Title: Danforth's Obstetrics and Gynecology, 10th Edition

Editors: Gibbs, Ronald S.; Karlan, Beth Y.; Haney, Arthur F.; Nygaard, Ingrid E. Title: Danforth's Obstetrics and Gynecology, 10th Edition Copyright ©2008 Lippincott Williams & Wilkins > Front of Book > Editors

Editors Ronald S. Gibbs MD Professor and Chair Department of Obstetrics and Gynecology; E. Stewart Taylor Chair in Obstetrics and Gynecology, University of Colorado Health Sciences Center, Denver, Colorado Beth Y. Karlan MD Director Women's Cancer Research Institute and Division of Gynecologic Oncology, Cedars-Sinai Medical Center; Professor, Department of Obstetrics and Gynecology, David Geffen School of Medicine at UCLA, Los Angeles, California Arthur F. Haney MD The Catherine Lindsay Dobson Professor and Chairman Department of Obstetrics and Gynecology, Division of Biologic Sciences and the Pritzker School of Medicine, The University of Chicago, Chicago, Illinois Ingrid E. Nygaard MD Professor Department of Obstetrics and Gynecology, School of Medicine, The University of Utah, Salt Lake City, Utah

Contributors Kjersti Aagaard-Tillery MD, PhD Assistant Professor of Obstetrics and Gynecology Baylor College of Medicine, Waco, Texas Baharak Amir MD Assistant Professor Department of Obstetrics and Gynecology, Dalhousie University; Active Medical Staff and Faculty, Department of Obstetrics and Gynecology, Division of Urogynecology and Pelvic Floor Surgery, IWK Health Centre, Halifax, Nova Scotia Ricardo Azziz MD, MPH, MBA Vice Chairman

Department of Obstetrics and Gynecology, David Geffen School of Medicine; UCLA Chair, Department of Obstetrics and Gynecology, Cedar-Sinai Medical Center, Los Angeles, California Kurt T. Barnhart MD, MSCE Associate Professor Department of Obstetrics and Gynecology and Epidemiology, University of Pennsylvania School of Medicine; Staff, University of Pennsylvania Medical Center, Department of Obstetrics and Gynecology, Philadelphia, Pennsylvania Rosemary Basson MD Clincial Professor Department of Psychiatry, University of British Columbia; Director, Sexual Medicine Program, Department of Psychiatry, Vancouver Hospital, British Columbia Jason K. Baxter MD Assistant Professor Department of Obstetrics and Gynecology, Thomas Jefferson University, Philadelphia, Pennsylvania Alfred Bent MD Professor Department of Obstetrics and Gynecology, Dalhousie University; Head, Division of Gynecology, Department of Obstetrics and Gynecology, IWK Health Centre, Halifax, Nova Scotia Lori A. Boardman MD, ScM Associate Professor Department of Obstetrics and Gynecology, The Warren Alpert Medical School of Brown University; Director of Colposcopy and Vulvar Clinics, Department of Obstetrics and Gynecology, Women and Infants' Hospital of Rhode Island, Providence, Rhode Island James A. Bofill MD Professor; Director; Maternal-Fetal Medicine Fellowship University of Mississippi Medical Center; Staff, Department of Obstetrics and Gynecology, University of Mississippi Medical Center, Jackson, Mississippi D. Ware Branch MD Professor Department of Obstetrics and Gynecology, University of Utah; Physician, University of Utah Hospital, Salt Lake City, Utah Robert E. Bristow MD

Associate Professor Department of Obstetrics and Gynecology, The Johns Hopkins University School of Medicine; Director, The Kelly Gynecologic Oncology Service, Department of Obstetrics and Gynecology, The Johns Hopkins Medical Institutions, Baltimore, Maryland J. Chris Carey MD Professor Department of Obstetrics and Gynecology, University of Colorado School of Medicine; Director, Denver Health and Hospital Authority, Denver, Colorado Ilana Cass MD Director; Gynecologic Oncology Fellowship; Associate Clinical Professor Program Department of Obstetrics and Gynecology, David Geffen School of Medicine at UCLA; Faculty Physician, Associate Clinical Professor and Director of Obstetrics and Gynecology, Department of Obstetrics and Gynecologic Oncology, Cedar-Sinai Medical Center, Los Angeles, California Marcelle I. Cedars MD Professor Department of Obstetrics, Gynecology, and Reproductive Sciences, University of California at San Francisco; Director, Center for Reproductive Health, University of California at San Francisco, San Francisco, California David P. Cohen MD Associate Professor and Chief Section of Reproductive Endocrinology and Infertility, University of Chicago Medical Center, Chicago, Illinois Charles C. Coddington III MD Director Department of Obstetrics and Gynecology, Denver Health Medical Center; Professor, Department of Obstetrics and Gynecology, University of Colorado School of Medicine, Denver, Colorado Dwight P. Cruikshank MD The Jack A. and Elaine D. Klieger Professor and Chairman Department of Obstetrics and Gynecology, Medical College of Wisconsin; Chairman, Department of Obstetrics and Gynecology, Froedtert Memorial Lutheran Hospital, Milwaukee, Wisconsin Marian D. Damewood MD Clinical Professor of Obstetrics and Gynecology Johns Hopkins University School of Medicine, Baltimore, Maryland; Chairman, Department

of Obstetrics and Gynecology; Director, Women and Children's Services, York Hospital/WellSpan Health Systems, York, Pennsylvania Susan A. Davidson MD Associate Professor Department of Obstetrics and Gynecology, University of Colorado at Denver and Health Sciences Center; Chief, Gynecologic Oncology, Department of Obstetrics and Gynecology, University of Colorado Hospital, Aurora, Colorado Jill K. Davies MD Associate Professor Department of Obstetrics and Gynecology, University of Colorado Health Sciences Center, Aurora, Colorado Ann J. Davis MD Departments of Pediatrics and Obstetrics and Gynecology, Tufts-New England Medical Center, Boston, Massachusetts John O. L. DeLancey MD Norman F. Miller Professor of Gynecology; Director of Pelvic Floor Research The University of Michigan, Ann Arbor, Michigan Donald J. Dudley MD Professor Department of Obstetrics and Gynecology, University of Texas Health Science Center at San Antonio, San Antonio, Texas Lorraine Dugoff MD Associate Professor Department of Obstetrics and Gynecology, University of Colorado Health Sciences Center, Aurora, Colorado David A. Eschenbach MD Professor and Chair Department of Obstetrics and Gynecology, University of Washington School of Medicine, Seattle, Washington Michele Evans MD Clinical Fellow Division of Reproductive Endocrinology and Infertility, Departments of Obstetrics, Gynecology, and Reproductive Sciences, University of California—WHCRC, San Francisco, California

Dee E. Fenner MD Harold A. Furlong Professor of Obstetrics and Gynecology; Director of Gynecology; Associate Chair for Surgical Services Department of Obstetrics and Gynecology, University of Michigan, Ann Arbor, Michigan Henry L. Galan MD Associate Professor; Chief of Maternal-Fetal Medicine Department of Obstetrics and Gynecology, University of Colorado at Denver Health Sciences Center, Aurora, Colorado Mary L. Gemignani MD, MPH Assistant Professor Department of Surgery, New York Hospital—Cornell Medical Center; Assistant Attending, Department of Surgery/Breast Science, Memorial Sloan-Kettering Cancer Center, New York, New York Ronald S. Gibbs MD Professor and Chair Department of Obstetrics and Gynecology; E. Stewart Taylor Chair in Obstetrics and Gynecology, University of Colorado Health Sciences Center, Denver, Colorado Melissa Gilliam MD, MPH Associate Professor Department of Obstetrics and Gynecology, The University of Chicago; Chief, Section of Family Planning and Contraceptive Research, Department of Obstetrics and Gynecology, The University of Chicago, Chicago, Illinois Larry C. Gilstrap MD Clinical Professor Department of Obstetrics and Gynecology, University of Texas Southwest Medical School; Chair Emeritus, Department of Obstetrics and Gynecology, University of Texas at Houston Health Science Center, Houston, Texas Robert L. Giuntoli II MD Assistant Professor The Kelly Gynecologic Oncology Service, Department of Obstetrics and Gynecology, The Johns Hopkins Medical Institutions, Baltimore, Maryland Steven R. Goldstein MD Professor Department of Obstetrics and Gynecology, New York University School of Medicine; Director of Gynecologic Ultrasound; Co-Director of Bone Densitometry, New York University Medical Center, New York, New York

Natalie S. Gould MD Gynecologic Oncologist Department of Obstetrics and Gynecology; Carilion Gyn Oncology Associates, Roanoke, Virginia Mounira Habli MD Department of Obstetrics and Gynecology, Maternal-Fetal Medicine Division, University of Cincinnati, Cincinnati, Ohio Sarah Hammil MD Department of Obstetrics and Gynecology, University of Washington School of Medicine, Seattle, Washington Authur F. Haney MD The Catherine Lindsay Dobson Professor and Chairman Department of Obstetrics and Gynecology, Division of Biologic Sciences and the Pritzker School of Medicine, The University of Chicago, Chicago, Illinois Joy Hawkins MD Professor Department of Anesthesiology, The University of Colorado School of Medicine; Director of Obstetric Anesthesia, Department of Anesthesiology, University of Colorado Hospital, Aurora, Colorado John C. Hobbins MD Professor Department of Obstetrics and Gynecology, University of Colorado School of Medicine, Aurora, Colorado Sabrina Holmquist MD Assistant Professor Section of Family Planning and Contraceptive Research, Department of Obstetrics and Gynecology, University of Chicago, Chicago, Illinois Christine H. Holschneider MD Assistant Professor Department of Obstetrics and Gynecology, David Geffen School of Medicine at UCLA; Chair, Department of Obstetrics and Gynecology, Olive View–UCLA Medical Center, Sylmar, California Carol J. Homko RN, PhD, CDE Assistant Professor

Department of Obstetrics and Gynecology and Medicine, Temple University School of Medicine; Nurse Manager, Department of GCRC, Temple University Hospital, Philadelphia, Pennsylvania Julia V. Johnson MD Professor Department of Obstetrics and Gynecology, University of Vermont; Vice Chair, Department of Obstetrics and Gynecology, Fletcher Allen Health Care, Burlington, Vermont Bronwen F. Kahn MD Fellow/Instructor Maternal-Fetal Medicine, Department of Obstetrics and Gynecology, University of Colorado Health Sciences Center, Denver, Colorado Amy R. Kane MD Resident Department of Reproductive Medicine, University of California—San Diego, San Diego, California Beth Y. Karlan MD Professor Department of Obstetrics and Gynecology, David Geffen School of Medicine at UCLA; Director, Women's Cancer Research Institute; Director, Division of Gynecologic Oncology, Cedars-Sinai Medical Center, Los Angeles, California Vern L. Katz MD Clinical Assistant Professor Department of Obstetrics and Gynecology, Oregon Health Science University, Portland, Oregon; Medical Director, Perinatal Services, Sacred Heart Medical Center, Eugene, Oregon Helen H. Kay MD Professor; Section Chief Maternal-Fetal Medicine; Chief of Obstetrics, Chicago Lying-In Hospital, University of Chicago, Chicago, Illinois Colleen M. Kennedy MD, MS Assistant Professor Department of Obstetrics and Gynecology, University of Iowa; Director, Vulvar Vaginal Disease and Colposcopy Clinics, Department of Obstetrics and Gynecology, University of Iowa Hospital, Iowa City, Iowa William R. Keye Jr. MD Director

Division of Reproductive Endocrinology and Infertility, Beaumont Medical Services, Royal Oak, Michigan Timothy E. Klatt MD Assistant Professor Department of Obstetrics and Gynecology, Medical College of Wisconsin; Medical Director, Obstetrical Services, Froedtert Memorial Lutheran Hospital, Milwaukee, Wisconsin Deborah Krakow MD Medical Genetics Institute, Cedars-Sinai Medical Center, Departments of Obstetrics and Gynecology and Human Genetics, David Geffen School of Medicine at UCLA, Los Angeles, California Richard S. Legro MD Professor Department of Obstetrics and Gynecology, Pennsylvania State University, Hershey Medical Center, Hershey, Pennsylvania Andrew John Lim MD Assistant Professor Department of Obstetrics and Gynecology, David Geffen School of Medicine at UCLA; Faculty Physician, Department of Obstetrics and Gynecology, Cedars-Sinai Medical Center, Los Angeles, California Kirsten J. Lund MD Associate Professor Department of Obstetrics and Gynecology, University of Colorado School of Medicine, Denver, Colorado James N. Martin Jr. MD Professor Department of Obstetrics and Gynecology, University of Mississippi Medical Center; Chief, Division of Maternal-Fetal Medicine and Obstetrics, Winfred L. Wiser Hospital for Women and Infants, Jackson, Mississippi Lisa Memmel MD Fellow Family Planning, Section of Family Planning and Contraceptive Research, Department of Obstetrics and Gynecology, University of Chicago, Chicago, Illinois Catherine Ann Matthews MD Associate Professor Department of Obstetrics and Gynecology, Virginia Commonwealth University, Richmond,

Virginia James McManaman MD Professor Departments of Obstetrics, Gynecology, Physiology and Biophysics, University of Colorado Health Sciences Center, Denver, Colorado Lisa Memmel MD Fellow Family Planning, Section of Family Planning and Contraceptive Research, Department of Obstetrics and Gynecology, University of Chicago, Chicago, Illinois Howard Minkoff MD Distinguished Professor Department of Obstetrics and Gynecology, SUNY Downstate; Chairman, Department of Obstetrics and Gynecology, Maimonides Medical Center, Brooklyn, New York David G. Mutch MD Judith and Ira Gall Professor; Director of the Division of Gynecologic Oncology Washington University School of Medicine, St. Louis, Missouri Charles W. Nager MD Professor Department of Reproductive Medicine, University of California, San Diego; Division Director, Urogynecology, Department of Reproductive Medicine, University of California, San Diego Medical Center, San Diego, California Roger B. Newman MD Professor Department of Obstetrics and Gynecology, Medical University of South Carolina; Vice Chairman for Academic Affairs and Women's Health Research, Department of Obstetrics and Gynecology, Medical University Hospital, Charleston, South Carolina Peggy A. Norton MD Professor Department of Obstetrics and Gynecology; Chief, Department of Urogynecology and Reconstructive Pelvic Surgery, University of Utah School of Medicine, Salt Lake City, Utah Ingrid E. Nygaard MD Professor Department of Obstetrics and Gynecology School of Medicine, University of Utah, Salt Lake City, Utah

Michael W. O'Hara PhD Professor of Psychology and Starch Faculty Fellow; Vice President; Faculty Senate Department of Psychology, University of Iowa, Iowa City, Iowa Santosh Pandipati MD Paranatologist Northwest Perinatal Center, Portland, Oregon Jeff Peipert MD, PhD Robert J. Terry Professor; Vice Chair of Clinical Research Department of Obstetrics and Gynecology, Washington University School of Medicine; Attending Physician, Department of Obstetrics and Gynecology, Barnes-Jewish Hospital, St. Louis, Missouri T. Flint Porter MD, MSPH Associate Professor Department of Obstetrics and Gynecology, University of Utah Health Sciences; Medical Director, Department of Maternal-Fetal Medicine, Intermountain Medical Center, Murray, Utah E. Albert Reece MD, PhD, MBA Vice President for Medical Affairs University of Maryland; John Z. and Akiko K. Bowers Distinguished Professor and Dean, School of Medicine, University of Maryland School of Medicine, Baltimore, Maryland Robert L. Reid MD Professor Department of Obstetrics and Gynecology, Queen's University; Chair, Division of Reproductive Endocrinology and Infertility, Department of Obstetrics and Gynecology, Kingston General Hospital, Ontario, Canada Holly E. Richter MD, PhD Professor; Division Director Department of Obstetrics and Gynecology, University of Alabama at Birmingham Medical Center, Birmingham, Alabama Charles Rittenberg MD Fellow Maternal-Fetal Medicine, Department of Obstetrics and Gynecology, Medical University of South Carolina; Instructor, Department of Obstetrics and Gynecology, Medical University of South Carolina, Medical Center, Charleston, South Carolina Lisa M. Roberts MD

Gynecology and Laparoscopy Surgeons PC, Raleigh, North Carolina Joseph S. Sanfilippo MD Professor University of Pittsburgh Medical School; Vice Chair and Director, Center for Reproductive Endocrinology and Infertility, Division of Obstetric Gynecology and Reproductive Sciences, McGee Women's Hospital, Pittsburgh, Pennsylvania Robert S. Schenken MD Professor and Chairman Department of Obstetrics and Gynecology, The University of Texas Health Science Center at San Antonio; Chairman, Department of Obstetrics and Gynecology, University Hospital, San Antonio, Texas James R. Scott MD Professor Department of Obstetrics and Gynecology, University of Utah Medical Center, Salt Lake City, Utah Beata E. Seeber MD, MSCE Assistant Professor Division of Gynecologic Endocrinology and Reproductive Medicine, Medical University of Innsbruck, Innsbruck, Austria Lisa S. Segre PhD Associate Research Scientist Department of Psychology, University of Iowa, Iowa City, Iowa Howard T. Sharp MD Associate Professor and Chief General Division of Obstetrics and Gynecology, University of Utah School of Medicine; Assistant Professor, Department of Obstetrics and Gynecology, University of Utah Medical Center, Salt Lake City, Utah Baha M. Sibai MD Professor Department of Obstetrics and Gynecology, University of Cincinnati College of Medicine, Cincinnati, Ohio Robert M. Silver MD Professor; Chief Maternal-Fetal Medicine, Department of Obstetrics and Gynecology, University of Utah

School of Medicine, Salt Lake City, Utah Catherine Y. Spong MD Chief Pregnancy and Perinatology Research, NICHD, NIH, Bethesda, Maryland; Maternal Fetal Medicine Specialist, Perinatal Diagnostic Center, INOVA Alexandria, Alexandria, Virginia Kris Strohbehn MD Associate Professor Department of Obstetrics and Gynecology, Dartmouth School of Medicine; Director, Division of Urogynecology/ Re-cons- tructive Pelvic Surgery, Dartmouth-Hitchcock Medical Center, Lebanon, New Hampshire Mika Thomas MD Fellow Department of Reproductive Endocrinology, University of Iowa Hospitals and Clinics, Iowa City, Iowa Bradley J. Van Voorhis MD Professor Department of Obstetrics and Gynecology, University of Iowa College of Medicine, Iowa City, Iowa Joan L. Walker MD The James A. Merrill Chair and Professor Section of Gynecologic Oncology, Department of Obstetrics and Gynecology, University of Oklahoma Health Sciences Center, Oklahoma City, Oklahoma Kenneth Ward MD Professor and Chair Departments of Obstetrics, Gynecology, and Women's Health, John A. Burns School of Medicine, University of Hawaii, Honolulu, Hawaii Louis Weinstein MD Paul A. and Eloise B. Bowers Professor and Chairman Department of Obstetrics and Gynecology, Thomas Jefferson University, Philadelphia, Pennsylvania R. Stan Williams MD Harry Prystowsky Professor of Reproductive Medicine; Iterim Chairman Department of Obstetrics and Gynecology; Chief, Division of Reproductive Endocrinology and Fertility, University of Florida, Gainesville, Florida

Kristen P. Wright MD Women and Children's Hospital, Department of Obstetrics and Gynecology, Burlington, Vermont Jerome Yankowitz MD Professor Department of Obstetrics and Gynecology, Roy J. and Lucille A. Carver College of Medicine; Director, Division of Maternal-Fetal Medicine, Department of Obstetrics and Gynecology, University of Iowa Hospitals and Clinics, Iowa City, Iowa Edward R. Yeomans MD Associate Professor Department of Obstetrics and Gynecology, Universiity of Texas—Houston; Chief of Obstetrics, LBJ General Hospital, Houston, Texas

Editors: Gibbs, Ronald S.; Karlan, Beth Y.; Haney, Arthur F.; Nygaard, Ingrid E. Title: Danforth's Obstetrics and Gynecology, 10th Edition Copyright ÂŠ2008 Lippincott Williams & Wilkins > Front of Book > Dedication

Dedication This hallmark 10th Edition of Danforth's Obstetrics and Gynecology is dedicated to our mentors and our teachers who have guided us to where we are; to our residents and students who have stimulated and prodded us; to our patients who have given us great gratification and inspiration; and to our families and friends who have given us love and support and make all that we do so meaningful.

Preface Welcome to the hallmark 10th Edition of Danforth's Obstetrics and Gynecology. In the 42 years since the first edition of this text appeared, it has been widely recognized as a standard text book for practicing physicians, residents, medical students and nurses. Previous editions have been translated into several languages and the text has enjoyed wide readership over the face of the globe. As medical practice changes continually, we also have made important changes in the 10th Edition. Important new topics have been added including stillbirth, group B streptococci and a whole new section on pelvic reconstructive surgery. To add to the appeal of the text, we have added many two-color figures and there is an enlarged multi-color section. In the textbook's website, accessible to those who purchase the book, we will have the full text of the book including all figures and tables. Our objective throughout has been to provide in a single textbook, current cutting edge information on the practice of the breadth of obstetrics and gynecology. Our goal has been to provide this in a highly readable, user friendly and evidence-based fashion. We are also happy to announce that with this 10th edition, we have a new editor, Dr. Ingrid Nygaard, Professor of Obstetrics and Gynecology in the Division of Urogynecology and Reconstructive Pelvic Surgery at the University of Utah. Dr. Nygaard replaced Dr. James R. Scott who had served as editor from the 5th through the 10th Editions—a record that will be long lasting. We also are most pleased to welcome new contributing authors, all experts in their fields, and returning contributing authors who have updated their previous chapters. With all of the pressures on faculty in academic departments these days, we know that writing a chapter for this text becomes a labor of love and demonstrates great commitment on the part of the authors to education and translating knowledge to the bedside. We also wish to extend a heartfelt thanks to our administrative staff who labored extensively in the preparation of this text—Michelle Nelson at University of Colorado and Phyllis Lopez at Cedars Sinai Medical Center. Finally this book would not have been possible without the expertise and organization our trusty editors, Sonya Seigafuse and Ryan Shaw at Lippincott Williams & Wilkins. We wish all of our readers continued success and gratification in the practice of obstetrics and gynecology. Ronald S. Gibbs MD Beth Y. Karlyn MD Arthur F. Haney MD

Ingrid Nygaard MD

1 Prenatal Care Vern L. Katz The time period from the recognition of a pregnancy until delivery is one of the greatest physical and psychologic transitions that a woman undergoes in her lifetime. During these months, the obstetrician, family physician, or midwife serves a much larger role than just health care provider. The clinicians' role during this time is not only to assess the health of the mother and fetus, prescribe interventions, and try to influence behaviors but also to advise and help patients as they undergo this challenging psychologic passage. This chapter outlines the principles of prenatal care and addresses specific concerns of a woman's general health during gestation. Prenatal care has consisted of adherence to ritual and taboo for generations. Greek authors suggested that Spartan women exercised in pregnancy to give birth to better warriors. Roman physicians argued that strong and violent movements induced rupture of membranes. In the early twentieth century, hanging clothing to dry on a clothesline was said to increase the risk of the umbilical cord wrapping around the baby's neck. In the United States, the first organized prenatal care programs began in 1901 with home nurse visits. The first prenatal clinic was established in 1911. The goal of early prenatal care was to diagnose and treat preeclampsia in order to decrease maternal mortality. It is not surprising that this focus on maternal and infant health occurred as a direct outgrowth of the woman suffrage movement. The current emphasis on prenatal care stems from historic pronouncements and retrospective analyses concluding that women who receive prenatal care have less fetal, infant, and maternal morbidity and mortality. However, a conclusive scientific foundation is lacking for the content of prenatal care and the relationship of its components to good outcomes. As technology flourishes and resources dwindle, it has become increasingly important to obtain scientifically based evidence demonstrating which components of prenatal care are clinically appropriate, cost-effective, and deserving of preferential funding. At this time, the optimal content and delivery of prenatal care remains the subject of discussion and debate. Given the increasing number of tools of prenatal assessment, the current consensus is that the best prenatal care is individualized for the specific needs of the mother. Prenatal care has two areas of emphasis. The first is directed at ensuring appropriate fetal growth and development. This is accomplished through counseling with regard to health

behaviors of the mother as well as physical and laboratory evaluations. The second area of emphasis is more complex and involves assessment of the physical and psychologic adaptations of the mother during her pregnancy. Most aspects of pathology occur when there is either insufficient maternal adaptation or too much. Preeclampsia and diabetes are good examples of such pathologies, respectively. The two areas of attention—maternal and fetal well-being—are obviously intertwined. For the clinician facing complex problems, it sometimes helps to untangle these two themes to better address diagnosis and therapy. An example is the pregnant woman diagnosed with cancer or the mother with epilepsy. The evaluation of risk:benefit ratio of tests and treatments must be seen looking at both maternal and fetal health. This chapter will emphasize normal changes in pregnancy, and later chapters will build on this discussion to focus on pathology. Over the three trimesters of pregnancy, a woman must develop new aspects to her identity. Her self-image develops an additional sense of femininity beyond what was developed at puberty, and a maternal self-concept must develop as well. Reba Rubin, in her works on the maternal experience, describes a new mother's psychologic tasks as the woman grows into her new role. These tasks include: Accepting a new body image, which is often in conflict with accepted societal views of attractiveness Accepting the child who is growing inside her Reordering her identity with her mother, her friends, and the father of the pregnancy Symbolically finding acceptance and safety for her child (i.e., making a new home). For many women with good social support, these tasks are anticipated and desired roles that bring a sense of fulfillment. For other women, some or all of these tasks are unanticipated and difficult. The obstetric provider, in multiple ways, helps the mother through these transitions while at the same time ensures the physical health of both patients (mother and fetus). Many aspects of prenatal care have grown from their original role of health promotion to ritualized traditions that have acquired symbolic value in helping women and their families adapt to these psychologic transitions. For example, studies have found that for women of average weight, the practice of weighing a woman during each visit has minimal medical value. Yet, if the nurse forgets to weigh a patient, that woman usually remarks quite quickly about having her weight taken. Another example is the routine ultrasound. This is now a demand ritual. At this visit, a mother will usually bring several female family members or friends to see the sonogram. The new mother not only uses the sonogram to bond with her child but also shows the baby to the other women around her for their acceptance. Throughout the world, cultures and subcultures view prenatal care differently, but most all hold it with respect. A woman might miss her annual Pap smear, but she rarely misses a prenatal visit.

Primary and Preconception Care Philosophy

Care for preconception, pregnancy, and postpartum should be integrated and accessible, focus on the majority of personal health care needs, represent a sustained partnership between patient and provider, and occur within the context of family and community. For many women, pregnancy care occurs as a part of the continuum in a long-term relationship with the health care provider. The first visit may be a preconception visit or may occur after the woman is pregnant. If a woman is seen for a preconception visit, many issues need not be readdressed when she becomes pregnant.

Content of the Preconception Visit The preconception visit is a focused visit for the woman who is planning to become or is considering becoming pregnant in the near future. The content of this interval visit includes a complete history; when appropriate, a complete physical examination; risk assessment and intervention; selected laboratory testing based on the patient's age and the results of the foregoing evaluation; ongoing management of medical conditions; and a plan of care. A purposeful discussion of contraception, sexually transmitted disease prevention, and timing of conception is appropriate. Timely administration of routine immunizations, educational counseling, and advice complete the visit.

Risk Assessment A goal specific to the preconception interval visit is the systematic identification of potential risks to pregnancy and the implementation of early intervention as necessary. These risks fall into several categories, described in the following sections.

Unalterable Factors Unalterable factors are preexisting factors that cannot be altered in any medical way by clinical intervention. These include the patient's height, age, reproductive history, ethnicity, educational level, socioeconomic status, genetic composition, and to some extent her body mass index (BMI). Genetic and family histories, although unalterable, may lend themselves to screening and evaluation. A detailed family history should be obtained, including inquiry of thromboembolic disease, recurrent miscarriage, neonatal or early infant death, congenital cardiac disease, mental retardation, or other major disease affecting health in family members.

Factors Benefiting from Early Intervention Conditions that should or could be modified before pregnancy is attempted include poor nutrition; an underweight or obese BMI; and poorly controlled medical diseases such as diabetes mellitus, asthma, epilepsy, phenylketonuria, hypertension, and thyroid disease. Some prescription medications that are known teratogens should be discontinued and appropriate substitutions made. These include medications such as isotretinoin (Accutane), warfarin sodium (Coumadin), certain anticonvulsants, and angiotensin-converting enzyme inhibitors. However, many medications are safe, such as medications for asthma and most antihistamines. Some medications such as antidepressants need to be evaluated for the

risk:benefit ratio. Determining the status of a patient's immunity to rubella, varicella, and hepatitis is appropriate during the preconception visit. If needed, the influenza vaccine is safe. In high-risk populations or endemic geographic areas, patients should be assessed for active tuberculosis with skin testing and chest x-ray.

Social Risk Factors Inquiry should be made regarding occupational hazards involving exposure to toxins such as lead, mercury and other heavy metals, pesticides, and organic solvents (both liquid and vapors). Hazards in the home, such as exposure to toxoplasmosis or toxic chemicals (asbestos, pesticides), are important to identify. If a woman uses well water, it should be assessed for acidity, lead, and copper. Family violence is a particularly important household hazard. Nonjudgmental, open-ended evaluation should be applied. Judith MacFarland has recommended questions such as “Are you in a relationship in which you are being hit, kicked, slapped, or threatened?” “Do you feel threatened?” “Have you been forced to do things against your will?” These questions should be asked again at the first prenatal visit. Some studies have suggested that a written questionnaire, in addition to oral questions, will allow for greater identification of domestic abuse. Approximately 20% of all pregnant women are battered during their pregnancy. About one half of women who are physically abused prior to pregnancy continue to be battered during pregnancy. For some women, the violence begins with pregnancy. All such patients require information regarding their immediate safety and referrals for counseling and support.

Risky Health Habits The use of illicit drugs or abuse of alcohol represents a significant health hazard to pregnancy. Alcohol is a known teratogen. There is no consensus on the correlation between the quantity of alcohol consumed and the manifestation of adverse fetal effects. Therefore, the best advice to women who wish to become pregnant is to stop drinking. The T-A-C-E screen for alcohol abuse has been well studied. The letters stand for four questions asked in a nonjudgmental manner:

1. T—“How much do you drink to feel drunk?” (tolerance)

2. A—“Does your drinking annoy anyone?”

3. C—“Has anyone told you to cut down?”

4. E—“Do you drink in the morning to feel better?” (eye-opener). Smoking cigarettes is associated with adverse pregnancy outcomes, including low birth weight, premature birth, and perinatal death. Smoking by both the pregnant woman and members of the household should be avoided during pregnancy and, preferably, not resumed postpartum. The relative risk of intrauterine growth restriction (IUGR) among

pregnant smokers has been calculated at 2.2 to 4.2. Because of the morbidity associated with smoking, various methods to assist women to quit smoking should be encouraged prior to pregnancy. Numerous interventions are available. Use of the transdermal nicotine patch in pregnancy is thought to be preferable to smoking. One benefit of using a nicotine patch is the elimination of exposure to other toxins such as carbon monoxide inhaled in cigarette smoke. Its theoretic risk is that it creates a constant blood level of nicotine, as opposed to the vacillations that occur with smoking. Depending on the timing of the prescription, it may be a very appropriate intervention. Similarly, all illicit drugs have the potential of harming the pregnancy. Other behaviors that should be avoided are those that promote exposure to sexually transmitted and other infectious diseases. These include unprotected sexual intercourse in a nonmonogamous relationship and the sharing of needles between addicts.

Interventions The final phase of the preconception visit involves specific interventions derived from the information obtained during the history, physical examination, and risk assessment phases. The specific interventions may include immunization against rubella, varicella, or hepatitis; changes in prescribed medications; behavior modification; genetic screening for such conditions as Tay–Sachs disease, cystic fibrosis, thalassemia, and sickle cell anemia; and nutritional and physical activity recommendations. During the physical examination, evaluation of the thyroid and breasts is important. Signs or symptoms of thyroid disease should prompt laboratory evaluation with TSH and free T4. If a woman is 35 years of age or older, a screening mammogram should be ordered, since as much as two and a half years may pass before she will be able to have one (mammograms have significantly decreased sensitivity during pregnancy and for up to 6 months after lactation). If a woman has a family history of premenopausal breast cancer, a mammogram may be considered at younger ages. Additionally, if there is a body habitus or history suggestive of polycystic ovary disease, this condition should be evaluated (Chapter 38). If a Pap smear has not been done within a year, this test should be repeated at this time. Abnormalities of the Pap smear are more easily addressed prior to pregnancy. Additionally, it is valuable at this visit to examine the patient's skin. The incidence of melanoma is increasing faster than any other malignancy in the United States. The obstetrician has the unique opportunity to assess and teach at this visit regarding this cancer. An inquiry about periodontal disease and, when appropriate, assessment of dental hygiene is important. Periodontal disease is associated with a significant risk of preterm birth. Periodontal disease may be treated at any time in pregnancy but is best addressed preconception. Folic acid as a supplement can reduce the occurrence and recurrence of neural tube defects and may reduce the risk of other birth defects as well. Women who have had a previous pregnancy affected by neural tube defects should take 4 mg of folic acid per day, starting 4 weeks prior to conception through the first trimester. For all other women of reproductive age who have the potential to become pregnant, 1 mg of folic acid should be prescribed. Unfortunately, prenatal vitamins contain only 0.4 to 0.8 mg. Some patients purposely initiate a preconception visit to determine whether or not a

preexisting medical condition is an absolute contraindication to pregnancy. Pulmonary hypertension, for example, although rare, is associated with up to a 50% maternal mortality and a greater than 40% fetal mortality. It is possible to obtain epidemiologic studies that provide statistics on the morbidity and mortality for mother and fetus for most disease states. These cannot, however, provide specific data for any one patient with her own unique set of medical, demographic, and social variables. Many patients who make these inquiries will benefit by reading the relevant medical materials themselves and by obtaining more than one opinion. Consultation with other medical specialists may be necessary. For example, women with orthopedic problems often inquire about vaginal delivery. Another common concern is advanced maternal age. Specific risks of increased rates of aneuploidy and miscarriage should be discussed. Women over age 40 have been found to have higher rates of low birth weight, fetal demise, preterm birth, and operative delivery. It is also important to discuss how and when to discontinue contraceptive measures. Patients using medroxy-progesterone acetate (Depo-Provera) injections may experience a delay of several months in the return of regular ovulatory menstrual cycles. An intrauterine device (IUD) may be removed at any time in the cycle. It should be removed as soon as conception is considered, since removal during pregnancy (although preferable to leaving in place) is associated with a higher rate of pregnancy loss. Likewise, birth control pills and other hormone-based contraceptives should be discontinued prior to attempting conception. Many physicians believe that discontinuing the use of hormonebased contraceptives for one to two cycles allows better growth of the endometrium. Although definitive evidence is lacking, the thought is that this may be associated with better implantation of the fertilized egg. If a woman discontinues hormone-based contraception, she needs to be reminded that ovulation may occur in a variable time period after stopping the contraception. Thus, risky behaviors should be avoided at the time of discontinuation. The patient should be advised to seek early prenatal care by making an appointment after missed menses or on confirmation of pregnancy by a home pregnancy test. Unfortunately, in the United States, only 75% of pregnant women receive prenatal care beginning in the first trimester. Ongoing barriers to prenatal care access include lack of money or insurance to pay for care, system undercapacity for appointments, and inadequate transportation.

