolapse, 552 in urinary incontinence, 530 Estrogen potency, 365t Estrogen receptors, 339, 340f in endometrium, 357 Estrogen replacement therapy abnormal bleeding with, 191, 505 bioidentical hormones, 497 continuous use, 493, 494, 495 contraindications, 494–495 cyclic use, 493 depression treatment, 506 for dyspareunia, 505–506 formulations of, 494, 495, 497 indications, 494–495 major trials of, 492–94 for menopausal vasomotor symptoms, 495 for osteoporosis in mature woman, 501 urinary incontinence, 507, 515, 530 vaginal atrophy treatment, 505 Estrogens, in clinical practice, 362–363 Estrostep, 121t Eszopiclone, 18t, 304t Ethynodiol diacetate, 120t Etonogestrel implant, 112 effects of, 106 insertion of, 115, 115f safety of MR imaging with, 41t Von Willebrand disease and, 193 Eugonadotropic amenorrhea, 378–379 nonclassic congenital adrenal hyperplasia, 379 ovarian tumor, 379 polycystic ovarian syndrome, 379 Euploid abortion, 138–139 Eutopic endometrium, 231 Eversion cervical, 102, 625 endocervical, 991 urethral, 486t Exercise, 12 External anal sphincter (EAS), 561–562, 562f, 563 anatomy of, 821–822, 822f sphincteroplasty, 1125–1127, 1126f–1127f External beam radiation therapy, 610, 611f, 615–616 conformal radiation therapy, 615 for endometrial cancer, 716 intensity-modulated radiation therapy, 616 for squamous cell carcinoma, 697–698

External genitalia, 409, 624, 818, 820 abnormal, bladder exstrophy and, 414 of CAIS patient, 413 development of, 410f gender assignment using, 413 phenotypic appearance of, 413 virilization of, 410f External genital warts. See Condyloma acuminata External iliac artery, 798–799, 798f Hesselbach triangle, 799 in pelvic lymphadenectomy, 1168–1169 proximal portion of, 816 External iliac lymph nodes, 809, 823 anatomy, 810f in minimally invasive surgery, 1178 pattern of tumor spread, 659 in pelvic lymphadenectomy, 1168–1169 External oblique muscle, 796 External vulva, 679 Extravasation injury, chemotherapeutic agents associated with, 595t F Facial hirsutism, 389f Fallopian tube carcinoma, 747, 747f staging of, 747, 750t Fallopian tubes, 809 ampullary portion of, 163, 809 anatomy of, 809 anomalies, 423 blue dye spill onto ovarian surface, 441f cannulation, 1050–1051, 1050f–1051f intraoperative, 1050–1051 postoperative, 1051 preoperative, 1050 clip application around, 1007f dilated, HSG and, 38–39 in ectopic pregnancy, 161, 163, 163f, 166 epithelium, 741f fibrosis of, Filshie clip fall and, 1006f fimbriated portion of, 809 interstitial portion of, 809 isthmic portion of, 809 laparoscopic salpingo-oophorectomy, 1019–1020, 1020f laparoscopic sterilization of, 1006–1010, 1006f–1010f ligation of, 936, 936f occlusion chemical, 118 mechanical, 117 pathology, 224–225 benign neoplasms, 224–225 hydrosalpinx, 224, 224f tuboovarian abscess, 225 in pelvic inflammatory disease, 33–34, 34f, 66–67 salpingectomy of interval partial, 937–938, 937f–938f laparoscopic, 1011–1012, 1011f–1012f salpingostomy and, 939–940, 939f

1239

1240

Index Fallopian tubes (Continuedâ•›) serous carcinoma in situ of, 741f sonographic detection of, 25–26 surgical reanastomosis of, 459f tumor confined to, 250t Fallopian tubes reanastomosis of, 458–459, 459f Falope ring, 115 surgical application, 1008, 1008f–1009f Famciclovir, 57t Fascial incision, 927f for Cherney incision, 931, 931f for Maylard incision, 932, 932f for midline vertical incision, 927, 927f for Pfannenstiel incision, 929–930, 929f–930f FAST. See Focused assessment with sonography for trauma (FAST) FDG-PET imaging for cervical cancer, 666 FDG-PET imaging, 45 Febrile nonhemolytic transfusion reaction, 866 Fecal immunochemical test (FIT), 10t Fecal incontinence (FI) definition of, 561 epidemiology of, 561 evaluation of, 564–569 clinical history, 564–566 diagnostic testing, 567–569, 567t physical examination, 566–567 Fecal Incontinence Severity Index, 564 functional testing for patients with, 567t medical management of, 569–570, 570t risk factors for, 563–564, 563t surgical management of, 570–571 Fecal incontinence quality-of-life (FI-QOL) questionnaire, 565t Fecal Incontinence Severity Index, 564t Federation of Gynecology and Obstetrics (FIGO), 787 Female condom, 128, 128f FC2 Female Condom, 128 insertion and positioning, 129f Female genital mutilation, 578 Female sexuality, 312–313 drive/desire, 312 release and resolution, 313 sexual arousal, 312–313 sexual response, models of, 312f variations in physiologic response, 313 Female tubal sterilization, 115–117 counseling in, 116 interval partial salpingectomy, 937–938, 937f–938f laparoscopic sterilization, 1006–1010, 1006f–1010f method failure in, 116–117 other effects of, 116–117 regret about, 116 risk-reducing salpingectomy, 116 salpingectomy and salpingostomy, 939–940 tubal interruption methods, 115–116

Femcon, 120t Femcon Fe, 120t Femoral artery anatomy, 798 medial femoral circumflex artery, 1166 UAE and, 198, 209 Fentanyl, 910 Ferguson reflex, 346 Ferriman-Gallwey scoring system, for hirsutism, 390–391, 390f Fertility awareness-based methods, 130 Fertinex, for ovulation induction, 452t Fesoterodine, for urinary incontinence, 533–534 Fetiform teratoma, 220 Fever, postoperative, 919 Fibrin sealant (Tisseal, Evicel), 581 Fibroadenomas, 278–279 Fibroepithelial neoplasm breast, 278–280 vulva, 96, 96f Fibroids. See Leiomyoma Fibromas-fibrosarcomas, 771 FIGO. See Federation of Gynecology and Obstetrics (FIGO) Filgrastim, 607 Filshie clip, 115, 1007, 1007f Fimbria ovarica, 809 Flaxseed oil, 498 Flexible sigmoidoscopy (FSIG), 10t Floxin, 65t Fluid and electrolyte abnormalities hyperkalemia, 919 hypernatremiam, 918 hypokalemia, 918 hyponatremia, 918 hypovolemic shock, 918 Fluid media, hysteroscopy, 904 Fluid resuscitation, 864–865 clinical assessment, 864, 864t Fluoroquinolones, 54–55 5-Fluorouracil (5-FU), 598 for vaginal intraepithelial neoplasia, 646 Fluoxetine, 306 for chronic pain syndromes, 259t for premenstrual dysphoric disorder, 303, 304t for vasomotor symptoms, 497t Flurazepam, 18t Fluvoxamine, 304t Focal adenomyosis, 213 Focused assessment with sonography for trauma (FAST), 32–33, 165–167 Focused-ultrasound therapy. See Magnetic resonance-focused ultrasound therapy Follicle-stimulating hormone (FSH), 119, 318, 319f, 334, 336, 343–344, 345f, 350–355 in amenorrhea, 370t for fertility evaluation, 434t, 436, 444 during menopause, 472, 488–489 for ovarian remnant syndrome, 261

in ovulation induction, 452–453 in precocious puberty, 328 for premature ovarian failure, 373, 381 secretion of, 345 testing for, 381–382 without breast development, 370t Follistim, for ovulation induction, 452t Foreign body, in vagina, 101 Forteo, for osteoporosis, 500t Fortical, for osteoporosis, 500t Fosamax. See Alendronate Fossa ovalis, 823 Fourth-tier contraceptive methods contraceptive sponge, 130, 131f spermicides, 130, 130f Fracture Intervention Trial (FIT), 502 Frankenhäuser plexus, 841 Functional anorectal disorders, 572–573 functional anorectal pain, 572–573 functional defecation disorders, 273 functional fecal incontinence, 572 Functional anorectal pain, 572–573 Functional bowel disorders, 265–267, 266t Functional defecation disorders, 273 Functional fecal incontinence, 572 Functional ovarian cysts, 215 associated factors, 218 diagnosis and treatment, 218–219, 218f theca lutein cysts, 219 Fundus, uterine, 807, 807f Furosemide, and urinary incontinence, 525t G GABA. See Gamma-aminobutyric acid (GABA) Gabapentin for chronic pain syndromes, 259t for menopausal vasomotor symptoms, 497t, 498 Galactorrhea, 280 causes of, 281t PRL levels associated with, 358, 378 GALT gene, 375 Gamete intrafallopian transfer (GIFT), 465 Gamma-aminobutyric acid (GABA), 303 Gamma rays, 610 Gardnerella vaginalis, 51 Gartner duct cysts, 101–102, 404t Gas embolization, 905 Gastrointestinal bowel preparation, 834–835 Gastrointestinal complications bowel obstruction, 915–916 diarrhea, 916 ileus, 915 nutrition, 916 Gastrointestinal disease, and pelvic pain, 265–267 appendicitis, 251t celiac disease, 265 colitis, 251t colonic diverticular disease, 265 constipation, 251t

Index diverticulitis, 251t functional bowel disorders, 265–267, 266t gastroenteritis, 251t Gastrointestinal toxicity, of chemotherapy, 605–606, 606t G-CSF. See Granulocyte colony-stimulating factors (G-CSF) Gellhorn pessary placement, 552f, 553–553 GelPOINT advanced access system, 895 Gemcitabine, 597–598 Gender assignment, 330, 413 Gender dysphoria, 330 Gender identity, 329–330 Genital herpetic ulcers, 56f Genitalia, male, 431f Genital trauma, 324–325 Genital ulcer infections, 55–60 chancroid, 59 granuloma inguinale, 59, 59t herpes simplex virus infection, 55–57 diagnosis of, 56 oral agents for, 57t symptoms of, 55–56, 56f treatment of, 56–57 lymphogranuloma venereum, 59–60, 60f syphilis, 57–59 diagnosis, 58 latent, 58 pathophysiology, 57–58 primary, 57 secondary, 57–58, 58f tertiary, 58 treatment, 58–59 Genital warts, external. See Condyloma acuminata Genitourinary fistulas angiogenesis, 577 classification of, 577–578, 578t definition of, 577 diagnosis of, 579–581 cystourethroscopy, 580 physical examination, 579–580 tampon test, 580 VCUG, 581 etiology of, 578–579 malignancy, 579 obstetric trauma, 578–579 pelvic surgery, 579 radiation therapy, 579 pathophysiology, 577 symptoms of, 579 treatment of, 581–582 conservative, 581 surgical, 581–582, 1078–1082, 1079f–1082f Genitourinary syndrome of menopause (GSM), 486, 486t, 505 Genitourinary tract, female, embryonic development of, 406f Gentamicin, 835t for hospitalacquired pneumonia, 911t for pelvic infection, 53

for PID, 68t for postgynecologic surgery infections, 79t Geriatric Depression Scale (GDS), 307 Geriatric screening, 17, 17f Germ cell tumors, ovarian, 760–767 choriocarcinoma, 764 diagnosis, 760–761 dysgerminoma, 762–763, 763f embryonal carcinomas, 764 epidemiology, 760 generalist, role of, 761–762 histogenesis, 762, 762f immature teratomas, 765, 765f management during pregnancy, 767 mature cystic teratoma, malignant transformation of, 765–766, 766f mixed germ cell tumors, 764–765 origin of, 761f pathology, 762–766 polyembryoma, 764 prognosis, 767 serum tumor markers in, 761t treatment, 766–767 WHO classification, 762, 762t yolk sac tumors, 764 Gestational carrier surrogacy, 465 Gestational choriocarcinoma, 785–786, 786f Gestational trophoblastic disease (GTD), 779–794 epidemiology of, 779–780 gestational trophoblastic neoplasia, 779, 784–791 assessment, 787 diagnosis of, 786–787, 787t FIGO staging of, 787–788, 787t, 788f histologic classification, 785–786 metastasis sites of, 789f phantom b-hCG, 791 posttreatment, 791 treatment, 788–791 hydatidiform mole (molar pregnancy), 780–784, 780t coexistent fetus, 784, 785f complete, 780–781, 780f, 780t, 781f diagnosis of, 782–783 ectopic molar pregnancy, 784 partial, 780t, 781–782 postmolar surveillance, 783–784 prophylactic chemotherapy, 784 treatment, 783 risk factors for, 779–780 WHO classification of, 779t Gestational trophoblastic neoplasia (GTN), 779, 784–791 assessment, 787 diagnosis of, 786–787, 787t FIGO staging of, 787–788, 787t, 788f histologic classification, 785–786 epithelioid trophoblastic tumor, 786 gestational choriocarcinoma, 785–786, 786f

invasive mole, 785, 785f placental-site trophoblastic tumor, 786 metastasis sites of, 789f phantom b-hCG, 791 postmolar surveillance, 783–784 posttreatment, 791 treatment, 788–791 cerebral metastases, 790–791 chemotherapy, 789–790 surgical, 788–789 Gestrinone (ethylnorgestrienone; R2323), 242 gFOBT. See Guaiac-based fecal occult blood test (gFOBT) GIFT. See Gamete intrafallopian transfer (GIFT) Glandular cell abnormalities, cervix, 636– 637 GnRH. See Gonadotropin-releasing hormone (GnRH) GnRH agonists. See Gonadotropin-releasing hormone (GnRH) GnRH antagonists, 209 for endometriosis, 241 GnRH-R. See Gonadotropin-releasing hormone receptor (GnRH-R) GOG. See Gynecologic Oncology Group (GOG) Gompertzian growth pattern, 592, 593f Gonadal dysgenesis, 373–374, 374f, 409 mixed, 412 pure, 412 46,XX, 413 46,XY, 412 Gonadal dysgenesis partial, 412 Gonadal peptides, and menstrual cycle, 351, 352f Gonadoblastomas, 219t, 762, 764 Gonadotropin-releasing hormone (GnRH), 318, 342, 344 for abnormal uterine bleeding, 195t, 197 decapeptide, 344f for endometriosis, 240–241 for leiomyomas, 204, 208–209 neuronal migration, 344–345 for ovulation induction, 452–453, 452t for precocious puberty treatment, 327, 328t for puberty evaluation, 328 pulsatile release of, 336f, 345, 345f secretion into portal vasculature, 334 Gonadotropin-releasing hormone receptor (GnRH-R), 339 for ovulation induction, 452–453, 452t Gonadotropin surge-inhibiting/attenuating factor (GnSIF/AF), 354 Gonads and ductal systems in male, development of, 407f Gonal-f, for ovulation induction, 452t Gonorrhea. See Neisseria gonorrhoeae G-protein coupled receptors, 339 Gracilis muscle transposition, 571

1241

1242

Index Gracilis myocutaneous flap, 1166, 1166f Granulocyte colony-stimulating factors (G-CSF), 607 Granuloma inguinale, 59 Granulosa cells, 352, 353 Graves speculum, 5f Gray-scale imaging, 23 Greater sciatic foramen, 800 Growing teratoma syndrome, 765 Growth hormone-releasing hormone (GHRH), 346 Growth spurt, 320 GSM. See Genitourinary syndrome of menopause (GSM) GTD. See Gestational trophoblastic disease (GTD) GTN. See Gestational trophoblastic neoplasia (GTN) Guaiac-based fecal occult blood test (gFOBT), 10t Gynandroblastomas, 773 Gynazole-1, for candidiasis, 62t Gynecologic infection Actinomyces infection, 83 antibiotics, 52–55 aminoglycosides, 53–54 carbapenems, 54 cephalosporins, 53 clindamycin, 54 fluoroquinolones, 54–55 metronidazole, 54 monobactam, 54 penicillins, 52–53 tetracyclines, 55 vancomycin, 54 bartholin gland duct abscess, 82, 83f external genital warts, 70 genital ulcer infections, 55–60 chancroid, 59 granuloma inguinale, 59, 59t herpes simplex virus infection, 55–57 lymphogranuloma venereum, 59–60, 60f syphilis, 57–59 infectious vaginitis, 60–64 candidiasis, 61–62, 61f, 62t characteristics of, 61t fungal infection, 60–63 trichomoniasis, 63–64 infectious warts and papules, 70 molluscum contagiosum, 70–71, 70f pelvic inflammatory disease, 65–70 acute, 66–67 chronic, 69 diagnosis, 66–69 microbiology and pathogenesis, 66 risk factors, 66t silent, 66 treatment of, 68t, 69–70, 69t tuboovarian abscess, 67–68, 68f postoperative infection, 75–82 abdominal incision infection, 80 adnexal infection, 78, 78f

diagnosis of, 76–77 infected pelvic hematoma, 79–80, 79f, 80f MRSA, 82 necrotizing fasciitis, 81–82, 82f ovarian abscess, 78–79 pelvic abscess, 79–80, 79f pelvic cellulitis, 78, 78f surgical site infection, 76 toxic shock syndrome, 80–81, 81t vaginal cuff cellulitis, 77–78, 78f wounds, 75–76 pruritic infestations, 71–72 pediculosis, 72 scabies, 71–72 suppurative cervicitis, 64–65 Chlamydia trachomatis, 64–65 Mycoplasma genitalium, 65 Neisseria gonorrhoeae, 64 urinary tract infections, 72–75 acute bacterial cystitis, 73–75 acute pyelonephritis, 75 asymptomatic bacteriuria, 75 treatment of, 74t vaginal flora, 50–52, 51t altered flora, 50 bacterial vaginosis, 51–52, 51f, 51t, 52t vaginal pH and, 50 vulvar abscess, 82 Gynecologic malignancies, surgeries for, 1134–1224 appendectomy, 1205–1206, 1205f colostomy, 1191–1193, 1192f–1193f diaphragmatic surgery, 1189–1190, 1189f en bloc pelvic resection, 1181–1184, 1181f–1183f ileostomy, 1196, 1196f inguinofemoral lymphadenectomy, 1215–1217, 1215f–1217f intestinal bypass, 1203–1204, 1203f–1204f large bowel resection, 1194–1195, 1194f–1195f low anterior resection, 1199–1202, 1200f–1202f lymphadenectomy paraaortic, 1171–1174, 1172f–1173f pelvic, 1168–1170, 1169f–1170f minimally invasive radical hysterectomy, 1142–1147, 1143f–1147f minimally invasive staging, 1175–1180, 1176f–1179f modified radical abdominal hysterectomy (type II), 1140–1141, 1140f–1141f omentectomy, 1185–1186, 1186f pelvic exenteration anterior, 1154, 1154f posterior, 1155, 1155f total, 1148–1153, 1148t, 1149f–1153f radical abdominal hysterectomy (type III), 1134–1139, 1136f–1138f

radical complete vulvectomy, 1212–1214, 1212f–1214f radical partial vulvectomy, 1209–1211, 1209f–1211f reconstructive grafts and flaps, 1218–1220, 1218f–1219f skinning vulvectomy, 1207–1208, 1207f–1208f small bowel resection, 1197–1198, 1197f–1198f splenectomy, 1187–1188, 1187f–1188f urinary conduit continent, 1160–1163, 1160f–1163f incontinent, 1156–1159, 1157f–1159f vaginal reconstruction, 1164–1167, 1164f–1166f Gynecologic malignancy, 40 Gynecologic Oncology Group (GOG), 707 Gyne-Lotrimin 3, for candidiasis, 62t Gyne-Lotrimin 7, for candidiasis, 62t H HAART. See Highly active antiretroviral therapy (HAART) Habitrol, 11t Haemophilus ducreyi, 59 Haemophilus influenzae, 324 HAIRAN syndrome. See Hyperandrogenicinsulin resistant-acanthosis nigricans (HAIRAN) syndrome Hair removal, in hirsutism, 399 Halban culdoplasty, 1118, 1118f Haloperidol, and urinary incontinence, 525t Handheld retractors, 851, 851f Hand-Schuller-Christian syndrome, 377 H2 antagonists, 281t Harmonic imaging, 23 Harmonic scalpel, 859 Hashimoto thyroiditis, 149 HBV. See Honor-based violence (HBV) hCG. See Human chorionic gonadotropin (hCG) Health Outcomes and Reduced Incidence with Zoledronic Acid Once Yearly (HORIZON) Pivotal Fracture Trial, 503 Heart and Estrogen/Progestin Replacement Study (HERS), 493 Heavy menstrual bleeding (HMB), 180. See also Abnormal uterine bleeding coagulopathy and, 192 hysterectomy in, 198 in kidney, liver, and thyroid disease, 192 LNG-IUS for, 195–196 uterine artery embolization for, 197–198 vWD-related chronic, 193 Hematogenous dissemination, of endometrial cancer, 712 Hematologic evaluation anemia, 184, 830 Hematologic evaluation autologous blood donation, 830

Index coagulopathies, 830 oral anticoagulation, 830 Hematologic toxicity, radiation therapy and, 621 Hematoma pelvic, 79–80, 79f, 80f vulva, 100–101 Hematometra, 212–213, 212f Hemoperitoneum, 32f, 67, 167, 770 Hemorrhage, intraoperative, 905. See also Abnormal uterine bleeding hemostatic agents, 861t heparin for, 859 management of, 859–860 steps of, 860 surgical method, 860 Hemostasis, 900 Heparin for hemorrhage, 859 for interstitial cystitis/painful bladder syndrome, 264 low-molecular-weight for antiphospholipid antibody syndrome, 149 characteristics of, 914t and osteoporosis risk, 481t prophylaxis, 837–838 for pulmonary embolism, 912–913 thrombocytopenia associated with, 836t unfractionated, 830–832, 831t Hepatic adenoma, benign, 126 Hepatic focal nodular hyperplasia, 126 Hepatitis A vaccine, 8t Hepatitis B counseling in, 19t vaccine, 8t Hepatitis C, counseling in, 19t Hereditary breast-ovarian cancer syndrome, 288 BRCA1 and BRCA2 genes, 736–737, 737f genetic testing, 737 Hereditary leiomyomatosis and renal cell cancer (HLRCC) syndrome, 203 Hereditary nonpolyposis colorectal cancer (HNPCC), 703, 736 Herlyn-Werner-Wunderlich syndrome, 417 Hernias, 267–268, 268f femoral, 267f incisional, 878 inguinal, 267f involve anterior abdominal wall, 267f obturator, 267 sciatic, 267 surgical risk factors, 878, 897, 926 Herpes simplex virus infection, 55–57 diagnosis of, 56 oral agents for, 57t symptoms of, 55–56, 56f treatment of, 56–57 and vulvar cancer, 681 HERS. See Heart and Estrogen/Progestin Replacement Study (HERS) Hesselbach triangle, 799