Initial Prenatal Visit This visit represents the first detailed assessment of the pregnant patient. The optimal timing of this visit may vary. For women who have not undergone the comprehensive preconception visit, prenatal visits should begin as soon as pregnancy is recognized. For these women, much of the content of the preconception visit will need to be addressed at this time—for example, screening for domestic abuse and alcohol use. All other women should be seen by about 8 menstrual weeks (6 weeks after conception) gestation. For all patients, the appropriate content of prenatal care and the first prenatal visit is contained in the antepartum record published by the American College of Obstetrics and Gynecology

(ACOG). Identifying data, a menstrual history, and a pregnancy history are obtained. Past medical, surgical, and social history are recorded, along with symptoms of pregnancy. The patient's current medications, including over-the-counter (OTC) and herbal supplements should be evaluated. A focused genetic screen, infection history, and risk status evaluation are performed or reconfirmed.

Diagnosis of Pregnancy The two aspects of pregnancy diagnoses include confirmation of an intrauterine pregnancy and assessment of viability. Evaluation of the signs and symptoms associated with the presumptive diagnosis of pregnancy, while a useful adjunct, has been largely superseded by the widely available urine pregnancy test and ultrasound. The detection of greater than 35 mIU of human chorionic gonadotropin (hCG) in the first morning void has a very high specificity for pregnancy. OTC pregnancy tests can confirm a pregnancy prior to the missed period. Other tests for confirming the presence of pregnancy include a positive serum βhCG and demonstration of the fetal heart by either auscultation or ultrasound. Using a transvaginal probe, an intrauterine pregnancy may be confirmed (gestational sac– intradecidual sign) at the time a β-hCG reaches 1,500 IU. Fetal cardiac activity should be seen by postconception week 3. Ultrasound imaging is not routinely indicated to diagnose pregnancy but is often used in the evaluation of a patient who is unsure of her last period, at increased risk for ectopic pregnancy, or showing signs of miscarriage. In conjunction with early quantitative serum β-hCG assessments, these conditions can be clearly differentiated from a normal intrauterine pregnancy and timely therapy initiated (Chapter 5).

Gestational Age The Nägele rule is commonly applied in calculating an estimated date of confinement (EDC). The clinician should remember that this is an approximate rule. Using the date of the patient's last menstrual period minus 3 months plus 1 week and 1 year, the rule is based on the assumptions that a normal gestation is 280 days and that all patients have 28-day menstrual cycles. Although several studies have found the average length of gestation for primiparous women to be 282 to 283 days, for convention, 280 days is the currently accepted average gestation. After adjustment for a patient's actual cycle length, natality statistics indicate that the majority of pregnancies deliver within 2 weeks before or after this estimated date. During prenatal care, the week of gestation can be obtained based on the calculated EDC. When the last menstrual period is unknown or the cycle is irregular, ultrasound measurements between the 14 and 20 weeks gestation provide an accurate determination of gestational age (Chapter 9). Care should be taken not to change the EDC unless the ultrasound differs by 10 or more days from the menstrual dates. Once dates are appropriately confirmed, continued alterations of EDC based on fetal size are problematic and ill advised.

Physical Examination A targeted physical examination during the first prenatal visit includes special attention to the patient's BMI, blood pressure, thyroid, skin, breasts, and pelvis. On pelvic

examination, the cervix is inspected for anomalies and for the presence of condylomata, neoplasia, or infection. A Pap smear is performed, and cultures for gonorrhea and chlamydia are taken, if indicated. A small amount of bright red bleeding may occur after these manipulations, and the patient can be assured that this is normal. On bimanual examination, the cervix is palpated to assess consistency and length as well as to detect the presence of cervical motion tenderness. Size, position, and contour of the uterus are noted. The adnexa are palpated to assess for masses. The pelvic examination may include evaluation of the bony pelvis—specifically, the diagonal conjugate, the ischial spines, the sacral hollow, and the arch of the symphysis pubis. This evaluation need only be performed once during the pregnancy.

Laboratory Evaluation Several laboratory tests are routinely done at the first prenatal visit.

Blood Tests Hematologic testing includes a white blood cell count, hemoglobin, hematocrit, and platelet count. Full red cell indices are advised for women of Asian descent to evaluate for thalassemia, a serologic test for syphilis (RPR, rapid plasma reagin or VDRL), a rubella titer, a hepatitis B surface antigen, a blood group (ABO), and Rh type and antibody screen. HIV testing should be recommended to all pregnant patients and documented in the chart. Routine assessment for toxoplasmosis, cytomegalovirus, and varicella immunity is not necessary but may be obtained if indicated. The National Institutes of Health and ACOG recommend offering all white women testing for cystic fibrosis status. Women with histories suggestive of thrombophilia, or a personal or family history for thromboembolic disease, should be evaluated at this time. Women with a history suggestive of thyroid disease should also be evaluated. Although TSH is normally used to evaluate for thyroid disease, TSH may be affected by other pregnancy hormones and not accurately affect thyroid status. Thus, a free T4 should always be obtained when evaluating thyroid disease in pregnancy. Appropriate screening for genetic carrier status, if not performed at the preconception visit, includes but is not limited to Tay–Sachs disease, Canavan disease in women of Jewish ancestry, α- and β-thalassemia in women of Asian and Mediterranean descent, and sickle cell disease in women of African descent. Women with a suggestive history of mental retardation should be screened for fragile X syndrome.

Urine Tests All women should have a clean-catch urine sent for culture. Asymptotic bacteriuria occurs in 5% to 8% of pregnant women. Urinary stasis is present during pregnancy secondary to physiologic changes in the urinary system, including decreased ureteral peristalsis and mechanical uterine compression of the ureter at the pelvic brim as pregnancy progresses. Bacteriuria combined with urinary stasis predisposes the patient to pyelonephritis, the most common nonobstetric cause for hospitalization during pregnancy. Urinary tract

infection is also associated with preterm labor, preterm premature rupture of the membranes, and preterm birth. Asymptomatic bacteriuria is identified by using microscopic urine analysis, urine culture (>100,000 colonies per milliliter), or a leukocyte esterase–nitrite dipstick on a clean-catch voided urine. Group B streptococcal (GBS) colonization of the urinary tract will not always induce a positive leukocyte esterase reaction. Thus, full urine culture at the first visit is indicated, even with negative leukocyte esterase.

Cultures and Infections The use of routine genital tract cultures in pregnancy is controversial. While it is clear that chlamydia, gonorrhea, GBS disease, herpes infection, and potentially bacterial vaginosis can be detrimental to the ultimate health of the fetus or newborn, the indications for and timing of cultures for these infections are debated. The ACOG recommends assessment for chlamydiosis and gonorrhea at the first prenatal visit for high-risk patients. The high-risk patient is defined as less than 25 years of age with a past history or current evidence of any sexually transmitted disease, a new sexual partner within the preceding 3 months, or multiple sexual partners. Any abnormal discharge should be assessed with a wet prep or Gram stain. Symptomatic patients should be treated. Symptomatic bacterial vaginosis may be treated in the first trimester. Tuberculosis skin testing in high-risk populations or in certain geographic areas should be done if the patient has not been vaccinated with BCG vaccine. BCG vaccinations are not given in the United States.

Discussions with the Patient The first prenatal visit is a time for the caregiver and patient to exchange expectations, to answer questions, and to set the stage for what will occur throughout the rest of normal prenatal care. The timing and content of future visits and the timing and rationale behind further laboratory testing should be explained. The patient should be given educational resources and materials that are written at the appropriate reading level. She and her partner are encouraged to ask questions about what they will read and to share the concerns they have about the pregnancy. It is important to reinforce that there is no such thing as a meaningless, “dumb,” or trivial question. Emergency and routine phone numbers should be given to the patient in writing. Social services and community resources, such as Women, Infants, and Children (WIC) programs, may be identified for the patient on an as-needed basis. Discussion regarding sexual activities, physical activities, and nutrition are usually initiated at this time. Instructions on safe and unsafe OTC medications (i.e., acetaminophen vs. ibuprofen) are also initiated. Instruction on the use of seat belts and domestic abuse is also recommended. For women with previous pregnancies, a discussion of issues and problems from that pregnancy and the past delivery experience should be entertained at this time. Many fears and tensions can be alleviated with simple discussions now and obviate anxieties that may linger and build over pregnancy. A note in the chart to

further discuss a particular point at a later time may also be helpful. Finally, the patient should be made aware of the warning signs and symptoms of infection (fevers, chills, dysuria, and hematuria) or threatened pregnancy loss (bleeding, cramping, passage of tissue). Should any of these occur, the patient should seek immediate medical attention. At the completion of the first visit, the next prenatal appointment is made.

Routine Antepartum Surveillance The rationale and guiding principles of prenatal care are listed in Table 1.1. It is at this point in the patients' care that individualization should occur. For women in high-risk categories—such as those with previous preterm birth, chronic medical diseases, family history of problems, and the like—an individualized frequency of visits should be established and documented. For example, a woman with a previous unexplained secondtrimester loss that was suspicious but not diagnostic for incompetent cervix might be observed weekly between 17 and 24 weeks, or a woman with chronic hypertension might be seen every 2 weeks throughout the first and second trimesters. In contrast, a woman with previous uncomplicated pregnancies might be seen every 6 weeks in the first and second trimesters and every other week in the last 8 weeks. The traditional timing of 14 prenatal visits was established empirically in the 1930s and has never been validated. In the mid 1980s and 1990s, several randomized trials demonstrated that for low-risk women, 6 to 8 total prenatal visits were equally effective in achieving good pregnancy outcomes. A systematic review and the current standard of care allow for individualized scheduling of visits. Fourteen visits for a low-risk woman would be more than necessary. Table 1.2 lists the traditional timing of visits. From this outline, each woman's needs may be individualized and the prenatal course altered, based on necessary assessments and interventions. A U.S. Public Health Service report delineated the interventions and tests deemed minimally necessary in a normal pregnancy and the suggested the timing for each (Table 1.3).

TABLE 1.1 Rationale for Routine Prenatal Care Prenatal care involves the following goals for pregnant women: to provide continuing, ongoing primary preventive health care to maintain or increase maternal health and the capability for self-care and to improve self-image before, during, and after pregnancy to reduce the risk of maternal mortality and morbidity as well as unnecessary pregnancy intervention

to reduce the risks to health before subsequent pregnancies and beyond the childbearing years to promote the development of parenting skills, including breast-feeding. The goals of prenatal care for the fetus are as follows: to reduce the risk of preterm birth, IUGR, retardation, and congenital anomalies to enhance fetal health and reduce the need for extended hospitalization after birth to promote healthy growth and development, immunization, and health supervision of the infant to reduce the risk of neurologic, developmental, and other morbidities to reduce the risk of child abuse and neglect, injuries, and preventable acute and chronic illness. The goals of prenatal care for the family during pregnancy and the first year of an infant's life are the following: to promote family development and positive parent–infant interaction to reduce the number of unintended pregnancies to identify and treat behavioral disorders that can lead to child neglect and family violence.

Content of Subsequent Prenatal Visits The two components of each prenatal visit are the assessments of fetal growth and health and the evaluation of maternal well-being. Maternal health is assessed first with the taking of an interval history, risk assessment and identification, and intervention as necessary. Fetal assessment is via physical examination and inquiry of fetal movements. It is important that the assessments be recorded in an ongoing database. The final aspect of the visit is education, advice, and support of the patient and her family.

TABLE 1.2 The Traditional Timing and Number of Prenatal Visits

Preconception:

Up to 1 year before conception

First prenatal:

6 to 8 weeks after missed menses

Monthly:

Up to 28 weeks

Bimonthly:

Up to 36 weeks

Weekly:

Until delivery

This schedule is modified and individualized for the needs of each woman, 6 prenatal visits may be sufficient for most lowrisk women, whereas 20 or more may be necessary for some high-risk women.

TABLE 1.3 Timing of Prenatal Care Based on Specific Interventi (in weeks)

First 6– 16– 26– 32 36 38 39 Visit 8a 18 28

History Medical

Psychosocial

Update

Physical

General

Blood pressure

Height

Weight

Body mass index

Pelvic exam

Breast exam

Fundal height

Fetal position

Fetal heart

Cervical exam

Laboratory

Hemoglobin/hematocrit

Rh factorb

Blood type

Antibody screen

Pap smear

GDM screen

Fetal testing for aneuploidy (12 weeks)

Urine

Dipstick

Protein

Sugar

Culture/urinalysis

Infections

Rubella

Syphilis

Hepatitis B

HIV (offer)

Genetic screen

GDM, gestational diabetes mellitus; HIV, human immunodeficiency virus. a If the patient had a preconception visit, some elements will be omitted. b If Rh negative, rescreen at 26 to 28 weeks.

Interval History Each prenatal visit begins with information gathering. Patients should be asked questions about their general health (see Concerns and Questions Particular to Pregnancy later in the chapter), their diet, sleeping patterns, and fetal movement. Questions regarding warning signs such as bleeding, contractions, leaking of fluid, headache, or visual disturbances are also appropriate. Importantly, patients should be given the opportunity to raise their own questions and concerns at each visit, with open-ended inquiries.

Physical Examination

The patient's weight is measured, and total weight gain and trends are evaluated (see Nutrition later in the chapter). The blood pressure is taken and trends are assessed for possible pregnancy-induced hypertension. As blood pressure tends to decrease during the second trimester, increases of 30 mm Hg systolic or 15 mm Hg diastolic over first-trimester pressures are considered abnormal and warrant further evaluation. The fundal height is measured with a tape from the top of the symphysis pubis, over the uterine curve, to the top of the fundus (Figs. 1.1, 1.2). This technique places an emphasis on change in growth patterns rather than the absolute measurement in centimeters, which can vary between patients. In women who are obese, periodic ultrasound assessments of fetal growth may be necessary. Gestational age is approximately equal to fundal height in centimeters from 16 to 36 weeks gestation. Measurements that are more than 2 cm smaller than expected for week of gestation are suspicious for oligohydramnios, IUGR, fetal anomaly, abnormal fetal lie, or premature fetal descent into the pelvis. Conversely, larger than expected measurements may indicate multiple gestation, polyhydramnios, fetal macrosomia, or leiomyomata. These concerns can be resolved with ultrasound examination.

Figure 1.1 The height of the fundus at comparable gestational dates varies among patients. Those shown are the most common. A convenient rule of thumb is that at 20 weeks gestation, the fundus is at or slightly above the umbilicus.

Fetal heart rate is auscultated, with care taken to differentiate fetal from maternal rates.

The normal fetal heart rate throughout pregnancy is between 110 and 160 beats per minute. Fetal position has been traditionally evaluated with the use of Leopold maneuvers. These are initiated at midpregnancy, when fetal body parts are more clearly identified. The maneuvers consist of four parts; the first three are performed with the examiner standing to one side of the patient and facing her head and the last with the examiner facing the patient's feet.

Figure 1.2 Fundal heights versus gestational age.

Figure 1.3 The first Leopold maneuver reveals what fetal part occupies the fundus.

The first maneuver answers the question, “What fetal part occupies the fundus?” (Fig. 1.3). The examiner palpates the fundal area and differentiates between the irregular, firm breech and the round, hard head. The second maneuver answers the question, “On which side is the fetal back?” (Fig. 1.4). The palms of the hands are placed on either side of the abdomen. On one side, the linear continuous ridge of the back is felt; on the other side, compressible areas and nodular parts are found.

Figure 1.4 The second Leopold maneuver reveals the position of the fetal back.

Figure 1.5 The third Leopold maneuver reveals what fetal part lies over the pelvic inlet.

The third maneuver answers the question, “What fetal part lies over the pelvic inlet?” (Fig. 1.5). A single examining hand is placed just above the symphysis. The fetal part that overrides the symphysis is grasped between the thumb and third finger. If the head is unengaged, it is readily recognized as a round, hard object that frequently can be displaced upward. After engagement, the back of the head or a shoulder is felt as a relatively fixed, knoblike part. In breech presentations, the irregular, nodular breech is felt in direct continuity with the fetal back. The fourth maneuver answers the question, “On which side is the cephalic prominence?” (Figs. 1.6, 1.7). This maneuver can be performed only when the head is engaged; if the head is floating, the maneuver is inapplicable. The examiner faces the patient's feet and places a hand on either side of the uterus, just above the pelvic inlet. When pressure is exerted in the direction of the inlet, one hand can descend farther than the other. The part of the fetus that prevents the deep descent of one hand is called the cephalic prominence. The routine examination is completed by evaluating the patient for edema. A finding of new-onset edema of the face and hands in association with proteinuria and elevated blood pressure is consistent with preeclampsia. Dependent pitting edema of the ankles and legs in the absence of other findings is normal in late pregnancy. It responds well to resting, with the legs elevated, and therefore is usually absent on rising in the morning. Another treatment for edema is immersion in a bathtub or swimming pool. Sudden weight gain in

the third trimester to a large extent reflects an increase in edema. The amount of weight gain that is pathologic is not known. However, more than 5 lb in a week is generally considered problematic. Routine examination of the cervix is not necessary unless the patient is at risk for cervical incompetence or is being evaluated for preterm labor.

Figure 1.6 The fourth Leopold maneuver reveals the position of the cephalic prominence. In a flexion attitude, the cephalic prominence is on the same side as the small parts.

Laboratory Evaluation Several laboratory evaluations are offered to all patients after the initial prenatal labs. These include screening for aneuploidy, which may be done at 11 to 13 weeks or at 16 to 20 weeks (Chapters 6, 7), screening for gestational diabetes mellitus (GBM) with a glucose challenge, and screening for maternal antibodies to fetal blood type.

Figure 1.7 In the fourth Leopold maneuver, in an extension attitude, the cephalic prominence is on the same side as the back.

Maternal Serum Screening Tests Screening with maternal serum alpha-fetoprotein (MSAFP) was originally adopted in the mid 1980s to detect fetal neural tube defects and fetal ventral wall defects. Further evaluation of maternal serum levels noted associations with aneuploidy. Several serum markers have been established as independent markers for fetal chromosome abnormalities. Different acolytes are used at different times in gestation, in conjunction with ultrasound evaluation. These are detailed in Chapters 6 and 7. During pregnancy, AFP is produced in sequence by the fetal yolk sac; the fetal gastrointestinal tract; and finally, the fetal liver. Its peak concentration in fetal serum occurs at the end of the first trimester. Transfer of AFP to the maternal serum occurs via the placenta and transamniotically. MSAFP levels are reported as multiples of the median from the database of the individual laboratory. Elevated maternal serum and amniotic fluid levels of AFP detect 85% of open neural tube defects (open spina bifida and anencephaly). Other causes for elevated MSAFP levels include omphalocele, gastroschisis, multiple gestation, fetal demise, incorrect dates, and adverse pregnancy outcomes. Patients with abnormal MSAFP levels require evaluation with targeted fetal ultrasonography (Chapters 6, 7, 9). Maternal serum markers and ultrasound evaluation should be offered to all women regardless of age; however, local availability and timing of initial maternal presentation to the health care system will influence the best test to offer each patient. First-trimester screening has a sensitivity of 80% to 85% for the detection of aneuploidy in women over age 35. The quad screen at 16 to 20 weeks has a slightly lower sensitivity. Many couples will decline serum screening but desire ultrasound evaluation of the pregnancy. Ultrasound has at best a 50% sensitivity to identify fetuses at risk for trisomy 21 and 90% sensitivity to predict more dimples

aneuploidy.

Screening for Gestational Diabetes The 1-hour, 50-g oral glucose screen is used to detect glucose intolerance in pregnancy. Following an abnormal screen, a 3-hour glucose tolerance test, commencing with a fasting blood sugar, followed by a 100-g glucola, is currently recommended. Two or more abnormal values on this test are considered diagnostic of GDM. GDM is discussed in greater detail in Chapter 15. Some clinicians feel that only women with risk factors (Table 1.4) should be screened. Proponents of universal screening argue that screening only those patients with risk factors will detect no more than half of patients with glucose intolerance. Opponents argue that the inconvenience and expense of testing are not necessary in patients without these risk factors, because the incidence of frank GDM in this population is so low. Most clinicians in the United States have adopted universal screening.

TABLE 1.4 Risk Factors for Gestational Diabetes Mellitus Maternal age greater than 30 years Previous macrosomic, malformed, or stillborn infant GDM in a previous pregnancy Family history of diabetes Maternal obesity Persistent glucosuria Chronic use of certain drugs such as β-sympathomimetics or corticosteroids GDM, gestational diabetes mellitus. Universal screening is offered to all patients between 26 and 28 weeks gestation. Selective screening based on risks may be performed earlier and repeated as needed if negative at earlier gestations. A patient may be tested in the fasting or nonfasting state. One hour after administration of a 50-g glucose load, the patient's blood is drawn. A patient with a glucose value greater than 140 mg/dL of serum is a candidate for a 3-hour, 100-g glucose tolerance test. If the value exceeds 180 mg/dL, most clinicians will not proceed with the 100-g test but rather will assign the woman a diagnosis of GDM. Women who are at high risk, such as those with a previous history of GDM or polycystic ovary syndrome, should have a cutoff of 130 mg/dL by which to proceed to the 100-g full test. The sensitivity of a serum glucose of 140 mg is 80% in predicting GDM, and women at significantly increased risk benefit from a higher sensitivity.

The significance of GDM lies not in an increased risk of fetal loss but in the risk of excessive fetal growth with its attendant birth-related morbidities. In addition, women with GDM have a 60% likelihood of developing overt diabetes mellitus within 16 years.

Rescreening for Rh Antibodies and Other Irregular Antibodies All Rh-negative women who are unsensitized at the beginning of pregnancy should be retested at approximately 26 to 28 weeks gestation. If the antibody screen remains negative, the mother should receive Rh0(D) immune globulin 300 mcg at 28 weeks to prevent isoimmunization in the third trimester. Approximately 1% of Rh-negative women will become sensitized if not given Rh immune globulins. Any woman with a positive indirect Coombs (antibody screen) in early pregnancy should be followed with serial antibody screens (Chapter 17).

Screening for Bacterial Vaginosis Bacterial vaginosis (BV) is a condition in which the normal flora of the vagina (specifically lactobacilli) are reduced in number and replaced by an overgrowth of anaerobic organisms. Studies have linked BV with an increased incidence of preterm labor, endometritis, and premature rupture of the membranes. A simple and effective screen performed late in the second trimester consists of a pelvic examination and wet mount to detect BV. A Gram stain is an alternative diagnostic tool. The treatment for women who are positive for BV includes either metronidazole (Flagyl) or clindamycin (Cleocin). Both are safe in pregnancy. Because BV is often asymptomatic, a test of cure may be appropriate. Routine screening is not recommended, as studies have not shown that screening and treatment decrease preterm labor and delivery. However, symptomatic women, women with cerclage, or women with preterm dilated cervices should be screened and treated.

Screening for Group B Streptococcus GBS are part of the normal vaginal, genitourinary, and gastrointestinal tract flora in up to 30% of healthy women. GBS have been implicated in amnionitis, endometritis, pyelonephritis, and wound infection in the mother. Vertical transmission during pregnancy, labor, and delivery may result in generalized sepsis in the newborn and related long-term morbidity or neonatal death. Prevention strategies have focused on detection of the bacteria in the mother and prophylaxis to decrease the incidence of early-onset GBS disease in the newborn. The recommended strategy involves routine anogenital cultures of all pregnant women at 35 to 37 weeks gestation. Cultures are obtained from the lower third of the vagina and perianal area. Cervical cultures are not reliable, and a speculum is not necessary to obtain an adequate culture sample. Culture-positive women are treated during labor with antibiotic prophylaxis to prevent fetal–neonatal GBS infection. Women with a positive urine culture for GBS at any time in pregnancy should be given antibiotic prophylaxis in labor.

These women do not need to be recultured. Treatment is with penicillin or ampicillin. Women with penicillin allergies may receive a cephalosporin or clindamycin. However, up to 15% of GBS colonies will be resistant to clindamycin. Thus, in the penicillin-allergic patient who cannot take cephalosporins, a sensitivity should be obtained at the time of anogenital cultures.

Testing Based on Symptoms or Clinical Risk Assessment A part of prenatal care of the normal patient consists of ongoing risk assessment and intervention or referral if a risk is identified. Several clinical signs or symptoms warrant further evaluation. Symptoms suggestive of urinary tract infections should prompt examination of a clean-catch urine specimen and cultures when appropriate. High-risk behaviors, identified during the course of a pregnancy, should prompt a test (or retest) for HIV infection and sexually transmitted diseases (STDs) or performance of a urinary drug screen. Repeated testing of hemoglobin should be done if the patient is symptomatic or at nutritional risk for anemia. Other testing, performed on an as-needed basis, includes ultrasound to detect abnormal fetal growth, antepartum fetal monitoring to assess fetal oxygenation status, or comprehensive targeted ultrasound examinations. A more thorough discussion of antepartum fetal monitoring can be found in Chapter 10.

Routine Ultrasound Most clinicians will obtain a detailed anatomic fetal evaluation in the mid second trimester by ultrasound (Chapter 9). This ultrasound helps document fetal age and fetal well-being as well as placental position. The fetal evaluation by ultrasound should be performed before 20 weeks so that appropriate referrals and consultation can be obtained if abnormalities are discovered.

Discussion with Patients and Families: Answering Questions Patients need the opportunity to engage in dialogue with their health care provider and to feel confident that their concerns are heard. Patients and families will often interact with a nurse or triage person in a physician's office. These individuals need to be trained in careful assessment and evaluation. The value of information that ancillary personnel can provide cannot be overemphasized. The prenatal visits are a time to stress the involvement of the entire family in the pregnancy process, including the role of the father and siblings. Therefore, an important part of the prenatal visit is discussion with the patient, her partner, or her family, both to exchange questions and answers and to provide reassurance and education. The exact content of these discussions will vary from visit to visit. Reaffirming the importance of appropriate social behaviors, such as smoking cessation, is beneficial, as are periodic evaluations of the social support systems and help in the home, both now and after the birth of the infant. Ongoing risk assessment requires that the patient be educated about the signs and

symptoms of preterm labor and preeclampsia. The list of warning signs for which an emergent telephone call is warranted includes the following: Vaginal bleeding Leaking of fluid from the vagina Rhythmic cramping pains of more than six per hour Abdominal pain of a prolonged or increasing nature Fever or chills Burning with urination Prolonged vomiting with inability to hold down liquids or solids for more than 24 hours Severe continuous headache, visual changes, or generalized edema A pronounced decrease in the frequency or intensity of fetal movements.

Concerns and Questions Particular to Pregnancy Pregnancy is a time of change, expectation, and anticipation. It may also be a time of heightened anxiety, emotionality, concern, and uncertainty. Many symptoms that the nonpregnant patient might view as minor may indicate a cause for alarm during pregnancy. The provision of direct, concise, and accurate information in a compassionate and reassuring manner will assuage many of these worries and provide direction for day-to-day activities. One of the roles of clinicians is to judge whether the symptoms a mother asks about and whether the physical findings measured are physiologic or pathologic. These judgments are most easily made and most easily explained to the patient and her family in the context of a few basic maternal physiologic adaptations. The first major maternal adaptation is cardiovascular. The maternal cardiovascular system must deliver enough nutrition and oxygen to the fetoplacental unit to ensure healthy development while at the same time not compromise the mother. During times of maternal activity when blood would normally be shunted from the viscera (including the uterus) to exercising muscles, there must be enough cardiovascular reserve to perfuse the uterus. This is accomplished through a series of steps that begin before the missed menses. Rising levels of progesterone induce increasing venous compliance. To maintain cardiac output, blood volume is increased. Blood volume reaches approximately 140% of normal by the early third trimester. Since only 25% of body water is intravascular, there is a compensatory increase in total body water. The clinician usually has to explain this to the woman who asks why at 8 weeks pregnant she already has to change pant size. The increased blood volume produces increased renal blood flow and increased glomerular filtration. Most medications are excreted much more quickly in pregnancy and level-dependent medications such as antiepileptics need to be adjusted. Blood vessel responsiveness to catecholamines and other pressors is reduced to inhibit shunting of circulation away from the growing uterus during stress, which leads to a generalized lower arterial and venous pressure. An additional effect of the relaxation of

smooth muscle by progesterone is the greater ability of the uterus to grow and stretch without the usual compensatory contractions. However, most other smooth muscle in the body is also affected, particularly in the gastrointestinal system. The following sets of topics and problems are centered on the most frequently asked questions and most important areas of concern.

Nutrition and Weight Gain The objectives of nutritional assessment and counseling are to develop, in concert with the patient, an analysis of maternal nutritional risk, a goal for total weight gain, and a diet plan that will fit the patient's lifestyle and is ethnically sensitive. The principle of good nutrition is that there is a positive linear relationship between maternal weight gain and newborn weight and that prepregnant maternal BMI can affect fetal weight independently of the amount gained by the mother during pregnancy. Together, initial weight and weight gain have an impact on IUGR and low birth weight. However, for a woman of normal weight and normal nutrition, the relationship between poor weight gain and fetal growth restriction may be an association, not a cause and effect. Importantly, excess maternal weight gain is also directly proportional to adverse perinatal outcome. The BMI is a calculation that relates the patient's weight to her height, thereby providing a more accurate indirect estimate of the patient's body fat distribution than can be obtained by weight alone. The BMI is calculated by dividing weight in kilograms by height in meters squared. If pounds and inches are used, the quotient is multiplied by 700. The BMI of a patient is categorized as underweight, normal weight, overweight, or obese.

Maternal Weight Gain Although dependent on many factors, the ideal weight gain during pregnancy can be simplified into three recommendations based on the prepregnant BMI (for singleton pregnancies). Women with a prepregnant BMI Table of Contents > 4 - Early Pregnancy Loss

4 Early Pregnancy Loss T. Flint Porter D. Ware Branch James R. Scott Miscarriage, also termed spontaneous abortion, is most commonly used to describe firsttrimester loss, although it has also been used to describe loss before 20 weeks. These arbitrary time limits have become less useful with advances in developmental biology and diagnostic sonography. Early pregnancy loss is more precisely defined as preembryonic (conception through the first 5 weeks of pregnancy from the first day of the last menstrual period), embryonic (6 to 9 weeks gestation), or fetal (10 weeks until delivery).

Epidemiology Miscarriage is the most common complication of pregnancy, occurring in at least 15% of clinically recognized pregnancies. Histologically defective ova found in hysterectomy specimens (Fig. 4.1) and data on early pregnancies detected with sensitive β-human chorionic gonadotropin (β-hCG) assays indicate that the rate is two to three times higher in early, unrecognized pregnancies. Miscarriage rates also vary with maternal age, ranging from 12% in women younger than 20 years of age to over 50% in women older than 45 years of age (Fig. 4.2). The likelihood of miscarriage is heavily dependent on past obstetric history, being higher among women with prior miscarriages and lower among women whose past pregnancy or pregnancies ended in live births.

Embryology Successful pregnancy is dependent on integration of several complex processes involving genetic, hormonal, immunologic, and cellular events, all working together in perfect order to achieve fertilization, implantation, and embryonic development. It is not surprising that early pregnancy loss can occur because of a number of embryonic and parental factors.

Embryonic Factors Most single, sporadic miscarriages are caused by nonrepetitive intrinsic defects in the developing conceptus, such as abnormal germ cells, chromosomal abnormalities in the

conceptus, defective implantation, defects in the developing placenta or embryo, accidental injuries to the fetus, and probably other causes as yet unrecognized. Fifty percent of women presenting with spotting or cramping already have a nonviable conceptus by sonogram, and many of these embryos are morphologically abnormal. About one third of abortus specimens from losses occurring before 9 weeks gestation are anembryonic. Some cases of empty gestational sacs or “blighted ova” actually represent pregnancy failures with subsequent embryonic resorption. The high proportion of abnormal aborted concepti is apparently the result of a selective process that eliminates about 95% of morphologic and cytogenetic errors. The frequency of chromosomally abnormal spontaneously aborted products of conception in the first trimester is approximately 60%, decreasing to 7% by the end of the 24th week (Fig. 4.3). The rate of genetic abnormalities is higher in anembryonic miscarriages. Autosomal trisomies are the most common (51.9%), arising de novo as a result of meiotic nondisjunction during gametogenesis in parents with normal karyotypes. The relative frequency of each type of trisomy differs considerably. Trisomy 16, which accounts for about one third of all trisomic abortions, has not been reported in live-born infants and is therefore uniformly lethal. Trisomy 22 and 21 follow in frequency. The next most common chromosomal abnormalities, in decreasing order, are monosomy 45,X (the single most common karyotypic abnormality), triploidy, tetraploidy, translocations, and mosaicism. Media publicity tends to give the impression that a variety of agents such as infections, video display terminals, cigarette smoking, coffee, ethanol, chemical agents, and drugs markedly increase the risk of miscarriage. In reality, there is little credible supportive evidence.

Figure 4.1 Histologic comparison of (A) a morphologically normally implanted human ovum estimated to be about 11 to 12 days of age with (B) an abnormal conceptus, showing a defective trophoblast with pathologically large lacunae and an empty chorionic sac that is destined to abort. (From Hertig AT, Rock J, Adams EC. Am J Anat 1956;98:435, with permission.)

Figure 4.2 Relation of maternal age to the risk of spontaneous abortion. (Data from Warburtin D, Kline J, Stein Z, et al. Cytogenetic abnormalities in spontaneous abortions of recognized conceptions. In: Porter IH, ed. Perinatal genetics: diagnosis and treatment. New York: Academic Press, 1986:133.)

Figure 4.3 The frequencies of chromosomal anomalies among 3040 spontaneously aborted fetuses related to the duration of pregnancy. For comparison, the frequency of chromosomal anomalies among 54,749 newborn infants is shown. (Data from Shiota K, Uwabe C, Nishimaura H. High prevalence of defective human embryos at the early implantation period. Teratology 1987;35:309; Boue J, Boue A, Lazar P. Retrospective and prospective epidemiological studies of 1500 karyotyped spontaneous human abortions. Teratology 1975;12:11; Lauritsen JG. Aetiology of spontaneous abortion: a

cytogenetic and epidemiological study of 288 abortuses and their parents. Acta Obstet Gynecol Scand Suppl 1976;52:1; and Creasy MR, Crolla JA, Alberman ED. A cytogenetic study of human spontaneous abortions using banding techniques. Hum Genet 1976;31:177.)

Pathology Most miscarriages occur within a few weeks after the death of the embryo or rudimentary analog. Initially, there is hemorrhage into the decidua basalis, with necrosis and inflammation in the region of implantation. The gestational sac is partially or entirely detached. Subsequent uterine contractions and dilation of the cervix eventually result in expulsion of most or all of the products of conception. When the sac is opened, fluid is often found surrounding a small macerated embryo, although no visible embryo may be present. Histologically, hydropic degeneration of the placental villi caused by retention of tissue fluid is common.

Clinical Features and Treatment An unrecognized pregnancy should always be considered in any woman of reproductive age with abnormal bleeding or pain. Likewise, a patient with known pregnancy should notify her physician promptly about vaginal bleeding or uterine cramps. Since management depends on several clinical factors, it is useful to consider miscarriage under the following subgroups.

Threatened Miscarriage Any bloody vaginal discharge or uterine bleeding that occurs during the first half of pregnancy has traditionally been assumed to be a threatened miscarriage. Spotting or bleeding during the early months of gestation occurs quite commonly, in as many as 25% of pregnant women. Bleeding is typically scanty, varying from a brownish discharge to bright red bleeding. It may occur repeatedly over the course of many days and usually precedes uterine cramping or low backache. On pelvic examination, the cervix is closed and uneffaced, and no tissue has passed. The differential diagnosis includes ectopic pregnancy, molar pregnancy, vaginal ulcerations, cervicitis with bleeding, cervical erosions, polyps, and carcinoma. Women presenting with threatened miscarriage should receive an ultrasound examination to determine location, viability, and gestational age. Accurate knowledge of gestational age is necessary for proper interpretation, as a sonographically empty uterus may imply an abnormal intrauterine or ectopic pregnancy when it actually represents a normal early gestation. Serial testing of β-hCG measurements is a useful adjunct if the diagnosis remains uncertain, along with a follow-up sonogram a few days later. A viable conceptus can be detected with modern ultrasound as early as 5.5 weeks

gestation. It is possible to visualize the yolk sac and gestational sac starting at 5 to 6 weeks by using transvaginal ultrasound, with cardiac activity seen thereafter. Ultrasound findings suggesting impending pregnancy loss include an abnormally sized or shaped gestational sac and yolk sac, an embryo small for dates, and slow embryonic heart rate. In the absence of signs of miscarriage, more than 95% of pregnancies continue if a live embryo is demonstrated sonographically at 8 weeks gestation. Even in the setting of uterine bleeding, more than two thirds survive as long as ultrasound demonstrates an appropriately sized embryo with a normal cardiac rate. The subsequent pregnancy loss rate is only 1% if a live fetus is seen at 14 to 16 weeks gestation. Although there is no convincing evidence that any treatment favorably influences the course of threatened miscarriage, a sympathetic attitude by the physician along with continuing support and follow-up are important to patients. This includes a tactful explanation about the pathologic process and favorable prognosis when the pregnancy is viable. An optimistic but cautious approach is prudent, since a few of these women will have a later embryonic or fetal death. It is reasonable to advise patients to remain available to medical care until it can be determined whether the symptoms will persist or cease. Continued observation is indicated as long as bleeding and cramping are mild, the cervix remains closed, quantitative β-hCG levels are increasing normally, and a normal embryo or fetus is evident on follow-up sonogram. If the bleeding and cramping progressively increase, the prognosis becomes worse. An unfavorable outcome is also associated with negative or falling β-hCG values, sonographic evidence of an embryo or fetus decreasing in size (Fig. 4.4), a slow heart rate, and a uterus that is not increasing in size on pelvic examination.

Inevitable and Incomplete Miscarriage Miscarriage is considered inevitable when bleeding and cramping is accompanied by gross rupture of the membranes or cervical dilation. The miscarriage is incomplete when the products of conception have partially passed from the uterine cavity, are protruding from the external os, or are in the vagina with persistent bleeding and cramping. There is no viable conceptus in most instances of inevitable or incomplete miscarriages. Rarely, a single twin may survive and continue to term after miscarriage of the other conceptus. Women with incomplete or inevitable miscarriage typically present with bleeding that can be profuse occasionally and produce hemodynamic instability. A careful pelvic examination is usually sufficient to establish the diagnosis, although ultrasound examination is often performed. Evacuation of the uterus is advisable to prevent further maternal hemorrhage or infection. Clinically stable patients can be treated as outpatients by either medical or surgical means. However, patients with uncontrolled bleeding should be transferred to the operating room for an examination under anesthesia and immediate surgical evacuation of the uterus. They should be observed postoperatively for several hours and discharged when considered stable.

Figure 4.4 Ultrasonic comparison of (A) an anembryonic pregnancy with no fetal tissue that is destined to abort with (B) a normal gestational sac with a transonic area, echogenic rim, and fetal pole.

Suction curettage can be performed promptly and safely in an inpatient or outpatient setting by using analgesia, a paracervical block, and an intravenous infusion of normal saline containing 10 to 20 U of oxytocin. The cervix is sometimes dilated, and ring forceps can be used to remove products of conception from the cervical canal and lower uterine segment, thereby facilitating uterine contractions and hemostasis. Suction curettage with a plastic curette and vacuum pressure is used to remove the remaining tissue. The curette is rotated 360 degrees clockwise as it is withdrawn, and the procedure is repeated in a counterclockwise direction. When a grating sensation is noted and no more tissue is obtained, the endometrial cavity has been emptied. The tissue obtained should be examined to confirm the presence of products of conception and rule out the possibility of ectopic pregnancy. Problems that can occur include allergic reactions to medication, uterine atony, uterine perforation, seizure, or cardiac arrest. A complete blood count level should be obtained, and blood replacement may be necessary if hemorrhage occurs. Rh-negative women should receive 50 g (in the first trimester) or the standard 300-g (in the second trimester) dose of Rh immune globulin to prevent Rh immunization. Medical management of incomplete miscarriage has been studied in well-designed trials and may be used instead of surgical evacuation in clinically stable patients, although uterine curettage may eventually be required. In one randomized, controlled trial, an 80% complete abortion rate was achieved by using 800 mg of misoprostol (four 200-mg tablets) per vagina every 4 hours. Most patients responded to the first dose. Curettage was necessary in 28% of patients. When successful, misoprostol treatment of incomplete miscarriage is associated with lower rates of short- and long-term complications compared with surgical evacuation. Combinations of misoprostol with methotrexate or RU-486 appear promising but are not available for clinical use.

Complete Miscarriage Patients followed for a threatened miscarriage should be instructed to save all tissue passed for later inspection. When the entire products of conception have passed, pain and bleeding soon cease. If the diagnosis is certain, no further therapy is necessary. In questionable cases, ultrasound is useful to confirm an empty uterus. In some cases, curettage may be necessary to be sure that the uterus is completely evacuated. Removal of remaining necrotic decidua decreases the incidence of bleeding and shortens the recovery time.

Missed Miscarriage The reason that expulsion of a dead conceptus does not occur despite a prolonged period is uncertain. The patient's symptoms of pregnancy typically regress, quantitative β-hCG levels fall, and no fetal heart motion is detected by ultrasound. While most patients eventually abort spontaneously, and coagulation defects due to retention of the conceptus are rare, expectant management is emotionally trying, and many women prefer to have the uterus evacuated. Either medical or surgical evacuation of uterine contents is acceptable. In the second trimester, the uterus can be emptied by dilation and evacuation (D&E) or induction of labor with intravaginal prostaglandin E2 (PGE2) or misoprostol. D&E is an extension of the traditional dilation and curettage (D&C) and vacuum curettage. It is especially appropriate at 13 to 16 weeks gestation, although many proponents use this procedure through 20 weeks. The cervix is usually first prepared by using misoprostol or passively dilated with laminaria to avoid trauma, and the fetus and placenta are mechanically removed with suction and instruments. If induction of labor is chosen, vaginal PGE2 may be used; one 20-mg suppository is placed high in the posterior vaginal vault every 4 hours until the fetus and placenta are expelled. Between 2.5 and 5.0 mg of diphenoxylate given orally and 10 mg of prochlorperazine given intramuscularly can control diarrhea and nausea, and narcotics or epidural anesthesia can be used to control pain. In this situation, a retained placenta is relatively common and may require manual removal and uterine curettage. Misoprostol has become more commonly used in recent years because of its equal efficacy and markedly lower incidence of unpleasant side effects; 200-mg tablets are placed high in the vagina every 4 hours until delivery of the fetus and placenta. Medical treatment of nausea, vomiting, diarrhea, and fever are rarely necessary, although retained placenta is not uncommon.

Septic Miscarriage Septic abortion, once a leading cause of maternal mortality, has become less frequent, primarily because of changes in abortion laws making pregnancy terminations more easily available to women with unwanted pregnancies. However, any type of spontaneous miscarriage can also be complicated by endometritis, which can progress to parametritis

and peritonitis. The clinical presentation typically includes fever, abdominal tenderness, and uterine pain. Septicemia and shock may occur if the local infection is left untreated. The polymicrobial infection mirrors the endogenous vaginal flora and includes Escherichia coli and other aerobic, enteric, gram-negative rods, group B-hemolytic streptococci, anaerobic streptococci, Bacteroides species, staphylococci, and microaerophilic bacteria. The initial evaluation and management of septic abortion should include: Physical and pelvic examination Complete blood cell count and determination of electrolyte, blood urea nitrogen, and creatinine levels Type and screen or cross match of blood Smears from cervix for Gram stain Aerobic and anaerobic cultures of endocervix, blood, and available products of conception Placement of indwelling Foley catheter Administration of intravenous fluids (e.g., saline, Ringer lactate) through a large-bore angiocatheter Administration of 0.5 mL of tetanus toxoid, given subcutaneously for immunized patients, or 250 U of tetanus immune globulin, administered deep within the muscle Abdominal x-rays to detect free air or foreign bodies. Optimal therapy consists of evacuation of the uterus and aggressive use of parenteral antibiotics before, during, and after removal of necrotic tissue by curettage (Table 4.1). Prompt removal of the infected tissue is important and should be performed within a few hours after beginning intravenous antibiotics. Numerous antibiotic regimens have been recommended, but high-dose, broad-spectrum coverage as outlined in Table 4.1 is essential. Although most patients with septic abortions respond favorably to treatment, septic shock syndrome is a serious complication that requires aggressive management in an intensive care setting.

TABLE 4.1 Antibiotic Regimens for Septic Abortion Gram-positive anaerobe and aerobic organism coverage: 1. Aqueous penicillin G, 4–5 million U i.v. q4–6h (20–30 million U each 24 h); or 2. Ampicillin, 2 g i.v. q4–6h; or 3. Clindamycin (Cleocin), 600 mg i.v. q6h or 900 mg i.v. q8h; or

4. Cefoxitin (Mefoxin) (or other cephalosporin), 1–2 g i.v. 6h (for penicillin-allergic patients, there is a 10% cross allergy); or 5. Imipenem-cilastatin (Primax), 250–500 mg q6h (must decrease dose for patients weighing 32,000 genes 3,200,000,000 base pairs

Figure 6.12 The DNA code consists of four characters and is read three characters at a time. It is transcribed into a ribonucleic acid (RNA) message, which instructs cells how to assemble proteins from amino acids.

The genetic code is spelled out with the four nitrogenous bases: adenine, thiamine, cytosine, and guanine (Fig. 6.12). The purine and pyrimidine bases are arranged in a ladderlike, double helix arrangement that is very stable (i.e., theoretical dissociation constant = 10-23). During cell division, DNA is duplicated with extremely high fidelity by synthesis of a new strand of one side of the molecular ladder (Fig. 6.13).

Figure 6.13 Normal cell cycle.

Although the human genome consists of at least 32,000 genes, genes comprise only one tenth of the encoded information. Most of the genome is of unknown function, but it probably codes for the proper spacing, alignment, and punctuation of the genetic instructions. About 99.8% of the DNA sequence is identical from one person to the next. Stated another way, there are many minor differences between any two persons; on average, there is a variation of one nucleotide for every 200 to 500 base pairs. When these sequence differences occur within genes, they can lead to genetic diseases or genetic variation. Most of the minor differences have no observable effect since they occur in the noncoding regions of the genome, regions of DNA that do not contain genes. These otherwise unimportant differences have been the basis of the current explosion of genetic knowledge, because much of our ability to study genes or diagnose genetic illness exploits differences (i.e., DNA sequence polymorphisms) in these regions to track or find neighboring genes. Cellular enzymes read the DNA sequence three bases at a time, and each triplet directs the positioning of a particular amino acid within the structure of a protein (Fig. 6.12). The protein coding instructions are transmitted to the cellular machinery through messenger RNA, a transient, intermediary molecule that is similar to a single strand of DNA (Fig. 6.14). The RNA strand is transcribed from the DNA template in the nucleus and has an opposite or complementary genetic sequence. Messenger RNA moves from the nucleus into the cytoplasm, where the protein manufacturing organelles build a protein. Analysis of messenger RNA molecules is extremely useful in the laboratory for detecting genes.

Figure 6.14 Anatomy of a gene. Regulatory regions are present in the 5′ region. Introns are spliced out of the final messenger RNA.

Some heritable variations in gene regulation and the resulting phenotypes occur without any change in the DNA sequence. In fact several “epigenetic” mechanisms have been uncovered that affect transcriptional control and regulate gene expression. These include RNA-associated silencing, DNA methylation, and histone modification. DNA methylation is the best understood; it is involved in transcriptional silencing of genes, regulation of expression of imprinted genes, controlling tumor suppressor, and silencing (lyonization) of genes located on the inactive X chromosome. Several advances in molecular biology have enabled the molecular genetics revolution to take place. The first was the discovery of restriction enzymes, which are bacterial proteins that can cut DNA molecules at specific sites by recognizing the DNA sequence at those sites. Over 400 restriction enzymes have been discovered, many are commercially available, and about 25 are used commonly. Restriction fragment length polymorphisms (RFLPs) occur because of minor sequence changes (usually single base substitutions) that abolish or create a recognition site, altering the length of a digestion fragment. Restriction sites occur frequently, and several restriction sites can occur in the vicinity of any given gene. When these RFLPs are polymorphic, they become useful markers for linkage studies, diagnostic testing, and paternity testing (Fig. 6.7). RFLPs and other DNA polymorphisms provide the landmarks for genetic maps. The polymerase chain reaction (PCR) is used to exponentially amplify DNA, via enzymatic replication, without using a living organism. The basic reaction is the workhorse behind a wide array of genetic manipulations. PCR is commonly used for mutation detection, DNA sequencing, the identification of genetic fingerprints, the diagnosis of infectious diseases, paternity testing, and disease gene discovery. PCR is designed to amplify only a specific small region of a DNA strand (usually between 50 and 10,000 base pairs). One or more primers (small fragments of DNA synthesized to be complementary to the DNA regions at the 5′ and 3′ ends of the DNA region that is to be amplified) provide the specificity as to which genetic region will be amplified. DNA sequencing is the process of determining the order of the nucleotide bases of a DNA sample. Most clinical sequencing depends on the PCR reaction. Fluorescently labeled chemically modified nucleotides are included as part of the PCR reaction. Each of the four nucleotides is labeled with a separate fluorescent dye, which fluoresces at a different wavelength. The labeled nucleotides are designed to stop the PCR reaction each time they are incorporated into the complementary strand, thus when the products are separated by size (usually by capillary electrophoresis through a polymer), a multicolored “ladder” is obtained that reflects the DNA sequence of the sample being tested (Fig. 6.15). Automated DNA sequencers can test thousands of samples each day, but current methods can directly sequence only short lengths of DNA at a time (usually Table of Contents > 7 - Prenatal Diagnosis

7 Prenatal Diagnosis Lorraine Dugoff The ongoing advances in molecular genetics and discoveries in cytogenetics are increasing the potential indications for prenatal diagnosis. It is now possible to identify hundreds of genetic syndromes prenatally by using technology including florescence in situ hybridization (FISH), mutation analysis, and biochemical markers. There have been recent advances in prenatal screening for Down syndrome. The use of nuchal translucency and first-trimester maternal serum marker screening has made it possible to detect 85% of cases of Down syndrome as early as 10½ weeks gestation. This chapter will review prenatal screening for aneuploidy and neural tube defects and the invasive techniques currently available in prenatal diagnosis, including chorionic villus sampling (CVS), amniocentesis, and percutaneous umbilical blood sampling.

Screening for Chromosomal Abnormalities Down syndrome occurs in approximately 1 of 800 live births. In 95% of cases, it is a result of meiotic nondisjunction of the chromosome 21 pair, usually in the mother's gamete, resulting in a 47, +21 karyotype. The risk of a fetus with Down syndrome, as well as trisomy 13 and 18, increases with maternal age. The incidence of karyotypic abnormalities at birth including Down syndrome in relation to maternal age is shown in Table 6.8 in this book. Four percent of cases of Down syndrome result from a translocation, and approximately 1% result from mosaicism. These cases are not related to advanced maternal age. A number of maternal serum markers have proven useful in screening for Down syndrome. Historically, a maternal age at delivery of 35 years was used as a cutoff to identify women at the highest risk for having a baby with Down syndrome. Various combinations of serum biochemical markers have been used to screen for Down syndrome since 1984, when it was found that low second-trimester maternal serum α-fetoprotein (MSAFP) levels were associated with Down syndrome. In the 1990s, it was reported that elevated human chorionic gonadotropin (hCG) levels and decreased unconjugated estriol (uE3) levels were associated with Down syndrome. The combination of these three markers in combination with maternal age, the triple screen, or triple test yields a 69% detection rate for Down syndrome at a 5% positive screen rate. A fourth marker, inhibin A, which may be increased in the serum of women carrying a fetus with Down syndrome, further increases the detection rate for Down syndrome in the second trimester. When inhibin A is included in the

second-trimester screening test, known as the quadruple or quad screen, the estimated detection rate increases to 81% with a 5% false positive rate. The triple and quadruple screens should ideally be offered between 15 and 18 weeks gestation, although they can be performed between 15 and 22 weeks. It is critical to know the precise gestational age, because the median values for the biochemical markers and the risk ratios are based on gestational age. First-trimester screening for Down syndrome using fetal nuchal translucency, a measurement obtained by ultrasound, and maternal serum markers, pregnancy-associated plasma protein A (PAPP-A) and the free beta subunit of human chorionic gonadotropin (fβhCG) in conjunction with maternal age (combined screening), yields a detection rate of approximately 85% at a 5% false-positive rate. The optimal gestational age for firsttrimester screening appears to be 11 weeks, as the detection rate may be the highest (87%) at this time. First-trimester screening may be performed between 10 weeks/3 days and 13 weeks/6 days. The first-trimester combined screen may also be used to screen for trisomy 18. Nuchal translucency alone is associated with detection rates of 75% rate for trisomy 18, 72% for trisomy 13, 87% for Turner syndrome, 59% for triploidy, and 55% for other significant chromosomal abnormalities. Down syndrome screening strategies that involve a combination of first- and secondtrimester markers yield the highest detection rates. There are a variety of possible approaches to combined first- and second-trimester screening. The various Down screening tests and their detection rates are listed in Table 7.1. The integrated screen determines a Down syndrome risk assessment based on a combination of maternal age, first-trimester nuchal translucency, and PAPP-A and the second-trimester quad screen markers. The patient is provided with a single risk for Down syndrome after the quad screen has been interpreted. The integrated screen yields a 94% to 96% detection rate at a 5% positive screen rate. A potential disadvantage of the integrated screen is that the patient does not receive any information regarding Down syndrome risk until the second trimester. The serum integrated screen is similar to the integrated screen except that the patient does not have a nuchal translucency measurement in the first trimester. The serum integrated screen is an effective screening option for patients who do not have access to a center that can perform nuchal translucency measurement This yields a detection rate of 88% at a 5% positive screen rate. The stepwise sequential screen consists of the measurement of nuchal translucency, PAPPA, and fβ-hCG in the first trimester and the quad screen in the second trimester. The results are provided to the patient after each test. An advantage of the stepwise sequential screen is that Down syndrome risk assessment is provided after the firsttrimester screen, which gives the patient the option of having CVS if her initial risk is high. The stepwise sequential screen has a 95% detection rate at a 5% positive screen rate. The contingent sequential screen determines an initial Down syndrome risk based on firsttrimester nuchal translucency, PAPP-A, and fβ-hCG measurements. Women with the highest risk from first-trimester screening are offered invasive testing by CVS, and women with the lowest risks are told that second-trimester testing is not necessary. Women with intermediate risks after the first-trimester screen have their risks reassessed by integrating

their first-trimester results with second-trimester quad screen results.

TABLE 7.1 Down Syndrome Screening Tests and Detection Rates (at a 5% positive screen rate) Detection Rate (%)

Screening Test First trimester NT measurement

64–70

NT, PAPP-A, free or total β-hCG (combined screen)

82–87

Second trimester MSAFP, hCG, unconjugated estriol (triple screen)

MSAFP, hCG, unconjugated estriol, inhibin A (quad screen)

First and second trimester Integrated (NT, PAPP-A, quad screen)

94–96

Serum integrated (PAPP-A, quad screen)

85–88

Stepwise sequential First-trimester test result: Positive: CVS offered Negative: quad screen offered Final: risk assessment incorporates first and second results

Contingent sequential First-trimester test result: Positive: CVS offered Negative: no further testing Intermediate: quad screen offered Final: risk assessment incorporates first and second results

88 to 94

NT, nuchal translucency; PAPP-A, pregnancy-associated plasma protein A; β-hCG, beta human chorionic gonadotropin; MSAFP, maternal serum alpha feto protein; CVS, chorionic villus sampling. American College of Obstetricians and Gynecologists. Clinical management guidelines for obstetrician-gynecologists. Screening for chromosomal abnormalities. ACOG Practice Bulletin No. 77, January 2007, with permission. In cases of first-trimester screening where the fetal nuchal translucency is 3.5 mm or greater, patients should be offered a targeted ultrasound examination and fetal echocardiogram. In addition to the increased risk for aneuploidies, these fetuses are at increased risk for having structural abnormalities, including heart defects as well as genetic syndromes. Women with an increased nuchal translucency measurement or abnormal first-trimester serum markers may be at increased risk for adverse obstetric outcomes, including preeclampsia, preterm birth, low birth weight, spontaneous fetal loss before 24 weeks gestation, and fetal demise later in gestation. Currently, there are no data to indicate whether or not fetal surveillance in the later pregnancy will be helpful in the care of these patients. In addition to nuchal translucency, other ultrasonographic markers for Down syndrome have proven to be useful adjunctive noninvasive screening tools. Absence of the fetal nasal bone in the first trimester has been observed in fetuses with Down syndrome. The assessment of absence of the fetal nasal bone, increased resistance to flow in the ductus venosus, or the presence of tricuspid regurgitation may be used to further modify firsttrimester Down syndrome risk assessment. The American College of Obstetrics and Gynecology published an updated technical bulletin on Screening for Fetal Chromosomal Abnormalities in January, 2007. The previous bulletin had recommended that screening for aneuploidy should be offered to all women younger than 35 at their estimated date of delivery and that invasive prenatal diagnostic testing should be offered to all women who will be 35 years or older at the estimated date of their delivery and to women with risk factors for having a fetus with aneuploidy including a significant family history, a positive screening test or an abnormality noted on prenatal

ultrasound. The updated bulletin recommends that screening and invasive testing should be available to all women who present for prenatal care before 20 weeks of gestation regardless of maternal age. It is likely that new markers may be implemented in the future to improve the sensitivity and specificity of maternal serum screening. ADAM 12, a metalloprotease that binds insulin growth factor binding protein-3 (IGFBP-3), appears to be an effective early Down syndrome marker. Decreased levels of ADAM 12 may be detected in cases of trisomy 21 as early as 8 to 10 weeks gestation. Maternal serum ADAM 12 and PAPP-A levels at 8 to 9 weeks gestation in combination with maternal age yielded a 91% detection rate for Down syndrome at a 5% false-positive rate. When nuchal translucency data from approximately 12 weeks gestation was added, this increased the detection rate to 97%. Cellfree fetal DNA was first detected in the maternal circulation over a decade ago. Fetal epigenetic markers such as DNA methylation or a placental epigenetic marker called maspin can be utilized to discriminate fetal DNA from maternal DNA. The detection of fetal DNA in the maternal circulation holds great promise for prenatal diagnosis of fetal disorders and pregnancy complications. To date, cellfree DNA has been used for fetal rhesus D blood typing and fetal gender determination for carriers of X-linked recessive disease and fetuses at risk for congenital adrenal hyperplasia.

Screening for Neural Tube Defects Neural tube defects are an etiologically heterogeneous group of conditions characterized by failure of closure of the embryonic neural tube. These abnormalities of the brain and vertebral column can occur as an isolated defect or as part of a genetic syndrome. Isolated neural tube defects occur in approximately 1.4 to 2 per 1,000 pregnancies and are the second most common major congenital anomaly. They are thought to result from a combination of genetic predisposition and environmental influences. Approximately 90% to 95% of all infants with neural tube defects are born to women with no history of a child with a neural tube defect. Factors known to be associated with neural tube defects include low folic acid intake, geographic region, ethnicity, maternal valproic acid and carbamazepine exposure, high maternal core temperature, and maternal diabetes. MSAFP screening for neural tube defects was introduced in the 1980s. MSAFP evaluation is an effective screening test for neural tube defects and should be offered to all pregnant women. This type of screening is most accurate from weeks 16 to 18, as there is the widest margin between abnormal and normal distributions at this period in gestation. Although screening for neural tube defects should optimally be performed between 16 and 18 weeks gestation, it can be done between 15 and 22 weeks. In the United States, a screen-positive cutoff of 2.5 multiples of the median (MoM) is commonly used, yielding a screen-positive rate of approximately 5%. This results in the detection of more than 95% of anencephalic fetuses and 80% of fetuses with open spina bifida. It is important to adjust MSAFP values for diabetes, race, maternal weight, and multiple gestation. In insulin-dependent diabetics, the MSAFP level is approximately 60% of

nondiabetic controls, and it is inversely correlated with the hemoglobin A1C levels. Blacks have approximately 1.1 times the MSAFP level of whites, and Asians have an intermediate level between blacks and whites. The median twin MSAFP level from 16 to 20 weeks is approximately 2.5 multiples of the median for a singleton pregnancy. The detection rate for twins is approximately 80%. An inaccurate gestational age determination is the most common reason for an abnormally elevated MSAFP. The false-positive rate can be lowered by performing an ultrasound examination before MSAFP screening to verify the gestational age and diagnose multiple gestations and cases of intrauterine fetal demise, which may also be associated with elevated MSAFP levels. Table 7.2 lists conditions that may be associated with an elevated MSAFP level. Women with MSAFP levels higher than the predetermined cutoff (usually 2.0 to 2.5 MOM) and women with risk factors for carrying a fetus with a neural tube defect including a positive family history or previous affected pregnancy, diabetes, or first-trimester valproic acid or carbamzepine use should be referred for genetic counseling and consideration of a diagnostic test. All women with a positive MSAFP screen should have a specialized ultrasound to further assess the risk of neural tube defects and rule out other fetal anomalies. According to the ACOG bulletin, genetic amniocentesis is the traditional diagnostic test offered to women with an elevated MSAFP. An elevated amniotic fluid AFP in association with the presence of acetylcholinesterase in the amniotic fluid is considered diagnostic for a fetal neural tube defect. If an amniocentesis is performed secondary to an elevated MSAFP, a sample of amniotic fluid should also be sent for cytogenetic analysis, as there are several studies that have reported an association between elevated MSAFP levels and fetal aneuploidy.

TABLE 7.2 Conditions Associated with an Elevated Maternal Serum Alpha-fetoprotein Level Neural tube defects Fetal demise Multiple gestation Selective fetal reduction Ventral wall defects: Gastroschisis Omphalocele Esophageal or duodenal atresia Urinary tract disease: Renal agenesis Congenital nephrosis

Polycystic kidney disease Obstructive lesion Integumental defects: Congenital ichthyosiform erythroderma Epidemolysis bullosa Hydrops or ascites Cystic hygroma Placental abnormalities: Placental lakes Retroplacental hemorrhage Hemangiomas of placenta and cord Maternal hepatoma There are many centers in the United States that use ultrasound as a diagnostic tool in women with a high risk for neural tube defects. Studies have shown that in experienced centers, ultrasound can yield a 97% sensitivity and a 100% specificity in the diagnosis of neural tube defects. If the fetal anatomy is well visualized and no abnormalities are detected, the risks and benefits of both amniocentesis and specialized ultrasound examination can be discussed with the patient. Many high-risk patients decline to have amniocentesis performed after a reassuring specialized ultrasound examination. Alternatively, amniocentesis should be offered if ultrasound visualization of the fetus is suboptimal and in patients in whom a fetal defect is identified.

Indications for Prenatal Diagnosis The most common indications for consideration of invasive prenatal diagnostic testing include an abnormal prenatal screen conferring an increased risk for fetal aneuploidy or spina bifida, a thickened nuchal translucency >3 mm, increased risk for a genetic condition based on parental carrier status, and identification of a fetal anomaly on prenatal ultrasound. Table 7.3 lists indications for consideration of invasive prenatal diagnostic testing.

TABLE 7.3 Indications for Invasive Prenatal Diagnostic Testing Abnormal biochemical screening result Fetal anomaly diagnosed on ultrasound Thickened nuchal translucency (>3 mm) Cystic hygroma Patient request for invasive testing for fetal karyotype Parent or previous fetus/child with a chromosomal abnormality

Parents are carriers for a monogenic disorder (i.e., Tay–Sachs disease, Huntington disease, myotonic dystrophy)

Invasive Prenatal Diagnosis Procedures Amniocentesis Amniocentesis was introduced in the 1950s for fetal sex determination. The first prenatal diagnosis case of trisomy 21 was reported in 1968. Since that time, the role of amniocentesis has dramatically expanded to include the diagnosis of various cytogenetic and biochemical abnormalities, fetal infections, and a multitude of mendelian disorders. Amniocentesis is the most extensively used fetal sampling technique.

Technique for Amniocentesis Amniocentesis is typically performed at 15 to 16 weeks gestation. Prior to the amniocentesis, an ultrasound examination is performed to assess fetal viability and number, gestational age, and fetal anatomy. Next, an optimal pocket of amniotic fluid is identified, ideally avoiding the fetus, umbilical cord, and placenta. The abdomen is then prepped with an antiseptic solution. Then, using continuous ultrasound guidance, the physician introduces a 20- to 22-gauge spinal needle into the pocket of fluid (Fig. 7.1). Approximately 20 mL of fluid is aspirated. The first 1 to 2 mL of amniotic fluid is generally aspirated in a separate syringe and is discarded to minimize the chances of maternal cell contamination.

Multiple Gestation Prior to the procedure, an ultrasound examination should be performed to determine the position of the fetuses, the placenta(s), and the membrane(s) separating the sacs. Chorionicity should be determined. It is important to describe the location of the fetuses and their placentas at the time the procedure is performed, as it may be necessary to later identify a fetus with abnormal results. Although the fetuses can change their relative positions, their placentas cannot. Thus, it is valuable to trace the umbilical cords to their placentas and to describe any other ultrasound features, including phenotypic gender, that may help to identify the fetuses at a later date.

Figure 7.1 Amniocentesis.

A number of techniques involving amniocentesis in twin gestations have been described. The most common technique used to ensure that the same sac is not sampled twice involves the injection of indigo carmine into the first sac after the amniotic fluid sample has been withdrawn. When higher-order multiples are sampled, indigo carmine can be injected into each successive sac. Methylene blue should not be used, as it has been reported to cause methemoglobinemia, hemolytic anemia, and intestinal obstruction. A single needle puncture technique has been reported for twin gestations. After the first sac has been sampled, the same needle is advanced into the sac of the second twin. The first 1 to 2 mL of amniotic fluid is discarded to avoid contamination from the first twin. Another reported technique involves simultaneous visualization of two needles on each side of the separating membrane by using a curvilinear or linear transducer. Both of these techniques eliminate the need to inject dye into the amniotic cavity.

Potential Complications and Risks Fetal Loss Several large prospective trials have been undertaken to establish the safety of midtrimester amniocentesis. A multicenter study sponsored by the National Institute of Child Health and Human Development (NICHD) found no significant difference in fetal loss rates between 1,040 patients who underwent midtrimester amniocentesis (3.5%) and matched controls (3.2%). A Canadian trial also reported similar fetal loss rates in the amniocentesis group and a matched control group. A British study published in 1978 was not as reassuring as the two previous collaborative studies. The group of 2,428 women who underwent amniocentesis had a 1.0% to 1.5% increased fetal loss rate compared with the matched control group. This study has been criticized for ascertainment bias, as many of

the matched controls were not selected until a later gestation than the subjects at the time of the amniocentesis, so some potentially eligible controls may have aborted before they had the opportunity to be selected. In addition, some of the patients in the amniocentesis group had elevated MSAFP levels, which may be associated with adverse pregnancy outcomes including fetal loss. None of these studies was randomized, and all were performed in the 1970s before ultrasound guidance was routinely used. The only randomized trial addressing the safety of amniocentesis was performed in Denmark and published in 1986. In this trial, 4,606 low-risk women between 14 and 20 weeks gestation were randomized into two groups: amniocentesis under ultrasound guidance or no procedure. The total fetal loss rate was noted to be significantly higher in the amniocentesis group (1.7%) compared with the control group (0.7%) (P 10 - Assessment of Fetal Well-Being

10 Assessment of Fetal Well-Being Catherine Y. Spong In the beginning of the 19th century, reports on the presence of fetal heart tones were published, and nearly 150 years later, continuous fetal heart rate (FHR) monitoring became a reality. By 1998, electronic fetal monitoring was used in 84% of all U.S. births, regardless of whether the primary caregiver was a physician or a midwife. With the advent of these technologies, fetal monitoring is implemented in nearly all pregnancies, either in the antepartum or intrapartum period. The challenge of fetal surveillance is to identify those fetuses whose physiologic defense mechanisms are compromised in order to be able to act before decompensation has occurred. The goal is to prevent fetal and neonatal morbidity and especially mortality.