Heterosexual precocious puberty, 329 Heterotopic pregnancy, 175 Hidradenitis suppurativa, 93–94, 93f Higher-order multifetal pregnancy, 456 High-grade squamous intraepithelial lesion (HSIL), 636, 640f, 658 Highly active antiretroviral therapy (HAART), 126, 651–652 Hirsutism, 389–391 facial, 389f Ferriman-Gallwey scoring system for, 390–391, 390f medications causes, 389t pathophysiology of, 390, 390f treatment of, 398–399 HIV-infected women, 651–652 HIV postexposure prophylaxis, following sexual assault, 309, 309t HMB. See Heavy menstrual bleeding (HMB) HNPCC. See Hereditary nonpolyposis colorectal cancer (HNPCC) Honor-based violence (HBV), 311 Hormone communication, 334, 335f Hormone replacement therapy. See Estrogen replacement therapy HoxA9, 408 HoxA10, 408 HoxA11, 408 HSD3B2 mutation, 414 HSDD. See hypoactive sexual desire disorder (HSDD) HSG. See Hysterosalpingography (HSG) HSIL. See High-grade squamous intraepithelial lesion (HSIL) Hulka-Clemens clip, 115 Hulka clip. See Wolf clip Hulka uterine manipulator, 881f Humagon, for ovulation induction, 452t Human chorionic gonadotropin (hCG), 36, 280f, 334–336 in complete hydatidiform mole, 781 composite curve for, 141f in ectopic pregnancy, 163–164 for diagnosis, 164–165 during treatment of, 170–173, 170t in gestational trophoblastic disease, 791 in GTN, 786–787 in malignant ovarian germ cell tumors, 761t ovarian cysts diagnosis, 215–216 for ovulation induction, 452, 452t, 455–456, 457 partial hydatidiform mole clinical assessment, 782 postmolar surveillance, 784 phantom, 791 uterine pregnancy and, 141 Human papillomavirus infection, of lower genital tract, 627–630 basic virology, 627–628 diagnosis of, 629

latent infection, 628 life cycle, 627f outcomes, 628–629, 628f prevention of, 630 productive infections, 628–629 surgical excision of, 996–997 transmission, 628 treatment of, 70, 71t, 629–630 vaccines for, 9t, 630 HyCoSy. See Hysterosalpingo-contrast sonography (HyCoSy) Hydatidiform mole, 780–784, 780t coexistent fetus, 784, 785f complete, 780–781, 780f, 780t, 781f diagnosis of, 782–783 ectopic molar pregnancy, 784 partial, 780t, 781–782 postmolar surveillance, 783–784 prophylactic chemotherapy, 784 treatment, 783 Hydrochlorothiazide (HCTZ), and urinary incontinence, 525t Hydromorphone, 910 Hydrosalpinx, 224, 224f surgical treatment of, 459, 464 Hydroxyzine, 304t Hymeneal defects, 320, 321f, 323, 415–416, 415f Hymenectomy, 969–970, 969f intraoperative, 969–970 postoperative, 970 preoperative, 969 Hyperandrogenic-insulin resistantacanthosis nigricans (HAIRAN) syndrome definition of, 386 Hyperandrogenism, 389–391 acne vulgaris, 391 alopecia, 391 differential diagnoses of, 394t evaluation of, 393–397, 395f hirsutism, 389–391 facial, 389f Ferriman-Gallwey scoring system for, 390–391, 390f medications causes, 389t pathophysiology of, 389–390, 390f treatment of, 397–400 Hypercholesterolemia, 15–16, 15t, 392 Hyperemesis gravidarum, 140, 781 Hypergonadotropic hypogonadism, 373–375 acquired abnormalities, 375 heritable disorders, 373–375 gonadal dysgenesis, 373–374, 374f specific genetic defects, 374–375 Hyperkalemia, 919 Hypernatremiam, 918 Hyperprolactinemia, 150, 357–359, 358f, 379 associated amenorrhea, 359 diagnosis, 358–359, 358f etiology, 357–358 and ovarian dysfunction, 450 treatment of, 360–361, 361f

1243

1244

Index Hyperreactio lutealis, 219 Hypertension, 827 chronic, 14–15 identifiable causes of, 15t initial drug therapy for, 15t Hyperthyroidism, 832 Hypertriglyceridemia, 15t, 16 Hypoactive sexual desire disorder (HSDD), 506 Hypogastric artery. See Internal iliac artery Hypogonadotropic hypogonadism, 358, 375–378 anterior pituitary gland disorders, 378 causes of, 378 hypothalamic disorders, 375–377 Hypokalemia, 918 Hyponatremia, 918 Hypospermia, 462 Hypothalamic disorders, 375–377 Hypothalamic kisspeptin neurons, 343 Hypothalamic neuroendocrinology, 342–343 Hypothalamic-pituitary axis, 342–346 abnormalities in, 357–361 hyperprolactinemia, 357–359, 358f pituitary adenomas, 359–360, 359t, 360f, 361f treatment of, 360–361, 362f anatomy, 342, 342f anterior pituitary hormones, 343 corticotropin-releasing hormone, 345 dopamine, 345 growth hormone–releasing hormone, 345–346 hypothalamic neuroendocrinology, 342 hypothalamic-releasing peptides, 344–345 other hypothalamic neuropeptides, 343 posterior pituitary peptides, 346 prolactin, 345 thyrotropin-releasing hormone, 345 Hypothalamic-pituitary-ovarian (HPO) axis, 318 positive and negative feedback loops with, 336f Hypothalamic-releasing peptides, 344–345 Hypothyroidism, 379, 832 and abnormal bleeding, 181t and delayed puberty, 329t fertility effects, 149, 329 menstrual disturbances by, 192 and ovarian dysfunction, 450 and precocious puberty, 328t pregnancy loss and, 149 preoperative evaluation, 832 PRL levels in, 358 treatment of, 383 Hypovolemic shock, 918 Hysterectomy, 835t abdominal, 950–956, 952f–956f. See also Hysterectomy abdominal incision infection following, 80 disadvantages of, 950

femoral nerve injury and, 844 intraoperative, 951–956 lower urinary tract injury during, 867 modified radical, 1140–1141, 1140f–1141f modified radical (type II), 1140–1141, 1140f–1141f obesity risk and, 75t for ovarian cancer, 751 and pelvic cellulitis, 78 pelvic infection following, 80, 80f postoperative, 956 postoperative infection, 76 preoperative, 950–951 radical (type III), 669t, 1134–1139, 1136f–1138f vesicocervical and vesicovaginal spaces during, 811 for adenomyosis, 214 adjuvant, following radiation, 672 for atypical endometrial hyperplasia, 706–707 for cervical cancer, 668–670 early-stage, 668–670 extrafascial (Type I), 668 modified radical (Type II), 669 radical (Type III), 669–670, 669f tissues resected during, 669t in cervical pregnancy, 174–175, 175f for chronic pelvic pain, 260 for CIN, 645 for endometriosis, 243 for epithelioid trophoblastic tumor, 786 in heavy menstrual bleeding, 198 laparoscopic, 950, 1026–1029, 1027f–1028f intraoperative, 1026–1029 postoperative, 1029 preoperative, 1026 laparoscopic supracervical, 1030–1032, 1030f–1032f for leiomyomas, 211 minimally invasive radical, 1142–1147, 1143f–1147f intraoperative, 1142–1147 postoperative, 1147 preoperative, 1142 for nonmetastatic PSTT, 786 for pelvic rgan prolapse, 556 in permanent contraception, 118 in primary endometrial dysfunction, 198 radical abdominal, 1134–1139 and risk of urinary incontinence, 516 roles in GTN treatment, 788–789 as sterilization, 118 supracervical, 950–951, 950f at time of prolapse repair, 556 tissues resected during simple and extended, 669t total laparoscopic, 1033–1036, 1034f–1036f urinary incontinence, risk of, 516 vaginal, 950, 957–961, 957f–961f. See also Hysterectomy

intraoperative, 957–961 ovarian abscess and, 78–79 pelvic cellulitis and, 78 postoperative, 961 preoperative, 957 radical, 669t vs. myomectomy, for leiomyomas, 212 Hysterosalpingo-contrast sonography (HyCoSy), 25–26, 26f Hysterosalpingography (HSG), 26–27, 38–39 for bicornuate uterus, 422 for diethylstilbestrol-induced reproductive tract abnormalities, 423 for evaluating pelvic anatomy, 438–440 for evaluation of amenorrhea, 382t of intrauterine cavity, 438, 439f mechanical tubal occlusion, 117 for müllerian anomalies, 418, 440f in transcervical Essure, 1047, 1047f for uterine anomalies, 438–440, 440f Hysteroscopic complications gas embolization, 905 hemorrhage, 905 uterine perforation, 905 Hysteroscopic instruments Bettochi hysteroscope, 902 flexible hysteroscope, 902–903 hysteroscopic morcellator, 903 rigid hysteroscope, 901–902 Hysteroscopic media. See Distention media Hysteroscopic morcellator, 903 Hysteroscopic myomectomy, 1040–1042, 1041f intraoperative, 1040–1042 instruments, 1040 surgical steps, 1040–1042 postoperative, 1042 preoperative, 1040 Hysteroscopic polypectomy, 1038–1039, 1038f intraoperative, 1038–1039 instruments, 1038 surgical steps, 1038–1039 postoperative, 1039 preoperative, 1038 Hysteroscopic preoperative considerations, 901 Hysteroscopic septoplasty, 1048–1049, 1048f–1049f intraoperative, 1048 postoperative, 1049 preoperative, 1048 Hysteroscopic transcervical sterilization. See Essure Permanent Birth Control System Hysteroscopy, 1037, 1037f I IAS. See Internal anal sphincter (IAS) Ibandronate, for osteoporosis, 500t, 503 ICON Group. See International Collaborative Ovarian Neoplasm (ICON) Group

Index Idiopathic granulomatous mastitis (IGM), 282 Idiopathic hypogonadotropic hypogonadism (IHH), 375 Ifosfamide (Ifex), 598–599, 599f IGRT. See Image-guided radiation therapy (IGRT) IHH. See Idiopathic hypogonadotropic hypogonadism (IHH) Ileal conduit, 1156–1159, 1156f–1159f, 1166 Ileostomy, 1196, 1196f Ileus, 915 Iliac crest, 800f Iliococcygeus muscle, 542, 803–804 804f Iliopsoas muscle, 823 Ilium, 799, 800f Image-guided radiation therapy (IGRT), 616 Imipramine, 123t and urinary incontinence, 525t, 534 Immature teratomas, 765, 765f Immunization, 7 recommendations for, 8t–9t Impaired glucose tolerance (IGT), 392 diagnosis of, 396t and type 2 DM, 392 Impedance, 858 Imperforate hymen, 321f Implanon, 41t, 112, 115 Implants, 41t IMRT. See Intensity-modulated radiation therapy (IMRT) Incisional hernia, 878 Incisions of bartholin gland duct, 971–972, 971f–972f Cherney, 931, 931f fascial, 927f Maylard, 932, 932f midline vertical, 926–928, 927f–928f intraoperative, 927–928 postoperative, 928 preoperative, 926–927 ovarian, 933f peritoneal, 928f Pfannenstiel, 929–930, 929f–930f intraoperative, 929–930 postoperative, 930 preoperative, 929 surgical, 846–847 midline vertical incision, 846 transverse incisions, 846–847 of vulvar abscess, 977–978, 977f–978f Incompetent cervix, 147 Incomplete abortion, 142 Incontinent urinary conduit, 1156–1159, 1157f–1159f patient preparation, 1156–1159 postoperative, 1159 preoperative, 1156 Induced abortion, 150–152 classification, 151

complications of, 155 counseling before elective abortion, 152 legislation of, 151–152 prophylaxis, 835t rates, 150 sequela of, 155 techniques, 152–155 medical, 154–155 surgical, 153–154 training in, 152 in the United States, 151–152 Inevitable abortion, 142 Infected pelvic hematoma, 79–80, 79f, 80f Infectious complications, associated with packed RBC transfusion, 866 Infectious disease, counseling in, 19t Infectious vaginitis, 60–64 candidiasis, 61–62, 61f, 62t topical agents for, 62t uncomplicated, 61–62 vulvovaginal, 61 characteristics of, 61t fungal, 60–63 fungal infection, 60–63 trichomoniasis, 63–64 diagnosis, 63, 63f treatment of, 64 Infectious warts and papules, 70 Inferior hypogastric plexus, 518f, 806 Infertility, 427–445, 449–470 anatomic abnormalities, correction of, 458–461 distal tubal occlusion, 458 endometrial polyps and, 460 intrauterine adhesions and, 460 leiomyomas and, 459 midtubal occlusion, 458 peritoneal disease, 460–461 proximal tubal occlusion, 458 tubal cannulation, 458 tubal factors, 458–459 tubal reconstruction, 458–459 uterine factors, 459–460 anovulation, evaluation for, 433–435 basal body temperature chart, 434, 434f clinical evaluation, 434 endometrial biopsy, 435 ovulation predictor kits, 435 serum progesterone, 435 sonography, 435 assisted reproductive technology for, 463–468 complications of, 466–468 egg donation, 465 embryo, oocyte, or ovarian tissue cryopreservation, 466 gamete or zygote intrafallopian transfer, 465 gestational carrier surrogacy, 465 intracytoplasmic sperm injection, 465 preimplantation genetic diagnosis/ screening, 466

in vitro fertilization, 464, 464f, 467t, 468t in vitro maturation, 466 cervical abnormalities in, correction of, 461, 462f definition of, 427 diagnostic algorithm for evaluation of, 445f diminished ovarian reserve, correction of, 458 diminished ovarian reserve, evaluation for, 435–437 antimüllerian hormone measurement, 436–437 antral follicle count, 437 follicle-stimulating hormone and estradiol measurement, 436 reproductive aging, 435–436, 435t etiology of, 428, 428t female anatomic abnormalities, evaluation for, 437–441 anatomic evaluation, 438–441, 438t Asherman syndrome, 438 cervical factors, 441, 441f endometrial polyps, 437–438 hysterosalpingography, 438–440, 439f–440f hysteroscopy, 441 laparoscopy, 440–441, 441f salpingitis isthmica nodosa, 437 transvaginal pelvic sonography, 440 tubal and pelvic factors, 437 uterine abnormalities, 437–438 female medical history, 428–430 environmental factors and, 429–430 ethnicity and family history, 430 gynecologic history, 428 social history, 428–429 surgical history, 428 female patient, physical examination of, 433 intrauterine insemination, 463 lifestyle therapies, 449–450 exercise, 450 nutrition, 450 stress management, 450 weight optimization, 449–450 luteal phase defect, 435 male, correction of, 462–463 abnormal semen volume, 462 abnormal sperm count, 462–463 abnormal sperm motility/morphology, 463 varicocele, 463 male, evaluation of, 442–445 additional sperm testing, 444 DNA fragmentation, 443–444 genetic testing, 444–445 hormonal evaluation, 444 normal spermatogenesis, 442 semen analysis, 442–443, 442t testicular biopsy, 445

1245

1246

Index Infertility (Continuedâ•›) male medical history, 430–433 male patient, physical examination of, 433 ovarian dysfunction, correction of, 450–458 hyperprolactinemia, 450 hypothyroidism, 450 ovulation induction, 450–458 physical examination, 433 primary, 427 secondary, 427 tests for, 434t unexplained, 460t unexplained infertility, 463 Inflamed Skene gland cyst, 587 Inflammatory bowel disease associated with chronic pelvic pain, 254t preconceptional counseling in, 19t rectovaginal fistula and, 573t Inflammatory breast cancer, 291–292, 292f Inflammatory dermatoses, 91–94 aphthous ulcers, 94 atopic eczema, 91 contact dermatitis, 91, 91f, 91t hidradenitis suppurativa, 93–94, 93f intertrigo, 91 lichen planus, 92–93, 92f, 92t psoriasis, 91–92, 92f Inflammatory pain, 249–250 Inflammatory vaginitis, desquamative, 101 Influenza vaccine, 8t Informed consent, 833 Infundibulopelvic ligament, 809 bleeding from, 862 transection during oophorectomy, 953f, 1027, 1027f twisting of, 222f Infundibulopelvic ligament coagulation, 1019, 1020f Infundibulopelvic ligament ligation, 935–936, 936f Inguinofemoral lymphadenectomy, 1215–1217, 1215f–1217f anatomy of, 822–823, 823f intraoperative, 1215–1217 postoperative, 1217 preoperative, 1215 for vulvar cancer, 685–686, 686t Injectable progestins for acute hemorrhage, 195 effects of, 127–128 effects on growth of leiomyomas, 204, 207 for endometrial cancer, 716 for endometrial hyperplasia, 706–707 in endometrial vascular fragility, 191 for endometriosis, 239–240 formulations, 127 Innominate bones, 799, 800f Insomnia, 18 Instrument, surgical, 848–853 for abdominal sacrocolpopexy, 1098 blades, 848–849, 849f

laparoscopic, 879–886. See also Laparoscopic instruments needle, 853–855, 854f needle holders, 849–850, 850f retractors, 850–852 abdominal surgery, 850–851, 851f vaginal surgery, 851–852, 852f scalpel, 848–849, 849f scissors, 849, 849f, 850f, 882 self-retaining retractor, 883 suction tips, 853–854, 854f tissue clamps, 852, 853f tissue forceps, 850, 851f vascular clamps, 853f Insulin-like growth factors (IGF), 352 Insulin-sensitizing agents, for ovulation induction, 452 Intensity-modulated radiation therapy (IMRT), 616, 616f Interischial line, 820 Intermenstrual bleeding. See Abnormal uterine bleeding Intermezzo, 18t Intermittent positive-pressure breathing (IPPB), 827 Internal anal sphincter (IAS), 561 Internal iliac artery, 808, 815–816 blood supply to vagina, 813 internal pudendal artery, 822 ligation, 862, 863, 863f pelvic blood supply by, 804, 805t uterine blood supply, 809 Internal iliac lymph nodes, 659, 694 distal common, 1170 in pelvic lymphadenectomy, 1169 uterine lymphatic drainage to, 809, 810f Internal oblique muscle, 796 International Collaboration of Epidemiological Studies of Cervical Cancer, 658 International Collaborative Ovarian Neoplasm (ICON) Group, 752 International Federation of Gynecology and Obstetrics (FIGO), 722 International Society for the Study of Vulvar Disease (ISSVD), 88, 647 International Society for the Study of Women’s Sexual Health (ISSWSH), 486 Interstitial cells, 442 Interstitial pregnancy, 173–174, 174f cornuostomy and cornual wedge resection in, 941–944, 941f–943f Intertrigo, 91 Interval partial salpingectomy, 937–938, 937f–938f for female tubal sterilization, 116 intraoperative, 937–938 postoperative, 938 preoperative, 937 Interventional radiology, 45–46 Intestinal bypass, 1203–1204, 1203f–1204f intraoperative, 1203

postoperative, 1204 preoperative, 1203 Intimate partner violence (IPV), 311–312 diagnosis, 311 management, 311–312 risks, 311 Intracytoplasmic sperm injection, 461f, 465 Intramural leiomyomas, 204. See also Leiomyoma Intraoperative radiation therapy (IORT), 619 Intrauterine adhesions. See Asherman syndrome Intrauterine device (IUD), 41t, 107–112 Actinomyces infection, 83 associated infections, 109–110 associated pelvic inflammatory disease, 69 bleeding treatment, 195–197, 214 bleeding with, 190–191 complication of, 53 contraceptive, 109f counseling for, 109–111 Cu-T 380A, 102t, 109, 131t, 132 ectopic pregnancy, 111 emergency contraception, 131t, 132 endometrial hyperplasia treatment, 706, 707 endometriosis treatment, 207 imaging of, 22, 28, 28f insertion procedures, 111–112 levonorgestrel-releasing intrauterine system, 108–109 low parity and adolescent candidates for, 110 magnetic resonance imaging of, 41t manufacturer contraindications to, 109t marker strings, 111 positioning, 28 postabortal or postpartum placement, 110 postadhesiolysis, 1053 Intrauterine pregnancy, 142f Intravenous leiomyomatosis, 204 Intravenous pyelography, 37–38 Intrinsic sphincteric defect (ISD), 522 TVT procedure for, 1063–1065, 1064f–1065f Intrinsic sphincteric deficiency, 522 Invasive mole, 785, 785f Invasive vulvar cancer, 682, 682t. See also Vulvar cancer Ionizing radiation with chemotherapy, 618 direct vs. indirect actions of, 613, 614f IORT. See Intraoperative radiation therapy (IORT) IPPB. See Intermittent positive-pressure breathing (IPPB) IPV. See Intimate partner violence (IPV) Irregular menstrual-type bleeding. See Abnormal uterine bleeding Ischioanal fossa, 815f Ischiocavernosus muscle, 820

Index Ischiorectal fossa, 821 Ischium, 799, 800f Isotretinoin, 400 ISSVD. See International Society for the Study of Vulvar Disease (ISSVD) ISSWSH. See International Society for the Study of Women’s Sexual Health (ISSWSH) Itch-scratch cycle, 88 J Jejunal conduit, 1166 K KAL1 gene, 375 Kallmann syndrome, 375–376, 376f, 444 Kariva, 120t Kegel exercises, 529 Kelnor, 120t Keratoacanthoma, 96 Klebsiella pneumoniae, 73, 911 Klinefelter syndrome, 145, 411, 444, 463 Knots, surgical, 856–857, 856f Krukenberg tumor, 747, 748f L Labial adhesion, 321–322, 322f Labial agglutination, 321 Labia majora, 818–819, 818f Labia minora, 322f, 818f, 819 reduction, 981–982 intraoperative, 981–982 postoperative, 982 preoperative, 981 LAIV. See Live attenuated influenza vaccine (LAIV) Laminaria, 153, 966 Lamotrigine, 123t Langer lines, 796, 797f Laparoscopic hysterectomy, 950, 1026–1029, 1027f–1028f intraoperative, 1026–1029 postoperative, 1029 preoperative, 1026 radical hysterectomy, 1142–1147, 1143f–1147f Laparoscopic instruments, 879–886 Acessa system for myolysis, 885f atraumatic manipulators, 880, 880f bipolar tools, 885f disposable vs. reusable, 880 endoscopic retrieval pouches, 883, 883f energy systems in minimally invasive surgery, 884–885 flexible laparoscopes, 886 laparoscopic optics, 886 monopolar tools, 885f morcellators, 883 parts of, 879–880, 879f scissors, 882 self-retaining retractors, 883–884 suction and irrigation devices, 882–883, 882f

traumatic graspers, 880–881, 881f uterine manipulators, 881–882, 881f, 882f Laparoscopic instruments, 879f Laparoscopic myomectomy, 1022–1025, 1023f–1025f intraoperative, 1022–1025 instruments, 1022 surgical steps, 1022–1025 postoperative, 1025 preoperative, 1022 Laparoscopic optics, 886 angles of view, 886 flexible laparoscopes, 886 lighting, 886 Laparoscopic ovarian cystectomy, 1015–1018, 1015f–1018f intraoperative, 1015–1018 instruments, 1015 surgical steps, 1015–1018 postoperative, 1018 preoperative, 1015 Laparoscopic salpingectomy, 1011–1012, 1011f–1012f intraoperative, 1011–1012 instruments, 1011 surgical steps, 1011–1012 postoperative, 1012 preoperative, 1011 Laparoscopic salpingo-oophorectomy, 1019–1020, 1020f Laparoscopic salpingostomy, 1013–1014, 1013f–1014f intraoperative, 1013–1014 instruments, 1013 surgical steps, 1013–1014 postoperative, 1014 preoperative, 1013 Laparoscopic sterilization, 1006–1010, 1006f–1010f intraoperative, 1006–1010 postoperative, 1010 preoperative, 1006 Laparoscopic supracervical hysterectomy (LSH), 1030–1032, 1030f–1032f intraoperative, 1030–1032 instruments, 1030 surgical steps, 1030–1032 postoperative, 1032 preoperative, 1030 Laparoscopic surgery anterior abdominal wall anatomy, 888– 889 factors, 874 health conditions, 875 obesity, 875 operating equipment, 878, 878f patient positioning, 879 physiology, 874–875 pregnancy, 876 retroperitoneal anatomy, 889 Laparoscopic uterine nerve ablation (LUNA), 243

Laparoscopy, 1003–1005 diagnostic, 1003–1005 intraoperative, 1004–1005 postoperative, 1005 preoperative, 1003–1004 for endometriosis, 237, 237f in infertility, 440–441, 441f intraoperative, 1004–1005 instruments, 1004 surgical steps, 1004–1005 in pelvic inflammatory disease, 67 pelvic pain, 253 postoperative, 1005 preoperative, 1003–1004 consent, 1003 patient preparation, 1003–1004 Laparotomy, 835t, 844–845, 844f Cherney, 931, 931f of femoral nerve, 844–845, 844f of genitofemoral nerve, 845 of lateral femoral cutaneous nerve, 845 Maylard, 932, 932f midline vertical, 926 –928, 927f –928f Pfannenstiel, 929 –930, 929f –930f LARC. See Long-acting reversible contraceptives (LARC) Large bowel resection, 1194–1195, 1194f–1195f intraoperative, 1194–1195 postoperative, 1195 preoperative, 1194 Laser conization, 644, 993–994 Lateral sacral vein, 817 Latzko technique, 582 LCIS. See Lobular carcinoma in situ (LCIS) LEEP conization, 993, 993f for CIN, 644 Leiomyomas, 202–212 appearance of, 203f diagnosis, 206–207 imaging of hysterosalpingography, 438, 439f magnetic resonance imaging, 42–43, 42f sonography, 206, 207 indications for medical treatment, 207t and infertility, 459 intramural, 206f management, 207–212 GnRH agonist treatment, 208–209 levonorgestrel-releasing intrauterine system, 207 magnetic resonance-guided focused ultrasound, 210–211, 211f myolysis, 212, 885, 885f observation, 207 sex steroid hormones, 207–208 surgery, 211–212 tranexamic acid, 209 uterine artery embolization, 209–210, 209f, 210f, 210t medroxyprogesterone acetate associated with, 204 myomectomy for

1247

1248

Index Leiomyomas (Continuedâ•›) abdominal, 945–947, 946f–947f hysteroscopic, 1040–1042, 1041f laparoscopic, 1022–1025, 1023f–1025f parasitic, 204 pathophysiology, 202–204 pedunculated, 204 prolapsed, vaginal myomectomy for, 948–949, 948f–949f submucous, 204, 206f, 207f subserosal, 204 symptoms, 205–206 uterine, 147, 725f uterine leiomyoma classification, 204–205, 204f of vulva, 96 Leiomyomatosis, 204–205 Leiomyosarcoma diagnosis, 722–724 epidemiology, 722 generalist, role of, 723–724 imaging of, 723 pathogenesis, 722 pathology, 724 prognosis, 732 risk factors, 722 treatment of, 729–732 vaginal, 699 Lesser sciatic foramen, 800 Leucovorin rescue, 170, 597 Levator ani muscles, 542–543, 802–804 examination of, 268, 268f iliococcygeus muscle, 803–804 804f pubococcygeus muscle, 802 puborectalis muscle, 803, 803f Levator ani syndrome, 269 Levator plate, 803 Levofloxacin for acute cystitis, 74t for chlamydial infection, 65t for postgynecologic surgery infections, 79t Levomilnacipran, 304t Levonorgestrel, 120t, 121t Levonorgestrel-releasing intrauterine system (LNG-IUS), 108–109, 108t for AUB, 195–196, 195t bleeding from, 191 for chronic HMB, 191 for endometrial cancer, 716 for endometriosis, 240 lactation and, 106 for leiomyomas, 207, 207t for menstrual blood loss, 110 Mirena, 109f, 162, 191 Leydig cell tumors, 773 Lichen planus, 92–93 diagnosis, 92–93, 92t oral, 92f vaginal, treatment of, 93 vulvar, treatment of, 93 Lichen sclerosus, 323–324, 323f, 681 vulvar, 88–91, 89f corticosteroids for, 89–90

diagnosis of, 89 estrogen cream for, 90 phototherapy, 90 retinoids for, 90 surgical intervention of, 90–91 surveillance of, 89–91 topical calcineurin inhibitors in, 90 topical medication guide for, 90t treatment of, 89–91, 90t Lifestyle changes, 10–12 exercise, 12 smoking, 10–11, 11t Ligaments of pelvis, 801 Linac, 610 Linear accelerator, 610, 611f, 612f Linear quadratic mammalian cell survival curve, 614f Linum usitatissimum, 498 Lipoma, vulvar, 96 Liposomal doxorubicin, 600 Listeria monocytogenes, 139 Live attenuated influenza vaccine (LAIV), 8t LMP tumors. See Low-malignant-potential (LMP) tumors LNG-IUS. See Levonorgestrel-releasing intrauterine system (LNG-IUS) Lobular carcinoma in situ (LCIS), 284 Loestrin, 120t Loestrin 1.5/30, 120t Loestrin 1/20, 120t Loestrin Fe 1.5/30, 120t Loestrin Fe 1/20, 120t Loestrin 24 Fe, 120t Lo Loestrin Fe, 120t Long-acting reversible contraceptives (LARC), 107, 330 Longitudinal vaginal septum, 416–417, 416f Loop electrosurgical excision procedure (LEEP) for cervical neoplasia, 441 for CIN, 644, 644t, 988–989, 988f–989f for HSIL, 636 Lo/Ovral, 120t LoSeasonique, 121t Low anterior resection, 1199–1202, 1200f–1202f intraoperative, 1199–1201 instruments, 1199 surgical steps, 1199–1201 postoperative, 1202 preoperative, 1199 Low-density lipoprotein cholesterol (LDL), 15–16 Lower genital tract human papillomavirus infection of, 627–630 basic virology, 627–628 diagnosis of, 629 latent infection, 628 life cycle, 627f outcomes, 628–629, 628f prevention of, 630

productive infections, 628–629 transmission, 628 treatment of, 629–630 preinvasive lesions of, 624–656 anal intraepithelial neoplasia, 650–651 anatomic considerations, 624–627 cervical intraepithelial neoplasia, 630–632 cervical neoplasia diagnosis, 632–641 HIV-infected patients, 651–652 human papillomavirus infection, 627–630 lower genital tract neoplasia, 624 postcolposcopy surveillance without treatment, 642–643 vaginal, 645–646 vulvar preinvasive lesions, 646–650 Lower outflow tract obstruction, 370–371 Lower reproductive tract disorders cervical lesions, 102 cervical stenosis, 102 cystic vulvar tumors, 97, 97f endocervical polyp, 102 epidermal and dermal lesions, 96, 96f eversion, 102 nabothian cyst, cervical, 102, 102f pigmentation, disorders of, 95, 95f solid vulvar tumors, 95–96 subcutaneous masses, 96 systemic illnesses, vulvar manifestations of, 94–95 acanthosis nigricans, 94 Behçet disease, 95 Crohn disease, 94, 94f vaginal conditions, 101–102 desquamative inflammatory vaginitis, 101 diethylstilbestrol-induced reproductive tract abnormalities, 101 foreign body in vagina, 101 Gartner duct cysts, 101–102 vulvar dermatoses, 88–94 inflammatory dermatoses, 91–94 lichen sclerosus, 88–91, 89f lichen simplex chronicus, 87 vulvar lesions, 86–88 diagnosis of, 86–88 pain, assessment of, 87f physical examination in, 87 vulvar biopsy, 87–88, 88f vulvar complaints, approach to, 86 vulvodynia, 97–100 behavioral therapy for, 99–100 definition of, 97 diagnosis of, 98–99, 98t, 99f ISSVD classification, 98t medical agents for, 100 surgery for, 100 treatment of, 99–100 vulvovaginal trauma, 100–101 hematoma, 100–101 laceration, 101

Index Lower urinary tract structures bladder, 813, 813f rectum, 814, 815f urethra, 814, 814f Low-grade squamous intraepithelial lesion (LSIL), 636, 640f Low-malignant-potential (LMP) ovarian tumors, 739–740 clinical features of, 739 pathology of, 739 prognosis of, 740 treatment of, 739–740, 740f Low-molecular-weight heparin (LMWH) for antiphospholipid antibody syndrome, 149 characteristics of, 914t for venous thromboembolism, 830–832, 831t, 836t LPD. See Luteal phase defect (LPD) LSH. See Laparoscopic supracervical hysterectomy (LSH) LSIL. See Low-grade squamous intraepithelial lesion (LSIL) Lumbar veins, 817 Lumbosacral plexus nerve plexus (L1-S4), 744t LUNA. See Laparoscopic uterine nerve ablation (LUNA) Lung cancer, 10 Luteal phase defect (LPD), 149, 357, 435 Luteinizing hormone (LH), 241, 318, 319f, 343–344, 345f infertility, 411f, 412–413, 435 in polycystic ovarian syndrome, 150, 387, 388f Lymphatic drainage anatomy of, 810f, 823f of breast, 275, 277f of cervix, 660f of ovary, 809 to perineum, 822–823, 823f of uterus, 809 of vagina, 812–813 of vulva, 822–823, 823f Lymphatic vascular space invasion (LVSI) of cervix, 659, 660f, 667, 668t, 669, 671t, 675 of uterus, 712 of vulva, 684 Lymph node dissection anatomy of, 810f, 823f in cervical cancer, 666 inguinal, 681f, 823f inguinofemoral, 1215–1217, 1215f–1217f in ovarian cancer, 751 paraaortic nodes, 713t, 714, 716t, 1176–1177 pelvic nodes, 810f, 1168–1170, 1169f–1170f, 1175–1180, 1176f–1179f in uterine cancer, 714 in uterine sarcoma, 730–731 in vulvar cancer, 685–687

Lymph node metastasis, in vulvar cancer, 683 Lymphogranuloma venereum (LGV), 59–60, 60f Lynch syndrome, 703, 736 genetic screening recommendation, 707t Lysis of intrauterine adhesions, 1052–1053, 1052f indications for, 260–261 intraoperative, 1052–1053 postoperative, 1053 preoperative, 1052 M Mackenrodt ligaments, 808 Magnetic resonance-guided focused ultrasound (MRgFUS), 43, 210–211 Magnetic resonance high intensity focused ultrasound (MR-HIFU) therapy, 43 Magnetic resonance imaging (MRI), 40–45 acute pelvic pain, 253 of adenomyosis, 43–44, 214 of anal incontinence, 568–569 of benign disease, 42–44 of breast cancer, 289 for cervical cancer, 666 of congenital anomalies, 43–44, 43f of cervical agenesis, 420 of congenital vaginal cysts, 417 of müllerian anomalies, 418 echo delay time, 40 endometrial cancer, 709 of endometriosis, 237 gynecologic malignancies, 44–45 in gynecology, 42 imaging technique, 41 with implants, 41t of leiomyoma, 42–43, 43f, 206–207 MRgFUS therapy, 43, 210–211 normal findings, 42, 42f of other gynecologic indications, 44, 44f of ovarian cysts, 216 for ovarian endometriomas, 44 of paratubal/paraovarian cysts, 223 relaxation time, 40 repetition time, 40 safety of, 41–42, 41t urogynecology, 45 Male condom, 128 Male infertility, correction of, 462–463 abnormal semen volume, 462 abnormal sperm count, 462–463 abnormal sperm motility/morphology, 463 varicocele, 463 Male sterilization, 118 fertility restoration, 118 long-term effects of, 118 vasectomy, 118, 118f Malignant mixed müllerian tumor (MMMT). See Carcinosarcoma

Mammalian target of rapamycin (mTOR), 605 Maprotiline, 304t Martius bulbocavernosus fat pad flap, 1083–1084, 1083f–1084f intraoperative, 1083–1084 surgical steps, 1083–1084 postoperative, 1084 preoperative, 1083 consent, 1083 patient evaluation, 1083 patient preparation, 1083 Mastalgia, 282 cyclic, 282 diagnostic algorithm for evaluation of, 283f noncyclic, 282 Matrix metalloproteinases (MMPs), 357 Mature cystic teratoma, 202, 217t, 219–221 characteristics of, 221f computed tomography for, 325 dermoid cyst, 219 following cystectomy, 220f malignant transformation of, 765–766, 766f sonography for, 221, 221f surgical removal of, 221 46,XX karyotype in, 221 Mature cystic teratoma, 219–221, 220f, 221f Maximum tolerated dose (MTD), 607, 608 Maximum urethral closure pressure (MUCP), 527–528 Mayer-Rokitansky-Küster-Hauser syndrome (MRKHS), 420 Maylard incision, 932, 932f McCall culdoplasty, 1116–1117, 1117f McIndoe procedure, 985–987, 985f–986f intraoperative, 985–987 instruments, 985 surgical steps, 985–987 for müllerian agenesis, 420 postoperative, 987 preoperative, 985 Measure of disease (MOD), 607 Medical abortion. See also Induced abortion contraindications, 155 of early pregnancy, 154t Medical disorders, combined hormonal contraceptives and, 124–126 cardiovascular disease, 124–125 cerebrovascular disorders, 125 diabetes mellitus, 124 HIV infections and antiretroviral therapy, 126 neoplastic diseases, 126 obese and overweight women, 124 seizure disorders, 125–126 systemic lupus erythematosus, 125 venous thromboembolism, 125 Medroxyprogesterone acetate associated with leiomyomas, 204

1249

1250

Index Medroxyprogesterone acetate (MPA), 326, 364, 365t for abnormal uterine bleeding, 194 for anovulation, 398 bleeding, 381 for endometrial hyperplasia, 706 for endometrial stromal tumors, 732 for hormone replacement, 493 injectable, 784 for leiomyoma, 204, 208 for ovarian SCST, 775 Megestrol acetate (Megace), 603, 707, 717 Meigs syndrome, 771 Melanoma, 10 of vagina, 699–700, 699–700 BRAF and KIT mutation, 700 ipilimumab, 700 staging, 699 treatment, 699–700 of vulva, 680t, 688f diagnosis, 681–682 epidemiology, 679–680 pathology, 688–689 prognosis, 682–684 risk factors, 680–681 staging, 688–689 treatment, 689–690 Melatonin-receptor agonist, 18t Melbourne Women’s Midlife Health Project, 474 Menopausal transition, 306–307, 471–491 abnormal uterine bleeding during, 474 antimüllerian hormone levels in, 472 and cognitive function, 485 definition of, 471 dyspareunia in, 487 follicle-stimulating hormone levels in, 472 influential factors, 471–472 ovarian changes in, 473, 473f parathyroid hormone levels, 478–479 patient evaluation, 487–489 estrogen maturation index, 489 gonadotropin and estrogen levels, 488–489 physiologic changes, 472–487 adrenal steroid levels, 473–474 in bone structure and metabolism, 476–477 breast changes, 484 cardiovascular changes, 483 in central nervous system, 484–485 in central thermoregulation, 474–476 dental changes, 484 dermatologic changes, 484 in endometrium, 474 in hypothalamus-pituitary-ovarian axis, 472 libido changes, 486 lower reproductive tract changes, 486–487, 488f menstrual disturbances, 474 osteopenia and osteoporosis, 477–483

psychosocial changes, 485–486 weight gain and fat distribution, 483–484 sexual dysfunction in, 487 sleep dysfunction and fatigue in, 484–485, 485t symptoms associated with, 471t urogenital changes in, 487 vasomotor symptoms in, 474–475, 475f. See also Menopausal vasomotor symptoms, treatment of genetic polymorphisms and, 475–476 pathophysiology of, 475–476 risk factors for, 476 vulvovaginal changes in, 486–487 Menopausal vasomotor symptoms, treatment of, 495–499 central nervous system agents, 497–498, 497t black cohosh, 498–499 citalopram (Celexa), 498 clonidine (Catapres), 498 dong quai, 498 flaxseed oil, 498 gabapentin (Neurontin), 498 norepinephrine, 497–498 paroxetine (Paxil), 498 red clover, 498 serotonin, 497–498 soy products, 498 venlafaxine, 498 complementary and alternative medicine for, 498–499 lifestyle changes, 499 phytoestrogens, 498–499 phytoprogestins, 499 vitamin E, 499 hormonal therapy for, 495–497, 496t bazedoxifene, 497 bioidentical hormones, 497 estrogen, 495 progestins, 495–497 lifestyle changes, 499 Menopause, 306–307, 492–508 definition of, 471, 492 dementia prevention in, 507 dental disease and tooth loss in, prevention of depression in, treatment of, 506–507 genitourinary symptoms of, selected preparations for, 505t hormone replacement administration, 494–495 contraindications of, 494–495 indications for, 494–495 risks and benefits of, 494 hormone treatment for, 492–494 estrogen administration, 492–493, 495t HERS study, 493 PEPI Trial, 493 Women’s Health Initiative, 493–494 libido of, decline in, 506

mortality in, leading causes of, 507t osteoporosis, treatment of, 499–505 hormonal therapy, 504 indications for, 499–501 nonhormonal antiresorptive agents, 501–503 nonpharmacologic therapy, 504–505 parathyroid hormone, 503–504 preventive health care for, 507–508 sex-related issues, treatment of, 505–506 skin aging in, treatment of, 507 urogynecologic disease in, prevention of, 507–508 vasomotor symptoms in, treatment of, 495–499 central nervous system agents, 497–498, 497t complementary and alternative medicine for, 498–499 hormonal therapy for, 495–497, 496t lifestyle changes, 499 Menopause-Specific Quality of Life (MENQOL) questionnaire score, 497 Menopur, for ovulation induction, 452t Menstrual cycle, 346–355, 347f characteristics, 347t endometrium and, 355–357 follicular development, 352–353 estrogen-dominant microenvironment for, 353 follicle stages, 352 selection window, concept of, 352–353 gonadal peptides and, 351, 352f ovarian hormone production, 348–351, 349f steroidogenesis across life span, 350–351, 351f two-cell theory, 350, 350f ovary and, 346–348, 348f, 349f embryology of, 346–347 morphology of, 346, 348f oocyte loss with aging, 347–348 oocyte maturation, 348, 349f stromal cells in, 348 phases, 353–355 follicular phase, 353 luteal phase, 354–355 ovulation, 353–354, 354f Menstruation-related psychologic disorders, 302–305 diagnosis, 303 pathophysiology, 303 treatment, 303–305, 304t Mental health, 17–18 aging and sexuality role in, 313 assessment of, 306 depression, 17–18 insomnia, 18 partner violence, 17–18 Meperidine, 123t Meralgia paresthetica, 845