Why Perform Fetal Monitoring? Since its inception, the primary objective of FHR monitoring has been to identify the fetus in distress so that measures might be taken in time to avert permanent fetal damage or death. However, a clear consensus regarding the definition of fetal distress has not been established. It has been described as “a condition in which fetal physiology is so altered as to make death or permanent injury a probability within a relatively short period of time” and is usually considered to denote disruption of normal fetal oxygenation, ranging from mild hypoxia to profound fetal asphyxia. The term hypoxia refers to the reduction of tissue oxygen supply below physiologic levels. Asphyxia, derived from the Greek word meaning “a stopping of the pulse,” implies a combination of hypoxia and metabolic acidosis. Historically, the clinical diagnosis of birth asphyxia has been based on findings such as meconium-stained amniotic fluid, abnormal FHR patterns, low Apgar scores, abnormal blood gases, and neonatal neurologic abnormalities. When present together, these findings are highly suggestive of a recent asphyxial insult. Isolated abnormalities, however, correlate poorly with birth-related asphyxia and subsequent neurologic impairment. In 2002, the American College of Obstetricians and Gynecologists Task Force on Neonatal Encephalopathy and Cerebral Palsy stated the criteria to define an acute intrapartum event sufficient to cause cerebral palsy (CP). Essential criteria (must meet all four):

1. Evidence of a metabolic acidosis in fetal umbilical cord arterial blood obtained at

delivery (pH 12 mmol/L).

2. Early onset of severe or moderate neonatal encephalopathy in infants born at 34 or more weeks gestation.

3. CP of the spastic quadriplegic or dyskinetic type.

4. Exclusion of other identifiable etiologies such as trauma, coagulation disorders, infectious conditions, or genetic disorders. Criteria that collectively suggest an intrapartum timing (within close proximity to labor and delivery, e.g., 0–48 hours) but are nonspecific to asphyxial insults:

1. A sentinel (signal) hypoxic event occurring immediately before or during labor.

2. A sudden and sustained fetal bradycardia or the absence of FHR variability in the presence of persistent, late, or variable decelerations, usually after a hypoxic sentinel event when the pattern was previously normal.

3. Apgar scores of 0–3 beyond 5 minutes.

4. Onset of multisystem involvement within 72 hours of birth.

5. Early imaging study showing evidence of acute nonfocal cerebral abnormality. At the cellular level, asphyxia triggers a cascade of events, including membrane depolarization, disruption of energy metabolism, altered neurotransmission, ion shifts, protease activation, free radical production, and phospholipid degradation. Profound and prolonged asphyxia may result in cell death and, eventually, death of the organism. Sublethal asphyxia may lead to multiorgan system dysfunction. Severe asphyxial brain injury may lead to long-term neurodevelopmental impairment. Cerebral palsy is a major disorder of neurodevelopment, defined as “a chronic disability, characterized by aberrant control of movement and posture, appearing early in life and not the result of recognized progressive disease.” It may be accompanied by mental retardation (41%), seizures (23%), or cortical visual impairment. The insult responsible for the development of CP may occur at any time during the prenatal, perinatal, or postnatal periods. Unlike other major neurodevelopmental disorders, the relationship between CP and abnormal or difficult birth has long been recognized, publicly dating back to a treatise presented by William John Little in 1862. In 1943, Windle demonstrated clinical and histopathologic evidence of neural damage in experimentally asphyxiated fetal guinea pigs. He later reported the effects of prolonged anoxia on fetal rhesus monkeys. Total anoxia for less than 8 minutes did not produce consistent injury, whereas anoxia for more than 10 minutes invariably resulted in neuropathology. There were no survivors beyond 20 to 25 minutes of anoxia. The pattern of injury produced by prolonged anoxia, however, did not correlate with the cerebral injury, mental retardation, and spasticity seen in CP. Later work demonstrated that prolonged partial asphyxia in monkeys produced acidosis, late FHR decelerations, and neuropathologic defects consistent with the findings in the common forms of CP. In addition to lesions in the thalamus and basal ganglia, prolonged partial asphyxia caused generalized cerebral necrosis or focal necrosis in the parasagittal regions and the border zones between the parietal and occipital lobes.

Although early studies created and fostered the assumption that birth-related asphyxia was the primary cause of CP, recent evidence challenges this assumption. In 1986, Nelson and Ellenberg reported a multivariate analysis of risk in 189 cases of CP. After accounting for major congenital malformations, low birth weight, microcephaly, and alternative explanations for the disorder, they were able to attribute only 9% of CP cases to birth asphyxia. Others have reached similar conclusions. Although birth asphyxia nearly tripled the odds of developing CP, only 8.2% of CP cases were potentially attributable to birth asphyxia. As early as the 19th century, researchers using auscultation recognized that certain FHR patterns were associated with adverse perinatal outcome. The introduction of direct electronic fetal monitoring and fetal scalp blood sampling in the 1960s provided tools for evaluating the fetus. FHR decelerations have been found to be correlated with fetal acidosis. Fetuses with no decelerations, early decelerations, or mild variable decelerations had average scalp pH values greater than or equal to 7.29, whereas those with severe variable or late decelerations had pH values less than or equal to 7.15. In addition, FHR variability was found to be correlated with scalp pH values, as fetuses with normal FHR variability had higher scalp pH values than those with decreased variability. The absence of FHR accelerations was correlated with poor perinatal outcome, and the presence of FHR accelerations has been shown to predict normal scalp pH values. With the development of indirect monitoring techniques, the experience derived from direct intrapartum monitoring became applicable to the antepartum period, leading to the development of antepartum testing. Antepartum fetal monitoring has the goal of identifying the fetus at risk, allowing sufficient time to intervene before permanent injury or death occur. Intrapartum fetal monitoring should be able to identify three groups of fetuses: The fetus that is not affected by labor The fetus that is negatively affected by labor but has enough reserve to compensate fully and is in no immediate danger The fetus that is negatively affected and lacks the reserve to compensate, thus uses its key resources to survive and is in danger for morbidity/mortality. It is the third group that would most benefit from intervention.

Who Should Be Monitored? Antepartum fetal monitoring typically is offered to patients at increased risk of fetal or neonatal morbidity/mortality. These include maternal medical complications, fetal conditions, and pregnancy complications. Overall, the studies supporting the methods of testing, the timing, and initiation are extremely varied; thus, absolute guidelines based on scientific evidence cannot be established. However, recommended gestational ages for initiation of testing, timing, and methods for specific maternal conditions and the supportive evidence can be found in Table 10.1. Intrapartum fetal monitoring has remained controversial since its inception. The FHR may

be evaluated by auscultation or by electronic monitoring. Auscultation is typically performed with a DeLee stethoscope or Doppler ultrasound. Electronic monitoring can be either performed externally or internally. External monitors use a Doppler device with computerized logic to interpret and count the signals. Internal monitoring uses a fetal electrode that records the fetal electrocardiogram (ECG). Well-controlled studies have shown the equivalence of intermittent auscultation to continuous fetal heart monitoring when auscultation was performed at specific intervals with a 1:1 nurse-to-patient ratio. The intensity of monitoring is based on risk factors, with more intensive surveillance required for high-risk pregnancies.

TABLE 10.1 General Guidelines for Initiation of Antenatal Testing Indication

Decreased fetal movement

Gestational Testing Age Schedule

Reference

At diagnosis

NST

Whitty 1991

At diagnosis

MBPP

Nageotte 1994, Miller 1996

40 wk

NST twice weekly

Landon 1996, Kjos 1995

40 wk

MBPP twice weekly

Nageotte 1994

32 wk

CST/wk, midwk NST

Lagrew 1993

32 wk

NST or BPP 2×wk

Landon 1996

Diabetes

A2, B, C, D without HTN

34 wk

NST 2×/wk + AFI/wk

Kjos 1995

26 wk

CST/wk, midwk NST

Lagrew 1993

26 wk

CST/wk, midwk NST

Lagrew 1993

28 wk

NST or BPP 2×/wk

Landon 1996

At diagnosis

BPP 2x/wk

—

26 wk

NST, AFI 2x/wk

Devoe 1991

33 wk

MBPP 2×/wk

Pircon 1991, Nageotte 1994

Chronic HTN with SLE or SGA or DM or PIH

Viability

NST, AFI 2×/wk

Pircon 1991

Mild preeclampsia

At diagnosis

NST, AFI 2×/wk

Miller 1996, Nageotte 1994

Suspected

At diagnosis

NST, AFI/wk

—

Confirmed

At diagnosis

NST, AFI 2×/wk

Miller 1996, Nageotte 1994

32 wk

NST,

—

R, F

Any class with HTN, ren dz, SGA

Fetal arrthymia

Chronic HTN or nonproteinuric PIH

FGR

Multiple gestation Concordant

growth

AFI/wk

Discordant growth

At diagnosis

NST, AFI 2×/wk

Miller 1996

High order

28 wk

BPP, 2×/wk

Elliott 1995

Oligohydramnios

At diagnosis

NST, AFI 2×/wk

—

Polyhydramnios

At diagnosis

BPP/wk

Miller 1996

Postdates

41–42 wk

NST, AFI 2×/wk

Druzin 1992, Nageotte 1994, El-Damarawy 1993

Preterm labor on tocolysis

At diagnosis

NST p.r.n.

—

At diagnosis

NST/d

Lewis 1999, Harding 1991

BPP/d

Vintzileos 1994, Hanley 1996

32 wk

MBPP 2×/wk or BPP/wk or CST/wk

Weeks 1995, Nageotte 1994

34a wk

MBPP/wk

Miller 1996

26 wk

CST, BPP, or NST/wk

Adams 1992

PPROM

History of stillbirth

SLE

NST, nonstress test; MBPP, modified biophysical profile; HTN, hypertension; BPP, biophysical profile; AFI, amniotic fluid index; ren dz, renal disease; SGA, small for gestational age; PIH, pregnancy-induced hypertension; SLE, systemic lupus erythematosus; DM, diabetes mellitus; FGR, fetal growth restriction; PPROM, preterm premature rupture of membranes. aOr 1 week prior to earlier stillbirth. Adapted from Queenan JT, ed. Management of high-risk pregnancy, 4th ed. Boston: Blackwell Science, 1999.

What Can We Monitor? Fetal Heart Rate The FHR can be monitored and recorded indirectly through the use of an ultrasound transducer or directly via a subcutaneous ECG electrode placed on the fetus (Fig. 10.1). The indirect method can be used throughout pregnancy and has no contraindications. Using the indirect method, ultrasound waves originating from the transducer penetrate the tissues and are reflected by tissue interfaces. Waves reflected from the moving structures of the fetal heart return to the transducer and are translated into electrical signals. In the direct method, the subcutaneously placed ECG electrode detects electrical impulses originating in the fetal heart. Amplified signals are processed by a cardiotachometer, comparing each incoming QRS complex to the one immediately preceding it. The interval between the two complexes is used to calculate a heart rate. The process is repeated, with each cardiac cycle yielding a graphic beat-to-beat display of the FHR. The direct method requires rupture of the fetal membranes for placement of the ECG electrode. In addition, in light of the potential risk of infection, the

electrode for direct assessment only should be used when the benefits outweigh this risk.

Figure 10.1 Direct and indirect fetal monitoring. A: Direct method. Recordings are made from a fetal electrocardiograph electrode applied directly to the fetus. A transcervical intrauterine pressure catheter is used to monitor the strength of uterine contractions. B: Indirect method. The FHR is derived from a Doppler ultrasound transducer applied to the maternal abdominal wall. A pressure sensor (tocodynamometer) detects uterine contractions. (Courtesy of Richard H. Paul.)

Uterine Activity Similar to FHR, the detection and measurement of uterine activity can be performed indirectly or directly (Fig. 10.1). Indirect assessment of uterine activity is performed with a pressure transducer (tocodynamometer) applied snugly to the maternal abdomen over the uterine fundus. Uterine contractions exert pressure on the abdominal wall that is transmitted to the tocodynamometer. Changes in pressure are converted into signals and

plotted on the uterine activity graph. The indirect method is noninvasive and can be performed at any time during pregnancy. The limitations of the indirect method are that the readout can be used only to determine contraction frequency, not strength of the contraction (a tightly fit belt will record larger contractions than a loosely fitting or misplaced belt), and the ability to detect contractions in extremely obese women may be difficult. Direct assessment of uterine activity employs a thin, flexible intrauterine pressure catheter (IUPC) placed transcervically into the amniotic cavity. Intrauterine pressure is transmitted from the amniotic fluid through the fluid-filled IUPC to a pressure transducer. The transducer converts pressure measurements into electrical signals, and continuous pressure readings are displayed on the uterine activity graph. The direct assessment is invasive and requires ruptured membranes. The direct method allows the readout of both the frequency and the strength of the uterine contractions. This can be especially useful in the evaluation and assessment of patients with prolonged labor.

Fetal State (Tone/Breathing/Movements) Using real-time ultrasound, the state of the fetus can be evaluated. Typically included in this evaluation are assessments of fetal tone, movements, and breathing. Fetal voiding and swallowing also can be evaluated. Specific assessments of fetal tone, breathing, and movements are discussed later in the section Biophysical Profile.

Amniotic Fluid Volume The volume of amniotic fluid is a measure of fetal well-being. By the second trimester, the predominant source of amniotic fluid is fetal urine. The level of amniotic fluid is thought to represent “long-term” fetal well-being. A compromised fetus will preferentially shunt blood to the major organs, such as the central nervous system [CNS] and adrenals, and away from others, such as the kidney. Decreased fetal renal perfusion results in a decrease in fetal renal function and subsequent oligohydramnios. The amniotic fluid can be assessed ultrasonographically. There are a number of methods to quantitate the volume, including the amniotic fluid index (AFI), single deepest pocket, two-dimensional pocket, and a subjective assessment.

How Do We Monitor? Equipment The fetal monitor tracing is a continuous paper strip composed of two cartesian graphs. The FHR tracing is displayed on the upper graph, with time on the x-axis and heart rate on the y-axis (range 30 to 240 beats per minute). Uterine activity is displayed on the lower graph, with time on the x-axis and pressure on the y-axis (range 0 to 100 mm Hg). Heart rate and uterine activity are plotted separately on the heat-sensitive paper by two thermal pens. On both grids, fine vertical lines represent 10-second intervals, and heavy lines denote 1-minute intervals. In the United States, the standard paper speed is 3 cm per minute.

Interpretation of the Fetal Monitor Tracing Analysis of the fetal monitor strip requires a systematic approach. First, the FHR is analyzed with respect to (a) the baseline, (b) variability, and (c) periodic patterns, including FHR accelerations and decelerations (Table 10.2). Uterine activity is evaluated with attention to the frequency, duration, and strength of contractions as well as the baseline uterine tone between contractions.

TABLE 10.2 Fetal Monitor Interpretation Uterine activity assessment Contraction frequency Contraction duration Baseline uterine tone Contraction strength FHR assessment Baseline rate Tachycardia Bradycardia Sinusoidal pattern Variability Increased variability Average or normal variability Decreased variability Absent variability Periodic patterns Accelerations Decelerations Early decelerations Variable decelerations Late decelerations

Fetal Heart Rate Interpretation Baseline Fetal Heart Rate The normal FHR baseline ranges from 120 to 160 beats per minute. Early in pregnancy, it is closer to 160 beats per minute, declining as gestational age advances. Likewise, the FHR may decrease gradually toward 120 beats per minute during the course of labor. An FHR

baseline below 120 beats per minute is termed bradycardia, and a rate in excess of 160 beats per minute is termed tachycardia. Abnormalities in the FHR baseline may have very different causes and consequences. It is important, therefore, to characterize the underlying etiology as accurately as possible and to institute appropriate therapy at the earliest possible time.

Bradycardia Bradycardia is defined as an abnormally low baseline FHR (110 mm Hg) or mild hypertension with evidence of organ involvement. Patients with low-risk chronic hypertension who do not develop superimposed preeclampsia have pregnancy outcomes similar to those of the general population. Studies have shown that antihypertensive treatment in this group does not affect perinatal outcome and is not necessary, provided they remain in the mild hypertension range by blood pressure criteria. Antihypertensive use may be discontinued at the first prenatal visit in any patient with mild hypertension. These patients should be observed closely throughout gestation, because they may become high risk at any time. Pharmacologic agents should be reinstituted if the SBP reaches 160 mm Hg, DBP reaches 105 mm Hg, or target organ damage develops. Prenatal care should include 24-hour urine collection for total protein determination in the first trimester and at least monthly visits in the first and second trimester. Visits should be every 1 to 2 weeks after 32 weeks, looking carefully for the development of superimposed preeclampsia. Fetal surveillance should include interval ultrasonography for fetal growth and amniotic fluid assessment every 4 weeks beginning at 32 weeks, unless there is suspicion of poor fetal growth, and then testing should be started earlier. Weekly fetal heart rate testing with nonstress tests should begin at 34 weeks. Fetal well-being assessment should be increased to twice weekly with evidence of growth restriction or oligohydramnios. The patient also should be instructed on fetal movement counts. Timing of delivery should be determined on an individual basis. Patients in the lowrisk group may continue their pregnancies up to 41 weeks, provided that blood pressure remains controlled and no evidence of superimposed preeclampsia or fetal growth restriction develops. Central to the management of the high-risk chronic hypertensive pregnancy is the use of antihypertensive pharmacotherapy. The choice of agent is dependent on its pharmacologic actions and will be covered in the next section. Prenatal care of the high-risk patient

includes a first-trimester 24-hour urine collection for total protein level. The frequency of visits in the first and second trimesters should be every 2 to 3 weeks, then weekly in the third trimester if clinically indicated. Fetal surveillance should include ultrasonography for estimated fetal weight and amniotic fluid volume every 4 weeks starting at 26 weeks. Weekly nonstress testing or biophysical profile assessments should begin at 28 weeks. The frequency of prenatal care visits and fetal testing may need to be increased dependent on clinical findings such as increasing hypertension, superimposed preeclampsia, decreased amniotic fluid volume, or fetal growth restriction. If superimposed preeclampsia is suspected or uncontrolled hypertension develops, the patient should be hospitalized, preferably at a tertiary care center. The timing of delivery is dependent on the development of confounding complications and gestational age. In general, pregnancies in patients with high-risk chronic hypertension should not be continued past 40 weeks.

Antihypertensive Agents Many agents are available for the control of hypertension. It is important to be familiar with the maternal and fetal side effects, as well as mode of action, in order to choose the most effective agent for the patient. Antihypertensive agents exert their activity through the following five methods: they decrease cardiac output, decrease peripheral vascular resistance, decrease blood pressure centrally, diurese, and inhibit angiotensin production. Commonly used drugs in pregnancy are listed in Table 16.25. For the postpartum patient who is breast-feeding, little information is known about most drugs regarding excretion in breast milk and neonatal effects. In general, ACE inhibitors are discouraged secondary to potential renal effects on the neonate.

Centrally Acting Drugs Methyldopa Methyldopa is the most commonly used antihypertensive in pregnancy. Its mode of action is by central inhibition of the sympathetic drive. The safety and efficacy of methyldopa is well established. Studies have documented no known congenital malformations or adverse long-term follow-up of children exposed in utero. Maternal side effects include tiredness, dry mouth, and somnolence. In addition, about 5% to 10% may have elevated liver enzyme values. Methyldopa is the agent of choice for long-term, nonemergent oral therapy.

Clonidine Clonidine is not commonly used, and there is limited data regarding the safety and efficacy of its use. Limited studies regarding congenital defects associated with the use of clonidine reveal no increased risk.

TABLE 16.25 Antihypertensive Drugs Commonly Used in Pregnancy Medication

Dosage

Maximum

Halflife

Methyldopa

250–500 mg p.o. q6– 12h

4 g/24 h

2 h

Labetalol

100 mg p.o. b.i.d.

2,400 mg/24 h

5–8 h

Thiazide diuretic

12.5 mg p.o. b.i.d.

50 mg/24 h

3 h

Nifedipine

10–20 mg p.o. q4–6h

240 mg/24 h

2 h

β-Blockers The main mode of action of β-adrenergic blockade is through the reduction in cardiac output. The drugs in this group are a heterogeneous mixture exerting their effects dependent on receptor selectivity, lipid solubility, and intrinsic sympathomimetic activity. Fetal effects of β-blockers may include growth restriction and neonatal hypoglycemia. Atenolol given in the first trimester, in particular, has been linked to intrauterine growth restriction. Labetalol is a nonselective β-blocker and a postsynaptic β-1 blocker. It has lower β-blocking effect than other β-blockers, which does not reduce cardiac output. Thus, it is probably less responsible for fetal growth restriction. The side effects are tremors, headache, and scalp tingling. The use of labetalol should be avoided in patients with asthma and acute congestive heart failure.

Calcium Channel Blockers Calcium channel blockers act by inhibiting extracellular calcium influx into cells through slow calcium channels. This, then, reduces peripheral vascular resistance. Studies have found no increase in congenital malformations associated with the long-term use of calcium channel blockers. However, adverse maternal and fetal outcomes have been associated with sublingual use of nifedipine, including maternal myocardial infarction and profound hypotension. Maternal side effects are flushing, headache, and palpitations.

Vasodilators

Hydralazine Hydralazine works through direct and potent vasodilatation. It may be used orally but is most effective as an intravenous agent to control hypertensive crisis. No congenital defects have been associated with hydralazine. It may cause hypotension in hypovolemic patients, so giving intravenous fluids may be warranted. Side effects include fluid retention, tachycardia, palpitations, headache, lupuslike syndrome, and neonatal thrombocytopenia.

Diuretics Diuretics, in general, are not contraindicated in pregnancy. There is no increased risk of congenital defects with their use, but their efficacy is uncertain. It is recommended that women receiving diuretics prior to pregnancy be continued on them throughout pregnancy. However, diuretics should be discontinued in patients with preeclampsia or oligohydramnios or if there is evidence of reduction in uteroplacental flow.

Thiazide The thiazide diuretics have minimal effect on lowering blood pressure in pregnancy and are rarely used. Limited studies show no increased congenital anomalies with the use of thiazide. The side effect profile includes maternal and fetal hyponatremia and acute pancreatitis, rise in blood uric acid levels, and neonatal thrombocytopenia. It also can precipitate hyperglycemia and glycosuria in the diabetic patient.

Furosemide Furosemide is rarely used as a sole pharmacologic agent but is useful in conjunction with other antihypertensives. Studies showed no increase in congenital anomalies with use in the second and third trimesters, but first-trimester use may be associated with hypospadias. Furosemide use in pregnancy should be limited to postpartum management of fluid overload and pulmonary edema in the preeclamptic patient.

Angiotensin-Converting Enzyme Inhibitors ACE inhibitors act by inhibiting the production of angiotensin II and by reducing peripheral vascular resistance. The use of ACE inhibitors has been associated with an increased risk of intrauterine demise, renal dysgenesis, oligohydramnios, pulmonary hypoplasia, fetal growth restriction, and neonatal renal dysfunction. The mechanism of action is thought to be due to continuous inhibition of the renin-angiotensin system, leading to the development of tubular dysfunction. Therefore, ACE inhibitors are contraindicated in pregnancy, mainly during the second and third trimesters. However, ACE inhibitors may be an excellent choice for hypertensive control in the postpartum period.

Contraception

Women with hypertensive diseases in pregnancy, whether preeclampsia or chronic hypertension, will seek advice regarding contraceptive methods postpartum. It is important to be familiar with options available to patients and to be able to discuss potential risk factors. No contraindications exist with the use of barrier methods with regard to hypertension. The user failure rate, however, may be significant if failure results in a pregnancy with increased morbidity due to hypertensive disease. There are no contraindications for hypertensive patients desiring to use an intrauterine device. It is important to be aware of any associated underlying medical problems or therapies that the patient may have that would prohibit the use of an intrauterine device. Natural family planning continues to be an acceptable form of contraception when used appropriately. The greatest concern in finding appropriate contraception for the hypertensive patient is with regard to hormonal contraception. Oral contraceptive pills are the most widely used reversible form of birth control in the United States. Combination oral contraceptives are known to elevate blood pressure minimally, increase clotting factors, and increase total cholesterol levels. Once again, it is extremely important to be familiar with any coexisting disease in a hypertensive patient. Hypertension may have associated underlying antiphospholipid syndrome, for example, which would be a contraindication to combination oral contraceptives, given the increased risk for thromboembolic phenomena. Progestinonly contraceptive methods may be a suitable alternative for women with underlying hypercoagulability because they do not interfere with coagulation. Overall, the contraceptive choices given to hypertensive patients are basically the same as in normotensive patients. The risks and benefits of contraception must be weighed and patients counseled accordingly. Avoiding the morbidity associated with pregnancy in some patients may be a benefit that outweighs the risk of contraceptive use.

Summary Points Making an appropriate diagnosis is essential in caring for women with hypertensive disease in pregnancy. There is no known etiology, prevention, or screening method for preeclampsia. The use of MgSO4 is warranted in patients with preeclampsia and eclampsia to prevent seizures. In patients with mild preeclampsia, the need for MgSO4 may be individualized. Fetal outcome in patients with preeclampsia is based largely on gestational age at delivery; as such, prolonging pregnancies in patients with preeclampsia should be done with close maternal and fetal observation. Blood pressure >170 mm Hg systolic and >110 mm Hg diastolic requires intervention. Any patient with symptoms of HELLP syndrome should have laboratory evaluation performed, regardless of blood pressure

measurements. Evaluation of a patient with chronic hypertension should include monitoring for target organ damage. Management of these patients is dependent on the degree of hypertension. Any patient with chronic hypertension is at increased risk of developing superimposed preeclampsia.

Suggested Readings Abramovici D, Friedman SA, Mercer BM, et al. Neonatal outcome in severe preeclampsia at 24 to 36 weeks' gestation: does the HELLP (hemolysis, elevated liver enzymes, and low platelet count) syndrome matter?. Am J Obstet Gynecol 1999;180:221– 225. American College of Obstetricians and Gynecologists. Chronic hypertension in pregnancy. ACOG Practice Bulletin No. 29. Obstet Gynecol 2001;98:177–185. American College of Obstetricians and Gynecologists. Diagnosis and management of preeclampsia and eclampsia. ACOG Practice Bulletin No. 33. Obstet Gynecol 2002;99:159– 167. Audibert F, Friedman SA, Frangieh AY, et al. Clinical utility of strict diagnostic criteria for the HELLP (hemolysis, elevated liver enzymes, and low platelets) syndrome. Am J Obstet Gynecol 1996;175:460–464. Barton JR, Bergauer NK, Jacques DL, et al. Does advanced maternal age effect pregnancy outcome in women with mild hypertension remote from term?. Am J Obstet Gynecol 1997;176:1236–1243. Barton JR, O'Brien JM, Bergauer NK, et al. Mild gestational hypertension remote from term: progression and outcome. Am J Obstet Gynecol 2001;184:979–983. Briggs R, Chari RS, Mercer B, et al. Postoperative incision complications after cesarean section in patients with antepartum syndrome of hemolysis, elevated liver enzymes, and low platelets (HELLP): does delayed primary closure make a difference?. Am J Obstet Gynecol 1996;175:893–896. Caritis, S, Sibai B, Hauth J, et al., and the National Institute of Child Health and Human Development Network of Maternal-Fetal Medicine Units. Predictors of pre-eclampsia in women at high-risk. Am J Obstet Gynecol 1998;179:946–951.

Chappell LC, Seed PT, Briley AL, et al. Effect of antioxidants on the occurrence of preeclampsia in women at increased risk: a randomised trial. Lancet 1999;354:810–816. Dekker GA, Sibai BM. Etiology and pathogenesis of preeclampsia: current concepts. Am J Obstet Gynecol 1998;179:1359–1375. Duley L, Galmezoglu AM, Henderson-Smart DJ. Magnesium sulfate and other anticonvulsants for women with preeclampsia. Cochrane Database Syst Rev 2003;issue 2. Levine RJ, Ewell MG, Hauth JC, et al. Should the definition of preeclampsia include a rise in diastolic blood pressure =15 mm Hg to a level 300 mg daily) are needed long term to control maternal hyperthyroidism. Medical thyroid ablation with 131I should not be considered during pregnancy because of the possibility of simultaneous fetal thyroid ablation. Antenatal treatment with 131I at the usual dosage results in 0.75 to 1.50 rad (0.0075 to 0.0150 Gy) of fetal radiation exposure. Patients with inadvertent first-trimester exposure can be reassured that the fetal thyroid gland does not begin concentrating iodine until 10 to 12 weeks gestation, and maternal thyroid ablation before this time would not be expected to affect the fetus. Exposure after 12 weeks gestation, however, may result in congenital hypothyroidism. Theoretically, 10

days of maternal PTU administration after accidental exposure may benefit the fetus by decreasing uptake of 131I iodine into the fetal thyroid gland.

TABLE 17.8 Treatment of Thyroid Storm Propylthiouracil: 600 mg p.o. (n.g.), then 300 mg q6h Sodium iodide: 1 g/500 empc i.v. q.d. Propranolol: 40–60 mg p.o. q4–6h Dexamethasone: 1 mg p.o. i.m. q6h Oxygen, acetaminophen, fluid replacement n.g., nasogastric tube administration. Adequate treatment of hyperthyroidism is important to decrease the risk of preeclampsia and preterm delivery as well as that of fetal demise, growth restriction, and fetal or neonatal thyroid dysfunction. The patient with a very serious complication of Graves disease, thyroid storm or crisis, can experience tachycardia, hyperpyrexia, circulatory collapse, and death. Thyroid storm involves a massive release of thyroid hormones and often is precipitated by a stressor, such as infection (e.g., pyelonephritis), thyroid gland palpation, or labor and delivery. Thyroid storm is an emergency and must be treated aggressively to prevent maternal decompensation (Table 17.8). Treatment may require the administration of multiple agents for up to 1 to 2 weeks. PTU should be given in large doses: 600 mg orally initially followed by 300 mg orally every 6 hours. The thioamides can be administered through a nasogastric tube if the patient cannot tolerate oral medications. In addition, sodium iodide, 1 g in 500 mL of fluid, should be given daily to inhibit the release of stored hormone. Propranolol may be added for control of tachycardia and other sympatheticlike symptoms if there is no evidence of cardiac failure. The initial propranolol dosage is 40 to 80 mg orally every 4 to 6 hours or 1 mg per minute intravenously for 2 to 10 minutes with concurrent maternal cardiac monitoring. The dosage may be adjusted, depending on the patient's cardiac response. Dexamethasone, 1 mg orally or intramuscularly every 6 hours, or hydrocortisone, 100 mg intravenously every 8 hours, can further inhibit peripheral T4 to T3 conversion. Oxygen, digitalis, fluid replacement, and acetaminophen (as an antipyretic) should be given as needed.

Thyroid Nodules and Cancer Evaluation of thyroid nodules discovered during pregnancy should begin with a complete physical exam, evaluation of thyroid function tests, and ultrasonography to document the nodule's presence and size. This is followed by a fine-needle aspiration, and if elected, surgical removal, preferably in the mid second trimester. Thyroid cancer is suspected if there is rapid growth unaccompanied by tenderness or hoarseness. Thyroid function test

results usually are normal. Thyroid cancer is more likely in a population irradiated in childhood; in this group, 30% of those with a thyroid nodule will have thyroid cancer at the time of surgery. In the pregnant patient, papillary cancer predominates and is no more aggressive than in the nonpregnant patient. Importantly, a delay in surgery does not alter outcome. In the presence of either a hyperfunctioning benign nodule or documented papillary carcinoma, thyroid function typically is suppressed with levothyroxine until definitively treated. In the presence of a more malignant cell type, such as medullary or undifferentiated carcinoma or lymphoma, some practitioners recommend pregnancy termination to pursue aggressive management with surgery, adjuvant radiation, and chemotherapy. There is no evidence that pregnancy affects the progression of thyroid cancer or that thyroid cancer affects the outcome of pregnancy. As a result, thyroid cancer or a history of it is not an absolute contraindication to pregnancy. Although pregnancy is not a contraindication to thyroid surgery, it is a contraindication to 131I treatment.

Fetal Thyroid Function The fetal thyroid gland is first gland that is capable of hormonal activity by the end of the first trimester, and there is normally a gradual increase in fetal T4 concentrations during pregnancy. This increase represents fetal production rather than transplacental transfer, because both T3 and T4 cross the placenta only minimally. However, iodides, antithyroid medications, and TSIs cross the placenta easily. Thyroid hormone deficiency during fetal development or during the first 2 years of life can cause irreversible brain damage, with the degree of disease related to the severity, duration, and gestational age at which the hypothyroidism occurs. Although neonatal hypothyroidism is not common (1 in 4,000 live births in the United States), it is a potentially treatable cause of mental retardation and thus is now included in newborn blood screening programs. Fetal hypothyroidism can be treated antenatally by direct hormone injection of the fetus via amniocentesis. Fetal hyperthyroidism also can be diagnosed before birth and may respond to prenatal treatment. Fetal or neonatal thyrotoxicosis occurs in 1 of 70 thyrotoxic mothers. It results from the transplacental transfer of TSIs and is a potentially serious disease, with mortality rates of 10% to 16% due to prematurity and congestive heart failure. Hyperthyroid pregnant patients should be evaluated frequently for fetal tachycardia, and appropriate interval fetal growth should be confirmed. Fetal goiter may be identified on ultrasonographic examination, and fetal thyroid function can be assessed with fetal blood sampling. Because PTU and methimazole cross the placenta, maternal dosage can be adjusted to correct the fetal hyperthyroidism; replacement T4 can then be given to the mother if necessary. The diagnosis of neonatal thyrotoxicosis usually is clinically apparent, as the infant may have a goiter, exophthalmos, tachycardia, irritability, and growth restriction. The mother likely has a history of hyperthyroidism and may have had previous infants affected by this

disease. Mild cases of neonatal thyrotoxicosis require no treatment; the symptoms resolve as maternal TSIs are cleared from the infant's system. Severely symptomatic babies are treated with propranolol and PTU.

Parathyroid Conditions The parathyroid glands function to maintain maternal calcium and phosphate homeostasis. Total calcium levels decline during pregnancy because the binding protein albumin declines, but the level of ionized, biologically active calcium is unchanged. The fetus contains approximately 30 mg of calcium, which is transported actively across the placenta. Maternal calcium requirements increase from 0.5 mg per day to 1.5 mg per day at term. Serum parathyroid hormone (PTH) levels gradually increase during pregnancy, reflecting the increased calcium transfer to the fetus plus the increases in extracellular fluid volume and glomerular filtration rate.

Hyperparathyroidism Hyperparathyroidism is a condition caused by excessive PTH production, often due to a clinically inapparent parathyroid adenoma. Hypercalcemia results and causes symptoms of fatigue, weakness, polyuria, polydipsia, nausea, anorexia, and constipation. During pregnancy, affected women may have prolonged nausea and vomiting. Increased renal excretion of calcium may predispose to nephrocalcinosis, renal calculi, and symptomatic bony resorption. Although serum calcium measurements remain the best single diagnostic test, the physiologic changes of pregnancy may make the diagnosis of hyperparathyroidism difficult. A total calcium concentration of 10.5 mg/dL or greater in late pregnancy must be considered suspicious, and a total calcium concentration of 12.0 mg/dL or greater is definite evidence of hyperparathyroidism. Palpable parathyroid adenomas are extremely uncommon. Hyperparathyroidism is associated with an increased incidence of perinatal morbidity and mortality; therapy is recommended. Up to 50% of infants of untreated mothers will develop hypocalcemia and tetany, which may be the first indicator of maternal disease. If the diagnosis is first established during pregnancy, surgical resection of the adenoma generally is indicated, although oral phosphate therapy (1.0 to 1.5 g daily in divided doses) may occasionally be attempted. Pregnancy termination need not be considered except in the rare case of advanced renal involvement.