Index Mesenchymal tumors, vaginal, 698–699 embryonal rhabdomyosarcoma, 698–699, 699f leiomyosarcoma, 699. See also Leiomyosarcoma Mesosalpinx, 809 in salpingectomy, 939–940, 939f, 942, 943f, 1011–1012, 1011f Mesoteres, 809 Mesovarium, 809 Metabolic syndrome, 17 PCOS and, 392, 392f Metastasizing leiomyomas, benign, 204 Metastatic tumors, of vulva, 691–692 Methicillin-resistant Staphylococcus aureus (MRSA), 53, 82, 282 Methotrexate, 596–597, 597f for ectopic pregnancy, 170–171 for GTN, 789, 790t for medical abortion, 154–155, 154t Metoprolol, 123t Metronidazole, 54, 835t MFPR. See Multifetal pregnancy reduction (MFPR) Miacalcin, for osteoporosis, 500t Miconazole, for candidiasis, 62t Miconazole combination pack, for candidiasis, 62t Microinvasion, 739 of cervical cancer, 667–672 of ovarian cancer, 739–740 of vaginal cancer, 699 of vulvar cancer, 687 Microinvasive cancers, of vulva, 687 Micronor, 121t Middle sacral artery, 817 Middle sacral vein, 817 Midline vertical incision, 926–928, 927f–928f intraoperative, 927–928 surgical steps, 927–928 postoperative, 928 preoperative, 926–927 consent, 926 prophylaxis, 926–927 Midtubal occlusion, 458 Midurethral sling release, 1074, 1074f intraoperative, 1074 surgical steps, 1074 postoperative, 1074 preoperative, 1074 consent, 1074 patient evaluation and preparation, 1074 Midurethral slings, in urinary incontinence, 531–532 Mifepristone, 153, 154 for medical abortion, 154–155, 154t Migraine headaches, 125 Mini-Cog Test, 17 Minimally invasive radical hysterectomy, 1142–1147, 1143f–1147f intraoperative, 1142–1147

instruments, 1142 surgical steps, 1142–1147 postoperative, 1147 preoperative, 1142 Minimally invasive sacrocolpopexy, 1103–1106, 1103f–1106f intraoperative, 1103–1106 surgical steps, 1103–1106 postoperative, 1106 preoperative, 1103–1106 Minimally invasive staging, for gynecologic malignancies, 1175–1180, 1176f–1179f intraoperative, 1175–1179 instruments, 1175 surgical steps, 1175–1179 postoperative, 1180 preoperative, 1175 Minimally invasive surgery (MIS), 1003–1053 diagnostic hysteroscopy, 1037, 1037f diagnostic laparoscopy, 1003–1005 endometrial ablation procedures, 1043–1045, 1044f–1045f hysteroscopic myomectomy, 1040–1042, 1041f hysteroscopic polypectomy, 1038–1039, 1038f hysteroscopic septoplasty, 1048–1049, 1048f–1049f laparoscopic hysterectomy, 1026–1029, 1027f–1028f laparoscopic myomectomy, 1022–1025, 1023f–1025f laparoscopic ovarian cystectomy, 1015–1018, 1015f–1018f laparoscopic salpingectomy, 1011–1012, 1011f–1012f laparoscopic salpingo-oophorectomy, 1019–1020, 1020f laparoscopic salpingostomy, 1013–1014, 1013f–1014f laparoscopic sterilization, 1006–1010, 1006f–1010f laparoscopic supracervical hysterectomy, 1030–1032, 1030f–1032f lysis of intrauterine adhesions, 1052–1053, 1052f ovarian drilling, 1021, 1021f proximal fallopian tube cannulation, 1050–1051, 1050f–1051f total laparoscopic hysterectomy, 1033–1036, 1034f–1036f transcervical sterilization, 1046–1047, 1046f–1047f Minimally invasive surgery (MIS), 874 laparoscopic leiomyoma ablation, 885 laser energy, 885 monopolar electrosurgery, 884, 885f ultrasonic energy, 884–885 Mini-pills, 126–127 Mirabegron, for urinary incontinence, 534

Mirena intrauterine system, insertion of, 114f Mirtazipine, 304t Misoprostol for cervical softening/dilatation, 112, 901, 1048, 1050, 1052 in hysteroscopic myomectomy, 1040 in lysis of intrauterine adhesions, 1052 for medical abortion, 154–155, 154t preprocedural, for cervical stenosis, 102 in proximal fallopian obstruction, 1050 in sharp dilatation and curettage, 964 in suction dilatation and curettage, 966 during surgical abortion, 153 Missed abortion, 140–142, 142–143 Mixed germ cell tumors, 764–765 Mixed gonadal dysgenesis, 412 Modified radical abdominal hysterectomy (type II), 667, 668t, 669, 1140–1141, 1140f–1141f intraoperative, 1140–1141 postoperative, 1141 preoperative, 1140 Molar pregnancy. See Hydatidiform mole Molluscum contagiosum, 70, 71f Monistat, for candidiasis, 62t Monistat-3, for candidiasis, 62t Monistat-7, for candidiasis, 62t Monobactam, 54 Monocryl. See Poliglecaprone Monodermal teratoma, 220 Monophasic pills, 119 Monosomy X (45,X), 138 Monostat-1, for candidiasis, 62t Monozygotic gestation, 456 Mons pubis, 818–819, 818f Mood disorders, 297–298, 298t MORE trial. See Multiple Outcomes of Raloxifene Evaluation (MORE) trial Morphine, 123t, 909 Moschcowitz culdoplasty, 1118–1119, 1119f MRgFUS. See Magnetic resonance-guided focused ultrasound (MRgFUS) MR-HIFU therapy. See Magnetic resonance high intensity focused ultrasound (MR-HIFU) therapy MRKHS. See Mayer-Rokitansky-KüsterHauser syndrome (MRKHS) MRSA. See Methicillin-resistant Staphylococcus aureus (MRSA) MTD. See Maximum tolerated dose (MTD) mTOR. See Mammalian target of rapamycin (mTOR) Mucinous adenocarcinomas, 661t borderline, 739, 739f of cervix, 745 of endometrium, 710–711, 712f of ovary, 745, 746f of ovary, 744t, 745 Mucinous tumors, benign, 221, 221f MUCP. See Maximum urethral closure pressure (MUCP)

1251

1252

Index Müllerian anomalies, 371–372, 372t, 417–423, 459 abortion, 147, 421–422 agenesis, 370t, 371t vs. androgen insensitivity syndrome, 372t agenesis, 418–420 arcuate uterus, 423 bicornuate uterus, 421–422, 422f classification of, 418t, 419f developmental, 440 diagnostic tools for, 418 diethylstilbestrol-induced reproductive tract abnormalities, 423 hysterosalpingogram appearance of, 440 imaging of, 29, 34 35f, 352 infertility, 418, 445f, 459 interstitial pregnancy and, 173 obstructed, 252 pain from, 417, 419, 420 segmental müllerian hypoplasia/agenesis, 418–420 septate uterus, 422 surgery for, 983–984, 983f–984f hysteroscopic septoplasty, 1048–1049 Mcindoe procedure, 985–987, 985f–986f vaginal septum excision, 983–984, 983f–984f unicornuate uterus, 420–421 uterine didelphys, 421 vaginal agenesis, 985 Multichannel cystometrics, 529f interpretation of, 528f for urinary incontinence, 527 Multifetal gestation, 456–457, 457f Multifetal pregnancy reduction (MFPR), 456 Multiple Outcomes of Raloxifene Evaluation (MORE) trial, 501 Muscles adductor longus, 823 bulbospongiosus, 820 coccygeus, 802 compressor urethrae, 516, 519f deep transverse perineal, 814 detrusor, 813 external anal sphincter, 516, 562f, 563, 804 external oblique, 796 gluteus maximus, 821 gracilis, 571 iliacus, 845 iliococcygeus, 542, 801f–804f, 802, 803– 804, 803–804 804f iliopsoas, 823 internal anal sphincter, 561, 568f, 821, 1125, 1126–1127, 1126f, 1129 internal oblique, 796, 845 ischiocavernosus, 820 levator ani, 542–543, 801f–803f, 802–804 obturator internus, 257, 269, 543, 544, 800f, 801–802, 812, 821 pectineus, 823 of pelvic floor

piriformis, 801 pubococcygeus, 802, 802f, 803f puborectalis, 542, 802f, 803, 803f pubovisceral, 802 rectus abdominis, 268–269 anatomy, 796 anterior abdominal wall nerve entrapment syndromes and, 269–270, 270f diastasis of, 256 infiltrated, 235 port placement, 895–896 Spigelian hernias along lateral border of, 267 transverse incisions, 846–847 sartorius, 823 sphincter urethrae, 516 striated urogenital sphincter complex, 516, 521f, 814 transversus abdominis, 796 urethovaginal sphincter, 516, 519f visceral fascia vs. parietal fascia of, 804t of walls of pelvis, 801–802, 802f Musculoskeletal etiologies, of pelvic pain, 267–269 hernias, 267–268, 268f myofascial pain syndrome, 268–269, 268f–269f peripartum pelvic pain syndrome, 269 Mycelex-3, for candidiasis, 62t Mycoplasma genitalium, 65, 139 Mycoplasma hominis, 51, 441 Mycostatin, for candidiasis, 62t Myelosuppression, 605 Myofascial pain syndrome, 268–269, 268f–269f Myomatous erythrocytosis syndrome, 205 Myomectomy abdominal, 945–947, 946f–947f hysteroscopic, 1040–1042, 1041f intraoperative, 1040–1042 postoperative, 1042 preoperative, 1040 laparoscopic, 1022–1025, 1023f–1025f intraoperative, 1022–1025 postoperative, 1025 preoperative, 1022 for leiomyoma, 211–212, 459 for leiomyomas, 211–212 abdominal, 945–947, 946f–947f hysteroscopic, 1040–1042, 1041f laparoscopic, 1022–1025, 1023f–1025f vaginal for prolapsed leiomyoma, 948–949, 948f–949f vs hysterectomy, 212 Myometrial contractility, 357 Myometrial hypertrophy, 214 Myometrium, 807 N NAAT. See Nucleic acid amplification tests (NAAT)

NAMS. See North American Menopause Society (NAMS) Nantes criteria, 270 Narcotic analgesics, and urinary incontinence, 525t Nasogastric decompression, 827 Nasogastric tubes (NGTs), 827 Natazia, 121t National Health and Nutrition Examination Survey (NHANES), 561 National Institute for Health and Clinical Excellence (NICE), 833 National Osteoporosis Risk Assessment (NORA), 501 Necrotizing fasciitis, 81–82, 82f Nefazodone, 304t Neisseria gonorrhoeae, 433, 441 bartholin gland duct abscess, 83, 97 bleeding from, 184, 191 clindamycin against, 54 diagnosis, 64 ectopic pregnancy, 163 infertility, 433 pelvic inflammatory disease, 52, 66, 67, 262 risks factors, 6t salpingitis associated with, 66 screening for, 5, 6t, 209, 310, 901 sexually transmission of, 63 symptoms treatment, 64 urethritis and paraurethral glands inflammation, 583 vulvar abscess, 97, 971 vulvovaginitis, 324 Neoplastic ovarian cysts, benign, 219–221 benign mucinous tumors, 221, 221f benign serous tumors, 221, 221f classification, 219t ovarian teratoma, 219–221, 220f Neosalpingostomy, 459f Nerve injury prevention, 843–846, 844f brachial plexus, 846 dorsal lithotomy, 845–846, 845f–846f laparotomy, 844–845, 844f of femoral nerve, 844–845, 844f of genitofemoral nerve, 845 of lateral femoral cutaneous nerve, 845 transverse incisions, 845 Nerves common fibular, 845 iliohypogastric, 799 ilioinguinal, 799 intercostal, 799 pelvic autonomic, 806f, 808 presacral, 806, 806 pudendal, 801, 804, 814, 821, 822f, 823 sacral, 801, 808, 816f, 817 subcostal, 799 Nervi erigentes, 823 NETA. See Norethindrone acetate (NETA) Neupogen. See Filgrastim Neuroendocrine tumors, of cervix, 662

Index Neurologic and psychiatric disorders, counseling in, 19t Neurologic etiologies, of pelvic pain, 269–270 anterior abdominal wall nerve entrapment syndromes, 269–270, 270f piriformis syndrome, 270–271 pudendal neuralgia, 270 Neuropathic pain, 250–251 Neuropeptide Y (NPY), 343 Neurotoxicity, of chemotherapy, 606 Nevus (nevi), 95 Nexplanon breast-feeding and, 106 efficacy of, 112 etonogestrel implant, 193 imaging of, 115 insertion, 115, 115f magnetic resonance imaging and, 41t, 115 subdermal contraceptive implant, 112 NHANES. See National Health and Nutrition Examination Survey (NHANES) NICE. See National Institute for Health and Clinical Excellence (NICE) Nicoderm CQ, 11t Nicorette, 11t Nicotine replacement, agents for, 11, 11t Nicotrol, 11t Nipple discharge, 280–281, 281f diagnostic algorithm, 280f galactorrhea, 280, 281t pathologic, 281, 281f N-methyl-d-aspartate receptors (NMDARs), 221 Nonatypical endometrial hyperplasia, 706 Noncyclic chronic pelvic pain, 234 Nonidentical sliding knots, 856 Nonproliferative benign breast disease, 283 Nonpuerperal breast abscesses, 282 Nonpuerperal infections, 282 Nonsteroidal antiinflammatory drugs (NSAIDs) for abnormal uterine bleeding, 184, 190–191, 192, 193, 195t, 196–197 for chronic pelvic pain, 258, 259 doses of, 239t for endometriosis, 239, 239t in endometriosis, 238, 239, 239t for leiomyomas, 207t, 209, 214 for postoperative pain, 909 NORA. See National Osteoporosis Risk Assessment (NORA) Nordette, 120t Norepinephrine, for menopausal vasomotor symptoms, 497–498 Norethindrone, 120t, 121t Norethindrone acetate (NETA), 120t, 121t, 194, 195 Norgestimate, 120t, 121t Norgestrel, 120t Norinyl, 120t

Norinyl 1+50, 120t Normal vaginal flora, 50–52 altered flora, 50 bacterial vaginosis, 51–52 vaginal pH, 50 North American Menopause Society (NAMS), 494, 499 Nortriptyline, 304t Nortriptyline, and urinary incontinence, 525t Nortriptyline, for smoking cessation, 11t NOS. See Steroid cell tumors not otherwise specified (NOS) NPY. See Neuropeptide Y (NPY) Nuclear medicine examinations, 45 Nucleic acid amplification tests (NAAT), 60, 63, 64, 65, 83 Nulliparity, 735 Nystatin, for candidiasis, 62t Nystatin powder, for candidiasis, 62t O Obesity, 12–14, 12t, 826, 875–876 and abnormal uterine bleeding, 181t antibiotic dosing, 834 contraceptive efficacy, 124 counseling, 18t definition of, 12t diagnosis of, 12–13 and endometrial cancer, 702 and infertility, 429, 429t, 449–450 and leiomyoma, 207 and miscarriage, 140, 151t and PCOS, 392 preoperative planning, 826 risk factors, 12–13, 12t treatment, 3t, 13–14 and urinary incontinence, 515 and wound infection, 921t Obstructed hemivagina, uterine didelphys with. See OHVIRA syndrome Obstructive sleep apnea, 392 Obturator canal, 800, 800f Obturator foramen, 800, 800f Obturator hernia, 267 Obturator neurovascular bundle, 818 Octyl-2-cyanoacrylate, 848 Ofloxacin for chlamydial infection, 65t for chlamydial infection, 65t for reducing CHC efficacy, 124t Ogestrel, 120t OHSS. See Ovarian hyperstimulation syndrome (OHSS) OHVIRA syndrome, 323, 417 Olaparib (AZD2281), 605 Oligospermia, 443, 463 Omental J-flap for radical hysterectomy, 1139 for total pelvic exenteration, 1152, 1153 for vaginal reconstruction, 1165–1166, 1165f, 1167 for vesicovaginal fistula, 1081–1082

Omentectomy, 1185–1186, 1186f intraoperative, 1185–1186 postoperative, 1186 preoperative, 1185 ONJ. See Osteonecrosis of jaw (ONJ) Onuf nucleus, 519f Oocytes, 318 chemoprotection of, 598 cryopreservation, 275, 465, 466 development of, 349f donation, chapter 20 endometriosisrelated infertility and, 234 extrusion of, 354 fertilization, 352, 442 genetic material in, 221 loss with aging, 348 maturation, 348–350, 349f in POF, 373, 676 in polycystic ovarian syndrome, 379 during prenatal and postnatal periods, 319f primary, 348 in vitro fertilization, 436, 465 Oophorectomy. See Salpingo-oophorectomy OPG. See Osteoprotegerin (OPG) Opiates, and urinary incontinence, 525t Opioids, 343 amenorrhea, 377 chronic pelvic pain, 258–259 postoperative pain, 909–910, 910t OPUS trial. See Outcomes Following Vaginal Prolapse Repair and Mid Urethral Sling (OPUS) trial Oral Ibandronate Osteoporosis Vertebral Fracture Trial in North America and Europe (BONE) trial, 503 Organ surgical injury, 867, 877 bladder injury, 867, 877 bowel injury, 869–870, 877 lower urinary tract injury, 867 universal cystoscopy, 869 ureteral injury, 868–869 urethral injury, 867–868 Orphenadrine, and urinary incontinence, 525t Ortho-Cyclen, 120t Ortho Evra patch, 122 Ortho-novum, 120t Ortho-Novum 1/35, 120t Ortho-Novum 7/7/7, 121t Ortho Tri-Cyclen, 121t Ortho Tri-Cyclen Lo, 120t Ospemifene, for dyspareunia, 506 Osteonecrosis of jaw (ONJ), 502 Osteoporosis, 477–483 clinical importance, 477 DEXA scans, 480f diagnosis of, 479 modifiable factors in, 482 nonmodifiable factors in, 481–482 pathophysiology of, 478–479 in postmenopausal women, 482t prevention of, 479–483

1253

1254

Index Osteoporosis (Continuedâ•›) primary, 478 risk factors, 481t screening of, 482–483 secondary, 478 secondary causes of, 479t Osteoporosis, treatment of, 499–505 hormonal therapy, 504 indications for, 499–501 nonhormonal antiresorptive agents, 501–503 bisphosphonates, 501–503, 502f calcitonin, 503 denosumab, 503 nonpharmacologic therapy, 504–505 calcium, 504 diet, 504 physical preventions, 504–505 vitamin D, 504 parathyroid hormone, 503–504 Osteoprotegerin (OPG), 476–477, 477f Outcomes Following Vaginal Prolapse Repair and Mid Urethral Sling (OPUS) trial, 558 Ovarian abscess, 78–79 Ovarian anomalies, 423 Ovarian cancer, 735–759 advanced, management of, 750–753 adjuvant chemotherapy, 752, 752t cytoreductive surgery, 750–752 neoadjuvant chemotherapy, 751–752 patients in remission, 752–753 early-stage, management of, 748–750 end-stage, palliation of, 754–755 epidemiology of, 735–737 epithelial ovarian cancer, 740–755 clear cell adenocarcinoma, 746, 746f diagnosis, 741–742 endometrioid adenocarcinomas, 745, 745f fallopian tube carcinoma, 747, 747f generalist, role of, 742–743 Krukenberg tumor, 747, 748f mixed carcinoma, 746 mucinous adenocarcinomas, 745, 746f paracentesis, 742 pathogenesis, 740–741, 741f pathology, 743–747 patterns of spread, 747–748 primary peritoneal carcinoma, 747, 747t prognostic factors, 753, 753t secondary tumors, 747 serous tumors, 744, 745f small cell carcinomas, 746–747 symptoms of, 741–742, 741f transitional cell carcinoma, 746 undifferentiated carcinomas, 746 FIGO staging, 748, 749f, 750t hereditary breast and, 736–737 BRCA1 and BRCA2 genes, 736–737, 737f genetic testing, 737

histological classification of, 744t low-malignant-potential tumors, 739– 740 clinical features of, 739 pathology of, 739 prognosis of, 740 treatment of, 739–740, 740f prevention, 737–739 prophylactic surgery, 738–739 recurrent ovarian cancer, management of, 753–754 salvage chemotherapy, 754 secondary cytoreductive surgery, 754 risk factors for, 735–737, 736t screening of, 737–739 biomarkers and proteomics, 738 general population, 738 high-risk women, 737–738 physical examination, 738 Ovarian cyst, 215 diagnosis, 215–216 functional, 215, 216–219 associated factors, 218 diagnosis and treatment, 218–219, 218f theca lutein cysts, 219 hemorrhagic, 217t, 218f imaging of, 34, 44, 216, 217t Magnetic resonance imaging, 216 management, 216, 223 neoplastic, 219–221 ovarian stimulation, 453, 455, 458, 464–466 pain from, 215 from progestins, 127 surgery for, 216, 933–934, 933f–934f symptoms, 215 torsion, 222 Ovarian cystectomy, 933–934, 933f–934f, 1015–1018, 1015f–1018f intraoperative, 933–934, 1015–1018 instruments, 1015 surgical steps, 933–934, 1015–1018 postoperative, 934, 1018 preoperative, 933, 1015 consent, 933 patient preparation, 933 Ovarian drilling, 1021, 1021f for ovulation induction, 457–458 for PCOS, 387–388 Ovarian dysfunction, correction of, 450–458 hyperprolactinemia, 450 hypothyroidism, 450 ovulation induction, 450–458 aromatase inhibitors for, 453 clomiphene citrate for, 451–452, 451f drug protocols for, 454f fertility drugs in, complications of, 453–457 gonadotropins for, 452–453, 452t insulin-sensitizing agents for, 452 ovarian drilling, 457–458

Ovarian follicular steroidogenesis, two-cell theory of, 350, 350f Ovarian hormone production, 348–351, 349f steroidogenesis across life span, 350–351, 351f two-cell theory, 350, 350f Ovarian hyperstimulation syndrome (OHSS), 453–456 abdominal pain in, 453 etiology of, 453 GnRH antagonist protocol in, 455f treatment of, 453–456 Ovarian hyperthecosis definition of, 386 Ovarian incision, 933f Ovarian pregnancy, 173 Ovarian remnant syndrome, 261 Ovarian retention syndrome, 261 Ovarian teratoma. See Mature cystic teratoma Ovarian tumors, 325 Ovary, 34, 346–350, 348f, 349f absent, 423 accessory, 423 adnexal mass separate from, 165, 166f adnexal torsion and, 222–223, 222f anatomy of, 809 blood supply to, 809 contralateral, 762, 763, 765, 766, 770 with echogenic bubbles, 26f ectopic implantation of fertilized egg in, 173 embryology of, 346–347 endometrioma in, 231f FIGO staging of carcinoma of, 750t follicular cyst in, 218f germ cell tumors, 750t hormone production, 350–351 inner medulla, 809 innervation, 809 lymphatic drainage of, 809 menopausal transition and, 473, 473f morphology of, 346–347, 348f oocyte loss with aging, 348 oocyte maturation, 348–350, 349f outer cortex, 809 polycystic, 397 postmenopausal, 473f and pregnancy outcomes, 620 premenopausal, 23f, 473f radiation therapy effects on, 620 reproductive-age, 473f sagittal plane of, 30f stromal cells in, 350 supernumerary, 423 Ovcon-35, 120t Overactive bladder, 514 pharmacologic treatment of, 533t sacral neuromodulation, 1085–1087, 1085f–1087f Overflow incontinence, 523 Overlapping sphincteroplasty, 1127f