Hypoparathyroidism Hypoparathyroidism results from inadequate production of PTH and is characterized by weakness, fatigue, mental status changes, numbness and paresthesias of the extremities, muscle cramps, and tetany. It must be distinguished from pseudohypoparathyroidism, in which parathyroid function is normal but end organs do not respond to PTH. The signs and symptoms of hypoparathyroidism are the result of a decreased serum ionized calcium level and increased neuromuscular irritability. It occurs most commonly as the result of parathyroid gland injury or removal

in association with thyroid surgery or irradiation, but it can be idiopathic. The increased calcium requirements of pregnancy may make patients with hypoparathyroidism more symptomatic. In addition, relative unavailability of calcium for the fetus may lead to secondary neonatal hyperparathyroidism. Symptomatic hypocalcemia can be prevented with calcitriol (1,25-dihydroxyvitamin D3), dihydrotachysterol, large doses of vitamin D, and calcium gluconate or lactate. The patient should be on a low-phosphate diet and consultation with an endocrinologist and a dietitian is warranted.

Adrenal Disease In normal pregnancy, plasma concentrations of adrenal steroid hormones typically increase with advancing gestation. Because the amount of cortisol bound to nuclear receptors actually is decreased slightly (due to competition by progesterone), both total plasma cortisol and cortisol-binding globulin levels increase. Free cortisol levels are increased, and a diurnal variation is maintained. Aldosterone levels also rise, although the factor or factors responsible remain unclear; no consistent correlations exist with observed elevations in angiotensin II or progesterone. Adrenal function tests are unaltered. As with other endocrine disorders, abnormalities in adrenal function usually are associated with infertility. However, adrenal insufficiency and hyperfunction can complicate pregnancy.

Adrenal Insufficiency Inadequate production of adrenal corticosteroids can be either chronic or acute. Although most cases of adrenal insufficiency are diagnosed outside of pregnancy, the disease may first occur during pregnancy and present a diagnostic challenge. The chronic form may become apparent with numerous nonspecific signs and symptoms, whereas the acute form may manifest as vascular collapse. The signs and symptoms of chronic adrenocortical insufficiency during pregnancy are identical to those in the nonpregnant state and include fatigue, hyperpigmentation, weakness, anorexia, nausea, vomiting, and weight loss. Because all of these problems may be encountered during the course of an otherwise normal gestation, the clinical diagnosis of adrenocortical insufficiency in pregnancy may be difficult. However, persistent weight loss or nausea and vomiting beyond the first trimester, particularly in association with any of the aforementioned signs or symptoms, should raise suspicions. The diagnosis and appropriate treatment of adrenocortical insufficiency during pregnancy are important because of the risks associated with the added stress of pregnancy and delivery and because of the increased likelihood of adrenal crisis, particularly during the puerperium. Adrenal insufficiency can be primary (Addison disease), due to autoimmune adrenal destruction or TB, or secondary, due most often to exogenous glucocorticoid intake (Table 17.9). When Addison disease is suspected, a blood sample for plasma cortisol and ACTH levels should be obtained. A cortisol level 7,500 U every 8 to 12 hours, adjusted to maintain the midinterval heparin levelsb in the therapeutic range Low-molecular-weight heparin: (1) Weight-adjusted (e.g., enoxaparin 1 mg/kg every 12 hours or dalteparin 200 U/kg every 12 hours) a

See text for postpartum thromboprophylaxis recommendations. bHeparin levels denotes anti-factor Xa levels. Women without a lupus anticoagulant in whom the activated partial thromboplastin time is normal can be followed by using the activated partial thromboplastin time. Modified from Branch DW, Khamashta MA. Antiphospholipid syndrome. In: Queenan J, ed. High-risk pregnancy. Washington, DC: American College of Obstetricians and Gynecologists, 2008. Healthy women with recurrent embryonic and preembryonic loss who have low or negative aPL titers do not require anticoagulation. Women with APS should be counseled about the potential risks of heparin therapy during pregnancy, including heparin-induced osteoporosis (1% to 2%) and heparin-induced thrombocytopenia (HIT). Women who are treated with heparin should be encouraged to take daily supplemental calcium at a dose of 1,500 to 2,000 mg per day and vitamin D (e.g., prenatal vitamins) and perform daily axial skeleton weight-bearing exercise (e.g., walking). Alhough uncommon, HIT potentially is very serious. Most cases have their onset 3 to 15 days after heparin initiation and are relatively mild in nature. A more severe form of HIT

paradoxically involves venous and arterial thromboses resulting in limb ischemia, cerebrovascular accidents, and myocardial infarctions as well as venous thromboses. The authors obtain platelet counts every several days for the first 2 weeks of heparin treatment and discontinue heparin if the platelet count falls to subnormal or by 50% from baseline.

Catastrophic Antiphospholipid Syndrome Catastrophic APS is a rare but devastating syndrome characterized by multiple simultaneous vascular occlusions throughout the body, often resulting in death. The diagnosis should be suspected if at least three organ systems are affected and confirmed if there is histopathologic evidence of acute thrombotic microangiopathy affecting small vessels. Renal involvement occurs in nearly three fourths of patients. Most patients have hypertension, and 25% eventually require dialysis. Other common manifestations include adult respiratory distress syndrome (65%), cerebral microthrombi and microinfarctions (55%), myocardial microthrombi (50%), dermatologic abnormalities (50%), and disseminated intravascular coagulation (25%). Death from multiorgan failure occurs in 50% of patients. The pathophysiology of catastrophic APS is poorly understood. However, the onset may be presaged by several factors, including infection, trauma, surgical procedures, discontinuation of anticoagulant therapy, and the use of drugs such as oral contraceptives. The condition has been reported in a modest number of pregnant women, with about half of reported cases during pregnancy and about half in the postpartum period. Severe preeclampsia may be a trigger for catastrophic APS. Early and aggressive treatment of catastrophic APS is necessary to avoid death. Patients should be transferred to an intensive care unit where supportive care can be provided. Hypertension should be treated aggressively with appropriate antihypertensive medication. While no one treatment has been shown to be superior to another, a combination of anticoagulants (usually heparin) and high-dose steroids plus either plasmapheresis or IVIG has been successful in some patients. Streptokinase and urokinase also have been used to treat acute vascular thrombosis. Women suspected of catastrophic APS during pregnancy probably should be delivered.

Rheumatoid Arthritis RA is a chronic inflammatory process that primarily involves synovial-lined joints, resulting in swelling and pain. Established criteria are used to make the diagnosis of classic, definite, and probable or possible RA and include morning stiffness, pain and tenderness in at least one joint, swelling of at least one joint, swelling of at least one other joint, symmetric joint swelling, subcutaneous nodules, x-ray changes typical of RA, a positive test result for rheumatoid factor, and other features. Though many cases are mild and may be treated with NSAIDs, the disease may be characterized by intermittent exacerbations with ultimate progression over many years to typical joint deformities. Pregnancy is associated with clinical improvement in at least 50% of patients, a phenomenon that may be related to elevated blood levels of free cortisol or to enhanced phagocytosis of immune complexes. Rheumatoid factor (IgM antibodies against autologous IgG) do not cross the placenta, and there is no fetal or neonatal involvement.

Management of RA during pregnancy should include an appropriate balance of medication, rest and exercise, heat, and physical therapy. Obviously, methotrexate, now widely used in the treatment of RA, must be discontinued prior to pregnancy. Inhibitors of tumor necrosis factor-α also are efficacious for the treatment of RA. Although experience with these drugs during pregnancy is limited, preliminary evidence is that they are not teratogenic; they are Food and Drug Administration (FDA) pregnancy category B agents. The basic reliance on large doses of salicylates, NSAIDs, and analgesics must be modified during pregnancy. Lowdose steroids (e.g., prednisone 5 mg per day) and low-dose aspirin are recommended. Though gold compounds cross the placenta, no fetal adverse effects or teratogenicity have been reported. Gold therapy can be continued in selected pregnant patients with RA who are unresponsive to glucocorticoids. Other NSAIDs and penicillamine are not recommended because of potential detrimental fetal effects. As in SLE, antimalarials (hydroxychloroquine) appear to be another safe option during pregnancy. Specialized antenatal surveillance is unnecessary for women with RA. Serial ultrasounds and antenatal surveillance should be reserved for the usual obstetric indications. Joint deformities rarely preclude vaginal delivery, but mechanical obstacles may occur in women with hip deformities. Cesarean delivery usually can be reserved for standard obstetric indications. The type of anesthesia (regional vs. general) chosen depends on the presence of skeletal deformities or special problems such as atlantoaxial subluxation.

Other Rheumatic (Collagen Vascular) Diseases Most disorders of undetermined origin, which are characterized by inflammation of various tissues, have been termed systemic rheumatic or collagen vascular diseases. More recently, many have been classified as autoimmune disorders because of their association with the production of autoantibodies and other immunologic aberrations. This group includes mixed connective tissue disorder, Sjögren syndrome, polyarteritis nodosa, dermatomyositis, and scleroderma. The risk of serious maternal and perinatal complications, including death, is concerningly elevated in patients with polyarteritis nodosa and scleroderma complicated by renal disease or cardiopulmonary disease. Scleroderma worsens in at least 10% of women during pregnancy. At least 5% have life-threatening complications, usually related to renal or cardiopulmonary disease.

Myasthenia Gravis Myasthenia gravis (MG) is a chronic neuromuscular autoimmune disease characterized by fatigue and weakness, usually involving the extraocular, facial, pharyngeal, and respiratory muscles. It is worsened by exertion and relieved by rest and anticholinesterase drugs. Antibodies to human acetylcholine receptors (AChR) are detectable in up to 90% of patients with MG. The anti-AChR antibodies are involved in complement-dependent destruction of the postsynaptic membrane of the myoneural junction, resulting in decreased nerve impulse transmission. Thymoma, thymic hyperplasia, and other autoimmune diseases often accompany MG. The functional abnormalities associated with the disease are similar to

those induced by curare. The course during pregnancy is variable, although there may be a tendency for relapse during the puerperium. The cholinesterase inhibitors and their equivalent doses most commonly used to alleviate symptoms are 0.5 mg of intravenous neostigmine, 1.5 mg of subcutaneous neostigmine, 15 mg of oral neostigmine, 60 mg of oral pyridostigmine, and 5 mg of oral ambenonium. Drugs are adjusted to the dose at which the patient's muscle strength is optimal with a minimum of cholinergic adverse effects. Oral pyridostigmine, or a sustained-release preparation of pyridostigmine, is the most commonly used medication for MG. Overmedication results in unpleasant effects such as abdominal cramps, flatulence, diarrhea, nausea, vomiting, and excessive secretion of saliva and tears. Toxic levels of pyridostigmine lead to a myasthenic crisislike syndrome involving profound muscle weakness and eventually respiratory failure. Treatment with high-dose glucocorticosteroids also has been used successfully in some patients. Regular rest periods with limited physical activity should be prescribed for the pregnant patient with MG. Infections should be treated aggressively because of their propensity to exacerbate MG. Careful plans should be made for drug therapy during pregnancy, labor, delivery, and the postpartum period. Some antibiotics, such as the aminoglycosides, may produce a myasthenic crisis and should be avoided. Other medications also may be harmful in women with MG (Table 18.10). Many patients with MG are sensitive to sedatives, analgesics, tranquilizers, and narcotics. Muscle relaxants should be avoided. Local or regional anesthetics are preferable. Magnesium sulfate is contraindicated because the drug diminishes the acetylcholine effect and has been known to induce a myasthenic crisis.

TABLE 18.10 Medications That May Exacerbate or Cause Muscle Weakness in Patients with Myasthenia Gravis Aminoglycosides Barbiturates Cholistin Ether Halothane Lincomycin Lithium salts Magnesum salts Penicillamine Polymyxin B Procainamide Propranolol Quinine Tetracycline Trichlorethylene

Labor typically progresses normally because smooth muscle is unaffected. Cesarean delivery should be reserved for obstetric reasons. Assisted ventilation should be available in the event of respiratory difficulty. During labor, the patient's oral dose of anticholinesterase should be discontinued and replaced with an intramuscular equivalent. Approximately 12% to 20% of infants born to women with MG exhibit neonatal MG, which lasts from a few hours to several days. The manifestations are caused by the transplacental transfer of acetylcholine-blocking factor. The classic features of neonatal MG differ from those seen in adults. The symptoms usually do not develop until day 1 or 2 of life, probably because of some protection to the infant from the maternal blood levels of anticholinesterase agents. A high index of suspicion is necessary to recognize this phenomenon, because an infant who appears healthy at birth may later develop respiratory failure with asphyxia. The involved infant shows generalized muscle weakness and hypotonic limbs and is limp and motionless. The Moro reflex often is weak or absent, and there may be a feeble cry, inability to suck, and associated difficulty in swallowing and breathing. Arthrogryposis (i.e., joint contractures), which may develop as a result of reduced intrauterine movement, has been reported in several infants born to mothers with MG.

Summary Points Rh immune globulin should be given to Rh D–negative, unsensitized women at 28 weeks gestation, within 72 hours after delivery, and in the event of antenatal procedures and complications associated with fetomaternal hemorrhage. Rh D alloimmunized women with anti-D titers 1:16 or greater should be referred for assessment of possible fetal anemia. MCA Doppler peak systolic velocity measurements are used to evaluate fetuses at risk for significant fetal anemia. Intravascular IUT is most efficacious for the treatment of severely anemic fetuses with hydrops. Platelet alloimmunization results in severe fetal and neonatal thrombocytopenia, which may be ameliorated with maternal administration of IVIG. Gestational thrombocytopenia is a benign disorder that is characterized by mild thrombocytopenia (>70,000 per mL), no history of excessive bleeding, no history of thrombocytopenia, resolution of thrombocytopenia 1 to 2 weeks after delivery, and no serious risk to the mother or the fetus. Autoimmune thrombocytopenia is characterized by thrombocytopenia before and after pregnancy, megathrombocytes on peripheral smears, bone marrow aspirate with normal or

increased numbers of megakaryocytes, history of excessive bleeding, and absence of splenomegaly. Antiplatelet antibodies are not useful in differentiating between gestational thrombocytopenia and autoimmune thrombocytopenia. Autoimmune thrombocytopenia is not associated with a significant risk of fetal thrombocytopenia leading to intracranial hemorrhage. The diagnosis of SLE is based on specific clinical criteria. A positive ANA test is confirmatory in 98% of patients, but elevated levels of antibodies to double-stranded DNA are most specific for disease activity. Most SLE flares during pregnancy are easily treated with glucocorticoids. Prophylaxis with glucocorticoid medication is not indicated to prevent flare during pregnancy. SLE flare during pregnancy is best detected by frequent and thorough clinical assessment. Congenital cardiac heart block associated with neonatal lupus is characterized by fetal bradycardia diagnosed in the second trimester in a fetus with a structurally normal heart. The diagnosis of APS should be based on the presence of thromboembolism or pregnancy morbidity in combination with the presence of LA or medium to high titers of β2-glycoprotein I– dependent IgG or IgM isotype aCL or medium to high titers of antiβ2-GPI. A regimen of heparin and low-dose aspirin reduces the risk of pregnancy loss in women with APS. Pregnancy is associated with clinical improvement in at least 50% of patients with RA. MG is a chronic neuromuscular autoimmune disease characterized by fatigue and weakness, usually involving the extraocular, facial, pharyngeal, and respiratory muscles. Women with MG should avoid magnesium sulfate and aminoglycoside preparations, narcotics, and muscle relaxants. Neonatal MG occurs in 12% to 20% of infants born to mothers affected with MG.

Suggested Readings Erythroblastosis Fetalis

American College of Obstetricians and Gynecologists. Management of alloimmunization during pregnancy. ACOG Practice Bulletin No. 75, August 2006. American College of Obstetricians and Gynecologists. Prevention of Rh D alloimmunization. ACOG Practice Bulletin No. 4, May 1999. Mari G. Noninvasive diagnosis by Doppler ultrasonography of fetal anemia due to maternal red-cell alloimmunization. N Engl J Med 2000;342:9. Moise KJ Jr. Management of rhesus alloimmunization in pregnancy. Obstet Gynecol 2002;100:600–611.

Platelet Alloimmunization American College of Obstetricians and Gynecologists. Thrombocytopenia in pregnancy. ACOG Practice Bulletin No. 6, September 1999. Berkowitz RL, Bussel JB, McFarland JG. Alloimmune thrombocytopenia: state of the art 2006. Am J Obstet Gynecol 2006;195:907–913. Berkowitz RL, Kolb A, McFarland JG, et al. Parallel randomized trials of risk-based therapy for fetal alloimmune thrombocytopenia. Obstet Gynecol 2006;107:91–96. Bussel JB, Zabusky MR, Berkowitz RL, et al. Fetal alloimmune thrombocytopenia. N Engl J Med 1997;337:22. Silver RM, Porter TF, Branch DW, et al. Neonatal alloimmune thrombocytopenia: antenatal management. Am J Obstet Gynecol 2000;182:1233.

Autoimmune Thrombocytopenia American College of Obstetricians and Gynecologists.Thrombocytopenia in pregnancy. ACOG Practice Bulletin No. 6, September 1999. Cines DB, Blanchette VS. Immune thrombocytopenic purpura. N Engl J Med 2002;346:995– 1008. Webert KE, Mittai R, Sigouin C, et al. A retrospective 11-year analysis of obstetric patients with idiopathic thrombocytopenic purpura. Blood 2003;102:4306–4311.

Systemic Lupus Erythematosus Buyon JP, Hiebert R, Copel J, et al. Autoimmune-associated congenital heart block: demographics, mortality, morbidity and recurrence rates obtained from a national neonatal lupus registry. J Am Coll Cardiol 1998;31:1658–1666.

Le Huong D, Wechsler B, Vauthier-Brouzes D, et al. Outcome of planned pregnancies in systemic lupus erythematosus: a prospective study on 62 pregnancies. Br J Rheumatol 199;36:772–777. Levy RA, Vilela VS, Cataldo MJ, et al. Hydroxychloroquine (HCQ) in lupus pregnancy: double-blind and placebo-controlled study. Lupus 2001;10:401–404. Moroni G, Ponticelli C. The risk of pregnancy in patients with lupus nephritis. J Nephrol 2003;16:161–167. Ruiz-Irastorza G, Khamashta MA, Gordon C, et al. Measuring systemic lupus erhthematosus flares during pregnancy: validation of the lupus activity index in pregnancy scale. Arthritis Rheum 2004;51:78–82. Thung SF, Grobman WA. The cost effectiveness of empiric intravenous immunoglobulin for the antepartum treatment of fetal and neonatal alloimune thrombocytopenia. Am J Obstet Gynecol 2005;193:1094–1099.

Antiphospholipid Syndrome American College of Obstetricians and Gynecologists. Thromboembolism in pregnancy. ACOG Practice Bulletin No. 19, 2000. Backos M, Rai R, Baxter N, et al. Pregnancy complications in women with recurrent miscarriage associated with antiphospholipid antibodies treated with low dose aspirin and heparin. Br J Obstet Gynaecol 1999;106:102–107. Branch DW, Khamashta MA. Antiphospholipid syndrome. In: Queenan J, ed. High-risk pregnancy. Washington, DC: American College of Obstetricians and Gynecologists, 2008. Empson M, Lassere M, Craig JC, et al. Recurrent pregnancy loss with antiphospholipid antibody: a systematic review of therapeutic trials. Obstet Gynecol 2002;99:135–144. Levine J, Branch DW, Rauch J. The antiphospholipid syndrome. N Engl J Med

2002;346:752–763.

Rheumatoid Arthritis Kanik KS, Wilder RL. Hormonal alterations in rheumatoid arthritis, including the effects of pregnancy. Rheum Dis Clin North Am 2000;26:805–823.

Myasthenia Gravis Mitchell PJ, Bebbington M. Myasthenia gravis in pregnancy. Obstet Gynecol 1992;80:178.

19 Obstetric and Perinatal Infections Jill K. Davies Ronald S. Gibbs In this chapter, six important infections are discussed—group B streptococci (GBS), varicella-zoster virus (VZV), parvovirus B19, toxoplasmosis, cytomegalovirus (CMV), and herpes simplex virus (HSV)—focusing on their relevance during pregnancy to both the mother and the fetus. In addition, two common peripartum infections will be reviewed— intra-amniotic infection (IAI) and postpartum endometritis.

Group B Streptococci In the 1970s, GBS became recognized as the leading cause of neonatal infection and an important cause of maternal genital tract infection. Prior to the mid 1990s, early-onset neonatal GBS disease incidence ranged between 1.5 to 2.0 cases per 1,000 live births. As prevention measures then came into practice, disease incidence declined by 70% to a rate of 0.5 cases per 1,000 live births. Most recent surveillance data indicates the rate of early onset is now 0.34 cases in 1,000 live births, and the rate of late onset disease decreased to 0.38 cases in 1000 live births. In 1996, the first national consensus guidelines were released. Based on new evidence from a large retrospective cohort study, new national prevention guidelines from the Centers for Disease Control and Prevention (CDC), American Academy of Pediatrics (AAP), and American College of Obstetricians and Gynecologists (ACOG) were released in 2002, recommending a single prevention strategy—namely, universal antenatal culture-based screening at 35 to 37 weeks gestation.

Epidemiology It is estimated that 20% to 30% of all pregnant women are GBS carriers, but colonization can be intermittent or transient. Prenatal screening for GBS at 35 to 37 weeks gestation is recommended by the 2002 national guidelines. In newborns, the most common GBS infections are sepsis, pneumonia, and meningitis (Fig. 19.1). Early-onset disease occurs within the first week of life; late-onset disease occurs after the first week. Outcome survival has improved recently. For term infants, survival for

GBS sepsis is about 98%, but for preterm infants the survival is lower, at 90% for cases at 34 to 36 weeks gestation and 70% for cases at less than 33 weeks. Risk factors for early-onset disease are maternal GBS colonization, prolonged rupture of membranes, preterm delivery, GBS bacteriuria during pregnancy, birth of a previous infant with invasive GBS disease, maternal chorioamnionitis as evidenced by intrapartum fever, young maternal age, African American race, Hispanic ethnicity, and low levels of antibody to type-specific capsular polysaccharide antigens. Manifestations of maternal GBS infection include urinary tract infection, chorioamnionitis, endometritis, bacteremia, and stillbirth. GBS are isolated in 15% of cases of amnionitis, 15% of cases of endometritis, 2% to 15% of infected abdominal wounds after cesarean delivery, and about 15% of cases of bacteriuria in obstetric patients.

Diagnosis The 2002 CDC guidelines provide directions for collecting and processing these specimens (Table 19.1). These guidelines recommend a rectogenital specimen to obtain optimal yield of GBS. There has been intense interest in tests for rapid identification of GBS. In one study, a polymerase chain reaction (PCR) test reported excellent sensitivity, specificity, positive predictive value, and negative predictive value when compared with conventional anovaginal cultures. The reported laboratory turnaround time was 40 to 100 minutes for these PCR methods. The FDA approved an intrapartum rapid PCR test (IDI-Strep B, Infection Diagnostic Inc., Quebec, Canada). However, there are “real-world” limitations to this test, including turnaround time on a 24-hour, 7-day per week basis and inability to determine antibiotic susceptibility in women who cannot take penicillin or a cephalosporin. One role for PCR tests may be in testing women whose GBS status is unknown on admission in labor.

Figure 19.1 Neonatal autopsy showing congenital pneumonia due to GBS. (From Gibbs RS, Schrag S, Schuchat A. Perinatal infections due to group B streptocci. Obstet Gynecol 2004;104[5]:1064.)

Tests from genital specimens other than PCR (such as antigen detection) are not sufficiently sensitive for clinical use.

Therapy Because resistance to penicillin or ampicillin has not been detected in GBS, penicillin, because of its narrow spectrum of activity, remains the agent of choice for GBS prophylaxis, with ampicillin as an alternative. Resistance to clindamycin and erythromycin among GBS isolates is widely prevalent, ranging from 7% to 30% for erythromycin and 3% to 15% for clindamycin. Resistance to also has been detected. These resistance trends led to a revision of the first- and second-line antibiotics (Table 19.2). Because of the possibility of inducible resistance, the 2002 guidelines recommend that clindamycin or erythromycin be used only if a given patient's GBS isolate was shown to have in vitro susceptibility to both. If there is in vitro resistance to either in a patient at high risk for penicillin anaphylaxis, then vancomycin should be used. For women at high risk of penicillin allergy colonized by clindamycin-resistant or erythromycin-resistant isolates, the 2002 guidelines recommend vancomycin. Because vancomycin use is restricted due to concerns regarding emerging vancomycin resistance, vancomycin should be

reserved, in GBS prophylaxis, for highly penicillin-allergic women with isolates of unknown susceptibility and isolates with resistance to either erythromycin or clindamycin. Because of its uniform activity, penicillin G remains the drug of choice for clinically evident maternal infection with GBS. Ampicillin is used widely and is an acceptable alternative. The usual dose of penicillin G is 5.0 million units intravenously initially, then 2.5 million units intravenously every 4 to 6 hours. Note that for prevention of GBS perinatal infections, the dosing interval is every 4 hours until delivery. For ampicillin, the usual adult dose is 2 g intravenously initially, then 1 g intravenously every 4 to 6 hours. Again, note that for GBS prophylaxis, the dosing interval is every 4 hours until delivery.

Prevention The indications for prophylaxis under this universal prenatal screening strategy are shown in Figure 19.2.

Obstetric Procedures Membrane sweeping (or stripping) among term patients hastens the onset of labor, with no increases in overall perinatal or peripartum infection. However, because studies using this technique did not report GBS status, there are no data to advise whether this procedure should or should not be avoided in GBS-positive women. Nevertheless, because the benefits of membrane sweeping are limited (such as a significantly greater likelihood of onset of labor within 48 hours). The authors avoid membrane sweeping in GBS-positive women. If there is an indication for delivery, there are many alternative interventions to membrane sweeping, such as vaginal prostaglandin preparations.

Vaccine Development Immunization holds promise to prevent a larger burden of disease, protecting against both early- and late-onset infections. Moreover, vaccination may prevent some adverse pregnancy outcomes associated with GBS, such as preterm delivery, spontaneous abortion, or stillbirth, particularly if vaccination of adolescent girls before pregnancy is a viable strategy. Additionally, immunization strategies would not contribute to emerging antimicrobial resistance among GBS. Promising GBS vaccine candidates now exist but are not available commercially.

TABLE 19.1 Procedures for Collecting and Processing Clinical Specimens for Group B Streptococcal Culture and Performing Susceptibility Testing to Clindamycin and Erythromycin

Procedure for collecting clinical specimens for culture of group B streptococcus at 35–37 weeks' gestation Swab the lower vagina (vaginal introitus), followed by the rectum (i.e., insert swab through the anal sphincter) using the same swab or two different swabs. Cultures should be collected in the outpatient setting by the healthcare provider or the patient herself, with appropriate instruction. Cervical cultures are not recommended and a speculum should not be used for culture collection. Place the swab(s) in to a non-nutritive transport medium. Appropriate transport systems (e.g., Amies or Stuart's without charcoal) are commercially available. If vaginal and rectal swabs were collected separately, both swabs can be placed into the same container of medium. Transport media will maintain GBS viability for up to 4 days at room temperature or under refrigeration. Specimen labels should clearly identify that specimens are for group B streptococcal culture. If susceptibility testing is ordered for penicillin-allergic women (Table 19.2), specimen labels should also identify the patient as penicillin allergic and should specify that susceptibility testing for clindamycin and erythromycin should be performed if GBS is isolated. Procedure for processing clinical specimens for culture of group B streptococcus Remove swab (s) from transport medium.* Inoculate swab(s) into a recommended selective broth medium, such as ToddHewitt broth supplemented with either gentamicin (8 µg/ml) and nalidixic acid (15 µg/ml), or with colistin (10 µg/ml) and nalidixic acid (15 µg/ml). Examples of appropriate commercially available options include TransVag broth supplemented with 5% defibrinated sheep blood of LIM broth.† Incubate inoculated selective broth for 18–24 hours at 35°– 37°C in ambient air or 5% CO2. Subculture the broth to a sheep blood agar plate (e.g., tryptic soy agar with 5% defibrinated sheep blood). Inspect and identify organisms suggestive of GBS (i.e., narrow zone of beta hemolysis, gram-positive cocci, catalase negative). Note that hemolysis may be difficult to observe, so typical colonies without hemolysis should also be further tested. If GBS is not identified after incubation for 18–24 hours, reincubate and inspect at 48 hours to identify suspected organisms.

Various treptococcus grouping latex agglutination tests or other tests for GBS antigen detection (e.g., genetic probe) may be used for specific indentification, or the CAMP test may be employed for presumptive identification. Procedure for clindamycin and erythromycin disk susceptibility testing of isolates, when ordered for penicillin-allergic patients.‡ Use a cotton swab to make a suspension from 18–24 hour growth of the organism in saline of Mueller-Hinton broth to match a 0.5 McFarland turbidity standard. Within 15 minutes of adjusting the turbidity, dip a sterile cotton swab into the adjusted suspension. The swab should be rotated several times and pressed firmly on the inside wall of the tube above the fluid level. Use the swab to inoculate the entire surface of a Mueller-Hinton sheep blood agar plate. After the plate is dry, use sterile forceps to place a clindamycin (2 µg) disk on to half of the plate and an erythromycin (15 µg) disk onto the other half. Incubate at 35°C in 5% CO2 for 20–24 hours. Measure the diameter of the zone of inhibition using a ruler of calipers. Interpret according to NCCLS guidelines for Streptococcus species other than S. pneumoniae (2002 breakpoints:‡ clindamycin: ≥19 mm = susceptible, 16–18 = intermediate, ≤15 = resistant; erythromycin: ≥21 mm = susceptible, 16–20 = intermediate, ≤15 = resistant). *Before inoculation step, some laboratories may choose to roll swab(s) on a single sheep blood agar plate or CNA sheep blood agar plate. This should be done only in addition to, and not instead of, inoculation into selective broth. The plate should be streaked for isolation, incubated at 35–37°C in ambient air of 5% CO2 for 18–24 hours and inspected for organisms suggestive of GBS as described above. If suspected colonies are confirmed as GBS, the broth can be discarded, thus shortening the time to obtaining culture results. †Sources Fenton, LJ, Harper MH. Evaluation of colistin and nalidixic acid in Todd-Hewitt broth for selective isolation of group B streptococci. J Clin Microbiol 1979;9:167–9. Although Trans-Vag medium is often available without sheep blood, direct comparison of medium with and without blood has shown higher yield when blood is added. LIM broth may also benefit from the addition of sheep blood, although the

improvement in yield is smaller and sufficient data are not yet available to support a recommendation. ‡Source NCCLS, Performance standard for antimicrobial susceptibility testing. M100-S12, Table 2H, Wayne, Pa.: NCCLS, 2002, NCCLS recommends disk diffusion (M-2) or broth microdilution testing (M-7) for susceptibility testing of GBS. Commercial systems that have been cleared or approved for testing of streptococci other than S. pneumoniae may also be used. Penicillin susceptibility testing is not routinely recommended for GBS because penicillin-resistant isolates have not been confirmed to date. From Centers for Disease Control and Prevention. Prevention of perinatal group B streptococcal disease. MMWR 2002;51(RR-11):4.

Varicella-zoster Virus (VZV) VZV, a member of the herpesvirus family, is the etiologic agent that causes chicken pox, an almost universal infection of children and adolescents. Its reactivation is the cause of herpes zoster. Ninety percent of individuals will be immune prior to adulthood. Infection during pregnancy complicates 0.7 per 1,000 pregnancies. The incubation period for varicella zoster is 10 to 21 days, and infected individuals are contagious from 1 to 2 days before the rash begins until all of the skin lesions are crusted over. The lesions are classically described as “dew drops on a rose petal.” During the prodrome and early infection, there is characteristic fever and malaise followed by development of the pruritic rash. Following varicella-zoster infection, the virus lays dormant in the dorsal horn cells of the spinal cord. Reactivation causes herpes zoster.

TABLE 19.2 Recommended Regimens for Intrapartum Antimicrobial Prophylaxis for Perinatal Group B Streptococci Disease Prevention*

Recommended

Penicillin G, 5 million units IV initial dose, then 2.5 million units IV every 4 hours until delivery Ampicillin, 2 g IV initial dose,

Alternative

then 1 g IV every 4 hours until delivery

If penicillin allergic†

Patients not at high risk for anaphylaxis

Cefazolin, 2 g IV initial dose, then 1 g IV every 8 hours until delivery

Patients at high risk for anaphylaxis‡

GBS susceptible to clindamycin and erythromycin§

Clindamycin, 900 mg IV every 8 hours until delivery

Erythromycin, 500 mg IV every 6 hours until delivery

GBS resistant to clindamycin or erythromycin or susceptibility unknown

Vancomycin,¶ 1 g IV every 12 hours until delivery

GBS, group B streptococci. *Broader-spectrum agents, including an agent active against GBS, may be necessary for treatment of chorioamnionitis †History of penicillin allergy should be assessed to determine whether a high risk for anaphylaxis is present. Penicillinallergic patients at high risk for anaphylaxis are those who have experienced immediate hypersensitivity to penicillin including a history of penicillin-related anaphylaxis; other high-risk patients are those with asthma or other diseases that would make anaphylaxis more dangerous or difficult to treat, such as persons being treated with beta-adrenergicblocking agents.

‡If laboratory facilities are adequate, clindamycin and

erythromycin susceptibility testing (Table 19.1) should be performed on prenatal GBS isolates from penicillin-allergic women at high risk for anaphylaxis. §Resistance to erythromycin is often but not always associated with clindamycin resistance. If a strain is resistant to erythromycin but appears susceptible to clindamycin, it may still have inducible resistance to clindamycin. ¶Cefazolin is preferred over vancomycin for women with a history of penicillin allergy other than immediate hypersensitivity reactions, and pharmacologic data suggest it achieves effective intraaminiotic concentration. Vancomycin should be reserved for penicillin-allergic women at high risk for anaphylaxis. From Centers for Disease Control and Prevention. Prevention of perinatal group B streptoccal disease. MMWR 2002:51(RR11):10. Most women are immune to varicella prior to adulthood due to a history of typical varicella infection as a child, which is considered sufficient for immunity. As most women are immune to varicella before reproductive age, most who do not specifically recall a history of chicken pox infection as a child are immune as well. Varicella vaccine (Varivax, Merck, Whitehouse Station, NJ) is now available and recommended for administration during childhood. Thus, the overwhelming majority of pregnant women are immune to varicella prior to pregnancy. Immunocompetent individuals will not get chicken pox again.