Index Ovulation induction, 450–458 aromatase inhibitors for, 453 clomiphene citrate for, 451–452, 451f drug protocols for, 454f fertility drugs in, complications of, 453–457 multifetal gestation, 456–457 ovarian hyperstimulation syndrome, 453–456 gonadotropins for, 452–453, 452t insulin-sensitizing agents for, 452 ovarian drilling, 457–458, 1021, 1021f Ovulatory disorders, 194–195 acute hemorrhage management, 194–195 chronic management, 194 Oxybutynin, for urinary incontinence, 533–534 P PACAP. See Pituitary adenylate cyclaseactivating peptide (PACAP) Paclitaxel (Taxol), 601 Paget disease, of nipple, 285–286, 286f Palmar-plantar erythrodysesthesia (PPE), 597t, 599t, 600 Pap testing, endometrial cancer, 708 Paraaortic lymphadenectomy, 1171–1174, 1172f–1173f anatomy of, 810 for cervical cancer, 666, 668 intraoperative, 1171–1174 for ovarian cancer, 748–749, 1171–1174, 1172f–1173f postoperative, 1174 preoperative, 1171 for uterine cancer, 713–715 Paracervical block, 841–843, 842f Paracrine communication, 334 ParaGard T 380A, insertion of, 113f. See Copper-containing intrauterine devices Parallel sliding knot, 856 Parametrial and paravaginal vessels, 863 Parametrium, 808 Paraovarian masses, 223 Paraplatin. See Carboplatin Parasitic leiomyomas, 204 Parathyroid hormone (PTH), for osteoporosis, 503–504 Paraurethral glands, complex configuration of, 583f Paravaginal defect repair abdominal surgery for, 1091–1092, 1091f–1092f indications for, 532–533 vaginal surgery for, 1088–1090, 1088f–1090f Parental chromosomal abnormalities, 145–148 infertility evaluation, 441–445 parental karyotype, 145, 146f screening products of conception, 146

sperm DNA testing, 145–146 treatment of, 146 Parietal fascia, 802 Parietal peritoneum, 797–798, 797f Paroophoron, 423 Paroxetine, 304t for menopausal vasomotor symptoms, 498 PARP inhibitors. See Poly(ADP) ribose polymerase (PARP) inhibitors Partial diverticular ablation, 1076–1077, 1076f–1077f Partial gonadal dysgenesis, 412 Partial hydatidiform mole, 780t, 781–782 Particle radiation, 610 Partner violence, 17–18 Pathologic nipple discharge, 281, 281f PATSS. See Postablation tubal sterilization syndrome (PATSS) PBAC. See Pictorial blood assessment chart (PBAC) PCOS. See Polycystic ovarian syndrome (PCOS) Pectineus muscles, 823 Pederson speculum, 5f Pediatric gynecology, 318–332 anatomy, 318–319 breast development and disease absent breast development, 326 breast mass/infection, 326–327 breast shape, 326 normal vs. tuberous breast development, 326f polythelia, 325 premature thelarche, 326 tuberous breasts, 326 congenital anatomic anomalies, 323 delayed puberty, 329, 329t genital trauma, 324–325 gynecologic examination, 320–321, 321f, 322f hypothalamic-pituitary-ovarian (HPO) axis, 318 labial adhesion, 321–322, 322f ovarian tumors, 325 physiology, 318–320 precocious puberty, 327–329 central (GnRH-dependent), 327–328, 328t evaluation of, 328t heterosexual, 329 peripheral (GnRH-independent), 328–329, 328t variations of normal puberty, 329 pubertal changes, 319–320 sexuality, 329–331 adolescent, 330 contraception, 330–331 gender identity, 329–330 Tanner stages, 319–320, 320f vaginal bleeding, 327, 327f, 327t vulvitis, 323–324 allergic and contact dermatitis, 323

infection, 324 lichen sclerosus, 323–324, 323f vulvovaginitis, 324, 324t, 325f Pediatric Pederson speculum, 5f Pediculosis, 72 Pediculus humanus capitis, 72, 72f Pedunculated leiomyomas, 204 Pegfilgrastim (Neulasta), 607 Pelvic abscess, 79–80, 79f Pelvic adhesions, 461 Pelvic arteries, 804, 805f Pelvic autonomic nerves, 806f Pelvic blood supply, 805–806, 805t Pelvic cellulitis, 78, 78f Pelvic congestion syndrome, 261–262, 261f Pelvic diaphragm, 801f–803f, 802 Pelvic floor anatomy, 802–804, 803f–804f inferior view of, 803f muscles of iliococcygeus muscle, 801f–804f, 803–804 levator ani muscles, 801f–803f, 802 pubococcygeus muscle, 802, 802f, 803f puborectalis muscle, 802f, 803, 803f visceral fascia vs. parietal fascia of, 804t muscle training, 529, 530 sonography findings of, 31–32 strengthening exercises, 528–530 Pelvic floor disorders, surgeries for, 1057–1130 abdominal culdoplasty procedures, 1118–1119, 1118f–1119f abdominal paravaginal defect repair, 1091–1092, 1091f–1092f abdominal sacrocolpopexy, 1098–1102, 1100f–1102f anal sphincteroplasty, 1125–1127, 1126f–1127f anterior colporrhaphy, 1088–1090, 1088f–1090f Burch colposuspension, 1061–1062, 1061f–1062f colpocleisis, 1120–1124, 1120f–1124f diagnostic and operative cystoscopy and urethroscopy, 1057–1060, 1058f–1060f martius bulbocavernosus fat pad flap, 1083–1084, 1083f–1084f McCall culdoplasty, 1116–1117, 1117f midurethral sling release, 1074, 1074f minimally invasive sacrocolpopexy, 1103–1106, 1103f–1106f perineorrhaphy, 1096–1097, 1097f posterior colporrhaphy, 1093–1095, 1094f–1095f pubovaginal sling, 1068–1069, 1068f–1069f rectovaginal fistula repair, 1128–1130, 1128f–1129f sacral neuromodulation, 1085–1087, 1085f–1087f

1255

1256

Index Pelvic floor disorders, surgeries for (Continuedâ•›) sacrospinous ligament fixation, 1112–1115, 1113f–1115f tension-free vaginal tape procedure, 1063–1065, 1064f–1065f transobturator tape (TOT) sling, 1066–1067, 1066f–1067f urethral bulking injections, 1070–1071, 1071f urethral diverticulum repair, 1075–1077, 1075f–1077f urethrolysis, 1072–1073, 1072f–1073f uterosacral ligament suspension, abdominal, 1110–1111, 1110f–1111f vaginal uterosacral ligament suspension, 1107–1109, 1108f–1109f vesicovaginal fistula repair, 1078–1082, 1079f–1082f Pelvic Floor Distress Inventory, 523 Pelvic Floor Distress Inventory 22-Item (PFDI-22), 547t Pelvic Floor Impact Questionnaire, 523 Pelvic Floor Impact Questionnaire 7-Item (PFIQ-7), 546t Pelvic floor muscle assessment, 550f Pelvic floor muscle training (PFMT), 570 Pelvic inflammatory disease (PID), 33–34, 33f, 34f, 65–70, 66–67, 252 acute, 66–67 laparoscopy, 67 sonography, 67 symptoms and physical findings, 66–67 testing of, 67 bleeding from, 252 Chlamydia trachomatis, 52, 176 chronic, 69 chronic pelvic pain, 66, 252, 254t diagnosis, 66–69 ectopic pregnancy, 162t, 176 hydrosalpinx and, 224 infertility from, 427, 428, 433t microbiology and pathogenesis, 66 Neisseria gonorrhoeae, 52, 66, 67, 262 risk factors, 66t risks factors, 66t role in tubal adhesions and obstruction, 176 silent, 66 sonography of, 33–34 symptoms, 66–67 treatment of, 69–70 oral, 69 outpatient, 69t parenteral, 68t, 69–70, 69t tuboovarian abscess, 67–68, 68f Pelvic innervation, 806–807 Pelvic lymphadenectomy, 1168–1170, 1169f–1170f anatomy of, 822–823, 823f for cervical cancer, 666 intraoperative, 1168–1170

abdominal exploration, 1168 abdominal incision, 1168 anesthesia, 1168 distal common iliac lymph nodes dissection, 1170, 1170f external iliac nodes dissection, 1168–1169, 1169f internal iliac nodes dissection, 1169 obturator fossa nodes dissection, 1169–1170, 1169f patient positioning, 1168 retroperitoneal exploration, 1168 for ovarian cancer, 748–749, 750t, 751 postoperative, 1170 preoperative, 1168 consent, 1168 patient evaluation, 1168 patient preparation, 1168 for uterine cancer, 713–715 Pelvic lymph nodes, 810f Pelvic mass adenomyosis, 213–214, 213f diagnosis, 213–214 diffuse, 213 focal, 213 management, 214 pathophysiology, 213 adnexal torsion, 222–223, 222f diagnosis, 222–223 management, 223 benign neoplastic ovarian cysts, 219–221 benign mucinous tumors, 221, 221f benign serous tumors, 221, 221f classification, 219t ovarian teratoma, 219–221, 220f demographic factors, 202 fallopian tube pathology, 224–225 benign neoplasms, 224–225 hydrosalpinx, 224, 224f tuboovarian abscess, 225 functional ovarian cysts associated factors, 218 diagnosis and treatment, 218–219, 218f theca lutein cysts, 219 hematometra, 212–213, 212f leiomyomas, 202–212 appearance of, 203f diagnosis, 206–207 intramural, 206f management, 207–212 medroxyprogesterone acetate associated with, 204 pathophysiology, 202–204 round, hyperemic, 205f submucous, 206f, 207f symptoms, 205–206 uterine leiomyoma classification, 204–205, 204f other uterine entities diagnosis, 215–216 management, 216, 218f ovarian cysts as group, 215 symptoms, 215

paraovarian masses, 223 solid ovarian masses, 221–222 Pelvic organ prolapse (POP), 538–560 approach to treatment, 550–551 Baden-Walker halfway system for, 542, 542t classification, 539–542 defect theory of, 544, 544f epidemiology, 538 nonsurgical treatment, 551–554 pelvic floor muscle exercises, 554 pessaries, use of, 551–554, 551f–552f, 553t pathophysiology, 542–545 connective tissue, 543 levator ani muscle, 542–543 vaginal support, levels of, 544–545 vaginal wall, 543–544, 544f patient evaluation, 545–550 pelvic organ prolapse quantification (POP-Q), 540–541, 541f, 542t anterior vaginal wall points, 540 apical vaginal points, 540–541 assessment with, 541 genital hiatus and perineal body, 541 posterior vaginal wall points, 541 perineal examination of, 548 physical examination, 548–550, 549f–550f risk factors associated with, 538–539, 539t age, 539 connective tissue disease, 539 elective cesarean delivery, 538–539 increased abdominal pressure, 539 obstetric-related, 538–539 race, 539 vaginal childbirth, 538 signs and symptoms, 538 surgical treatment, 554–558 anterior compartment, 555 hysterectomy for, 556 and incontinence surgery, 557–558 laparoscopic and robotic approach for, 554–555 obliterative procedures, 554 perineum, 556 plan for, 555 posterior compartment, 556 reconstructive procedures, 554–556 use of mesh and materials in, 556–557, 557t vaginal apex, 555–556 symptoms associated with, 545–548, 545t anal incontinence, 546–547 bulge symptoms, 546 constipation, 546 digital decompression, 546 pelvic and back pain, 547–548 sexual dysfunction, 547 urinary symptoms, 546 vaginal examination of, 548–550, 549f–550f visual descriptors, 539–540, 540f

Index Pelvic organ prolapse quantification (POP-Q), 540–541 anatomic landmarks used during, 541f anterior vaginal wall points, 540 apical vaginal points, 540–541 assessment with, 541, 541f and degrees of uterine prolapse, 541f genital hiatus and perineal body, 541 grid system used for, 541f posterior vaginal wall points, 541 staging system of pelvic organ support, 542t Pelvic Organ Support Study (POSST), 538 Pelvic pain acute pain, 251–253, 251t computed tomography, 252–253 history, 251 laboratory testing, 252 laparoscopy, 253 physical examination, 251–252 radiologic imaging, 252–253 sonography, 252 chronic, 253–262, 254t concurrent lordosis and kyphosis in, 256f history, 253–255 musculoskeletal origins of, 256t physical examination, 255–258 questions relevant to, 255t specific causes of, 260–262 surgical treatment, 259–260 testing, 258 treatment, 258–260 dysmenorrhea, 262 dyspareunia and, 262–263 dysuria and, 263–265 gastrointestinal disease and, 265–267 celiac disease, 265 colonic diverticular disease, 265 functional bowel disorders, 265–267, 266t musculoskeletal etiologies, 267–269 hernias, 267–268, 268f myofascial pain syndrome, 268–269, 268f–269f peripartum pelvic pain syndrome, 269 neurologic etiologies, 269–270 anterior abdominal wall nerve entrapment syndromes, 269–270, 270f piriformis syndrome, 270–271 pudendal neuralgia, 270 pathophysiology, 249–251 inflammatory pain, 249–250 neuropathic pain, 250–251 somatic/visceral pain, 249, 250f with pessary use, 553–554 rating scales for, 255f Pelvic plexus, 806 Pelvic sidewalls, 814–816, 815f Pelvic ureter, 815f, 816 Pelvic vessels, 814–816, 815f Pelvic viscera, anatomy of

fallopian tubes, 809 lower urinary tract structures, 813–814, 813f, 814f bladder, 813, 813f ovaries, 809 rectum, 814, 815f uterus, 807–809 blood supply to, 809 broad ligaments, 807f, 809 cervix, 807, 807f corpus, 807, 807f endometrium and serosa, 807 innervation, 809 lymphatic drainage of, 809 round ligaments of, 807f, 808 uterine support, 808, 808f vagina, 809–813, 810f–812f Pelvis anatomy of, 40, 40f, 799–814 arcus tendineus fascia, 02, 543 blood supply to, 804–806, 805f, 805t bony pelvis and pelvic joints, 799–800, 800f connective tissue of, 804, 804f gray-scale imaging for, 23 innervation, 806, 806f ligaments of, 801, 801f pain in. See Pelvic pain pelvic floor innervation, 804 muscles, 802–804, 802f, 803f, 804t. See also Levator ani muscles site for endometriosis, 231 sonographic examination of, guidelines for, 22–23 ultrasound beyond, 36 viscera, 807–814 walls of muscles and fascia of, 801–802, 802f openings in, 800–801, 800f Penicillins, 52–53 Peptide hormones, 334–336 FSH, 334 human chorionic gonadotropin, 335–336 immunoassays for, 341–342 LH, 334–335 reproduction disorders, 362 thyroid-stimulating hormone, 335 Percutaneous tibial nerve stimulation (PTNS), 571–572 for fecal incontinence, 571–572 for urinary incontinence, 534–535 Pergonal, for ovulation induction, 452t Perimenopause, 107 definition of, 471 Perinatal depression, 305–306 antepartum, 305 postpartum, 305–306 postpartum blues, 305–306 postpartum depression, 306 postpartum psychosis, 306 Perinatal disorders, 305–306 other psychiatric disorders, 306

perinatal depression, 305–306 antepartum, 305 postpartum, 305–306 postpartum blues, 305–306 postpartum depression, 306 postpartum psychosis, 306 perinatal loss, 306 Perineal body, 822 Perineal membrane, 819–820 Perineorrhaphy, 1096–1097, 1097f intraoperative, 1096–1097 surgical steps, 1096–1097 postoperative, 1097 preoperative, 1096 consent, 1096 patient evaluation, 1096 patient preparation, 1096 Perineum anatomy of, 820–822 anterior (urogenital) triangle, 819f, 820–821, 827f blood vessels of, 822 defects of, 414 innervation to, 823 lymphatic drainage to, 822–823, 823f perineal body, 822 posterior (anal) triangle, 821–822 Perineum, defects of, 414 Peripartum pelvic pain syndrome, 269 Peripheral precocious puberty (GnRHindependent), 328–329 Peritoneal disease, 460–461 endometriosis, 460–461 pelvic adhesions, 461 Peritoneal incision, 928f Periurethral-perivesical venous plexus, 818 Permanent contraception, 115–118 female tubal sterilization, 115–117 counseling in, 116 method failure in, 116–117 other effects of, 116–117 regret about, 116 risk-reducing Salpingectomy, 116 tubal interruption methods, 115–116 hysterectomy, 118 male sterilization, 118 transcervical sterilization, 117–118 Persistent müllerian duct syndrome (PMDS), 413 Pessaries, for pelvic organ prolapse, 551–554, 551f–552f, 553t complications of, 553–554 guidelines for, 553t indications for, 551 patient evaluation and placement of, 552–553, 552f selection for, 551–552 types of, 551f Pessary ulcers, 553 PET-computed tomography (PET-CT) fusion, 45, 46

1257

1258

Index Pfannenstiel incision, 929–930, 929f–930f intraoperative, 929–930 postoperative, 930 preoperative, 929 PFDI-22. See Pelvic Floor Distress Inventory 22-Item (PFDI-22) PFIQ-7. See Pelvic Floor Impact Questionnaire 7-Item (PFIQ-7) PFMT. See Pelvic floor muscle training (PFMT) PGD. See Preimplantation genetic diagnosis (PGD) Phenothiazines, 281t Pheromones, 344 Photoelectric effect, 612 Photons (x-rays), 610 Phthirus pubis, 72, 72f Phyllodes tumors, 279–280 Physical examination, 2–7 bimanual examination, 5–6, 6f breast examination, 2–4, 3f–4f clinical evidence, 2–3 examination interval, 7 pelvic examination, 4–5 inguinal lymph nodes and perineal inspection, 4 speculum examination, 4–5, 5f rectovaginal examination, 6–7, 7f speculum examination, 4 Phytoestrogens, for menopausal vasomotor symptoms, 498–499 Phytoprogestins, for menopausal vasomotor symptoms, 499 Pictorial blood assessment chart (PBAC), 181f PID. See Pelvic inflammatory disease (PID) Pinopods, 357 Pioglitazone, 398 Pioglitazone, and urinary incontinence, 525t Piriformis muscle, 801 Piriformis syndrome, 270–271 Pituitary adenomas, 359–361, 359t, 360f, 361f, 378 algorithm for, 361f classification, 359, 360f clinical features of, 359t imaging of, 383 pregnancy and, 360 symptoms, 359–360 treatment of, 360–361, 361f, 362f Pituitary adenylate cyclase-activating peptide (PACAP), 343 Pituitary apoplexy, 360 Placental-site trophoblastic tumor (PSTT), 786 Planning target volume (PTV), 615 Plant-derived agents, chemotherapeutic, 600–602, 601t taxanes, 600–601, 600f, 601t topoisomerase inhibitors, 602 vinca alkaloids, 600f, 601–602 Platelet dysfunction, 193

PLCO trial. See Prostate, Lung, Colorectal and Ovarian (PLCO) trial Plexus of Santorini, 818 Plicae transversales recti, 814, 815f Ploidy, 138 PMDS. See Persistent müllerian duct syndrome (PMDS) Pneumococcal Polysaccharide vaccine (PPSV), 8t PNTML. See Pudendal nerve terminal motor latency (PNTML) POI. See Primary ovarian insufficiency (POI) Poliglecaprone, 847 Poly(ADP) ribose polymerase (PARP) inhibitors, 605 Polycystic ovarian syndrome (PCOS), 12, 150, 339, 379, 386–403, 397 consequences of, 387t definition, 386, 387t diagnosis, 393–397 in adolescence, 397 17-alpha hydroxyprogesterone, 394–395 antimüllerian hormone, 396 cortisol, 396 dehydroepiandrosterone sulfate, 394 endometrial biopsy, 397 gonadotropins, 394 insulin resistance and dyslipidemia measurement, 396–397 sonography, 397, 397f testosterone, 393–394 thyroid-stimulating hormone and prolactin, 393 etiology of, 386–387 incidence of, 386–387 initiation and maintenance, model for, 388f pathophysiology, 387–388 androgens, 387 anovulation, 387–388 gonadotropins, 387 insulin resistance, 387 sex hormone-binding globulin, 387–388 signs and symptoms, 389–393 complications in pregnancy, 393 endometrial neoplasia, 392–393 hyperandrogenism, 389–391 infertility, 393 menstrual dysfunction, 389 metabolic syndrome and cardiovascular disease, 392 obstructive sleep apnea, 392 other endocrine dysfunction, 391–392 pregnancy loss, 393 psychologic health, 393 treatment, 397–400 acanthosis nigricans, 400 acne, 399–400 conservative treatment, 397–398 hirsutism, 398–399 surgical therapy, 400, 1021, 1021f treatment of oligo- and anovulation, 398