Varicella Exposure and Management When exposure occurs in a pregnant woman, it is important to obtain her history regarding prior varicella infection. The diagnostic approach to the pregnant woman with possible varicella exposure is shown in Figure 19.3. With a prior history of typical chicken pox infection, she can be reassured. No serologic confirmation is required. In the setting of an inconclusive maternal history, a VCV immunoglobulin G (IgG) level should be checked urgently. Most laboratories can provide results of this in a day or so. If a woman's IgG is positive shortly after exposure, this indicates prior immunity and she can be reassured. If her IgG is negative, she is susceptible to infection from the exposure. A significant exposure to varicella consists of a household contact, a face-to-face contact with an infected individual for at least 5 minutes, or an indoor contact with chicken pox or herpes zoster for at least 1 hour. If the woman meets these criteria, her varicella immunoglobulin M (IgM) antibody level should be measured. If her IgM is negative, immune globulin should be given to prevent transmission of the virus or lessen its severity. She should be given postexposure prophylaxis with varicella-zoster–specific immune globulin (VariZIG, FFF Enterprises, Temecula, CA). The adult dosage of VZIG is 625 U and is most effective when given within

96 hours of exposure. If VZIG is not available, 0.6–1.2 mL/kg of intravenous immune globulin (IVIG) can be given. In one trial, administration of VZIG to pregnant women within 96 hours of exposure was demonstrated to be highly efficacious in preventing 80% (20 of 25) of clinical infection. The 16 of 18 women who did not receive VZIG contracted infection. In addition, when VZIG was given between 3 and 10 days after exposure, the same group described attenuation of maternal infection.

Natural History and Pathophysiology Although most pregnant women will have self-limited infection, VZV during pregnancy has been associated with increased morbidity and mortality compared with nonpregnant adult infection (http://www.fda.gov/cber/ infosheets/mphvzig092005.htm). Symptomatic therapy with antipyretics and antipruritic agents that are safe during pregnancy can be used. Because of the high infectivity of this virus, the patient should be properly isolated from other susceptible pregnant women. When diagnosis of maternal varicella is made, patients should be treated with acyclovir 800 mg orally five times daily for 7 days to decrease severity of infection, as it has been associated with a decrease in time to lesion healing and lessens fever and other symptoms. Five percent of women in the National Institute of Child Health and Development (NICHD) review of maternal varicella developed varicella pneumonia. Women with VZV infections during pregnancy should be given strict respiratory precautions, as a significant minority of women who develop varicella pneumonia will develop respiratory failure warranting mechanical ventilation, and their respiratory status can rapidly decompensate. Respiratory symptoms most likely will develop on the second day of rash, often consisting of dry cough, hemoptysis, pleuritic chest pain, and shortness of breath. Chest radiographs most often will show a miliary or diffuse nodular pattern. Varicella pneumonia should be treated aggressively with acyclovir 10 to 15 mg/kg given intravenously three times daily for 7 days. Higher doses of acyclovir are needed to treat varicella due to its lower specificity for VZV compared with HSV.

Figure 19.2 Indications for intrapartum antibiotic prophylaxis to prevent perinatal GBS disease under a universal prenatal screening strategy based on combined vaginal and rectal cultures collected at 35 to 37 weeks gestation from all pregnant women. (GBS, group B streptococci.) (From Centers for Disease Control and Prevention. Prevention of perinatal group B streptococcal disease. MMWR 2002;51[RR-11]:8.)

Neonatal Varicella Newborn infection can occur if maternal infection with rash and symptoms develop from approximately 5 days before delivery until 2 days after delivery. This is the period in which there is insufficient time for maternal IgG antibody development and passive transfer to protect the fetus. Infection in the neonate usually will occur within 5 to 10 days of life and is of variable course but can be quite severe. Passive immunization of the exposed neonate with 125 U of VZIG is recommended if maternal varicella infection occurs within 5 days of delivery to 2 days following delivery as well as to any exposed neonate born at less than 28 weeks gestation, as IgG antibody transfer at premature gestational ages is less efficient. Although VZIG will not protect all neonates from varicella, it should reduce the severity of infection. Appropriate isolation of exposed infants should occur as well.

Fetal Effects and Prenatal Diagnosis Varicella has been shown to cause fetal effects. Although first-trimester infection is associated with a low risk for miscarriage and anomalies (0.4%), the second trimester between approximately 12 and 20 weeks is the highest risk for vertical transmission causing serious fetal abnormalities (congenital varicella syndrome). Although vertical transmission has been estimated to be as high as 10%, more recent studies suggest this risk to be less than 2%. Fetal abnormalities include skin scarring, a variety of fetal central nervous system (CNS) abnormalities, ophthalmologic effects, limb anomalies, and gastrointestinal abnormalities. These fetal effects are thought to be as a result of immaturity of the fetal immune system as well as intrauterine herpes zoster resulting in a predilection for neuronal cells and their downstream innervated tissues. There is no clear information regarding whether maternal administration of VZIG or acyclovir will lessen or prevent these fetal effects.

Figure 19.3 Algorithm for assessment and management of varicella exposure in pregnancy. (IgG, immunoglobulin G.) (From Chapman SJ. Varicella in pregnancy. Semin Perinatol 1998;22:344.) * VZIG is not currently available in the US although available with IRB approval through FFF Enterprised (Temecula, California). Sample release forms are available through http://www.fda.gov/cber/infosheets/ mphvzig 020806form-pdf.

Approximately 4 to 6 weeks following resolution of maternal varicella infection, detailed ultrasound exams to evaluate for fetal effects should be performed. A subsequent ultrasound should be performed between 8 and 12 weeks to look for delayed effects.

Herpes Zoster Herpes zoster represents a reactivation of VZV and is commonly known as shingles. Although herpes zoster may be contagious to a nonimmune person by skin-to-skin contact, it is not spread by respiratory secretions. Fetal effects are not reportedly seen, as most herpes zoster infections do not result in viremia. Depending on dermatomal reactivation, intrauterine infection theoretically could be possible if the uterus were involved with reactivation of T10-L1 (which innervates the uterus). In most recent reviews, in utero

transmission has not been reported without dissemination. These painful infections should be treated with acyclovir.

Prevention Postpartum vaccination of varicella-nonimmune women should be offered when breastfeeding has been completed. Since it is a live, attenuated vaccine, the ACOG and AAP recommended that women avoid conception for 1 month following vaccine administration, although the manufacturer recommends a 3-month delay (http://www. merck.com/product/usa/pi_circulars/v/varivax/varivax_pi.pdf). However, since vaccine virus has not been found to be excreted into breast milk, it has been suggested that vaccine administration not be delayed in nonimmune breast-feeding women.

Parvovirus B19 Epidemiology Erythema infectiosum and fifth disease are two common names for parvovirus B19 infection. B19 is the only parvovirus known to cause human infection. It was not until 1984 that parvovirus B19 was first described as a cause of fetal infection and nonimmune hydrops. Only 30% to 60% of adults are immune to this virus. The incidence of parvovirus B19 seroconversion during pregnancy is 1% to 2% but may be higher than 10% during epidemics.

Pathophysiology Parvovirus is a highly contagious infection, with an attack rate of 60% to 80% of susceptible household contacts, whereas only 20% to 30% of susceptible schoolteachers or day care workers will become infected following exposure. Infection is most common in late winter or spring and is transmitted by respiratory droplets and contaminated blood. Transplacental fetal transmission occurs in one third of cases, with risk of adverse fetal outcome in approximately 10%. Parvovirus is a strong inhibitor of hematopoietic cells, including liver, myocardium, and erythroid precursor cells. The P antigen on the red blood cell is a receptor for parvovirus B19; fetal cardiac myocytes are another receptor for the P antigen. Although maternal infection can be asymptomatic, some will develop symptoms including fever, myalgias, and malaise initially followed by arthralgias and sometimes pruritis and rash—commonly a “slapped cheek”–appearing rash in children. Uncommonly, meningoencephalitis, hepatitis, or myocarditis may occur with seroconversion. Symptomatic fetal infection is seen in approximately 10% and is associated with myocarditis; nonimmune hydrops; fetal demise; spontaneous loss; and rarely, neurologic complications. When hydrops occurs, it usually does so within 2 to 6 weeks of fetal infection, although the reported range is 1 to 12 weeks, with the maximal risk for development of fetal hydrops between 17 and 24 weeks gestation. Although the mechanism behind development of hydrops is incompletely understood, severe anemia leading to highoutput cardiac failure is the likely pathophysiologic mechanism.

Diagnosis Diagnosis of maternal parvovirus B19 infection initially is made by serologic methods with enzyme immunoassay of B19 IgM and IgG. Antibodies of the IgM class will become measurable in 7 to 10 days following maternal infection, peaking at about 14 days then declining over 2 to 3 months. The IgG antibodies will rise more slowly, not peaking until about 4 months following acute infection. When IgG is positive on the initial specimen following exposure and IgM is negative, the patient demonstrates evidence of past infection. Immunity is lifelong, and she can be reassured that there is no fetal risk. If the first serum sample demonstrates negative IgM and IgG, acute seroconversion still may be occurring. Thus, repeat titers should be repeated 1 to 2 weeks after the initial titers were collected to study the evolution of the titers. To compare the sets of IgM/IgG antibodies most accurately, the laboratory should freeze the serum after running the first specimen to run together with the second specimen. Maternal B19 viremia will be present during acute seroconversion by DNA PCR, but persistent low-level viremia may persist for years following acute seroconversion. Thus, PCR testing for the virus is a less specific and a more expensive method of detection. New on the horizon include parvovirus B19 IgG avidity assays as well as IgG epitope specificity assays. These assays likely will be most useful in those patients with low-level parvovirus B19 IgM levels that may signify nonrecent seroconversion and may be associated with less, if any, fetal risk. Because fetal immunologic response is less pronounced, fetal and cord blood examinations should be confined to B19 DNA PCR.

Prenatal Diagnosis and Fetal Management Following confirmation of acute maternal seroconversion, fetal ultrasound examinations should be serially performed for 10 to 12 weeks following seroconversion to evaluate for fetal anemia as well as hydrops and other signs of fetal viral infection such as calcifications in the liver and myocarditis. Similar to Rh isoimmunization, anemic fetuses from parvovirus B19 infection will demonstrate increased blood velocity, as measured by peak systolic velocity in the middle cerebral artery. Ultrasound evidence of anemia usually will precede the development of fetal hydrops, allowing for optimization of fetal procedures such as percutaneous umbilical blood sampling (PUBS) and intrauterine transfusion (IUT). Hydrops, defined as fluid in two or more fetal body cavities, traditionally was defined as pleural effusions, pericardial effusions, ascites, and scalp edema but also may manifest as placental edema and be accompanied by amniotic fluid abnormalities. IUT to support the fetus during the parvovirus B19 suppression of hematopoiesis can prevent hydrops formation or cause it to resolve. Resolution of hydrops may take weeks despite correction of fetal anemia with IUT. Spontaneous recovery of parvovirus-induced hydrops has been described but is uncommon. Fetal mortality is higher when hydrops is present and is lessened with IUT. Prognosis following fetal recovery from in utero parvovirus infection usually is quite good, and only rare neurodevelopmental, cardiac, and hematologic sequelae have been reported.

Toxoplasmosis Primary maternal toxoplasmosis occurs in approximately 1 of every 900 pregnancies in the United States. This estimate is based on a prospective study of sera from 23,000 pregnant women done in early and late gestation. That study, conducted by the National Institutes of Health, also showed that 38% of the women tested had antibodies to Toxoplasma gondii, indicating previous infection with the organism. More recent data suggest that the seroprevalence may now be somewhat lower (15% among women of childbearing age); this reduction may be due to improved hygiene, education, and meat practices. In earlier data, the presence of antibodies correlated with increasing patient age and was twice as frequent among blacks as among whites. None of the mothers tested had evidence of significant clinical disease. It has been estimated that between 400 and 4,000 babies are born with congenital T. gondii infections each year. Some data suggest that congenital infections occur in approximately 1 in 10,000 births.

Microbiology: Transmission Cats The cat is the definitive host for T. gondii, which is a protozoan parasite (Fig. 19.4). About one half of the cats tested in the United States have antibodies to T. gondii. It is thought that cats acquire infection by eating infected wild rodents and birds. A week after infection, the cat begins to shed oocysts in its feces. Shedding of the oocysts persists for about 2 weeks only, then the cat recovers spontaneously. These animals are susceptible to reinfection and also may shed toxoplasma oocysts when infected with other organisms.

Figure 19.4 T. gondii in trophozoites or proliferative form. (From Jones JL, Lopez A, Wilson M, et al. Congenital toxoplasmosis: a review. Obstet Gynecol Surv 2001;50:297, with permission.)

Although the cats excrete unsporulated (i.e., noninfectious) oocysts in their feces, within days to weeks these oocysts sporulate and become extremely infectious. The fecal oocysts are an important source of infection to humans through inadvertent ingestion. Because sporulation of the organism occurs after days to weeks in cat litter, it is recommended that pregnant women not change the litter and instead it is changed daily by a nonpregant person. Care must be taken in disposing of cat litter because the oocysts can remain infectious for long periods in favorable climates.

Food In Europe, where the use of refrigeration is more limited and foods usually are not frozen, ingestion of contaminated food is an important cause of toxoplasmosis. Although meat is the most common infected food source discussed, produce from oocyte-contaminated soil as well as unpasteurized milk and unfiltered water sources also are at risk. In the United States, most meat is frozen at some point during storage or transport. Freezing is probably one of the factors responsible for the difference in incidence of toxoplasmosis here and in Europe. Worldwide, about 1% of cattle, 20% of hogs, and 30% of sheep have toxoplasmosis. To avoid contamination from meat, it should be cooked thoroughly at adequate temperatures. To avoid contamination of fruits and vegetables from potentially contaminated soils, thorough washing of fruits and vegetables is recommended. In addition, proper hand hygiene, prevention of cross contamination of cooking surfaces, and

cleaning of food preparation areas and kitchen knives is crucial. Organ transplantation is another less common risk factor.

Epidemiology T. gondii has a worldwide distribution and has been reported from wherever cats are found. It is somewhat more common in tropical and coastal regions and is less common in regions that are cold, warm and arid, or at high elevation. The infection rate in the United States is significantly lower than that in France. Within the United States, seroprevalence rates are lower in the western central and mountain states and higher in eastern Atlantic and eastern central states.

Pathophysiology Acute toxoplasmosis generally is well tolerated in immunocompetent adults but may result in vertical infection to the fetus and lead to potentially serious consequences. In the immunocompetent adult host, symptoms usually are mild or inapparent. In about 10%, fever, fatigue, malaise, headache, myalgias, and lymphadenopathy will be present. These symptoms will resolve in weeks to months without specific therapy. In immunosuppressed adult patients, signs and symptoms often will be more pronounced and can result in significant ocular and CNS abnormalities. Reactivation infection in immunosuppressed pregnant women also can cause fetal infection. T. gondii exists in three forms: trophozoites or proliferative form (Fig. 19.4), tissue cysts, and oocytes. The organism undergoes a substantial portion of its life cycle in the cat, where after between 5 and 8 days of infection, there is peak oocyte production. As many as ten million oocysts per day can be shed in feces for periods varying between 7 and 20 days. These oocytes sporulate within 1 to 3 days and can remain infectious for several months in moist soil. At that point, they may be carried from point of deposition by other animals (e.g., flies) and deposited in food. It also has been suggested that they can become airborne from a dried-out litter box and lead to human infection. Eating undercooked or raw meat that contains tissue cysts causes approximately one half of infections in most humans. In the human, the trophozoite form of T. gondii is seen in the acute phase of the infection, and it is during this phase that host cells are invaded. Thereafter, the organism multiplies every 4 to 6 hours until the cytoplasm becomes so filled with trophozoites that the cells rupture, releasing organisms to invade other cells.

In Utero Transmission Newborns with congenital toxoplasmosis become infected in utero by transplacental passage of the parasite when the mother has acute infection. Chronic infections (onset precedes pregnancy) do not lead to congenital infection except in the rare circumstance of an immunocompromised host (e.g., patient with systemic lupus erythematosus taking steroids, HIV infection) with reactivation. In general, the likelihood of fetal infection increases with each trimester of pregnancy, being approximately 15%, 25%, and 60% in the first, second, and third trimester, respectively. The severity of damage associated with congenital toxoplasmosis also is related to the timing of maternal infection, but in this

situation, the risks decrease toward term. Severe fetal disease or fetal death occurs in about 10% of cases when infection occurs during the first trimester and is extremely rare with infection during the third trimester. Mild damage is more frequent in the second and third trimesters (about 5%). Subclinical infections increase from about 2% with firsttrimester infections to 50% with third-trimester infections. The results of a case-control study of women with poor pregnancy outcomes and controls suggested that acute infection could be associated with preterm delivery and stillbirth but not with spontaneous abortion. Chronic infections were not associated with any untoward outcomes.

Diagnosis in Pregnancy Maternal Infection Maternal infection with T. gondii usually is asymptomatic, although 10% to 20% of infected mothers have lymphadenopathy. Posterior cervical lymphadenopathy is the most frequent finding associated with acute maternal toxoplasmosis. The infection also can result in a mononucleosislike syndrome with fatigue and lassitude and, rarely, can cause encephalitis. Acute toxoplasmosis should be considered in any pregnant woman who has lymphadenopathy, particularly involving the posterior cervical chain, or mononucleosislike symptoms. The vast majority, however, of those acutely infected with T. gondii are asymptomatic. The clinical picture can be much more severe in immunocompromised adults. Because of the wide clinical spectrum of toxoplasmosis, clinicians are forced to rely on serologic tools for the diagnosis of toxoplasmosis in pregnancy. The diagnosis of primary infection with T. gondii during pregnancy requires either (a) the demonstration of a seroconversion to this organism, (b) a significant rise in antibody titer obtained from maternal sera taken at two different times, or (c) the detection of toxoplasma-specific IgM antibody. Adults with primary infection develop IgG and IgM antibody to toxoplasma rapidly. Toxoplasma-specific IgG antibody develops within 2 weeks after infection, peaks in 6 to 8 weeks, drops down over the subsequent several months, and then persists for life. Toxoplasma-specific IgM develops within 10 days after infection and remains elevated for 6 months to more than 6 years. Because IgM antibody remains elevated for many months, IgM titers may not provide useful information to document recent primary infection in pregnant women. The enzyme-linked immunosorbent assay (ELISA) test for IgM frequently shows the development of high titers of IgM antibody that can persist for many months and even years. Indirect immunofluorescence antibody (IFA) tests for toxoplasma-specific IgM usually show high titers for only about 6 months after infection; thereafter, the titer rapidly drops. The IFA test, then, frequently is more useful than ELISA in differentiating remote from recent primary infection of a pregnant woman. In any case, the presence of IgG and the absence of IgM suggest an infection that is probably at least a year old. Because of difficulties with the reliability of some commercially available tests for IgM, it has been recommended that all positive test results be confirmed in a reference

laboratory. The authors recommend the laboratory of Jack Remington and colleagues, who can be reached at 650-853-4828 or [emailprotected]. Up to 40% of positive toxoplasmaspecific IgM results from commercial laboratories are false positives. Avidity testing is a newer type of testing that particularly can be helpful for testing for several of the infections discussed in this chapter, including toxplasma, CMV, and parvovirus. When antibodies are initially produced to a new antigen, the antibodies have low avidity for the antigen. As the antibody response matures, the avidity of the antibody increases. Avidity testing usually is expressed as an index, the percentage of the antibody bound to antigen following denaturation. Some researchers have suggested that the presence of high-avidity IgG antibodies exclude acute infection within the previous 3 months, thereby making it a useful test for first-trimester infections with serious fetal consequence such as toxoplasma and CMV, particularly when the IgM is elevated. If the IgM is falsely elevated, as reflected by nonprogression of acute and convalescent serum titers as well as high-avidity IgG antibodies, then there should be little fetal risk and much maternal anxiety can be averted. Approximately 50% of placentas of congenitally infected infants will show T. gondii cysts on histologic slides, and their presence supports the diagnosis of acute infection in the mother during pregnancy. Additional cases can be detected by the presence of parasites in the cord blood. The organism also has been isolated from placental tissue of acutely infected mothers in 2% to 25% of cases. Recovery was more frequent when infection occurred later in pregnancy. Isolation of organisms from tissue specimens, buffy coat heparinized blood, and body fluids can be used for diagnosis as well. These specimens produce the organism after inoculation into the intraperitoneal cavities of mice or into tissue culture.

Prenatal Diagnosis Antenatal diagnosis of fetal toxoplasmosis previously relied on culture of amniotic fluid (15 to 20 cc) or fetal blood (1.5 to 3.0 cc) obtained at the time of diagnostic amniocentesis or cordocentesis, respectively. The specimen commonly was cultured in mouse or fibroblast cells. The main difficulties with culture techniques have been that some assays may take up to several weeks to get complete results, and few laboratories are able to perform the assay. In addition, amniocentesis performed too early in gestation occasionally can be falsely negative. Toxoplasma-specific IgM, when present in fetal blood from cordocentesis, also has been used to diagnose fetal infection prenatally. Unfortunately, fetal-specific IgM antibody frequently does not develop until after 21 to 24 weeks gestation and is positive in only about 50% of infected cases. Additionally, cordocentesis is a procedure that entails some risk. More recently, the PCR has been used to detect T. gondii in amniotic fluid and has been shown to be useful in the detection of in utero infections. In one large series, PCR performed better than conventional tests (sensitivity 97.4% vs. 89.5%; negative predictive value 99.7% vs. 98.7%). In a more recent study, higher parasite concentrations (>100 per mL) were associated with more severe congenital infection outcomes. This information in particular may be useful for prenatal counseling. To a large extent, PCR of amniotic fluid

has rendered cordocentesis unnecessary for the purpose of diagnosing toxoplasma infections. Prenatal ultrasound also may demonstrate abnormalities. Many of these visualized abnormalities will signify a poor postnatal prognosis. Ventriculomegaly and hydrocephalus as well as microcephaly will be poor prognosticators. Intracranial calcifications, placentomegaly, hepatomegaly cataracts, and hydrops may be other signs. Intracranial replication of toxoplasma tachyzoites as well as its proinflammatory cytokine response will cause necrosis and then the development of the periventricular calcifications. Resultant ventriculomegaly occurs secondary to relative obstruction of cerebrospinal fluid outflow through narrow areas such as the foramina of Monro and the cerebral aqueduct. Due to the difficult nature of interpretation of this testing and the certain anxiety of the implications of a diagnosis of possible congenital toxoplasmosis, consultation with an expert is recommended for proper interpretation of serologic results and subsequent management recommendations.

Neonatal Infection Most congenitally infected newborns are asymptomatic at birth. Literature has shown that detection of toxoplasma-specific immunoglobulin A (IgA) may be a reliable method for the diagnosis of toxoplasmosis in the newborn. A number of these asymptomatic, untreated infants will go on to have delayed and potentially serious manifestations. The 20% with clinically obvious symptoms at birth will exhibit multiple findings. The most frequent clinical findings are chorioretinitis, jaundice, fever, and hepatosplenomegaly. Hydrocephaly or microcephaly and cerebral calcifications can be seen in severe cases. Demonstration of toxoplasma-specific IgM infection may be diagnostic, although in newborns, approximately 20% of infections are not detectable by toxoplasma-specific IgM at birth.

Treatment and Prevention Treatment of acute toxoplasmosis in immunocompetent, nonpregnant adults is primarily supportive. In general, the prognosis following acute infection is good, except in cases of profound immunosuppression. The treatment in pregnancy is a bit more complex. In Europe, where the seroprevalence and, hence, the clinical experience is greater, spiramycin is the first-line agent used. However, that agent generally does not cross the placenta, and if fetal infection is detected, women also are treated with a combination of pyrimethamine, folinic acid, and a sulfonamide. Although not definitive, treatment with these regimens may prevent maternal-to-fetal transmission of the infection or improve the outcome among infected fetuses. In one study from France, 163 mothers diagnosed with toxoplasmosis prior to 28 weeks gestation were treated with spiramycin (23 also received pyrithiamine and sulfadiazine). Three fetuses died in utero, and 27 were diagnosed with congenital toxoplasmosis. All 27 were free from symptoms and had normal neurologic development at

15 to 71 months. Most studies that control for gestational age at the time of infection suggest that transmission rates are not altered markedly by therapy, but the degree of fetal sequelae may be. The standard dosage is 25 mg of pyrimethamine by mouth given daily and 1 g of sulfadiazine by mouth four times daily for 1 year. Pyrimethamine is a folic acid antagonist and therefore may have teratogenic effects when given in the first trimester. Whenever possible, treatment with pyrimethamine in the first trimester should be weighed against the potential risk of drug teratogenicity to the infant. Folinic acid, 6 mg given intramuscularly or by mouth every other day, should be used to correct the depletion of folic acid induced by pyrimethamine. Spiramycin can be obtained in the United States through the CDC. It is used more commonly in Europe, and hence, there are no good controlled studies of its efficacy in this country. It has not been found to be teratogenic in humans or animals. Case-control studies in France, where women routinely receive serial assessments to detect seroconversion, have revealed that risk factors for acquisition of infection include poor hand washing, eating undercooked beef or lamb, and owning a cat. Based on these data, the CDC has recommended that serosusceptible pregnant women should be counseled to avoid eating raw or undercooked meats, which may contain T. gondii cysts. This can be accomplished by using a food thermometer to ensure that the meat is cooked all the way through. Fruits and vegetables should be peeled and washed before eating. Gloves should be used for gardening and during any contact with soil or sand because cat waste might be found there. Pregnant women should avoid close contact with cat feces, such as by avoiding changing cat litter. The CDC also highlights the need for obstetricians to educate pregnant patients about these important preventive steps. In countries such as France, with high seroprevalence rates, routine serologic screening programs have proven successful in diagnosing recent seroconverters, allowing for prenatal diagnosis of fetal status and either termination of pregnancy or prenatal therapy. There is no consensus for routine screening in the United States. Because of the low prevalence of the disease and the possibility of false-positive results, the ACOG does not recommend routine screening. Most recently, programs have been undertaken that focus on screening of newborns and the institution of treatment during the neonatal period to minimize the morbidity that would otherwise accrue to congenitally infected children. Many infections in children that otherwise would be missed on routine clinical examination can be detected with IgM assays. Treatment of these infected infants has been associated with very low rates of subsequent neurologic or retinal disease. Routine screening of newborns in the United States is not yet recommended.

Cytomegalovirus CMV, a member of the herpesvirus family, is the largest virus that infects humans. It can code for over 200 proteins, through which it can lead to substantial down regulation of the immune system and many diseases, such as infectious mononucleosis in young adults. It

also causes the most common congenital viral infection, affecting approximately 1% of all live births, which comprises about 35,000 infants annually in this country. Congenital CMV infection is acquired by the fetus in utero when the mother develops primary CMV infection while pregnant or with reactivation of a prior maternal infection. Although reactivated disease in the pregnant woman accounts for more than one half of the congenital infections, primary maternal CMV infection is much more likely to result in a severely affected and symptomatic infant. Passive in utero transfer of maternally derived CMVspecific IgG antibody appears to provide some protection to the fetus when CMV is reactivated during pregnancy. The majority of infants with congenital CMV are asymptomatic (90%), but some have evidence of disease during the newborn period (10%). About 10% of the symptomatic group has full-blown cytomegalic inclusion disease. An additional 10% of infected infants who are asymptomatic at birth later develop symptoms related to CMV infection. The most common late-onset symptoms in these cases are mental retardation and deafness. These infants usually shed high titers of virus in the urine and saliva for a number of months. CMV infections can be acquired by the child during the postpartum period through (a) exposure of the infant to infectious maternal body fluids such as cervical secretions, urine, saliva, and breast milk; (b) following blood transfusion or tissue transplantation from an infected donor; or (c) most frequently, through contact with infected individuals, such as in the newborn nursery, day care centers, or from other family members in the household. These cases are called acquired cytomegalovirus infections in contrast to congenital infections.

Virology CMV has a diameter of about 180 nm and is encapsulated by an icosahedral capsid containing 162 capsomeres. Within the capsid is double-stranded DNA of about 230 kb that is enclosed by a lipid bilayer envelope. The diagnosis of CMV requires laboratory confirmation and cannot be made on clinical grounds alone. Seroconversion, monoclonal antibody, and PCR are among the tools available for diagnosis. Antibody response (whether maternal or fetal) may play a less important role in transmission and, subsequently, in the development of symptomatic disease than other viral factors, such as the amount of maternal viremia or the timing in pregnancy during which infection and subsequent maternal-to-fetal transmission occurs.

Epidemiology Seroprevalence of CMV among adult populations shows significant geographic variability. Rates range from 40% to 100% depending on the region surveyed, with most infections being detected solely by serologic screening (i.e., asymptomatic). Countries or regions with low socioeconomic status usually demonstrate very high seroprevalence rates. The risk of seroconversion during pregnancy for a seronegative woman is approximately 2%. However,

because congenital infections can follow either primary disease (maternal seroconversion) or reactivation of disease, congenital infections may occur in a much higher percentage of cases. There are two periods in life when infection rates are particularly high—perinatal (related to mother-to-child transmission, breast-feeding, and child to child) and reproductive age (putatively related to sexual transmission). Pregnant women acquire CMV infection either through exposure to infected children (the infected children shed virus in urine, saliva, and nasopharyngeal secretions and are infectious for a prolonged period) or through sexual contact. About 1% to 2% of women in the United States shed CMV from their cervix at any given time, although that number is higher in women with multiple sexual partners.

Pathophysiology The incubation period for CMV is 20 to 60 days. Following primary infection, the virus goes into a latent phase within host tissues. Intermittent periods of reactivation occur frequently, and virus again is excreted in the nasopharynx, cervix, urine, saliva, and breast milk. Maternal viral shedding increases throughout pregnancy, and neonatal infection becomes increasingly likely as cervical shedding rates increase toward term. Acquisition of disease by neonates at the time of birth is much more common than congenital infection but is much less devastating. Perinatally acquired infection comes from CMV carried in the cervix during the late stages of pregnancy as well as from CMV in breast milk. After primary infection during the prenatal period, the congenital infection rate has been reported to be as high as 55%. Although the majority of infants with congenital CMV are asymptomatic, infants with symptomatic infection at birth usually have findings associated primarily with the reticuloendothelial and central nervous systems. The severe cases of congenitally acquired symptomatic infection result from primary rather than recurrent infection in the pregnant woman and from infections occurring early in pregnancy. The most common findings in these severe cases include hepatosplenomegaly, jaundice, a generalized petechial rash, microcephaly, and growth restriction. Less common findings include chorioretinitis with or without optic atrophy, pneumonitis, cerebral calcifications, microphthalmia, microcephaly, seizures, and cerebral and cerebellar atrophy. The mortality of newborns with symptomatic disease is approximately 30%. Most deaths are due to disseminated intravascular coagulation, hepatic disease, and bacterial superinfection. In those neonates with sequelae at birth, 13% will have mental impairment.

Diagnosis Maternal Infection The majority of primary maternal infections with CMV are asymptomatic and unrecognized. When symptoms do occur, they often are not recognized as being indicative of CMV because they appear as a mild, infectious, mononucleosislike illness, with lymphadenopathy, fatigue, and slight fever. Even though CMV is hepatotropic, elevations in liver enzyme levels rarely are seen in primary or recurrent infections. In primary infections, lymphocytosis may be present with increases in atypical lymphocytes and

thrombocytopenia. A diagnostic approach to the pregnant woman following CMV exposure is outlined in Figure 19.5. About one third to two thirds of all pregnant women have IgG antibodies to CMV, indicating previous infection. Detection of CMV-specific IgM during the acute phase of infection is useful for making the diagnosis of CMV infection, but only 80% of women with primary infection demonstrate this antibody. In addition, more than one third of mothers with recurrent CMV from latent infection will be positive for CMV-specific IgM. CMV-specific IgM antibodies may persist up to 18 months, and some test methods may give false-positive results because of cross reactions with other herpesviruses, antinuclear antibody, or rheumatoid factor. A microneutralization assay may be of some utility. In one study, antibodies did not appear until 15 weeks after infection and persisted thereafter. Thus, its absence, shortly after a presumed infection, can help to rule out infection. In a recent report from a referral center in Italy, about one half of pregnant women with a diagnosis of preliminary referring CMV infection had no evidence of active infection. Clinicians should be thoughtful in analyzing commercially available tests results for IgG and IgM anti-CMV antibodies.

Figure 19.5 Diagnosis of maternal CMV infection. (CVM, cytomegalovirus; IgG, immunoglobulin G; IgM, immunoglobulin M; AI, avidity index; NT, neutralization test; IEmRNA, intermediate-early messenger RNA.) (From Hollier LM, Grissom H. Human herpes viruses in pregnancy: cytomegalovirus, Epstein-Barr virus, and varicella zoster virus. Clin Perinatol 2005;32:674; adapted from Revello M, Gerna G. Diagnosis of congenital HCMV infection. Clin Microbiol Rev 2002;15[4]:680–715, with permission.)

Avidity studies, with similar methodology to that described previously for toxoplasmosis, also can be performed with CMV IgG to try to differentiate between primary and reactivation infection. Again, when antibodies are first made to an antigen, they are of low avidity. With time, as antibodies mature, the avidity increases. Thus, the presence of high avidity shortly after a suspected infection makes recent infection (and the highest fetal risk) highly unlikely. Viral culture is the gold standard for the diagnosis of CMV infection. Virus usually is detected in the cervix, nasopharynx, and urine of infected individuals. However, culture results are positive with both primary and recurrent infections. PCR also has proven to be quite useful in the detection of CMV. Quantitative PCR testing has been particularly useful in the management of AIDS and transplant in patients whose high serum levels augur complications, and it offers an early opportunity for the initiation of antiviral therapy.

Fetal Infection Sonography may be useful for identifying some abnormalities in the fetus that may be related to CMV infection. A spectrum of sonographic findings including fetal hydrops, intrauterine growth restriction, polyhydramnios, fetal ascites, and specific CNS anomalies (e.g., ventriculomegaly, periventricular calcifications, and microcephaly) as well as intra-abdominal pathology (hepatosplenomegaly, intra-abdominal calcifications) may suggest an intrauterine infection, possibly CMV, and invasive fetal testing should be considered. When multiple ultrasound markers are found (microcephaly in particular is worrisome), prognosis is often poor, whereas if only isolated markers are found such as isolated hepatic calcifications, prognosis may be better. Lynch and others reported the successful prenatal diagnosis of fetal infection by a combination of amniotic fluid culture and measurement of total and CMV-specific IgM and γ-glutamyl transpeptidase in fetal blood samples. In a study of 189 pregnancies with known outcome, Enders and colleagues reported 89.5% sensitivity with the use of amniotic fluid and fetal blood assessments for virus and anti-CMV IgM. They noted that the correct diagnosis of in utero infection with CMV by amniotic fluid analysis could be expected after 21 weeks gestation and at least 6 weeks following the diagnosis of infection in the mother. Other authors have reported similar sensitivities and have pointed out that those instances of false-negative results often are associated with infants with minimal stigmata of disease. Further studies are needed on the sensitivity and specificity of these methods in

identifying infected infants prior to birth. More recently, quantitative PCR from the amniotic fluid has been used to give additional direction to counseling when congenital CMV is diagnosed in the fetus by amniocentesis. Guerra and associates showed that if Table of Contents > 20 - Human Immunodeficiency Virus

20 Human Immunodeficiency Virus Howard Minkoff

Human Immunodeficiency Virus The HIV epidemic is a quarter of a century old and in that time frame has transformed from a uniformly lethal disease of unknown etiology to a manageable chronic disease, albeit one with complicated treatment regimens and mortality remaining an inherent risk. The success of treatment regimens has led to the emergence of two epidemics—one among those with access to highly active therapies as well as a larger one among those without. In this chapter, the pathophysiology and epidemiology of HIV will be summarized, and the management of obstetric and gynecologic patients who are infected will be detailed. Given the ability of U.S. providers to avail themselves of the most efficacious therapies, they should be able to assure their patients that perinatal transmission of HIV will be an extremely uncommon event and that gynecologic morbidities can be minimized.

Microbiology HIV is a lentivirus, from the family of retroviruses, which characteristically have an RNA genome contained within a capsid and a lipid envelope. Retroviruses constitute a large and diverse family of enveloped RNA viruses that use the transcription of virion RNA into linear double-stranded DNA as a replication strategy, with subsequent integration into the host genome. The characteristic enzyme used for this process, an RNA-dependent DNA polymerase that reverses the flow of genetic information, is known as reverse transcriptase. The unique lifestyle of the retrovirus involves two forms, a DNA provirus and an RNA-containing infectious virion. Infection is initiated by the binding of a protein on the surface of the virus (gp120 Env protein) to the CD4 molecule found on some T-cells, macrophages, and microglial cells. CD4 was first shown to be a viral receptor in a number of studies showing the susceptibility of CD4-bearing cells to infection and the ability to block infection with anti-CD4 monoclonal antibodies in culture. HIV is composed of core (p18, p24, and p27) and surface (gp120 and gp 41) proteins, genomic RNA, and the reverse transcriptase enzyme surrounded by a lipid bilayer envelope. The virion contains three structural genes (gag, pol, and env) as well as a complex set of regulatory genes (including tat, vif, nef, vpu, and ref) that control the rate of virion production. As noted, it preferentially infects cells with the CD4+ antigen,

particularly helper lymphocytes but also macrophages, cells of the central nervous system, and according to some evidence, cells of the placenta. At least two other cell surface molecules help HIV enter cells. These coreceptors for HIV, called CXCR4 and CCR5, are receptors for chemokines. Individuals who are homozygous for a deletion at the CCR5 gene appear less likely to acquire HIV, while deletion heterozygotes progress less rapidly if infected. On the basis of cell tropism, HIV strains can be broadly divided into two categories—macrophage-tropic (M-tropic) and T-cell tropic (T-tropic). M-tropic strains use CCR5 as a coreceptor and are referred as R5 viruses. They primarily infect macrophages and primary T cells and infect poorly CD4+ T-cell lines. In addition, these viruses tend to be transmitted sexually more easily. T-tropic strains use the CXCR4 coreceptor, which is most expressed in CD4+ T cells. Also referred to as X4 viruses, they induce the formation of syncytia in the infected cells. Early in the course of HIV infection, the R5 strain viruses predominate; however, eventually, both X4 and R5 strains are recovered (Fig. 20.1).

Figure 20.1 Early in the course of HIV infection, the R5 strain viruses predominate, but eventually both X4 and R5 strains are recovered. (From Levy JA. Infection by human immunodeficiency virus—CD4 is not enough. N Engl J Med 1996;335:1525–1527, Figure 1A. Illustrations © Massachusetts Medical Society, with permission.) (See Color Plate)

Epidemiology By the end of 2003, approximately 1,039,000 to 1,185,000 persons in the United States were living with HIV/AIDS, an estimated 24% to 27% of whom were unaware of their infection, with approximately 25% being women. AIDS cases increased rapidly in the 1980s and peaked in 1992 (an estimated 78,000 cases diagnosed that year) before stabilizing in 1998; since then, approximately 40,000 AIDS cases have been diagnosed annually. Over the course of the epidemic, even before effective treatments were widely utilized, the number of AIDS cases decreased 47% from 1992 to 1998. The majority of AIDS cases continue to occur among males; however, the proportion of all AIDS cases for females increased from 15% in

1981 to 1995 to 27% in 2001 to 2004. Not coincidently, the vast majority of cases of pediatric AIDS are secondary to vertical transmission of HIV from mother to fetus. The proportion of all AIDS cases attributable to high-risk heterosexual contact (i.e., sexual contact with a person at high risk for or infected with HIV) from 1981 to 1995 was 10% and increased to 30% from 2001 to 2004. Among males and females, case rates among blacks (males: 131.6 per 100,000; females: 67.0 per 100,000) were 7 and 21 times higher, respectively, than rates for whites (males: 18.7 per 100,000; females: 3.2 per 100,000). Other important trends characterize the epidemic in women. For example, an increasing proportion of AIDS cases are occurring in women in the South, perhaps reflecting the dramatic increase in other sexually transmitted diseases first seen in that region more than a decade ago. Poverty status also might vary with gender, with women substantially more likely to be covered by Medicaid and less likely to be privately insured. These data demonstrate, yet again, that poverty, drug use, and sexually transmitted diseases continue to fuel the HIV epidemic among women in the United States.

Pathophysiology HIV infection induces a profound immune dysfunction, with abnormalities in every arm of the immune system. While studies of long-term nonprogressors (HIV-infected patients who are asymptomatic and have normal CD4+ T-cell counts in the absence of treatment) have revealed several immune mechanisms that are significant in controlling HIV infection, the virus has several inherent strategies by which to escape this vigorous immune response and to continue replicating. The most studied of these strategies are antigenic variation, down regulation of the surface expression of major histocompatibility complex (MHC) molecules, and reduction of specific CD8+ T cells. Once the immune system has become debilitated, infected individuals are rendered susceptible to opportunistic infections (e.g., Pneumocystis carinii pneumonia [PCP] and central nervous system toxoplasmosis) and neoplasias (e.g., Kaposi's sarcoma) that rarely afflict patients with intact immune systems. An HIV-infected patient with one of several specific opportunistic infections, neoplasia, dementia encephalopathy, or wasting syndrome is diagnosed as having AIDS. The diagnosis of AIDS can be made in the absence of laboratory evidence of infection if the patient has no other known cause of immune deficiency and has the definitive diagnosis of one of a number of indicator diseases. In 1993, the Centers for Disease Control and Prevention (CDC) changed the case definition to include all individuals with HIV infection whose CD4 counts drop below 200 cells/mm3 as well as HIV-infected individuals with advanced cervical cancer, pulmonary tuberculosis, and recurrent pneumonia. At the time of initial infection, an individual may be asymptomatic or may develop an acute mononucleosislike syndrome that can be accompanied by aseptic meningitis. There is then an immediate viremia of substantive proportions (up to ten billion viral particles turned over per day) and an equally impressive immune responsive with similar levels of Tcell turnover. Antibodies can be detected in almost all individuals at 6 to 12 weeks after exposure, but in rare circumstances, this latent period (the so-called “window phase”) can be longer. After seroconversion has occurred, an asymptomatic period of variable length usually follows. The median clinical latency in the absence of effective therapy is

estimated at approximately 11 years. Very few infected persons (100,000 copies or when the CD4 count drops below 350 cells/mm3. In the nonpregnant state, when those thresholds are passed, HAART should be initiated. The appropriate guidelines for initiating therapy in pregnancy follow.

Resistance Testing Resistance testing has become a staple of care for HIV-infected individuals. The viral RNA is reverse transcribed into complementary DNA (cDNA) by the viral reverse transcriptase through use of a cellular lysine tRNA molecule as a primer; subsequently, the RNAase activity of the reverse transcriptase degrades the viral RNA template. The reverse transcriptase incorporates an incorrect nucleotide every 1,500 to 4,000 bases, which explains the rapid occurrence of mutations. Some of the resulting mutations provide a survival advantage, leading to drugresistant strains. There is accumulating evidence that transmitted resistant mutants may persist for indefinite periods after initial infection, these viral variants may be detectable by standard

assays used in clinical practice, the prevalence of resistance in antiretroviral-naive patients is increasing, and baseline resistance may be associated with adverse virologic outcomes. For these reasons, baseline HIV resistance testing is now recommended for all patients with established infection, including pregnant women, prior to initiating treatment. Most randomized trials of resistance testing have demonstrated that those assigned to study arms with access to resistance test results have a greater reduction in viral load after the initiation of salvage therapy, though follow-up generally has been short. These tests are recommended for individuals prior to commencing therapy or after failed therapy. Treatment failure is defined as the failure to attain an undetectable level of virus or the persistent presence of virus after it has become undetectable. Transient low-level viremia may not be the same as a drug failure, and sustained response to treatment can occur even in the setting of occasional low-level viremia. Blood for testing should be obtained before a failing regimen is discontinued lest wild-type virus overgrow before the test is performed. In that circumstance, an individual with no apparent resistance would still fail therapy when reexposed to drugs that favor the growth of the resistant virus over the wild-type strain. In essence, resistance testing is more useful for ruling out, than for ruling in, therapies to be utilized in a given patient. That is because, as noted, the absence of resistance may merely reflect the reemergence of a wild-type strain after an antiretroviral agent has been withdrawn. In that circumstance, the assays will not detect a low volume of a minority mutant strain. However, if the patient is reexposed to the offending agent, the resistant strain may again attain dominance. It is not possible to perform resistance studies if there are 100,000 copies/mL. Using two NRTIs alone does not achieve the goal of suppressing viremia to below detectable levels as consistently as does the other regimens discussed previously and should be used only if more potent treatment is not possible. Use of antiretroviral agents as monotherapy is contraindicated, except when there are no other options or in pregnancy to reduce perinatal transmission, as noted below. When initiating antiretroviral therapy, all drugs should be started simultaneously at full dose with the following three exceptions: dose escalation regimens are recommended for ritonavir; nevirapine (NVP); and in some cases, ritonavir plus saquinavir. Recent data confirm that four drugs are generally no better than three drugs when considering treatment with currently available NRTIs and PIs in treatment-naive patients who are not infected with drug-resistant virus. In order to determine whether a change in therapy is appropriate, the patient must undergo monitoring for immunologic and virologic response as well as for drug toxicity and acceptability. The aim of antiretroviral therapy remains the maintenance of a plasma HIV-1 RNA level below the limits of detection of the most sensitive assays available commercially (i.e., 250 CD4 cells/mm3. In women who become pregnant while taking NVP, this risk is substantially lower. Until more data are available that address concerns about bone formation in utero, tenofovir should be avoided unless resistance testing suggests that its use is advisable. Efavirenz is contraindicated in the first trimester of pregnancy. Nelfinavir has been used extensively in pregnancy, but concerns about its potency make it a less attractive agent. Ritonovir-boosted lopinavir remains an acceptable first-line option, although concerns about dosing have been raised and currently are being addressed. When possible, ZDV should be used as part of the antiviral regimen. In Pediatric AIDS Clinical Trials Group (PACTG) Protocol 076, which utilized a regimen of ZDV given during pregnancy and labor and to the newborn for 6 weeks, the antenatal dosing of 100 mg administered orally five times daily was selected on the basis of the standard ZDV dosage

for adults at the time of the study. However, administration of ZDV three times daily will maintain intracellular ZDV triphosphate at levels comparable with those observed with more frequent dosing. Comparable clinical response also has been observed in some clinical trials among persons receiving ZDV twice daily. Thus, the current standard dosing for ZDV, whether used as a part of a HAART regimen or as single drug therapy for transmission prevention (discussed below), is 200 mg three times daily or 300 mg two times daily. While it is possible that these dosing regimens may not have equivalent efficacy to that observed in PACTG 076, a regimen of two or three times daily is likely to enhance maternal adherence. Most data regarding the safety of ZDV have been reassuring. Almost 1,000 children have been tracked for 4 years with no increase in risks of neurodevelopmental delay or carcinogenesis. In regard to monitoring of the mother on ZDV, it only is necessary to measure the blood count and liver functions on a monthly basis. The only abnormality that occurs with any frequency is anemia. Other NRTIs generally have been well tolerated and have not been demonstrated to be teratogenic in humans. However, concerns have been raised about potential adverse effects on both mothers and infants related to the avidity of these drugs for mitochondria. By binding to mitochondrial γ-DNA polymerase and interfering with replication, these drugs can induce mitochondrial dysfunction. ddC demonstrates the greatest inhibition of mitochondrial γ-DNA polymerase, followed in order by ddI, d4T, 3TC, ZDV, and abacavir. Clinical disorders associated with mitochondrial toxicity include neuropathy, myopathy, cardiomyopathy, pancreatitis, hepatic steatosis, and lactic acidosis. In regard to potential maternal toxicity, several cases of lactic acidosis, three of which were fatal and two of which were accompanied by pancreatitis, have been reported among pregnant or recently delivered women who had been on ddI and d4T therapy along with a variety of third agents since before conception. Two cases of fatal liver failure in pregnant women on ZDV, 3TC, and nelfinavir also have been reported. These cases developed in late pregnancy, and in several cases, the presentation was similar to that seen with acute fatty liver of pregnancy, a condition that itself has been linked to mitochondrial fatty oxidation disorders in the fetus and mother. This has led to speculation that the metabolic changes of late pregnancy may enhance susceptibility to complications of nucleoside agents, especially those with greater inhibition of mitochondrial γ-DNA polymerase. That susceptibility is suggested both by the syndrome of acute fatty liver of pregnancy and animal data that demonstrate reduced mitochondrial fatty acid oxidation in late pregnancy and in animals treated with exogenous estradiol and progesterone to mimic pregnancy levels. However, many cases of death related to use of these medications outside of pregnancy have been reported as well. In any event, although these serious morbidities appear to be rare, providers caring for HIV-infected women receiving nucleoside analog agents should be cognizant of the risk and monitor accordingly. One approach would be to monitor hepatic enzyme levels during the last trimester and to aggressively investigate all new symptoms. Women with substantial elevations in transaminase levels above baseline or other new abnormalities, in the absence of other explanations such as preeclampsia, should have their nucleoside agents discontinued, either with substitution of agents from another class of antiretrovirals or discontinuation of all antiretrovirals. In view of the

reports of maternal

deaths and toxicity associated with prolonged use of d4T and ddI in pregnancy, this combination should be used in pregnancy with caution and only if other nucleoside agents cannot be used because of resistance or toxicity.

TABLE 20.3 Antiretroviral Drug Use in Pregnant HIV-Infe Pharmacokinetic and Toxicity Data in Human Pregnancy and Re Use in Pregnancy Antiretroviral Drug

Pharmacokinetics in Pregnancy

Concerns in Pregnancy

NRTIs/NtRTIs

Recommended agents

Zidovudine*

Pharmacokinetics not significantly altered in pregnancy; no change in dose indicated.

No evidence of human teratogenicity. Well-tolerated, short-term safety demonstrated for mother and infant.

Lamivudine*

Pharmacokinetics not significantly altered in pregnancy; no change in dose indicated.

No evidence of human teratogenicity. Well-tolerated, short-term safety demonstrated for mother and infant.

Pharmacokinetics not significantly altered in pregnancy; no change in dose

Cases of lactic acidosis, some fatal, have been reported in pregnant women receiving

Alternate agents

Didanosine

Emtricitabine†

Stavudine

Abacavir*

indicated.

didanosine and stavudine together.

No studies in human pregnancy.

Pharmacokinetics not significantly altered in pregnancy; no change in dose indicated.

No evidence of human teratogenicity. Cases of lactic acidosis, some fatal, have been reported in pregnant women receiving didanosine and stavudine together.

Pharmacokinetics are not significantly altered in pregnancy; no change in dose indicated.

Hypersensitivity reactions occur in ~58% of nonpregnant persons; a much smaller percentage are fatal and are usually associated with rechallenge. Rate in pregnancy unknown. Patient should be educated regarding symptoms of hypersensitivity

reaction. Insufficient data to recommend use

Tenofovir†

No studies in human pregnancy. Phase I study in late pregnancy in progress.

Studies in monkeys show decreased fetal growth and reduction in fetal bone porosity within two months of starting maternal therapy. Clinical studies in humans (particularly children) show bone demineralization with chronic use; clinical significance unknown.

No studies in human pregnancy.

Rodent studies indicate potential for teratogenicity and developmental toxicity.

Not recommended

Zalcitabine

NNRTIs Recommended agents

Nevirapine

Pharmacokinetics not significantly altered in pregnancy; no change in dose indicated.

No evidence of human teratogenicity. Increased risk of symptomatic, often rash associated, and potentially fatal liver toxicity among women with CD4+ counts >250/mm3 when first initiating therapy; unclear if pregnancy increases risk.

Not recommended

Efavirenz†

No studies in human pregnancy.

FDA Pregnancy Class D; significant malformations (anencephaly, anophthalmia, cleft palate) were observed in 3 (15%) of 20 infants born to cynomolgus monkeys receiving efavirenz during the first trimester at a dose giving plasma levels comparable to systemic human

therapeutic exposure; there are three case reports of neural tube defects in humans after first trimester exposure; relative risk unclear.

Delavirdine

Protease Inhibitors

Recommended agents

No studies in human pregnancy.

Rodent studies indicate potential for carcinogenicity and teratogenicity.

Hyperglycemia, new onset or exacerbation of diabetes mellitus, and diabetic ketoacidosis reported with PI use; unclear if pregnancy increases risk. Conflicting data regarding preterm delivery in women receiving PIs.

Lopinavir/ritonavir

Pharmacokinetic studies of standard dose of lopinavir/ritonavir capsules (3 capsules twice daily) during 3rd trimester indicated levels were significantly lower than during postpartum period and in nonpregnant adults; an increased dose of 4 capsules of lopinavir/ritonavir twice daily starting in the 3rd trimester resulted in adequate lopinavir exposure; by 2 weeks postpartum, standard dosing was again appropriate. Pharmacokinetic studies of the new lopinavir/ritonavir tablet formulation are underway, but data are not yet

No evidence of human teratogenicity. Well-tolerated, short-term safety demonstrated in phase I/II studies.

Nelfinavir

Alternate agents

Adequate drug levels are achieved in pregnant women with nelfinavir 1250 mg, given twice daily.

No evidence of human teratogenicity. Well-tolerated, short-term safety demonstrated for mother and infant. Nelfinavir dosing at 750 mg three times daily produced variable and generally low levels in pregnant women.

Indinavir

Ritonavir

Two studies including 18 women receiving indinavir 800 mg three times daily showed markedly lower levels during pregnancy compared to postpartum, although suppression of HIV RNA was seen.

Theoretical concern re: increased indirect bilirubin levels, which may exacerbate physiologic hyperbilirubinemia in the neonate, but minimal placental passage. Use of unboosted indinavir during pregnancy is not recommended.

Phase I/II study in pregnancy showed lower levels during pregnancy compared to postpartum.

Limited experience at full dose in human pregnancy; has been used as lowdose ritonavir boosting with other PIs.

Pharmacokinetic studies of saquinavir soft gel capsules (SGC) indicated that inadequate drug levels were observed in pregnant women given 1,200 mg of saquinavir-SGC as a sole PI three times daily [275], but adequate levels were

Saquinavirhard gel capsule [HGC] (Invirase®)/ritonavir

achieved when 800 mg saquinavir-SGC boosted with ritonavir 100 mg was given twice daily. However, saquinavir-SGC is no longer produced. Limited pharmacokinetic data on saquinavir hard gel capsule (HGC) suggest that 1,000 mg saquinavirHGC/100 mg ritonavir given twice daily will achieve adequate saquinavir drug levels in pregnant women.

Well-tolerated, short-term safety demonstrated for mother and infant for both saquinavir-SGC and -HGC in combination with low-dose ritonavir.

Insufficient data to recommend use

Amprenavir

Atazanavir

No studies in human pregnancy.

No studies in

Oral solution contraindicated in pregnant women because of high levels of propylene glycol, which may not be adequately metabolized during pregnancy. Theoretical concern re: increased indirect bilirubin levels, which may exacerbate physiologic

human pregnancy.

hyperbilirubinemia in the neonate, although transplacental passage of other PIs has been low.

Darunavir

No studies in human pregnancy.

No experience in human pregnancy.

Fosamprenavir

No studies in human pregnancy.

No experience in human pregnancy.

Tipranavir

No studies in human pregnancy.

No experience in human pregnancy.

Fusion Inhibitors Insufficient data to recommend use

Enfuvirtide

No studies in human pregnancy.

No experience in human pregnancy

NRTI, nucleoside reverse transcriptase inhibitor; NtRTI, nucleotide transcriptase inhibitor; NNRTI, non-nucleoside reverse transcripta

protease inhibitor; SGC, soft gel capsule; HGC, hard gel capsule. *Zidovudine and lamivudine are included as a fixed-dose combinat zidovudine, lamivudine, and abacavir are included as a fixed-dose Trizivir®. † Emtricitabine and tenofovir are included as a fixed-dose combina emtricitabine, tenofovir, and efavirenz are included as a fixeddose AtriplaTM . ‡ Triple NRTI regimens including abacavir have been less potent vir to PI-based HAART regimens. Triple NRTI regimens should be used or PI-based HAART regimen cannot be used (e.g., due to significan A study evaluating use of zidovudine/lamivudine/abacavir among p with HIV RNA 500 cells/mm3 and who had normal cervical cytology at baseline. They concluded that similar cervical cancer screening practices might be applicable to both groups, although they cautioned that such a strategy warranted evaluation in an appropriate clinical trial.

Menstrual Irregularities While a large number of studies have assessed the association between HIV infection and menstrual abnormalities, none has clearly demonstrated a link. Any such studies must consider a variety of confounding factors that might mediate such a relationship, such as weight loss (or gain secondary to HAART), smoking, or illicit drug use. One large study controlling for several of the aforementioned confounding factors demonstrated slightly shorter (1,000 copies should be offered elective cesarean sections at 38 weeks but should not undergo amniocentesis. Prophylactic antibiotics should be given. Efavirenz should be avoided in the first trimester, and NVP should not be initiated as part of a HAART regimen for women with a CD4 count over 250 cells/mm3. Women with unknown HIV status in labor should undergo rapid testing. If found to be positive, they should receive intrapartum therapy. Methergine should not be coadministered with PIs or with the NNRTIs efavirenz and delavirdine, because these drugs are potent CYP3A4 enzyme inhibitors. PIs may affect blood levels of hormones (and vice versa). Therefore, up-to-date sources on drug–drug interactions should be utilized prior to prescribing hormonal contraception. Condom use with emergency contraceptive backup is recommended because studies show that attempts at consistent

dual method use consisting of a condom plus use of a rigorous, client dependent, ongoing method of reversible contraception (e.g., combined hormonal contraceptives or progestin-only hormonal contraception) often results either in inconsistent use of the condom or inconsistent use of the ongoing pregnancy prevention method. Infertile HIV-infected couples should undergo the same evaluation as noninfected couples and have access to ART. HIV-infected women should have a baseline Pap smear, which should then be repeated at 6 months and then annually if the results are normal. Women with abnormal Pap tests, including ASCUS, ASC-H, or LSIL, should be referred for colposcopy and further evaluation that may include HPV DNA testing, cervical biopsy, cervical curettage, and endometrial biopsy, depending on cell type and the degree of cytological abnormality.

Suggested Readings Epidemiology/Pathophysiology Borrow P, Lewicki H, Wei X, et al. Antiviral pressure exerted by HIV-1 specific cytotoxic T-lymphocytes (CTLs) during primary infection demonstrated by rapid selection of CTL escape virus. Nat Med 1997;3:205–211. Cen S, Khorchid A, Javanbakht H, et al. Incorporation of lysyl-tRNA synthetase into human immunodeficiency virus type 1. J Virol 2001;75:5043–5048. Centers for Disease Control and Prevention. Epidemiology of HIV/AIDS—United States, 1981–2005. MMWR Morb Mortal Wkly Rep 2006;55(21):589–592. Chinen J, Shearer WT. Molecular virology and immunology of HIV infection. J Allergy Clin Immunol 2002;110(2):189–198. Colgrove RC, Pitt J, Chung PH, et al. Selective vertical transmission of HIV-1 antiretroviral resistance mutations. AIDS 1998;12(17):2281–2288. Goulder PJ, Phillips RE, Colbert RA, et al. Late escape from an immunodominant cytotoxic T-lymphocyte response associated with progression to AIDS. Nat Med 1997;3:212–217. Hader SL, Smith DK, Moore JS, et al. HIV infection in women in the United States. Status

at the millennium. JAMA 2001;285:1186–1192. Ho DD, Neumann AU, Perelson AS, et al. Rapid turnover of plasma virons and CD4 lymphocytes in HIV-1 infection. Nature 1995;373:123–126. Lansky A, Fleming PL, Byers RH Jr, et al. A method for classification of HIV exposure category for women without HIV risk information. MMWR Recomm Rep 2001;50(RR-6):31– 40. Liu R, Paxton WA, Choe S, et al. Hoozygous defect in HIV-1 co-receptor accounts for resistance for some multiply-exposed individuals to HIV-1 infection. Cell 1996;86:367– 377. Nijhuis M, Deeks S, Boucher C. Implications of antiretroviral resistance on viral fitness. Curr Opin Infect Dis 2001;14(1):23–28. Pantaleo G, Soudenys H, Demarest JF, et al. Evidence for rapid disappearance of initially expanded HIV-specific CD8+ T-cell clones during primary HIV infection. Proc Natl Acad Sci USA 1997;94:9448–9453. Pao D, Andrady U, Clarke J, et al. Long-term persistence of primary genotypic resistance after HIV-1 seroconversion. J Acquir Immune Defic Syndr 2004;37(5):1570–1573. Schneider MF, Gange SJ, Williams CM, et al. Patterns of the hazard of death after AIDS through the evolution of antiretroviral therapy: 1984–2004. AIDS 2005;19(17):2009–2018. Weinstock HS, Zaidi I, Heneine W, et al. The epidemiology of antiretroviral drug resistance among drug-naïve HIV-1 infected persons in 10 US cities. J Infect Dis 2004;189(12):2174–2180.

Management of the Human Immunodeficiency Virus Aberg JA, Gallant JE, Anderson J, et al. Primary care guidelines for the management of persons infected with human immunodeficiency virus; recommendations of the HIV Medicine Association of the Infectious Diseases Society of America. Clin Infect Dis 2004;39:609–629. Durant J, Clevenbergh P, Halfon P, et al. Drug-resistance in HIV-1 therapy: the VIRADAPT randomized control trial. Lancet 1999;353:2195–2199. Hammer SM, Saag MS, Schecter M, et al. Treatment for adult HIV infection: 2006

recommendations of the International AIDS Society–USA Panel. JAMA 2006;296:827–843. Hecht FM, Grant RM. Resistance testing in drug-naïve HIV-infected patients: is it time? Clin Infect Dis 2005;41(9):1324–1325. Robbins GK, De Gruttola V, Shafer RW, et al. Comparison of sequential three-drug regimens as initial therapy for HIV-1 infection. N Engl J Med 2003;349:2293–2303. Sax PE, Islam R, Walensky RP, et al. Should resistance testing be performed for treatment-naïve HIV-infected patients? A cost-effectiveness analysis. Clin Infect Dis 2005;41(9):1316–1323.

Pregnancy American College of Obstetricians and Gynecologists. Scheduled cesarean delivery and the prevention of vertical transmission of HIV infection. ACOG Committee Opinion No. 234, May 2000. Baylor MS, Johann-Liang R. Hepatotoxicity associated with nevirapine use. J Acquir Immune Defic Syndr 2004;35:S21–S33. Blanche S, Tardieu M, Rustin P, et al. Persistent mitochondrial dysfunction and perinatal exposure to antiretroviral nucleoside analogues. Lancet 1999;354:1084–1089. Connor EM, Sperling RS, Gelber R, et al. Reduction of maternal-infant transmission of human immunodeficiency virus type 1 with zidovudine treatment. N Engl J Med 1994;331:1173–1180. European Collaborative Study and the Swiss Mother + Child HIV Cohort Study. Combination antiretroviral study and duration of pregnancy. AIDS 2000;14:2913–2920. European Mode of Delivery Collaboration. Elective caesarian-section versus vaginal delivery in prevention of vertical HIV-1 transmission: a randomized clinical trial. Lancet 1999;353:1035–1039. French R, Brocklehurst P. The effect of pregnancy on survival in women infected with HIV: a systemic review of the literature and meta-analysis. Br J Obstet Gynecol 1998;105:827–835. Fundaro C, Genovese O, Rendeli C, et al. Myelomeningocele in a child with intrauterine

exposure to efavirenz. AIDS 2002;16:299–300. Garcia PM, Kalish KA, Pitt J, et al. Maternal levels of plasma human immunodeficinecy virus type 1 RNA and the risk of perinatal transmission. N Engl J Med 1999;341:394–402. Guay LA, Musoke P, Fleming T, et al. Intrapartum and single dose nevirapine compared with zidovudine for prevention of mother-to-child transmission of HIV-1 in Kampala, Uganda: HIVNET 012 randomised trial. Lancet 1999;354:795–802. Ibday JA, Yang Z, Bennett MJ. Liver disease in pregnancy and fetal fatty acid oxidation defects. Mol Genet Metab 2000;71:182–189. International Perinatal HIV Group. The mode of delivery and the risk of vertical transmission of human immunodeficiency virus type 1: a meta-analysis of 15 prospective cohort studies. N Engl J Med 1999;340:977–987. Ioannidis JPA, Abrams EJ, Ammann A, et al. Perinatal transmission of human immunodeficiency virus type 1 by pregnant women with RNA virus loads Table of Contents > 21 - Placenta Previa and Abruption

21 Placenta Previa and Abruption Helen H. Kay All bleeding during pregnancy should be investigated by an examination and imaging studies. There are many etiologies for bleeding in pregnancy, but the most clinically significant are placenta previa and placental abruption. These conditions can lead to serious fetal compromise and maternal death. Other causes of bleeding that should be excluded are cervical lesions such as carcinoma or polyps, vaginal lacerations from trauma or carcinoma, other uterine bleeding such as dehiscence of a prior cesarean section scar, and premature cervical dilation, although these usually do not present with large amounts of blood loss. The presence of either placenta previa or placental abruption places the patient in a high-risk situation that warrants close monitoring. A definitive diagnosis is extremely important because in many cases, both commit the patient to a prolonged period of bed rest and hospitalization.

Placenta Previa Incidence Placenta previa is encountered in approximately 0.50% to 1.00% of all pregnancies and is fatal in 0.03% of cases. Formerly, the diagnosis of milder degrees of placenta previa without hemorrhage may have gone unnoticed by clinical exam, but now with the widespread use of ultrasound scanning, the incidence appears to be rising. It is more common in multiparous than in nulliparous women, occurring in only 1 in 1,500 nulliparas and in as many as 1 in 20 grand multiparas. The incidence in the United States is declining, probably in part due to the smaller number of grand multiparous women.

Definition The definition of placenta previa has been complicated because the original descriptions referred to the location of the placenta in relation to a dilated cervix (i.e., in labor) determined by digital exam. By this diagnostic methodology, a complete previa is present when the placenta extends over and beyond the internal os. A partial previa refers to a placenta with its edge partially over the dilated cervix, meaning that if the cervix were visualized with a speculum, placental tissue would be seen over some part of the dilated

cervical area but not all. The last type of previa, the marginal previa, refers to a placenta where the edge lies very close to and up to the edge of the os but does not cover any of the dilated cervix. In those original descriptions, the distance between the placental edge and the internal os was never defined in terms of centimeters (Fig. 21.1). However, with the advent of transvaginal ultrasound imaging, the cervix can be routinely imaged, even when not dilated, and the internal os is seen as a point, not a dilated cervix—hence the confusion over the terminology. In today's practice, any suspected low-lying placenta seen by transabdominal scan should be further evaluated by a transvaginal scan to determine the distance between the edge of the placenta and the internal os (Fig. 21.2). Those cases where the placental edge completely covers the cervical os are labeled as a complete previa. Those with the placental edge at the cervical os should be labeled as partial or marginal (partial/marginal), as it is impossible to determine whether those placentas will remain covered over the dilated cervix during labor or whether they will remain at the edge of the dilated cervix. The cases in which the placental edge is located within 1 to 2 cm of the internal os are the most confusing. Studies that have evaluated the situation where a placental edge is 2 cm from the cervical os are considered to have normal placentas that are not previa. Patients with the placental edge between 1 and 2 cm of the internal os, however, remain in the gray zone. These patients will benefit from either a double setup at the time of labor or close observation in labor and an attempt for a vaginal delivery if there is no bleeding.

Figure 21.1 Diagrammatic illustration of the three classic types of previa: marginal, partial, and complete. These relate to diagnosis by digital or visual examination when the patient is in labor with a partially dilated cervix. The term central previa refers to a previa in which the central portion of the placenta lies directly over the cervical os.

Figure 21.2 Diagrammatic illustration of the classes of placenta previa diagnosed by transvaginal ultrasound. In the nonlaboring patient, the internal os is seen as a point, and the distance between this and the lower edge of the placenta becomes the more critical reference.

Pathophysiology Placenta previa is a condition of abnormal implantation (i.e., into the lower uterine segment rather than the corpus or fundal region). The exact pathophysiology is unknown, but because it is seen more frequently in patients who tend to be older, multiparous, and have had prior cesarean sections or prior uterine curettage, it is thought to result from scarring in the endometrium. This is theorized to lead to abnormal endometrial tissue, poor vascularization, thinner myometrium, and a less favorable location for implantation. Presumably, the embryo is attracted to healthier tissue, which would be the unaffected endometrium of the lower uterine segment. By this rationale, the anterior uterine segment after cesarean section would appear to be an unfavorable site for implantation, but for uncertain reasons, the uterine trauma from cesarean sections actually increases the risk of previa by as much as sixfold.

Risk Factors Several risk factors have been found that are associated with placenta previa (Table 21.1). The most significant is a prior cesarean section (approximately 1 in 200 deliveries; the incidence is higher if a woman has undergone two or more cesarean sections). Black or minority patients seem to be at higher risk, as are women over 35 years of age. Other risks include increased gravidity and parity and cigarette smoking, with a 2.6- to 4.4-fold increase. Interestingly, meta-analyses have shown a preponderance of male gender among the fetuses with placenta previa. The mechanism for this is unknown. Previous abortion has not been consistently shown to be associated with an increase in risk for previa.