Polycystic ovary appearance, 33 Polyembryoma, 764 Polyglactin, 847 Polythelia, 325 POP. See Progestin-only pills (POP) POP-Q. See Pelvic organ prolapse quantification (POP-Q) PORTEC-1 trial. See Post-Operative Radiation Therapy in Endometrial Carcinoma (PORTEC-1) trial Portio supravaginalis, 807, 807f Portio vaginalis, 807, 807f Port-site metastasis in endometrial cancer, 713 in laparoscopy, 878 Positron emission tomography (PET), 45, 46f for cervical cancer, 666 Positron emission tomography (PET) breast cancer, 289 POSST. See Pelvic Organ Support Study (POSST) Postablation tubal sterilization syndrome (PATSS), 197, 1043 Postabortal contraception, 155 Postcoital bleeding, 180 Postembolization syndrome, 209 Posterior colporrhaphy, 556, 1093–1095, 1094f–1095f intraoperative, 1093–1095 surgical steps, 1093–1095 mesh reinforcement with, 556 perineum in, 556 postoperative, 1095 preoperative, 1093 consent, 1093 patient evaluation, 1093 patient preparation, 1093 rectal injury during, 870 Posterior fornix, 810, 811f Posterior pelvic exenteration, 1155, 1155f Posterior pituitary peptides, 346 Postmenopausal Estrogen/Progestin Interventions (PEPI) Trial, 493 Postmenopause, definition of, 471 Postoperative fever, 919 Postoperative infection, 75–82 abdominal incision infection, 80 adnexal infection, 78, 78f bowel obstruction, 915–916 diagnosis of, 76–77 diarrhea, 916 infected pelvic hematoma, 79–80, 79f, 80f MRSA, 82 necrotizing fasciitis, 81–82, 82f ovarian abscess, 78–79 pelvic abscess, 79–80, 79f pelvic cellulitis, 78, 78f postoperative ileus, 915 prevention, 921t surgical site infection, 76 toxic shock syndrome, 80–81, 81t

Index vaginal cuff cellulitis, 77–78, 78f wound, 919–922 wounds, 75–76 Postoperative orders fluid and electrolytes, 908 pain management, 908 Post-Operative Radiation Therapy in Endometrial Carcinoma (PORTEC-1) trial, 621 Postoperative wound, 919 Postpartum, 305–306 Postpartum blues, 305–306 Postpartum depression, 306 Postpartum psychosis, 306 Power Doppler imaging, 24 PPE. See Palmar-plantar erythrodysesthesia (PPE) PPSV. See Pneumococcal Polysaccharide vaccine (PPSV) Prazosin, and urinary incontinence, 525t Precocious puberty, 327–329 central (GnRH-dependent), 327–328, 328t evaluation of, 328t heterosexual, 329 peripheral (GnRH-independent), 328–329, 328t variations of normal puberty, 329 Preconceptional counseling, 18, 18t–19t Pregnancy angular, 173–174 cervical, 174–175, 175f cesarean scar, 175–176, 175f ectopic, 161–179. See also Ectopic pregnancy heterotopic, 175 interstitial, 173–174, 174f intrauterine, 142f molar, 780–784, 780t ovarian, 173 prevention of, sexual assault and, 308–309, 309t vulvar cancer management during, 688 Pregnancy of unknown location (PUL) definition of, 137 diagnosis of, 165 transvaginal sonography, 141 treatment, 168–173 Preimplantation genetic diagnosis (PGD), 146 Preinvasive lesions, of lower genital tract, 624–656 anal intraepithelial neoplasia, 650–651 diagnosis, 650 histology, 650f management, 650–651 pathophysiology, 650 translucent acetowhite lesion of, 651f anatomic considerations, 624–627 cervix, 624–627 external genitalia, 624 vagina, 624 cervical intraepithelial neoplasia, 630–632

management, 641–643 natural history of, 631–632, 631t risk factors, 630–631, 631t treatment of, 643–645 cervical neoplasia diagnosis, 632–641 Bethesda system, 635–637, 635t, 636t biopsy, 640–641, 641f cervical cancer screening guidelines, 634–635 cervical cytology, 632–633 colposcopy, 637–640, 638t, 639f, 641f HPV testing, 633–634 Pap tests, 632–633 HIV-infected patients, 651–652 human papillomavirus infection, 627–630 basic virology, 627–628 diagnosis of, 629 latent infection, 628 life cycle, 627f outcomes, 628–629, 628f prevention of, 630 productive infections, 628–629 transmission, 628 treatment of, 629–630 lower genital tract neoplasia, 624 postcolposcopy surveillance without treatment, 642–643 ablation, 643 excision, 644 hysterectomy, 645 surveillance after treatment, 644, 645 vaginal, 645–646 diagnosis, 645 management, 645–646 pathophysiology, 645 prognosis, 646 vulvar preinvasive lesions, 646–650 characteristics, 647t classification, 647–648, 647t diagnosis, 648–649 management, 649 pathophysiology, 646–647, 647f prognosis and prevention, 649–650 Preinvasive lesions, of vagina, 645–646 CO2 laser ablation, 646 diagnosis of, 645 management, 645–646 pathophysiology of, 645 prognosis, 646 radiation therapy, 646 topical therapy, 646 wide local excision, 646 Premarin. See Conjugated equine estrogen; Estrogen replacement therapy Premature menarche, 329 Premature ovarian failure (POF), 373, 373t autoimmune disorders and, 375 definition, 471 fragile X syndrome and, 374–375 FSH level with, 381 infertility diagnosis, 433t infertility treatment, 458

Premature thelarche, 326, 329 Premenstrual dysphoric disorder (PMDD), 302–303 diagnosis, 303 diagnostic criteria for, 303t oral contraceptive for, 119 treatment of, 303–305 Prepubertal genitalia, 321f Presacral nerve, 806 Presacral space anatomy of, 816–817, 816f in presacral neurectomy, 260 in sacrocolpopexy, 1099, 1103 Pressure flowmetry, for urinary incontinence, 527 Preventive care, 7–19 cancer screening, 9–10 colon cancer, 9–10, 10t lung cancer, 10 skin cancers, 10 cardiovascular disease, 13–14, 14t chronic hypertension, 14–15, 15t diabetes mellitus, 16, 16t dyslipidemia, 15–16 hypercholesterolemia, 15–16, 15t hypertriglyceridemia, 15t, 16 geriatric screening, 17, 17f immunization, 7, 8t–9t lifestyle changes, 10–12 exercise, 12 smoking, 10–11, 11t mental health, 17–18 depression, 17–18 insomnia, 18 partner violence, 17–18 metabolic syndrome, 17, 17t obesity, 12–14, 12t diagnosis of, 12–13 risk factors, 12–13 treatment, 3t, 13–14 preconceptional counseling, 18, 18t–19t stroke, 14–15 thyroid disease, 17 Prevent Recurrence of Osteoporotic Fractures (PROOF) study, 503 Prevesical space. See Space of Retzius Primary endometrial dysfunction, 195–198 combination oral contraceptive pills, 196 iron therapy, 197 levonorgestrel-releasing intrauterine system, 195–196 medical treatment of, 195t nonsteroidal antiinflammatory drugs, 196–197 other hormonal agents, 197 tranexamic acid, 196, 196f uterine procedures, 197–198 Primary ovarian insufficiency (POI). See Premature ovarian failure Primary peritoneal carcinoma definition of, 747, 747t staging of, 750, 750t Primordial germ cells, in yolk sac, 348

1259

1260

Index Processus vaginalis, 819 Progesterone receptors, 339, 340f in endometrium, 357 Progestin implants, 112–115, 115f Progestin injectables. See Depot medroxyprogesterone acetate (DMPA) Progestin-only contraceptives, 126–128 injectable progestins, 127–128 progestin-only pills, 126–127 Progestin-only pills (POP), 126–127 Progestins for clinical practice, 363 for menopausal vasomotor symptoms, 495–497 Progestogens, in clinical practice, 364 Prolactin, 345 Prolapse ulcers, 553 Prolia, for osteoporosis, 500t PROOF study. See Prevent Recurrence of Osteoporotic Fractures (PROOF) study Proopiomelanocortin, 343 PROP1 gene, 378 Propionibacterium acnes, 391 Prostate, Lung, Colorectal and Ovarian (PLCO) trial, 738 Proteus mirabilis, 73 Proton dose distribution, patient with cervical cancer, 611f Provera. See Medroxyprogesterone acetate Proximal fallopian tube cannulation, 1050–1051, 1050f–1051f intraoperative, 1050–1051 instruments, 1050 surgical steps, 1050–1051 postoperative, 1051 preoperative, 1050 Proximal tubal obstruction, 458–459 Proximal tubal occlusion, 458 Pruritic infestations, 70–72 pediculosis, 72 scabies, 70–72 Pseudogestational sac (pseudosac), 142 Pseudo-Meigs syndrome, 206 Pseudomonas aeruginosa, 911 Psoriasis, 91–92, 92f PSTT. See Placental-site trophoblastic tumor (PSTT) Psychosocial issues, 297–317 anxiety disorders, 298, 300t biopsychosocial model, 297f child sexual abuse, 310–311, 310t depression. See Depression eating disorders, 301–302 anorexia nervosa, diagnosis of, 301t, 302 bulimia nervosa, diagnosis of, 302, 302t diagnosis, 302 treatment, 302 female sexuality and, 312–313 drive/desire, 312 release and resolution, 313 sexual arousal, 312–313 sexual response, models of, 312f variations in physiologic response, 313

intimate partner violence, 311–312 diagnosis, 311 management, 311–312 risks, 311 late life, 307 menopause transition and menopause, 306–307 menstruation-related disorders, 302–305 diagnosis, 303 pathophysiology, 303 treatment, 303–305, 304t mood disorders, 297–298, 298t perinatal disorders, 305–306 other psychiatric disorders, 306 perinatal depression, 305–306 perinatal loss, 306 sexual assault, 307–310 examination and documentation, 308 HIV postexposure prophylaxis after, 309, 309t physical findings, 308, 308t pregnancy prevention, 308–309, 309t psychological response to, 310 sexually transmitted disease prevention following, 309–310, 309t treatment, 308–309 sexual dysfunctions, 313–314, 314t diagnosis and treatment, 314 somatic symptom disorders, 307 substance use disorders, 301, 301t PTNS. See Percutaneous tibial nerve stimulation (PTNS) PTV. See Planning target volume (PTV) Pubarche, 320 Pubertal changes, 319–320 Pubis, 799, 800f Puboanalis muscle, 802 Pubococcygeus muscle, 802 Puboperinealis muscle, 802 Puborectalis muscle, 542, 561, 803, 803f Pubourethral ligament, 820 Pubovaginalis muscle, 802 Pubovaginal sling, 1068–1069, 1068f–1069f intraoperative, 1068–1069 surgical steps, 1068–1069 postoperative, 1069 preoperative, 1068 consent, 1068 patient evaluation, 1068 patient preparation, 1068 in urinary incontinence, 532 Pubovisceral muscle, 802 Pudendal artery, 822, 822f Pudendal nerve, 822f Pudendal nerve terminal motor latency (PNTML), 569 Pudendal neuralgia, 270 Pudendal vessels, 822f Puerperal infections, 281–282 Pulmonary complications, 802 acute respiratory distress syndrome, 913 acute respiratory failure, 911

aspiration, 911–912 asthma, 826 atelectasis, 911 hospital-acquired pneumonia, 911, 911t pulmonary embolism, 912–913, 913t Pulmonary embolism, 912 Pure gonadal dysgenesis, 412 Pyolene nystatin, for candidiasis, 62t Q QIDS-SR. See Quick Inventory of Depressive Symptomatology-Self Report (QIDS-SR) Quartette, 121t Quazepam, 18t Quick Inventory of Depressive Symptomatology-Self Report (QIDS-SR), 299t–300t Quiescent gestational trophoblastic disease, 791 Quinolone, 54–55, 835t for hospitalacquired pneumonia, 911t for surgical prophylaxis, 835t R RAAS. See Renin-angiotensinaldosterone system (RAAS) Radiation biology, 612–614 alpha/beta ratio, 614 cell death, 613 direct vs. indirect actions of ionizing radiation, 613, 614f DNA molecule as target for biologic effect, 612–613 four R’s of, 613–614 reassortment, 613–614 reoxygenation, 614 repair, 613 repopulation, 613 linear-quadratic theory, 614, 614f Radiation-induced carcinogenesis, 621, 621t Radiation-induced insufficiency fractures, 621 Radiation oncology practice, 614–621 fractionation schemes, 615 ionizing radiation with chemotherapy, 618 radiation therapy with surgery, 618–619 tumor control probability, 617–618 Radiation physics, 610–612 depth-dose curve, 612 electromagnetic radiation, 610 electromagnetic radiation energy deposition, 611–612 particle radiation, 610 radiation sources, 610, 611f linear accelerator, 610, 611f, 612f radionuclides, 610, 612t radiation unit, 612 Radiation therapy, principles of, 610–623 brachytherapy, 616–617. See also Brachytherapy

Index conformal, 615–616 external beam, 615–616 Heyman capsules, 715 image-guided, 616 intensity-modulated, 616, 616f intraoperative, 619 radiation biology, 612–614 alpha/beta ratio, 614 cell death, 613 direct vs. indirect actions of ionizing radiation, 613, 614f DNA molecule as target for biologic effect, 612–613 four R’s of, 613–614 linear-quadratic theory, 614, 614f radiation oncology practice, 614–621 fractionation schemes, 615 ionizing radiation with chemotherapy, 618 radiation therapy with surgery, 618–619 tumor control probability, 617–618 radiation physics, 610–612 depth-dose curve, 612 electromagnetic radiation, 610 electromagnetic radiation energy deposition, 611–612 particle radiation, 610 radiation sources, 610, 611f radiation unit, 612 role in management of gynecologic cancers, 611t stereotactic body, 616 tandem and ovoid device, 616, 616f tissue response to, 619–621 bladder, 620 bone, 621 epithelium and parenchyma, 619 hematologic toxicity, 621 kidney, 621 ovary and pregnancy outcomes, 620 rectosigmoid, 620–621 skin reactions, 619 small bowel, 620 vagina, 619–620 Radiation Therapy Oncology Group (RTOG) trial, 615 Radiation unit, 612 Radical abdominal hysterectomy (type III), 1134–1139, 1136f–1138f for cervical cancer, 669–670 intraoperative, 1135–1139 postoperative, 1139 preoperative, 1135 types of, 669t Radical complete vulvectomy, 1212–1214, 1212f–1214f intraoperative, 1212–1214 postoperative, 1214 preoperative, 1212 for vulvar cancer, 685, 685f Radical partial vulvectomy, 1209–1211, 1209f–1211f

intraoperative, 1209–1211 postoperative, 1211 preoperative, 1209 for vulvar cancer, 684–685, 684f, 685f Radical vaginal trachelectomy, 669t for cervical cancer, 670 Radiography, 37–39 bone densitometry, 39 breast imaging, 37 chest radiograph, 37, 826 cardiac testing, 828 for cervical cancer, 664t for GTN, 787 for pneumonia, 911 for vaginal cancer, 695, 695t hysterosalpingography, 38–39 intravenous pyelography, 37–38 positive pressure urethrography, 38 selective salpingography, 39 voiding cystourethrography, 38 Radionuclides, 610, 612t Radiosensitivity, tumor, 617, 617t RAIR. See Rectoanal inhibitory reflex (RAIR) Raloxifene, for osteoporosis, 500t, 501 Ramelteon, 18t, 304t Random-donor platelets, 866 Ranitidine, 281t RANK ligand. See Receptor activator of nuclear factor (RANK) ligand RCRI. See Revised Cardiac Risk Index (RCRI) Reactive dermatitis, benign, 286f Reanastomosis, of fallopian tube segments, 458–459, 459f, 459f Recentin. See Cediranib Receptor activator of nuclear factor (RANK) ligand, 476–477, 476t Receptor tyrosine kinases (RTKs), 604 Reconstructive grafts and flaps, 1218–1220, 1218f–1219f intraoperative, 1218–1219 postoperative, 1220 preoperative, 1218 Rectal accommodation, 563 Rectal compliance, 563 Rectal injury, 870 Rectoanal inhibitory reflex (RAIR), 563 Rectosigmoid, 620–621 Rectosigmoid lesions, 234–235 Rectouterine pouch. See Cul-de-sac of Douglas Rectovaginal examination, 6–7, 7f Rectovaginal fistula (RVF), 573–575 classification of, 573–574 definition of, 573–574 diagnosis of, 574 distal wall of posterior vagina, 574f risk factors, 573t surgical repair, 1128–1130, 1128f–1129f intraoperative, 1128–1130 postoperative, 1130 preoperative, 1128

treatment of, 574–575 in woman underwent midline episiotomy, 574f Rectovaginal space, 811, 811f, 812f Rectum, 814, 815f Rectus abdominis muscle, 268–269 anatomy, 796 anterior abdominal wall nerve entrapment syndromes and, 269–270, 270f in Cherney incision, 931 diastasis of, 256 infiltrated, 235 in Maylard incision, 932 in midline vertical incision, 927 in Pfannenstiel incision, 929–930, 930f port placement, 895–896 Spigelian hernias along lateral border of, 267 transection, 932f transverse incisions, 846–847 Rectus sheath, anterior abdominal wall, 796–798 797f Recurrent disease, vulvar, 688 distant recurrences, 688 vulvar recurrences, 688 Recurrent miscarriage, 144–150 alloimmune factors, 149 anatomic factors, 147–148 autoimmune factors, 148–149, 148t endocrinologic factors, 149–150 etiology, 145 evaluation and treatment, 150, 151t immunologic factors, 148–149 parental chromosomal abnormalities, 145–148 thrombophilias, 150 Red blood cell replacement clinical assessment, 865 complications, 865 transfusion, 865 Red clover, 498 Reid Colposcopic Index, 639, 640t Renal disease, preconceptional counseling in, 19t Renin-angiotensinaldosterone system (RAAS), 303 Reproductive aging female, 435–436, 435t stages of, 472f Reproductive endocrinology, 334–368 endocrine secretion, 334 endometrium, 355–357 hormone biosynthesis and mechanism of action, 334–339 peptide hormones, 334–336 steroid hormones, 336–339 hormone communication, 334, 335f hypothalamic-pituitary axis, 342–346 abnormalities in, 357–361 anatomy, 342, 342f anterior pituitary hormones, 343

1261

1262

Index Reproductive endocrinology (Continuedâ•›) corticotropin-releasing hormone, 346 dopamine, 345 growth hormone–releasing hormone, 345–346 hypothalamic neuroendocrinology, 343 hypothalamic-releasing peptides, 344–345 other hypothalamic neuropeptides, 343 posterior pituitary peptides, 346 prolactin, 345 thyrotropin-releasing hormone, 345 immunoassays for peptide and steroid hormones, 341–342, 341t reproductive steroids in adult human serum, 341t stimulation tests, 342 suppression tests, 342 menstrual cycle, 346–355, 347f characteristics, 347t endometrial changes during, 356f follicular development, 352–353 gonadal peptides, 351, 352f ovarian hormone production, 348–351, 349f ovary and, 346–348, 348f, 349f phases, 353–355 neuroendocrine signaling, 334 neurotransmitter secretion, 334, 335f receptor structure and function, 339–341 G-protein coupled receptors, 339 receptor expression and desensitization, 340–341 steroid hormone receptors, 339–340, 340f Reproductive Risks for Incontinence Study at Kaiser (RRISK) study, 539 Reproductive tract, female, development of, 409f Repronex, for ovulation induction, 452t Resistant ovary syndrome, 374 Retinoids, 90 Retractors. See Instruments, surgical Retrograde transtubal transport, in endometrial cancer, 712 Retroperitoneal entry, 935f Retroperitoneal surgical spaces, 814–818 pelvic sidewalls, 814–816, 815f presacral space, 816–817, 816f prevesical space, 817–818, 817f Retropubic space. See Prevesical space Retropubic urethropexy, 1061 for urinary incontinence, 532 Revised Cardiac Risk Index (RCRI), 828 Rhabdosphincter, 814, 814f Rigid hysteroscope, 901–902 Risedronate, for osteoporosis, 500t, 503 Risk of Ovarian Malignancy Algorithm (ROMA), 742 Rivaroxaban (Xarelto), 831t, 832 Robotic surgery, 886–887 Rocephin. See Ceftriaxone

ROMA. See Risk of Ovarian Malignancy Algorithm (ROMA) Rosiglitazone, and urinary incontinence, 525t RRISK study. See Reproductive Risks for Incontinence Study at Kaiser (RRISK) study RTKs. See Receptor tyrosine kinases (RTKs) RTOG trial. See Radiation Therapy Oncology Group (RTOG) trial Russell sign, 302 S Sacral nerve stimulation (SNS). See Sacral neuromodulation Sacral neuromodulation, 1085–1087, 1085f–1087f for fecal incontinence, 571 intraoperative, 1085–1087 surgical steps, 1085–1087 postoperative, 1087 preoperative, 1085 consent, 1085 patient evaluation, 1085 patient preparation, 1085 in urinary incontinence, 534 Sacral venous plexus, 817 Sacrospinous ligament fixation (SSLF), 1112–1115, 1113f–1115f intraoperative, 1112–1115 surgical instruments, 1112–1113 surgical steps, 1113–1115 postoperative, 1115 preoperative, 1112 Sacrospinous ligaments, 800 Sacrotuberous ligaments, 800 Sacrum, 799 Safyral, 120t Saline infusion sonography (SIS), 24–25, 25f, 28f Asherman syndrome, 34f, 147 for AUB, 186–187 congenital uterine anomalies, 418 endometrial polyp, 186–187 leiomyoma, 206 müllerian anomalies, 418 of normal endometrial cavity, 25f, 27f submucous fibroid, 206f Salmon calcitonin, for osteoporosis, 500t Salpingectomy, 939–940, 939f for ectopic pregnancy, 172 for hydrosalpinges, 224 at laparoscopy, 1011–1012, 1011f–1012f at laparotomy, 939–940, 939f risk reducing, 139 Salpingitis isthmica nodosa, 437 Salpingography, selective, 39 Salpingo-oophorectomy (SO), 935–936, 935f–936f intraoperative, 935–936 laparatomy surgical steps, 935–936 abdominal entry, 935 anesthesia, 935

exposure, 935 fallopian tube ligation, 936, 936f infundibulopelvic ligament ligation, 935–936, 936f patient positioning, 935 ureter location, 935, 935f uteroovarian ligament ligation, 936, 936f postoperative, 936 preoperative, 935 consent, 935 patient evaluation, 935 patient preparation, 935 Salpingostomy, 939–940 for ectopic pregnancy, 172 at laparoscopy, 1013–1014, 1013f–1014f at laparotomy, 939, 940 Sampson artery, 808 Saphenous opening, 823 Sarcoptes scabiei, 71, 71f SARMs. See Selective androgen-receptor modulators (SARMs) Sartorius muscle, 823 SBRT. See Stereotactic body radiation therapy (SBRT) Scabies, 71–72 Scarpa fascia, 796, 797f, 818 Schiller-Duval body, 764, 764f Sciatic hernia, 267 Scissors. See Instruments, surgical SCJ. See Squamocolumnar junction (SCJ) Sclerosing stromal tumors, 771–772 Scopolamine, and urinary incontinence, 525t SCSTs. See Sex cord-stromal tumors (SCSTs) SDAT. See Senile dementia of Alzheimer type (SDAT) Seasonale, 121t Seasonique, 121t Seborrheic keratosis, 96 Secca procedure, for fecal incontinence, 572 Second-tier contraceptive methods, 118–128 Segmental müllerian hypoplasia cervical agenesis, 419–420 müllerian agenesis, 420 vaginal atresia, 419 Selective estrogen-receptor modulators (SERMs), 363–364 agonist or antagonist effects of, 364t bleeding and, 191 chemical structures of, 363f for osteoporosis, 500t Selective estrogens, Menopause, and Response to Therapy (SMART-2) trial, 497 Selective muscarinic-receptor antagonists, for urinary incontinence, 534 Selective photothermolysis, 399 Selective progesterone-receptor modulators (SPRMs), 131t for endometriosis, 241 ulipristal acetate, 208

Index Selective salpingography, 39 Selective serotonin-reuptake inhibitors (SSRI) for depression, 303–304, 304t Self breast examination (SBE), 2–3 Self-retaining retractor. See Instruments, surgical Semen volume, abnormal, 461–462 Senile dementia of Alzheimer type (SDAT), 507 Sentinel lymph node biopsy (SLNB) for endometrial cancer, 686–687, 686f for vulvar cancer, 686–687, 686f Separation pain, 171 Septate uterus, 418, 422 bicornuate uterus vs., 422 diagnosis, 422 hysteroscopic septum resection in, 422 imaging of, 34–35, 35f, 422 infertility, 439f miscarriage, 147, 147t MR imaging, 43 surgery for, 1048–1049, 1048f–1049f SERMs. See Selective estrogen-receptor modulators (SERMs) Serotonergic pathway stimulation, 281t Serotonin-reuptake inhibitors for menopausal vasomotor symptoms, 497–498 Serous adenocarcinoma, 661t, 662, 744t borderline, 740f of cervix, 661t of endometrium, 709t, 710, 711f of ovary, 744f uterine papillary, 711f, 716–717 Serous cystadenomafibroma, 219 Serous tubal intraepithelial carcinoma (STIC), 741 Serous tumors, benign, 221, 221f Sertoli cells, 442 Sertoli cell tumors, 772 Sertoli-Leydig cell tumor (SLCT), 772–773, 772f Sertoli-stromal cell tumors, 772–773 Sertraline, 304t for depression, 304t for vasomotor symptoms, 497t, 498 for vulvar contact dermatitis, 91t Sex cord-stromal tumors (SCSTs), 767–775 classification of, 769–770, 769t diagnosis, 768–769 epidemiology, 768 FOXL2 gene mutation, 768 generalist, role of, 769 granulosa cell tumors, 770–771 adult, 769f, 770–771, 770f juvenile, 771 gynandroblastomas, 773 pathology, 769–773 prognosis, 775 Sertoli cell tumors, 772

Sertoli-Leydig cell tumor (SLCT), 772–773, 772f Sertoli-stromal cell tumors, 772–773 sex cord tumors with annular tubules, 773 stage and survival of, 771t steroid cell tumors, 773 thecoma-fibroma group, 771–772 treatment, 773–775 tumor markers for, 768t unclassified, 773 Sex cord tumors with annular tubules, 773 Sex-determining region of Y (SRY), 405, 407 Sex development, disorders of, 409–414 abnormal androgen production, 412 algorithm for, 414f chromosomal ovotesticular, 411 classification of, 409t definitions, 409–411 gender assignment, 413 sex chromosome, 411 46,XX disorders, 412–413 46,XY disorders, 411–412 Sex hormone-binding globulin (SHBG), 241, 338, 365, 387–388 Sex of rearing, 330 Sex steroid hormones, 207–208 Sex steroids, chemical structures of, 363f Sexual abuse, child, 310–311, 310t recommended testing, 310 sexual contact in, findings diagnostic of, 310t STD prophylaxis and, 311 Sexual arousal, in females, 312–313 Sexual assault, 307–310 examination and documentation, 308 HIV postexposure prophylaxis after, 309, 309t physical findings, 308, 308t pregnancy prevention, 308–309, 309t psychological response to, 310 sexually transmitted disease prevention following, 309–310, 309t treatment, 308–309 Sexual determination, 405 Sexual dysfunctions, in females, 313–314, 314t Sexual infantilism, 374 Sexuality, 329–331 adolescent, 330 contraception, 330–331 gender identity, 329–330 Sexually transmitted disease (STD) counseling in, 19t prevention, following sexual assault, 309– 310, 309t screening guidelines, 6t Sharp dilatation and curettage, 964–965, 964f–965f SHBG. See Sex hormone-binding globulin (SHBG) SHOX gene, 411

Sickle-cell disease, preconceptional counseling in, 19t Sigmoid conduits, 1166 Sims uterine sound, 964f Single-donor platelets, 866 Skeletal muscle relaxants, and urinary incontinence, 525t Skeletonizing, uterine artery, 860 Skene gland, 97, 814, 819 ductal occlusion of, 97 infection of, 583 Skin aging in mature woman, treatment of, 507 Skin cancers, 10 Ski needle, 897f Skinning vulvectomy, 1207–1208, 1207f–1208f intraoperative, 1207–1208 postoperative, 1208 preoperative, 1207 SLCT. See Sertoli-Leydig cell tumor (SLCT) SLE. See Systemic lupus erythematosus (SLE) Sliding-Scale Insulin, 833t SLNB. See Sentinel lymph node biopsy (SLNB) Small bowel resection, 1197–1198, 1197f–1198f intraoperative, 1197–1198 postoperative, 1198 preoperative, 1197 Small cell carcinomas, 746–747 Smoking, 10–11, 11t and assisted reproductive technology, 429 and ectopic pregnancy, 161 effects and assisted reproductive technology, 429 health risks associated with, 429t infertility, 429, 429t, 471 miscarriage, 140, 429 risk for pulmonary complications, 825–826 and urinary incontinence, 516 wound infection, 51t, 75t, 921t Smooth muscle tumor of uncertain malignant potential (STUMP), 724–725 Solid ovarian masses, 221–222 Somatic pain, 249, 250f Somatic symptom disorders, 307 Sonic hedgehog (SHH) gene, 408 Sonoelastography, 29–30 Sonography, 22–37 for acute pelvic pain, 252 clinical applications, 32–37 infertility, 34–36, 34f–35f intraabdominal fluid, 32–33, 32f malignant ovarian characteristics, 33 pelvic inflammatory disease, 33–34, 33f, 34f ultrasound beyond pelvis, 36–37

1263

1264

Index Sonography (Continuedâ•›) compression, 36–37, 36f examination techniques, 22–30 contrast-enhanced sonography, 29 Doppler technology, 23–24, 24f focused-ultrasound therapy, 30 gray-scale imaging, 23 harmonic imaging, 23 hysterosalpingo-contrast sonography, 25–26, 26f saline infusion sonography, 24–25, 25f sonoelastography, 29–30 three-dimensional sonography, 26–29, 27f–29f findings of, 30–32 endometrium, 31, 31f, 32f pelvic floor, 31–32 reproductive tract organs, 30, 30f physics of, 22, 23f transvaginal, 23, 23f Soy products, 498 Space of Retzius, 817 anatomy of, 817–818, 817f bleeding from, 862 and Burch colposuspension, 1061–1062, 1061f entry into, 1061–1062, 1061f, 1068f, 1073f and paravaginal defect repair, 1091, 1091f and pubovaginal sling, 1068, 1068f, 1069 and tension-free vaginal tape, 1063 and urethrolysis, 1072–1073, 1073f Spectrazole, for candidiasis, 62t Spermatogenesis, 430–431, 442 Sperm count, abnormal, 462–463 Spermicides, 130 Sperm morphology, abnormal, 443, 463 Sperm motility, 463 Sphincteric deficiency. See Intrinsic sphincteric deficiency Sphincteroplasty end-to-end, 1127f indications for, 571 overlapping, 1127f Sphincter urethrae, 516, 814 Spironolactone for hirsutism, 399 and urinary incontinence, 525t Splenectomy, 1187–1188, 1187f–1188f intraoperative, 1187–1188 postoperative, 1188 preoperative, 1187 Spontaneous abortion, 137–144 clinical classification, 140–143 complete abortion, 142–143 incomplete abortion, 142 inevitable abortion, 142 missed abortion, 143 septic abortion, 143 threatened abortion, 140–142, 141f, 141t, 142f

euploid abortion, 138–139 fetal factors, 138, 138f incidence, 137–138 management, 143–144, 144t maternal factors, 139–140 Squamocolumnar junction (SCJ), 102, 807 Squamous cell carcinoma cervical, 660, 661f of endometrium, 712 vaginal, 694–698, 695f diagnosis, 695 prognosis, 696 recurrent disease, 698 risks, 694–695 staging and classification, 695 surveillance, 698 treatment, 696–698 vulvar, 680f early-stage, 681f metastatic, 681f SRY. See Sex-determining region of Y (SRY) SSLF. See Sacrospinous ligament fixation (SSLF) St. Marks (Vaizey) Incontinence Score, 565t Stages of Reproductive Aging workshop (STRAW), 471 Staphylococcus aureus, 80, 324 Staphylococcus saprophyticus, 73 Stereotactic body radiation therapy (SBRT), 616 Sterilization female tubal, 115–117. See also Female tubal sterilization laparoscopic, 1006–1010, 1006f–1010f laparotomy, 937–938, 937f–938f male, 118. See also Male sterilization reversibility of, 459 risk-reducing salpingectomy, 116, 739 transcervical, 1046–1047, 1046f–1047f Steroid bioassays, 365 Steroid cell tumors, 773 Steroid hormone receptors, 339–340, 340f classification, 339 estrogen, progesterone, and androgen receptors, 339 nongenomic actions of steroids, 340 relative binding affinities of, 365f structure, 339, 340f Steroid hormones, 336–339 classification, 336 immunoassays for, 341–342 potency, 364–365, 365t reproduction disorders, 362 steroidogenesis, 336–338, 337f transport in circulation, 338–339 Steroidogenic enzymes, 337t STIC. See Serous tubal intraepithelial carcinoma (STIC) Stool DNA (sDNA), 10t Strassman metroplasty, 422f Stratum compactum, 355 STRAW. See Stages of Reproductive Aging workshop (STRAW)

Streak gonad, 409 Streptococcus pneumoniae, 324 Stress urinary incontinence (SUI), 514 Burch colposuspension for, 1061–1062, 1061f–1062f pubovaginal sling for, 1068–1069, 1068f–1069f surgical treatment of, 531–533 midurethral slings, 531–532 paravaginal defect repair, 532–533 pubovaginal slings, 532 retropubic urethropexy, 532 transvaginal needle procedures, 532–533 urethral bulking agent injection, 532 tension-free vaginal tape procedure for, 1063–1065, 1064f–1065f treatment of, 530–533 medications for, 530 pessary and urethral inserts, 530–531 urogenital changes and, 487 Striated urogenital sphincter anatomy, 519f Striated urogenital sphincter complex, 814 Stroke, 14–15 Stromal cells, 350 Stromal luteomas, 773 Struma ovarii, 220 Study of Women’s Health Across the Nation (SWAN), 313 STUMP. See Smooth muscle tumor of uncertain malignant potential (STUMP) Subfertile couples, 427. See also Infertility Submucous fibroid, 206f Submucous leiomyomas, 204, 206f Subserosal leiomyomas, 204 Substance use disorders, 301, 301t Suction dilatation and curettage, 153, 966–968, 966f–968f intraoperative, 967–968 instruments, 967 surgical steps, 967–968 postoperative, 968 preoperative, 966–967 consent, 966 patient evaluation, 966 patient preparation, 966–967 Suction-irrigator, 882f Sunitinib, 604, 604f Superficial perineal fascia, 818 Superficial transverse perineal muscles, 820 Supernumerary ovary, 423 Superovulation, 451 Suppurative cervicitis, 64–65 Chlamydia trachomatis, 64–65 Mycoplasma genitalium, 65 Neisseria gonorrhoeae, 64 Supracervical hysterectomy (SCH), 950–951, 950f Surgeries for benign gynecologic disorders, 926–1002

Index Surgical abortion, 153–154. See also Suction dilatation and curettage cervical preparation, 153 menstrual aspiration, 153 vacuum aspiration electric, 153 manual, 153–154 Surgical safety, 843 Surgical site infection, 76 anatomy of, 76f classification, 76, 76f definition, 76 criteria for, 77t prevention, 80, 921t prophylaxis for, 834, 835t risks, 75t treatment, 78, 921t Surveillance, Epidemiology, and End Results (SEER) database study, 724 Sutures, 422f, 855–856 bidirectional, 898 categorization of, 898 designation, 855t loops, 900 material, 855f unidirectional, 898 Symphysis pubis, 799 Synechiae. See Asherman syndrome Synthetic erythropoietins, 606–607 Syphilis, 57–59 diagnosis, 58 latent, 58 pathophysiology, 57–58 primary, 57 secondary, 57–58, 58f tertiary, 58 treatment, 58–59 Syringoma, vulvar, 96, 96f Systemic illnesses, vulvar manifestations of, 94–95 acanthosis nigricans, 94 Behçet disease, 95 Crohn disease, 94, 94f Systemic lupus erythematosus (SLE), 125 T Tamoxifen, 603, 703 in AUB, 181 bleeding and, 188 for breast cancer, 284, 285, 291 and endometrial cancer, 703 in LCIS, 284 for ovulation induction, 451 Tanner stages, 319–320, 320f TAP block. See Transversus abdominis plane (TAP) block Taxanes, 600–601, 600f, 601t TCRE. See Transcervical resection of endometrium (TCRE) Tegaserod, 266 Temazepam, 18t, 123t Tension-free vaginal tape, 1063–1065

intraoperative, 1063–1065 surgical steps, 1063–1065 postoperative, 1065 preoperative, 1063 consent, 1063 patient evaluation, 1063 patient preparation, 1063 Tension-free vaginal tape (TVT), 531, 862, 1063–1065, 1064f–1065f Teratospermia, 443 Teratozoospermia, 443, 463 Terazol 3, for candidiasis, 62t Terazol 7, for candidiasis, 62t Terazosin, and urinary incontinence, 525t Terconazole, for candidiasis, 62t Teriparatide, for osteoporosis, 500t TESE. See Testicular sperm extraction (TESE) Testicular regression, 412 Testicular sperm extraction (TESE), 463 Testis, male, anatomy of, 431f–432f TET. See Tubal embryo transfer (TET) Tetracyclines, 55 Thalassemias, preconceptional counseling in, 19t Theca lutein cysts, 219 hydatidiform mole, 781 Thecoma-fibroma group, 771–772 Thecomas, 771 Thelarche, 320 Thermal injury, laparoscopy, 878 Thiazolidinediones, and urinary incontinence, 525t Thioridazine, and urinary incontinence, 525t Third-tier contraceptive methods, 105, 128–130 barrier methods, 128–130 cervical cap, 129–130 diaphragm plus spermicide, 128–129 female condom, 128 cervical cap, 129–130 diaphragm plus spermicide, 128–129, 129f female condom, 128, 128f, 129f fertility awareness-based methods, 130 male condom, 128 Thoracic endometriosis, 235 Threatened abortion, 140–142 diagnosis of, 141–142, 141t outcomes in, 141t Three-dimensional sonography, 26–29, 27f–29f clinical use, 27–29, 28f–29f IUD, 111 leiomyoma, 206 Mullerian anomalies, 418 with power Doppler angiography, 28 technical aspects, 26–27, 27f Thrombocytopenia, and abnormal uterine bleeding, 192 Thromboembolism, 830 Caprini Risk Assessment Model, 836t

deep-vein thrombosis compression sonography for, 36–37 pretest probability for, 913t prevention, 835 hormone discontinuation, 837 prophylaxis options, 837–838 thrombophilias, 836–837 pulmonary embolism, 912–913, 913t treatment, 913t venous, 125, 830 Thrombophilias, 836, 837f factor V Leiden mutation, 837 and incidence of VTE, 125 and miscarriage, 150 preconceptional counseling in, 18t protein C deficiency, 837 protein S deficiency, 837 prothrombin G20210A mutation, 837 Thyroid disease, 17, 149–150 counseling in, 19t Thyroid peroxidase antibodies (TPOAb), 383 Thyroid-stimulating hormone (TSH), 335 abnormal uterine bleeding, 192 amenorrhea, 379, 380f, 382, 382t hydatidiform mole, 782 Thyrotropin, 344 Thyrotropin-releasing hormone (TRH) Tinzaparin (Innohep), 914t Tioconazole, for candidiasis, 62t Tissue clamps. See Instrument, surgical Tissue extraction techniques, 896, 896f Tissue plasminogen activator (TPA), 357 Tissue-selective estrogen complex (TSEC), 364, 497 for osteoporosis, 500t TIV. See Trivalent inactivated influenza vaccine (TIV) Tolterodine, for urinary incontinence, 533–534 Topical antibiotics, 400 Topical benzoyl peroxide, 400 Topical retinoids, 399–400 Topoisomerase inhibitors, 602 Top-tier contraceptive methods, 105, 107–118 contraceptive failure rates, 107t intrauterine contraception, 107–112 permanent contraception, 115–118 progestin implants, 112–115 Total laparoscopic hysterectomy, 1033–1036, 1034f–1036f postoperative, 1035–1036 preoperative, 1033–1035 Total pelvic exenteration, 1148–1153, 1148t, 1149f–1153f intraoperative, 1148–1152 instruments, 1148 surgical steps, 1148–1152 postoperative, 1153 preoperative, 1148 Total progressive motility, 443 Total vaginal length (TVL), 541

1265

1266

Index Toxic shock syndrome (TSS), 80–81, 81t Toxoplasma gondii, 139 TPA. See Tissue plasminogen activator (TPA) TPOAb. See Thyroid peroxidase antibodies (TPOAb) TPPP. See Typical pelvic pain posture (TPPP) Trachelectomy, 962–963, 962f–963f intraoperative, 962 postoperative, 963 preoperative, 962 TRALI. See Transfusion-related acute lung injury (TRALI) Tranexamic acid (TXA), 191, 196, 196f, 862 for abnormal uterine bleeding, 194t, 195, 195t, 196 contraindications, 196 for hemorrhage, 862 for leiomyoma, 209 mechanism of action, 196f Tranquilizers, 123t Transabdominal pelvic sonograms, 319f Transcervical resection of endometrium (TCRE), 1044 Transcervical sterilization, 117–118, 1046–1047, 1046f–1047f. See also Essure Permanent Birth Control System chemical tubal occlusion, 118 intraoperative, 1046–1047 instruments, 1046 surgical steps, 1046–1047 mechanical tubal occlusion, 117 postoperative, 1047 preoperative, 1046 Transformation zone (TZ) and cervical neoplasia, 627 component, 636 SCJ within, 639 Transfusion-related acute lung injury (TRALI), 866 Transitional cell carcinoma, 746 of endometrium, 712 Transobturator tape (TOT) sling, 532, 1066–1067, 1066f–1067f Transvaginal sonography (TVS), 23 adenomyosis, 214, 214f anteverted uterine corpus, 30f for AUB, 185–186 clinical applications of, 32–37 ectopic pregnancy, 165–167, 166f–167f ectopic pregnancy, 165–167 endocervical polyp, 44 endometrial cancer, 185–186 endometrial hyperplasia, 705–706, 705f endometrial polyp, 189 endometrioma, 236–237, 236f, 237f endometriosis, 236–237 hematometra, 212–213, 212f hemorrhagic cyst, 217t hydrosalpinx, 224f intrauterine pregnancy, 141

IUD positioning, 28 for leiomyoma, 206 mature cystic teratoma, 221, 221f missed abortion, 143, 143f ovarian cancer, 742 ovarian cyst, 26f, 456f ovarian hyperstimulation syndrome, 456 PCOS, 397, 397f pediatric uterus, 325 pelvic hematoma, 80, 80f for postoperative infection, 77 of pseudogestational sac, 166f theca lutein cysts, 782f tuboovarian abscess, 68, 68f of uterine cervix, 30f Transversalis fascia, anterior abdominal wall, 796–797, 797f Transverse cervical ligaments. See Mackenrodt ligaments Transverse colon conduit, 1159, 1159f, 1166 Transverse incisions, 845 advantages of, 929 Cherney incision, 931, 931f Maylard incision, 932, 932f Pfannenstiel incision, 929–930, 929f–930f Transverse vaginal septa, 416, 417f surgery for, 983–984, 983f–984f Transversus abdominis muscle, 796 Transversus abdominis plane (TAP) block, 843 Trazodone, 304t Treponema pallidum, 57, 310 Triazolam, 18t Trichomonads, 63f Trichomonas vaginalis bacterial vaginosis, 52 nonneoplastic findings, 637 testing for, child sexual abuse, 310, 310t trichomoniasis, 63 vulvovaginitis, 324 Trichomoniasis, 63–64 diagnosis, 63, 63f treatment of, 64 Tricyclic antidepressants, and urinary incontinence, 525t Trifolium pretense, 498 Trihexyphenidyl, and urinary incontinence, 525t Trimethoprim-sulfamethoxazole, for granuloma inguinale, 59t Tri-Norinyl, 121t Triphasic pills, 121 Triploid karyotype, 782 Triploidy, 138 Trivalent inactivated influenza vaccine (TIV), 8t Trivora, 121t Trocars, 892 Trocar-site metastasis, 878 Troglitazone, and urinary incontinence, 525t

Troleandomycin, 123t Trophectoderm biopsy, 467f TSEC. See Tissue-selective estrogen complex (TSEC) TSH. See Thyroid-stimulating hormone (TSH) Tubal abortion, 168 Tubal cannulation, 458 Tubal embryo transfer (TET), 465 Tubal ring. See Falope ring Tuberous breasts, 326 Tuboovarian abscess, 67–68, 68f, 225 Tuboovarian complex, 220 Tumor hypoxia, 618 Turner syndrome, 411 characteristic findings of, 411t karyotyping, 383 mosaicism (45,X/46,XY), 762 physical examination, 381 TVL. See Total vaginal length (TVL) TXA. See Tranexamic acid (TXA) Typical pelvic pain posture (TPPP), 255 U UAE. See Uterine artery embolization (UAE) UFH. See Unfractionated heparin (UFH) UKCTOCS. See United Kingdom Collaborative Trial of Ovarian Cancer Screening (UKCTOCS) Ulipristal acetate, 208 Ella, 132, 241 for emergency contraception, 131t for leiomyoma, 208 Ultrasonic energy, 859, 884 Umbilical entry, 889 Umbilical ligaments, 797–798, 798f, 889, 889f Uncomplicated cellulitis, 282 Undifferentiated carcinoma, of endometrium, 712 Unexplained infertility, 460t Unfractionated heparin (UFH), 830–832, 831t Unicornuate uterus, 418t imaging of, 35, 35f, 43, 43f impaired pregnancy with, 420–421 miscarriage, 147, 421 Unidirectional suture, 898 United Kingdom Collaborative Trial of Ovarian Cancer Screening (UKCTOCS), 738 Unopposed estrogen therapy, 702 UPSC. See Uterine papillary serous carcinoma (UPSC) Urachus, 797 Ureaplasma urealyticum bacterial vaginosis associated with, 51 cervical infection by, 441 in euploid abortions, 139 Ureterovaginal fistula, 580f Urethra, 814, 814f anatomy of, 520f and associated muscles, 814f

Index Urethral bulking injections, 1070–1071, 1071f intraoperative, 1070 choice of bulking agent, 1070 surgical steps, 1070 postoperative, 1070–1071 preoperative, 1070 consent, 1070 patient evaluation, 1070 patient preparation, 1070 in urinary incontinence, 532 Urethral coaptation, 519 Urethral diverticulum, 97, 582–587 classification of, 584 development, mechanism of, 583f diagnosis of, 585–587 cystourethroscopy, 585–586, 585f physical examination, 585 positive pressure urethrography, 586 Trattner double-balloon catheter used in, 586f voiding cystourethrogram, 586 diverticulectomy, 587 etiology of, 583–584 surgery for, 1075–1077, 1075f–1077f symptoms of, 584–585 transurethral expression of discharge with compression of, 585f treatment of, 587 Urethral diverticulum repair, 1075–1077, 1075f–1077f intraoperative, 1075–1077 diverticulectomy, 1075–1076 partial diverticular ablation, 1076–1077 Spence marsupialization, 1077 postoperative, 1077 preoperative, 1075 Urethral injury, 867–868 Urethral inserts, 531 Urethral integrity, 522 Urethral patches, 531 Urethral pressure profile, for urinary incontinence, 527–528 Urethrolysis, 1072–1073, 1072f–1073f intraoperative, 1072–1073 abdominal approach, 1073 vaginal approach, 1072–1073 postoperative, 1073 preoperative, 1072 Urethroscopy, 1057–1060, 1058f–1060f intraoperative, 1058–1060 surgical steps, 1058–1060 postoperative, 1060 preoperative, 1058 Urethrovaginal sphincter, 516, 814 Urgency urinary incontinence, treatment of, 533–535 anticholinergic medications, 533–534, 533t botulinum toxin A, 535 mirabegron, 534 percutaneous tibial nerve stimulation, 534–535 sacral neuromodulation, 534

Urinary complications oliguria, 916–917 urinary retention, 917 Urinary incontinence, 514–537 conservative treatment for biofeedback therapy, 630 diet, 530 electrical stimulation, 530 estrogen replacement, 530 Kegel exercises, 529 pelvic floor muscle training, 529, 530 pelvic floor strengthening exercises, 528–530 scheduled voiding, 530 definitions of, 514 diagnosis, 522–528 bimanual and rectovaginal examination in, 526 history, 522–524 neurologic evaluation in, 524 past medical history in, 524 patient questionnaire for, 523, 523t pelvic support assessment in, 524–525 physical examination, 524–526 postvoid residual volume measurement, 526 symptom clustering in, 522–523 tests for, 526–528 urinalysis and culture, 526 urinary symptoms in, 523–524 urodynamic studies, 526–528 voiding diary in, 523, 523f diverticulum and, 1075 epidemiology, 514 mixed, 514 pathophysiology, 516–522 bladder emptying, 521–522, 521f bladder filling, 516–519, 517f–520f continence, 516 continence theories, 522 prevalence of, by age group risks factors, 514–516, 515t age in, 514–515 childbirth and pregnancy, 515 chronic obstructive pulmonary disease, 515–516 family history, 515 hysterectomy, 516 menopause, 515 obesity, 515 race, 515 smoking, 516 stress, 514 Burch colposuspension for, 1061–1062, 1061f–1062f pubovaginal sling for, 1068–1069, 1068f–1069f tension-free vaginal tape procedure for, 1063–1065, 1064f–1065f treatment of, 530–533 treatment of, 528–535 urgency, 514

sacral neuromodulation for, 1085–1087, 1085f–1087f treatment of, 533–535 vaginal USLS of patient with, 1107 Urinary tract infections (UTI), 72–75 acute bacterial cystitis, 73–75 diagnosis of, 73–74 treatment of, 74–75 acute pyelonephritis, 75 asymptomatic bacteriuria, 75 treatment of, 74t Urinary tract lesions, 235 Urine evacuation, physiology of, 521f Urine storage, physiology of, 520f Urodynamic stress incontinence, 514 Uroepithelium, 516 Uroflowmetry, for urinary incontinence, 527 Urogenital diaphragm, 819–820 Urogenital hiatus, 802 Urogenital sphincter, 516 Urogenital triangle, 819f, 820–821 Urogynecologic disease, prevention of, 507–508 Urogynecology, 45 procedures, 835t Uterine abnormalities, 437–438 Uterine adenosarcoma, 728, 728f diagnosis of, 722–724 epidemiology, 722 FIGO staging of, 729t, 730f generalist, role of, 723–724 imaging of, 723 pathology, 728 prognosis, 732 treatment, 729–732 Uterine adnexa, 809 Uterine artery embolization (UAE), 45, 197–198 absolute and relative contraindications for, 210t cervical pregnancy and, 174–175 in leiomyomas, 209–211, 209f, 210f Uterine carcinosarcoma, 726–728, 727f as biphasic malignant neoplasm, 727f with heterologous elements, 727f ifosfamide for, 732 surgical treatment for, 731 treatment of, 732 Uterine curettage, 965, 965f. See also Suction dilatation and curettage Uterine curette, 965f Uterine didelphys, 421 diagnosis, 34–35, 35f, 437 imaging of, 43, 418 infertility, 35 miscarriage, 147, 440 with obstructed hemivagina, 417f Uterine diverticula, 215 Uterine enlargement, 188 Uterine isthmus, 807, 807f Uterine leiomyomas, 147

1267

1268

Index Uterine leiomyosarcoma, 723f, 724 diagnostic criteria for, 725t doxorubicin for, 732 FIGO staging of, 729t, 730f surgical treatment for, 730, 732 Uterine manipulators, 881 Uterine mesenchymal tumors, 724 histological classification of, 724t Uterine myomas, 202 Uterine papillary serous carcinoma (UPSC), 710, 711f management of, 716–717 Uterine perforation, 905 Uterine positions, 5f Uterine receptivity, 357 Uterine sarcomas, 722–734 adenosarcoma, 728, 728f advanced (stages III and IV), treatment of, 731–732 carcinosarcoma, 732 endometrial stromal tumors, 732 leiomyosarcoma, 732 carcinosarcoma, 726–728, 727f as biphasic malignant neoplasm, 727f with heterologous elements, 727f diagnosis, 722–724 endometrial sampling, 723 generalist, role of, 723–724 imaging studies, 723 laboratory testing, 723 signs and symptoms, 722–723, 723f early-stage disease (stages I and II), treatment of, 729–731 adjuvant chemotherapy, 731 adjuvant radiation, 731 fertility-sparing management, 731 surgery, 729–731 surveillance, 731 endometrial stromal tumors, 725–726 endometrial stromal nodule, 725 endometrial stromal sarcoma, 725–726, 726f high-grade undifferentiated sarcoma, 726 epidemiology of, 722 FIGO staging system for, 728–729, 729t, 730f leiomyosarcoma, 723f, 724, 725f pathogenesis, 722 pathology, 724–728 patterns of spread, 728 risk factors for, 722 staging, 728–729 STUMP, 724–725 survival and prognostic factors, 732 survival rates of women with, 732t Uteroovarian ligament, 809 Uterosacral ligaments, 543, 808, 808f Uterosacral ligament suspension (USLS), abdominal, 1110–1111, 1110f–1111f Uterus, 807–809 anatomy of, 807f, 814

arcuate, 35f bicornuate, 421–422, 422f blood supply to, 809 broad ligaments, 807f, 809 cervix, 807, 807f corpus, 807, 807f endometrium and serosa, 807 innervation, 809 lymphatic drainage of, 809 round ligaments of, 807f, 808 septate, 422–423 unicornuate, 421 uterine support, 808, 808f V Vagina, 624, 809 anatomy of, 809–813, 810f–812f blood supply to, 812 clear cell adenocarcinomas of, 698 foreign body in, 101 innervation, 812–813 lymphatics, 812 radiation therapy effects on, 619–620 rectovaginal space, 811, 811f, 812f support, 812 vesicocervical space, 811, 811f, 812f vesicovaginal space, 811, 811f, 812f Vaginal adenocarcinomas, 698 Vaginal adenosis, 101 Vaginal atresia, 419 surgery for, 420, 985–987, 985f–986f Vaginal bleeding, 327, 327f, 327t Vaginal cancer, 694–701 adenocarcinoma, 698 anatomy, 694 clear cell adenocarcinoma, 698 evaluation of, 695t FIGO staging of, 696f, 696t, 697f incidence, 694 malignant melanoma, 699–700 mesenchymal tumors, 698–699 embryonal rhabdomyosarcoma, 698–699, 699f leiomyosarcoma, 699 squamous cell carcinoma, 694–698, 695f diagnosis, 695 prognosis, 696 recurrent disease, 698 risks, 694–695 staging and classification, 695 surveillance, 698 treatment, 696–698 Vaginal contraceptive film, 130f Vaginal cuff cellulitis, 77–78, 78f Vaginal cuff dehiscence, 1036, 1147 Vaginal flora, 50–52, 51t altered flora, 50 bacterial vaginosis, 51–52, 51f, 51t, 52t vaginal pH and, 50 Vaginal hysterectomy, 950, 957–961, 957f–961f. See also Hysterectomy intraoperative, 957–961 ovarian abscess and, 78–79

pelvic cellulitis and, 78 postoperative, 961 preoperative, 957 radical, 669t Vaginal intraepithelial neoplasia (VaIN), 645 high-grade, 646 low-grade, 645–646 Vaginal moisturizers, 620 Vaginal myomectomy, for prolapsed leiomyoma, 948–949, 948f–949f intraoperative, 948–949 postoperative, 949 preoperative, 948 Vaginal pouch, 128 Vaginal preinvasive lesions, 645–646 CO2 laser ablation, 646 diagnosis of, 645 management, 645–646 pathophysiology of, 645 prognosis, 646 radiation therapy, 646 topical therapy, 646 wide local excision, 646 Vaginal reconstruction, 1164–1167, 1164f–1166f intraoperative, 1164–1167 postoperative, 1167 preoperative, 1164 Vaginal septum longitudinal, 416–417, 416f surgery for, 983–984, 983f–984f transverse, 416, 417f Vaginal septum excision, 983–984, 983f–984f Vaginal specula, 5f Vaginal uterosacral ligament suspension, 1107–1109, 1108f–1109f Vaginal vestibule, 818f, 819 Vaginal wall, 543–544, 544f Vaginal wall points anterior, 540 apical, 540–541 posterior, 541 VaIN. See Vaginal intraepithelial neoplasia (VaIN) Valacyclovir, 57t Valium. See Diazepam Valvular heart disease, 828 Vancomycin, 54 Varenicline, for smoking cessation, 11t Varicocele, 430, 463 Vascular clamps. See Instruments, surgical Vascular endothelial growth factor (VEGF), 604 Vasomotor symptoms, treatment of. See Menopausal vasomotor symptoms, treatment of VCUG. See Voiding cystourethrography (VCUG) VDRL. See Venereal Disease Research Laboratory (VDRL) VEGF. See Vascular endothelial growth factor (VEGF)

Index VEGF Trap, 604, 604f Venereal Disease Research Laboratory (VDRL), 58 Venlafaxine for chronic pain syndrome, 259t for depression, 304t for menopausal vasomotor symptoms, 497t, 498 for mood symptoms, 306 Venlafaxine XR, 304t Venous thromboembolism (VTE). See Thromboembolism Ventilation-perfusion (V/Q) scans, 45 Verapamil, 281t Veress needle, 890f–891f Verrucous carcinoma, 688 Versa Step System, 892, 892f Vertebral Efficacy with Risedronate Therapy (VERT) trial, 503 Vertioxetine, 304t VERT trial. See Vertebral Efficacy with Risedronate Therapy (VERT) trial Very-low-density lipoprotein (VLDL), 16 Vesical neck, 813 Vesical trigone, 813 Vesicocervical space, 811, 811f, 812f Vesicovaginal fistula repair, 1078–1082, 1079f–1082f intraoperative, 1078–1082 surgical steps—abdominal repair, 1079–1082 surgical steps—vaginal repair, 1078–1079 postoperative, 1082 preoperative, 1078 consent, 1078 patient preparation, 1078 Vesicovaginal fistulas classification of, 578t cystoscopic view of, 580f Vesicovaginal space, 811, 811f, 812f Vestibular bulbs, 819–820, 819f Vestibulectomy, 979–980, 979f–980f Vestibulitis, 97 Vicryl. See Polyglactin Vilazodone, 304t Villoglandular adenocarcinomas, 662 VIN. See Vulvar intraepithelial neoplasia (VIN) Vinca alkaloids, 600f, 601–602 Virilization clinical features of, 395f of external genitalia, 410f manifest by clitoromegaly, 395f Visceral pain, 249, 250f Viscerosomatic convergence, 249 Vitamin E, for menopausal vasomotor symptoms, 499 Vitiligo, 95, 95f VLDL. See Very-low-density lipoprotein (VLDL) Voiding cystourethrography (VCUG), 38 for genitourinary fistulas, 581 for urethral diverticulum, 586 Von Willebrand factor (vWF), 193–194, 193f

VTE. See Venous thromboembolism (VTE) Vulva anatomy of, 818–820, 818f bartholin glands, 819f, 820 blood vessels of, 822 clitoris, 819, 819f external, 679 innervation to, 823 labia minora, 818f, 819 lymphatic drainage to, 822–823, 823f mons pubis and labia majora, 818–819, 818f vaginal vestibule, 818f, 819 vestibular bulbs, 819–820, 819f Vulvar abscess, 82 incision and drainage, 977–978, 977f–978f Vulvar cancer, 679–693 anatomy, 679 bartholin gland carcinoma, 691 basal cell carcinoma, 690–691 diagnosis, 681–682 lesion evaluation, 681 patient evaluation, 681–682 staging systems, 682, 682t, 683f symptoms, 681 epidemiology, 679–680 histologic subtypes, 680t invasive, 682, 682t management during pregnancy, 688 melanoma, 688–690, 688f–689f clinical presentation, 688–689 staging, 389t, 688–689 treatment, 689–690 metastatic tumors, 691–692 prognosis, 682–684 depth of invasion, 683 lymphatic vascular space invasion, 684 lymph node metastasis, 683 surgical margins, 684 tumor diameter, 683 recurrent disease, 688 distant recurrences, 688 vulvar recurrences, 688 risk factors, 680–681 age, 680 chronic immunosuppression, 681 herpes simplex virus infection, 681 infection with high-risk HPV serotypes, 680 lichen sclerosus, 681 squamous cell carcinoma, 680f early-stage, 681f metastatic, 681f surveillance, 688 treatment, 684–687 inguinofemoral lymphadenectomy, 685–686, 686t microinvasive tumors (stage IA), 687 sentinel lymph node biopsy, 686–687, 686f stage IB–II, 687 stage III, 687 stage IVA, 687

surgery, 684–687, 684f, 685f, 686f vulvectomy, 684–685, 685f verrucous carcinoma, 688 vulvar Paget disease, 691 vulvar sarcoma, 691 Vulvar dermatoses, 88–94 inflammatory dermatoses, 91–94 aphthous ulcers, 94 atopic eczema, 91 contact dermatitis, 91, 91f, 91t hidradenitis suppurativa, 93–94, 93f intertrigo, 91 lichen planus, 92–93, 92f, 92t psoriasis, 91–92, 92f lichen sclerosus, 88–91, 89f corticosteroids for, 89–90 diagnosis of, 89 phototherapy, 90 surgical intervention of, 90–91 surveillance of, 89–91 topical medication guide for, 90t treatment of, 89–91, 90t lichen simplex chronicus, 87 Vulvar intraepithelial neoplasia (VIN), 646–650 bulky lesion of, 648f cavitational ultrasonic surgical aspiration, 649 characteristics, 647t classification, 647–648, 647t diagnosis, 648–649 clinical findings, 648 vulvoscopy, 648–649 differentiated type, 647–648 laser ablation of, 649 management, 649 pathophysiology, 646–647, 647f prognosis and prevention, 649–650 topical therapy, 649 treatment of, 995–998 usual type, 647–648 wide local excision for, 649 Vulvar lesions, 86–88 diagnosis of, 86–88 pain, assessment of, 87f physical examination in, 87 vulvar biopsy, 87–88, 88f vulvar complaints, approach to, 86 Vulvar melanomas, 688–690, 688f–689f clinical presentation, 688–689 staging, 389t, 688–689 treatment, 689–690 adjuvant therapy, 689 of metastatic melanoma, 689–690 surgery, 689 Vulvar Paget disease, 691, 692f Vulvar preinvasive lesions, 646–650 characteristics, 647t classification, 647–648, 647t diagnosis, 648–649 management, 649 pathophysiology, 646–647, 647f prognosis and prevention, 649–650

1269

1270

Index Vulvar sarcoma, 691 Vulvectomy, for vulvar cancer, 684–685, 685f radical partial, 684–685, 685f radical total, 685, 685f simple partial, 684 Vulvitis, 323–324 allergic and contact dermatitis, 323 infection, 324 lichen sclerosus, 323–324, 323f Vulvodynia, 97–100 behavioral therapy for, 99–100 definition of, 97 diagnosis of, 98–99, 98t, 99f ISSVD classification, 98t medical agents for, 100 surgery for, 100 treatment of, 99–100 Vulvovaginal trauma, 100–101 hematoma and, 100–101 laceration, 101 laceration and, 101 Vulvovaginitis, 324, 324t, 325f vWF. See Von Willebrand factor (vWF) W WAR. See Whole abdominal radiotherapy (WAR) Warfarin, 123 interactions with methotrexate, 595 protocol for, 831t teratogenicity, 18t for venous thromboembolism, 830–832, 831t, 912 Wellbutrin. See Bupropion Well woman care, 2–21 medical history, 2 physical examination, 2–7 bimanual examination, 5–6, 6f breast examination, 2–4, 3f examination interval, 7 pelvic examination, 4–5 rectovaginal examination, 6–7, 7f speculum examination, 4 preventive care, 7–19 cancer screening, 9–10, 10t

cardiovascular disease, 13–14, 14t chronic hypertension, 14–15, 15t diabetes mellitus, 16, 16t dyslipidemia, 15–16 geriatric screening, 17 immunization, 7, 8t–9t lifestyle changes, 10–12, 11 mental health, 17–18 metabolic syndrome, 17, 17t obesity, 12–14, 12t stroke, 14–15 thyroid disease, 17 WHI. See Women’s Health Initiative (WHI) WHIMS. See Women’s Health Initiative Memory Study (WHIMS) Whole abdominal radiotherapy (WAR), 731 Wide local excision, for vulvar intraepithelial neoplasia, 649, 995–996, 995f Williams Obstetrics, 305, 357 WISDOM. See Women’s International Study of Long Duration Oestrogen after Menopause (WISDOM) Witches’ milk, 325 Withdrawal bleeding, 180 Wolf clip, 115 application of, 1009 Women’s Health Initiative (WHI), 307, 493–494 Women’s Health Initiative Memory Study (WHIMS), 507 Women’s International Study of Long Duration Oestrogen after Menopause (WISDOM), 494 Word catheter placement, 972, 972f Wound closure of laparotomy incision, 847 peritoneum and fascia, 847 subcutaneous adipose layer and skin, 847–848, 848f Wound infection. See Surgical site infection Wounds, 75–76 clean, 75 clean contaminated, 75–76

closure, 847–848. See also Wound closure contaminated, 76 dehiscence, 919–920 X 23,X, 442 Xarelto. See Rivaroxaban 46,XX disorders of sex development, 362, 412–413 46,XX gonadal dysgenesis, 412 46,XX ovotesticular DSD, 412–413 46,XX testicular DSD, 413 45,X/46,XX, 373, 411 46,XX/46,XY karyotype, 411 45,X/46,XY, 373, 411 47,XXY, 145, 411 46,XY, 442 46,XY disorders of sex development, 411–412 46,XY gonadal dysgenesis, 412 Y 23,Y, 442 Yasmin, 120t, 304 Yaz, 119, 120t Yersinia species, 324 Yolk sac tumors, 760, 761t, 764 Schiller-Duval bodies in, 764, 764f tumor markers for, 761t Yuzpe method, 132 Z Zaleplon, 18t, 304t for insomnia, 18t Zantac. See Ranitidine Zelnorm. See Tegaserod ZIFT. See Zygote intrafallopian transfer (ZIFT) Zoledronate, for osteoporosis, 500t Zoledronate, for osteoporosis in mature woman, 503 Zolpidem, 18t, 304t Zovia 1/35, 120f Zovia 1/50, 120f, 120t Zygote intrafallopian transfer (ZIFT), 465