TABLE 21.1 Risk Factors Associated with Placenta Previa Black and minority Advanced maternal age High gravidity High parity Previous abortion—induced and spontaneous Prior cesarean section Cigarette smoking

Diagnosis The diagnosis of placenta previa can be made by transabdominal ultrasound. With the advent of the curvilinear probe, the cervical and lower uterine segment is much better imaged, and the relationship of the lower placental edge to the internal cervical os can be routinely visualized. However, the most common diagnostic pitfalls include a distended bladder and a lower uterine segment contraction that can lead to misdiagnosis. Of those placenta previas diagnosed in the second trimester, 90% to 95% resolve by the third trimester due to further development of the lower uterine segment, also referred to as “migration” of the placenta. However, if the placenta covers the internal os by 20 mm or more, meaning that it crosses the os by 20 mm, there is a 100% sensitivity rate for detection of previa at delivery, which requires a cesarean section. Three-dimensional scanning may further increase prenatal detection, but this technology remains a new investigational technique for previa at this time. Therefore, it is imperative that follow-up scanning be performed to determine if there is resolution of what appears to be a placenta previa. Marginal and partial placenta previa are significantly less likely to persist into the third trimester (i.e., Table of Contents > 23 - Stillbirth and Intrauterine Fetal Demise

23 Stillbirth and Intrauterine Fetal Demise Robert M. Silver Few obstetric complications are as emotionally devastating for families as antepartum stillbirth. Since the mid 20th century, there has been a tremendous decrease in the rate of stillbirth due to improved prevention and treatment of conditions such as diabetes, hypertension, and red cell alloimmunization. However, stillbirth rates have reached a plateau or have only modestly declined over the past several decades. This is in contrast to neonatal death rates, which continue to drop substantially. Currently, stillbirth after 20 weeks gestation affects over 1 in 200 pregnancies and is considerably more common than sudden infant death syndrome and intrapartum stillbirth in developed countries. Nonetheless, relatively more public attention and research have focused on infant rather than fetal mortality. Thus, fetal death remains a common, important, and poorly understood obstetric problem. This chapter will review the nomenclature, epidemiology, causes, risk factors for, management of, and recurrence risk for stillbirth. Emphasis will be placed on clinically relevant issues, recent developments, and areas of controversy.

Terminology The terminology of pregnancy loss can be confusing and often varies among and even within countries. Traditionally, abortions (or miscarriages) refer to pregnancy losses prior to 20 weeks gestation, while fetal deaths or stillbirths are used to describe losses after 20 weeks gestation. The threshold of 20 weeks is somewhat arbitrary, and it may be more useful to classify pregnancy losses by stages of gestational development. For example, pregnancy losses could be classified as pre-embryonic or anembryonic (conception to 5 weeks gestation), embryonic (6 to 9 weeks gestation), and fetal (after 10 weeks gestation) losses. In the past, anembryonic losses were termed blighted ova. This term is best avoided. Another approach would be to describe losses prior to 20 weeks gestation as early losses and those after 20 weeks gestation as late losses. It is important to specify the timing in gestation and nature of pregnancy loss as accurately as possible. This can be difficult because death or failure of growth of the conceptus may precede clinical symptoms of miscarriage by days or weeks. Thus, ultrasound findings, histologic examination, and human chorionic gonadotropin (hCG) levels often are more

useful than clinical data when characterizing pregnancy losses. The etiologies of pregnancy losses vary over gestation. Genetic problems are more common in pre-embryonic or anembryonic losses, while antiphospholipid syndrome (APS) and heritable thrombophilias are more likely in losses after 10 weeks gestation. Also, the recurrence risk of pregnancy loss is influenced by gestational age. Pregnancy losses tend to recur at similar times during gestation, and in patients with recurrent pregnancy loss, those with fetal deaths after 10 weeks gestation have worse subsequent pregnancy outcomes than women with recurrent early losses. Stillbirth often is defined as the death of a fetus after 20 completed weeks of gestation. In cases of uncertain gestational age, losses weighing >500 g are considered stillbirths. However, others believe that a more useful definition would include death of a fetus past the age of viability. This has prompted the use of 24 or even 28 weeks gestation as a threshold for defining stillbirth. Another controversial issue is whether or not to include both antepartum and intrapartum deaths as stillbirths. Some but not all studies distinguish between the two. This is an important distinction, as causes and strategies to reduce antepartum and intrapartum losses are quite different. Intentional fetal death (e.g., pregnancy termination in the setting of fetal anomalies or preterm premature rupture of membranes) poses another problem for vital statistics. Pregnancy terminations often are excluded when counting stillbirths, but the issue remains controversial. It seems appropriate to exclude terminations as a distinct entity. However, in many cases, these fetuses would be stillborn if the pregnancy were allowed to continue. As such, their exclusion might alter the true impact of stillbirth on a population.

Epidemiology In 2003, the stillbirth rate (after 20 weeks gestation) in the United States was 6.23 per 1,000 live births. This represents a slight and steady decline since 1990, when the rate was over 7.5 per 1,000 live births (Fig. 23.1). Just over one half of stillbirths in the United States occur between 20 and 27 weeks gestation. It is important to note that this may underestimate the true rate, as stillbirths are likely underreported. The scope of the problem is considerably higher in many parts of the world. Stillbirth rates are estimated to range from 5 per 1,000 births in rich countries to 32 per 1,000 births in southern Asia and sub-Saharan Africa. The estimated number of global stillbirths per year is 3.2 million.

Figure 23.1 Thousands of fetal and infant deaths in the United States, 1990–1993. (MacDorman MF, Hoyert DL, Martin JA, et al. Fetal and perinatal mortality, United States, 2003. Natl Vital Stat Rep 2007;55:1–18.)

In the United States, stillbirth rates continue to be increased in non-Hispanic black women. In 2003, the fetal mortality rate for non-Hispanic blacks was 11.56 per 1,000 births compared with 4.94 per 1,000 births for non-Hispanic whites. Fetal mortality also is relatively higher for teenagers, unmarried women, and women over 35 years of age. It is difficult to obtain an accurate estimate of the fetal death rate between 10 and 20 weeks gestation, because such data are not routinely collected. According to the National Survey of Family Growth, estimates of total fetal losses per year in the United States are about one million. The majority of these occur prior to 20 weeks gestation.

Classification Numerous classification schemes have been used to catalog stillbirths based on etiology. This has proved difficult for several reasons. First, it often is difficult to be certain of a “cause” of death. Many risk factors such as diabetes, obesity, or heritable thrombophilias are associated with an increased risk of fetal death. However, the vast majority of women with these risk factors have live-born infants. Thus, it is difficult to be certain that these factors led to the stillbirth. Second, there may be more than one potential cause of stillbirth in the same patient. For example, what would be considered the etiology in a fetus with trisomy 18 that also has evidence of bacterial infection? Stillbirth may be due to the additive or interactive effects of several disorders. Finally, a cause of death often is never determined. In many cases, this is due to a lack of systematic evaluation into potential etiologies. However, a cause of death may not be found despite a comprehensive evaluation. This is especially true in cases of term stillbirth. Because of these problems, no single classification scheme has been universally adopted, and new ones are being developed. Additional confusion arises from the use of different definitions for fetal death, the occasional inclusion of neonatal death, and different

standards regarding causes versus associations in the classification schemes. The Wigglesworth classification probably is in most widespread use today (Table 23.1). A problem with all of the classification systems is that many stillbirths remain unexplained. Recently, Gardosi and colleagues introduced a new system that explains a much larger proportion of fetal deaths than prior schemes (Table 23.2). However, many of the etiologies in the new system may be risk factors such as small-for-gestational-age fetus (SGA) rather than etiologies. Forthcoming international conferences hopefully will facilitate the development of uniform definitions and classification systems for fetal death.

TABLE 23.1 Wigglesworth Classification 1. Congenital defect/malformation (lethal or severe) 2. Unexplained antepartum fetal death 3. Death from intrapartum “asphyxia,” “anoxia,” or “trauma” 4. Immaturity 5. Infection 6. Death due to other specific causes 7. Death due to accident or nonintrapartum trauma 8. Sudden infant death, cause unknown 9. Unclassifiable Hey EN, Lloyd DJ, Wigglesworth JS. Classifying perinatal death: fetal and neonatal factors. Br J Obstet Gynaecol, 1986;93(12):1213–1223.

Etiologies and Risk Factors Fetal Conditions Congenital Abnormalities Genetic abnormalities and fetal malformations account for a significant proportion of stillbirths. Abnormal karyotypes are present in 6% to 12% of stillbirths after 20 weeks gestation. The rate of chromosomal abnormalities is considerably higher in first-trimester pregnancy losses and is probably intermediate in losses between 10 and 20 weeks gestation. This likely underestimates the true rate of chromosomal abnormalities, because karyotype is not always successfully obtained in cases of stillbirth. The odds of an abnormal karyotype are increased in the setting of fetal malformations, dysmorphic features, or SGA fetus. Conversely, the chances of an abnormal karyotyope is low (about 2%) in stillbirths greater

than 20 weeks gestation with no apparent phenotypic abnormalities. The most common single abnormality in stillbirths is monosomy X (Fig. 23.2), occurring in 23% of cases with abnormal karyotype. Trisomies including 21, 18, and 13 also are common. This is in contrast to first-trimester losses, wherein trisomy 16 accounts for the majority of abnormalities. Many fetuses have malformations or other congenital abnormalities without necessarily having chromosomal abnormalities. Up to 35% of stillborn infants undergoing perinatal autopsy have abnormalities including malformations, syndromes, and dysplasias. Approximately 25% of these will have an abnormal karyotype. However, it is likely that many of these fetuses have genetic abnormalities that are not identified by traditional karyotype. Some fetuses may have microdeletions or additions that are too small to be identified by cytogenetics. Newer molecular genetic technology using a technique termed comparative genomic hybridization (CGH) may identify these smaller lesions. Similar abnormalities have been reported in cases of unexplained mental retardation with normal karyotype. Other cases of stillbirth are due to single gene mutations that require specific targeted assays for diagnosis. Many are autosomal recessive conditions such as glycogen storage diseases, hemoglobinopathies, and other metabolic disorders. There are probably several other single gene disorders responsible for some cases of stillbirth. Another potential genetic cause of pregnancy loss is confined placental mosaicism. This refers to abnormal chromosomes in some or all of the placental tissue with normal fetal karyotype. In turn, this leads to abnormal placental function resulting in fetal growth impairment or death. Continued advancements in molecular genetic technology should enhance our ability to identify previously unrecognized genetic causes of stillbirth.

TABLE 23.2 Relevant Condition of Death (ReCoDe) Classification 1. Fetus 1. Lethal congenital anomaly 2. Infection 2.1. Chronic (e.g., TORCH) 2.2. Acute 3. Nonimmune hydrops 4. Isoimmunization 5. FMH 6. Twin–twin transfusion 7. Intrapartum asphyxia 8. Fetal growth restriction 9. Other

2. Umbilical Cord 1. Prolapse 2. Constricting loop or knot 3. Velamentous insertion 4. Other 3. Placenta 1. Abruptio 2. Previa 3. Vasa previa 4. Placental infarction 5. Other placental insufficiency 6. Other 4. Amniotic fluid 1. Chorioamnionitis 2. Oligohydramnios 3. Polyhydramnios 4. Other 5. Uterus 1. Rupture 2. Uterine anomalies 3. Other 6. Mother 1. Diabetes 2. Thyroid diseases 3. Essential hypertension 4. Hypertensive diseases in pregnancy 5. Lupus/APS 6. Cholestasis 7. Drug abuse 8. Other 7. Trauma 1. External 2. Iatrogenic 8. Unclassified 1. No relevant condition identified 2. No information available TORCH, serology for toxoplasmosis, rubella, cytomegalovirus, and herpes simplex virus; FMH, fetal–maternal hemorrhage; APS, antiphospholipid syndrome. Gardosi J, Kady SM, McGeown P, et al. Classification of stillbirth by relevant condition at death (ReCoDe): population

based cohort study. BMJ 2005;331(7525):1113–1117.

Figure 23.2 Second-trimester fetal death with cystic hygroma and nonimmune hydrops. The fetus had Turner syndrome. (Reprinted with permission from Silver RM. Fetal death. Obstet Gynecol 2007;109:153–167.)

Infection Infections are another biologically plausible, generally accepted cause of stillbirth, accounting for 10% to 25% of stillbirths in developed countries. The proportion of stillbirths due to infection (especially bacterial infection) is even higher in developing countries. It is important to be careful when attributing fetal death to infection. Mothers often have vaginal infection or colonization or systemic viral infections that may have nothing to do with a stillbirth. Fetal autopsy and placental histologic evaluation are extremely helpful in proving that infection truly is a cause of stillbirth. For example, positive cultures of group B streptococcus in fetal lungs is convincing evidence of causality, while positive maternal serology for cytomegalovirus (CMV) in a case with no evidence of infection on fetal autopsy is not.

Bacterial Infection Bacterial infections implicated in stillbirth are most commonly due to ascending organisms from the genital tract. Bacteria such as Escherichia coli, Klebsiella, Ureaplasma urealyticum, Mycoplasma hominus, Bacterioides species, and group B streptococcus track from the vagina, through the cervix, and into the amniotic fluid, where they may be

swallowed by the fetus, sometimes leading to infection. Less commonly, bacteria such as Listeria monocytogenes can be hematogenously transmitted to the fetus. It is noteworthy that some organisms usually cause clinically apparent intra-amniotic infection, while other indolent organisms such as L. monocytogenes may cause vague symptoms that are difficult to diagnose. Although rare, fetal death also may occur because of severe systemic maternal infection. This is thought to be due to the propagation of inflammatory mediators leading to uterine ischemia, hypoxia, and preterm labor.

Viral Infections The most common viral infection that has been linked to fetal death is parvovirus B19 (Fig. 23.3). This virus is trophic for erythrocyte precursors and myocardial cells. Death is thought to be caused by fetal anemia, hydrops, and/or myocardial dysfunction. Parvovirus is most likely to cause fetal death after infection in the first two trimesters. Late fetal death due to the virus is rare. The organism has been reported in up to 15% of cases of fetal death when polymerase chain reaction (PCR) was used to detect parvovirus nucleic acid in the fetus or placenta. However, parvovirus has been found in 20 h

Active phase

4.90

1.2 or less

—

Second stage

0.95

1.0 or less

Nonea

Multiparous labor

Latent phase

5.30

—

>14 h

Active phase

2.20

1.5 or less

—

Second stage

0.24

2.0 or less

Nonea

There is no limit to the length of the second stage as long as progress is being made and there is no fetal distress. Ineffective uterine contractions lead to increased tissue acid content in the myometrium, which further contributes to poor contractility. In one study, the pH of myometrial capillary blood obtained at the time of cesarean delivery from women with dysfunctional labor was lower than in women having cesarean for other indications. This also was associated with higher capillary lactate and lower oxygen saturation. Normal labor is characterized by coordinated uterine contractions, cervical dilation, gain in station of the fetal head, and normal progress in the cardinal movements of labor. With careful attention to achieving these milestones of normal labor, a successful vaginal delivery is likely. However, if the parturient does not achieve these milestones, prompt intervention is more likely to increase the chances for vaginal delivery. Although an aggressive approach with regard to diagnosing labor abnormalities may enhance maternal and fetal outcome, the last important key to the successful management of labor is to use clinical judgment on when to abandon medical therapy in favor of surgical intervention. If the judgment is made that continuing medical therapy may dangerously compromise either mother or fetus, then prompt surgical delivery (cesarean or operative vaginal delivery) should be considered.

Figure 24.3 Labor curve of nulliparas versus multiparas. Note that different labor

slopes are expected between nulliparous (solid line) and multiparous women (dotted line).

TABLE 24.3 The Cardinal Movements of Labor Engagement Descent Flexion Internal rotation Extension External rotation Shoulder rotation

Epidemiology of Dystocia The precise incidence of dystocia is difficult to determine and varies with different populations and different labor and delivery units based on local practice patterns. According to the National Center for Health Statistics, 28% of women who delivered in the United States in the year 2000 were diagnosed with labor abnormalities, with a primary cesarean delivery rate of 16.1%. The rate of primary cesarean delivery in 2004 increased to 20.6% of all deliveries in the United States. Dystocia is more common in nulliparous women than in multiparous women and is more common in the first stage of labor than in the second stage of labor. Labor abnormalities occur in approximately 25% to 30% of nulliparous women and in 10% to 15% of multiparous women. Dystocia occurs in the second stage of labor in about 5% to 10% of nulliparous women and is relatively rare in multiparas (38°C), fetal tachycardia (baseline fetal heart rate of >160 beats per minute), elevated maternal white cell count, uterine tenderness when the uterus is relaxed, and foul-smelling vaginal discharge. With the diagnosis of intrauterine infection, broad-spectrum antimicrobial agents should be administered and uterine activity stimulated with oxytocin if labor is not

progressing adequately. Because oxytocin often does not work well in this scenario, the obstetrician should be prepared to move to cesarean delivery if oxytocin is ineffective in order to avoid neonatal infectious morbidity.

Cephalopelvic Disproportion True cephalopelvic disproportion (CPD), or fetopelvic disproportion, commonly is diagnosed on the labor and delivery suite, although some authorities believe that CPD occurs in as few as 1 in 250 pregnancies. CPD occurs when the fetal birth weight or the fetal head is of sufficient size or orientation to preclude entry into the maternal pelvic inlet. This diagnosis often is made in retrospect after the birth weight is known and the positioning of the fetal head has been determined at the time of cesarean delivery. However, in the United States, the term cephalopelvic disproportion is used to describe almost any unsuccessful attempt at vaginal delivery. Further, the diagnosis of CPD often is used when labor progress is not sufficient and medical therapy is not successful or even not attempted. These cases often reflect inadequate use of oxytocin and are not problems with large fetal size or a small maternal pelvis. CPD is an important diagnosis because it has prognostic information for subsequent pregnancies when VBAC is considered. In women with a prior diagnosis of CPD, success rates of VBAC are only 50%. Additionally, these women should be managed differently during the VBAC, with prompt repeat cesarean if labor does not progress appropriately. Another important contribution to the fetopelvic relationship is the size of the fetus. Pregnancies with macrosomic fetuses (>4,000 g birth weight) have a greater risk of cesarean delivery for dystocia as a result of true CPD. In a study by Turner and colleagues, fetal macrosomia was associated with longer first and second stages of labor, a greater need for oxytocin therapy, and a greater risk for cesarean delivery for CPD refractory to oxytocin. In their patient population, the overall incidence of cesarean delivery of 5.2%, but if birth weight was between 4,000 and 4,500 g, the incidence of cesarean delivery was 13.8%. Also, forceps delivery was employed in 31.8% of infants with a birth weight between 4,000 and 4,500 g, whereas forceps were used in 13.6% of deliveries overall. Unfortunately, there are no good predictors of fetal weight to guide management. Sonographic estimates of fetal weight at term are notoriously spurious and can miscalculate birth weight by up to 20%. The obstetrician employing Leopold maneuvers to estimate fetal weight by palpation of the maternal abdomen can only estimate small, average, or large fetal size. Hence, it is not advisable to induce labor or perform a cesarean delivery for presumed macrosomia unless the obstetrician judges that a dangerous situation exists for vaginal delivery (e.g., high risk of shoulder dystocia). Numerous studies of induction of labor for presumed macrosomia consistently show an increase in the cesarean delivery rate with no decrease in neonatal morbidity or shoulder dystocia. When the diagnosis of a labor abnormality is made, clinical pelvimetry should be performed to assess the dimensions of the maternal pelvis (Fig. 24.6). Only in the rare cases in which the maternal pelvis is markedly small or if there is clear CPD should

cesarean delivery be performed without the prior use of oxytocin. For example, labor through a platypelloid pelvis with a normal term-sized fetus is rarely successful because of the markedly shortened anterior–posterior diameter that characterizes this pelvic architecture. After assessment of the pelvic type, approximations of the fetal size should be undertaken. Unless the fetus appears to be markedly macrosomic (>4,500 g), medical therapy with oxytocin should be instituted.

Figure 24.6 Pelvic types. There are four primary pelvic types: gynecoid, android, anthropoid, and platypelloid. Women may have a mixed pelvic type with features suggestive of different pelvic types that do not fit conveniently into one of these four types.

Abnormal Position of the Fetal Head Abnormal positions of the fetal head include occiput posterior (OP), deep transverse arrest, and deflexion abnormalities such as face and brow presentations and reflect fundamental abnormalities in the cardinal movements of labor. Different positions of the fetal head are depicted in Figure 24.7. An OP position is unfavorable for successful vaginal delivery, particularly if the parturient has an android pelvic structure, as the long diameter of the fetal head negotiates the maternal pelvis at a relatively high station, leading to poor descent. The OP position may occur in up to 10% of women in labor and can be corrected with oxytocin therapy. According to Cheng and associates, associated factors for OP position include epidural use, amniotomy, African American race, nulliparity, and birth weight >4,000 g. Operative vaginal delivery, either via a Scanzoni maneuver or via a straight OP application with traction, is another option for delivery. A Scanzoni maneuver involves rotating the OP fetus to an OA position with forceps and then completing the delivery with forceps from the OA position. A Scanzoni maneuver is associated with a higher incidence of maternal trauma (third- and fourth-degree lacerations of the perineum and sulcus tears of the vagina) and fetal

trauma. Hence, such deliveries should be performed only by obstetricians skilled in these techniques and thus have largely fallen into disfavor. Moreover, delivery of the OP fetus via forceps should probably be attempted only if the fetal head has attained at least a +2 station. At higher stations, cesarean delivery may be the safest alternative. The prudent obstetrician will realize that assigning station in a labor characterized by an OP position is more difficult than in an OA position and often leads to the impression of a lower station than actually is present. Care should be taken to accurately assess the biparietal diameter in relationship to the maternal ischial spines.

Figure 24.7 Position of the fetal head. The sutures of the fetal head should be palpated, and the fetal head position should be recorded to ensure that the normal cardinal movements of labor are being followed. The fetal occiput, with the maternal position, are the reference points. Hence, OA refers to the occiput anterior position; OP, occiput posterior; LOT, left occiput transverse; LOA, left occiput anterior; ROP, right occiput posterior. Any fetal position can occur and should be noted on the labor curve.

A deep transverse arrest occurs in the second stage, where the fetus maintains an OT position at a low pelvic station. Deep transverse arrests often are associated with abnormal maternal pelvic architecture and may not be easily delivered via forceps. Kielland. forceps were designed to address the problem of the deep transverse arrest. Vacuum delivery probably should be avoided in this circumstance, as excessive traction of the fetus with a deep transverse arrest can result in significant birth trauma. Cesarean delivery is the most prudent option if the fetal station is not sufficiently low for operative vaginal delivery or if excessive traction is required to effect delivery. Operative vaginal delivery for a deep transverse arrest should be performed only by obstetricians skilled in the use of forceps for this problem. Deflexion abnormalities also cause dystocia. The classic forms of deflexion abnormalities include brow and face presentations. Typically, a brow presentation is characterized by the long axis of the fetal head negotiating the short axis of the midpelvis, precluding vaginal delivery. A fetus in the brow presentation may spontaneously convert to a vertex or face presentation. Whereas fetuses with a brow presentation that do not convert rarely deliver

vaginally (except in women with generously sized midpelvic dimensions with a small fetus), face presentations often will deliver vaginally if the mentum, or chin, is positioned anteriorly (mentum anterior). Although these extreme flexion abnormalities usually are easily diagnosed and are relatively rare, other mild flexion abnormalities may not be so readily evident. Flexion abnormalities may be suspected in a prolonged or protracted labor that is unresponsive to oxytocin. Unfortunately, there are no safe and accepted means to correct flexion abnormalities of the fetal head. Often, abnormal fetal position may occur as the result of the maternal pelvic type (Fig. 24.6). For example, android pelvic types often lead to deep transverse arrest or OP position because of the progressive narrowing of the pelvis. Women with an anthropoid pelvis tend to have fetal positions persistently OA or OP, thus interfering with the normal cardinal movements of labor. Finally, women with a true platypelloid pelvis have transverse arrests, assuming that the fetal head negotiates the shortened pelvic inlet. Because many women have mixed pelvic types, careful clinical pelvimetry may provide valuable information in the management of dystocia.

Figure 24.8 Synclitism. The term synclitism refers to the relative orientation of the fetal sagittal suture with the maternal bony pelvis. A: Normal synclitism of a fetus in left OT position, with the sagittal suture equidistant between the anterior and posterior segments of the maternal pelvis. B: Posterior asynclitism, where the sagittal suture is closer to the posterior bony pelvis and more of the right parietal bone is palpated. C: Anterior asynclitism in which the sagittal suture is more anteriorly located, and the left parietal bone is more readily evident.

Asynclitism When asynclitism of the fetal head occurs, the sagittal suture of the head is either deviated posteriorly or anteriorly in relation to the maternal outlet (Fig. 24.8). As with

other abnormal positioning of the fetal head, a larger diameter of the fetal head is expected to negotiate the bony pelvis of the mother. In these situations, the second stage of labor often is prolonged and arrest of descent is common, leading to an increased need for operative vaginal delivery. An important aspect of performing operative vaginal delivery involves correction of the asynclitism of the fetal head. This correction often can be accomplished with forceps that have a sliding lock or via vacuum extraction of the fetus, where the precise attitude and positioning of the fetus is of less importance.

Fetal Abnormalities Specific fetal abnormalities may contribute to the etiology of dystocia. Fetuses with neuromuscular disease, and particularly those who have suffered an in utero demise, may have flexion abnormalities. Also, fetal conditions such as hydrocephalus, hydrops fetalis, and tumors of the head or sacrum can lead to mechanical obstruction of the birth canal and hence cause dystocia, which usually is not remedied except by cesarean delivery.

Specific Labor Abnormalities Only if the progress of labor is closely monitored can labor abnormalities be diagnosed. Moreover, the timely diagnosis of these labor abnormalities, with prompt medical therapy, should improve the chances of achieving a vaginal delivery. These labor abnormalities can be classified as either arrest disorders (Fig. 24.9) or protraction disorders (Fig. 24.10). Table 24.2 provides commonly used parameters for abnormal labor.

Prolonged Latent Phase A prolonged latent phase (Fig. 24.9A) occurs when regular painful uterine contractions are present for an extended period of time without entering the active phase of labor. Although a prolonged latent phase generally is not classified as an arrest disorder, some authorities believe that the latent phase is an example of a primary dysfunctional labor. In nulliparous women, the definition of a prolonged latent phase is a period of uterine activity without cervical change for more than 20 hours, and in multiparas this time period is 14 hours. The cervix may be dilated up to 4 cm and be completely effaced. The precise etiology is not clear but likely reflects ineffective uterine contractions without a dominant myometrial pacemaker. The management of a prolonged latent phase is controversial, and there are two commonly used approaches. Some obstetricians believe that a prolonged latent phase reflects an underlying labor abnormality that should be managed aggressively with amniotomy and oxytocin. The other approach is to provide supportive measures including intravenous hydration and narcotic pain relief. Studies comparing these approaches have not shown either to be a clearly superior choice, so either treatment plan is acceptable as long as the patient understands the plan and risks. The more aggressive approach in some cases may be an induction of labor with the attendant higher risk of cesarean delivery, whereas the more conservative approach runs of the risk of prolonging a potentially dysfunctional labor. Both options are acceptable and deciding which course to

take requires obstetric judgment and a motivated, informed patient.

Figure 24.9 Arrest disorders. A: Prolonged latent phase. Although it might be said that a prolonged latent phase is not strictly an arrest disorder, it reflects an abnormality in the normal progress of labor in which the change into the active phase is arrested. B: Arrest of dilation, in which the cervix achieves 6 cm of dilation but then does not change for 2 hours. C: Arrest of descent. The fetal head moves from a –2 station to a 0 to –1 station but then makes no further progress.

Figure 24.10 Protraction disorders. These examples of protraction disorders are exaggerated to depict each abnormality. In each case, these abnormalities should be detected early and appropriate therapy instituted. A: Protracted active phase. Note that the average slope is much less than 1.5 cm per hour. B: Protracted active phase that could be confused as a prolonged deceleration phase. C: Prolonged and neglected second stage. Intervention should occur sooner than indicated on this partogram.

Arrest of Dilation An arrest of dilation occurs when there is no cervical change after 2 hours in the active phase of labor (Fig. 24.9B). In most cases, arrest of dilation occurs as a result of ineffective uterine contractions. Uterine contractions may become dysfunctional and lose their synchronous rhythmic nature. Figure 24.4 shows an example of the loss of a dominant myometrial pacemaker with the expression of two pacemakers firing independently and without coordinated uterine contractions. In any case, prompt medical therapy with oxytocin usually corrects the underlying problem. In those rare cases where CPD is evident on evaluation of the patient, prompt cesarean delivery is indicated and oxytocin

administration should be avoided.

Arrest of Descent After complete dilation is achieved, the primary goal of the second stage of labor is to gain station of the fetal head through the maternal pelvis with eventual delivery. If the patient does not gain station of 1 cm after an hour of adequate pushing efforts, an arrest of descent is diagnosed (Fig. 24.9C). The cause of this arrest disorder may be one or a combination of several underlying abnormalities, including inadequate uterine contractions, CPD, abnormal fetal position, and asynclitism. If an arrest of descent is diagnosed, the obstetrician has several options including the use of oxytocin, operative vaginal delivery, or cesarean delivery. The choices for therapy should be guided by the fetal status, station of the fetal head, maternal status, and operator experience.

Protracted Active Phase When cervical change continues with adequate uterine contractions in the active phase of labor but over a longer time period than anticipated, then a prolonged active phase is the diagnosis (Fig. 24.10A). In nulliparous patients, cervical change is Table of Contents > 26 - Operative Vaginal Delivery

26 Operative Vaginal Delivery James A. Bofill James N. Martin Jr. Most likely, there has always been a desire of obstetric attendants to safely grasp the fetal head in order to accelerate delivery of the infant and shorten a woman's difficult labor. The story of the use of obstetric instruments to facilitate delivery—either forceps or vacuum devices—is both colorful and unique within the history of medicine. Properly used obstetric forceps may have saved more lives, both infant and maternal, than any other instrument devised by physicians. The heyday of obstetrical forceps use was in the early 20th century, when nearly half of deliveries were accomplished by their means. Obstetricians of that time considered that the obstetric forceps, with liberal use of episiotomy, protected the maternal genital tract and prevented more extensive injury. Similarly, the forceps were considered to provide the fetus, especially the preterm fetus, with a “helmet” that prevented rapid changes in cranial pressure during delivery. These notions have been discarded by the rigors of modern clinical studies. Early in the 21st century, the practice of operative vaginal delivery is considered by some obstetricians to be anachronistic, a “dying” art and not something to be mastered or practiced. The total rate of operative vaginal delivery in 2004, the last year for which complete data are available, was only 5.2% in the United States. Obstetric forceps were used in 1.1% of deliveries, and 4.1% were delivered via the vacuum extractor (Fig. 26.1). Since 1989, there has been an 80% decrease in the frequency of operative forceps use, steadily falling over 15 years from 5.5% in 1989 to 1.1% in 2004. During this time, the frequency of vacuum extractor procedures peaked in 1997 at 6.2%, thereafter decreasing by one third to a level of 4.1% in 2004. There are several possible causes that relate to diminishing operative vaginal delivery usage in the United States. Certainly, the crisis of litigation in the field of obstetrics is one cause. Yeomans and Hankins perceive a vicious cycle whereby (a) concern about litigation lessens usage and reduces teaching about obstetric forceps and vacuum in obstetrics and gynecology (OBGYN) residency training programs; (b) physician training and confidence with operative vaginal delivery is diminished; (c) usage of operative vaginal delivery decreases further, increasing the probability of poor clinical outcomes when used; and (d) poor clinical outcomes often lead to litigation in our society.

Utilization of operative vaginal delivery was very important to physicians during times when cesarean delivery was considered to present a significant health risk to an obstetric patient or its low frequency of use was considered to be a quality assurance barometer— both concerns were a driving force in minimizing abdominal delivery while encouraging vaginal delivery. Currently, there is a paradigm shift away from the former line of reasoning—cesarean delivery has become a very safe procedure, and a physician's personal cesarean delivery rate is rarely used today as a reflector of quality care. Hence, the rate of operative vaginal delivery in the United States has been declining as the frequency of primary and repeat cesarean delivery has been climbing—from 20.7% in 1996 to a record high of 29.1% in 2004. During the same time interval, trial of labor to accomplish vaginal birth after cesarean (VBAC) has decreased 67%. Not only has cesarean delivery become the most common surgical procedure in modern medicine, it has for the first time to any significant degree been considered appropriate for elective reasons when traditional obstetric indicators are absent. Nevertheless, teaching and clinical experience with some types of operative vaginal delivery are considered an integral part of contemporary residency training in obstetrics. Although very challenging instrumental deliveries are seldom undertaken when cesarean delivery is the better option, most physicians continue to learn outlet and low-forceps operations with some rotation as well as the proper techniques for vacuum extraction.

Figure 26.1 Trends in forceps and vacuum delivery from 1989 to 2004.

Delivery with the Vacuum Extractor The vacuum extractor has a history nearly as colorful as the obstetric forceps. Its early development and use have been described previously. Since inception and the earliest stages of development, the vacuum extractor has been considered an easier instrument to use than the obstetric forceps. For example, Arnott in 1829 considered that the vacuum extractor was “a substitute for steel forceps in the hands of men who are deficient in manual dexterity, whether from inexperience or natural ineptitude.” This, of course, is

inaccurate in today's practice. The history of the forceps and vacuum extractor are intertwined, a fact that is best personified by James Young Simpson of Scotland, who performed the first well-documented series of successful vacuum deliveries and also designed the popular obstetric forceps that bear his name. Simpson's report was met with skepticism and caution. The vacuum instrument was essentially discarded, probably due to lack of appropriate materials for the construction of a durable device. The modern era of vacuum extraction began in 1954, when Malmstrom introduced a metal cup that he termed the vacuum extractor. The original Malmstrom vacuum extractor consisted of a mushroom-shaped stainless steel cup with a smooth, inverted lip and an outside diameter of 60 mm. Unlike current obstetric practice, smaller Malmstrom devices were also commonly placed prior to full cervical dilatation late in the first stage of labor in order to overcome dystocia and hopefully accelerate delivery. The vacuum extractor was considered to be a simpler instrument as well as one that required less anesthesia than the obstetric forceps. Vacuum-assisted vaginal delivery did not become popular in the United States in part due the entrenched place of obstetric forceps and reports of fetal complications with vacuum delivery. The vacuum device often was associated with scalp abrasions, and the edematous area of the scalp raised by the device (the chignon) was cosmetically unpleasant. Several reports of life-threatening neonatal complications after vacuum extraction were published. Many of these patients may not have been appropriate candidates for vacuum delivery. Nevertheless, these reports of poor neonatal outcomes led to refinements in technique. Wider's group refined the vacuum procedure in the 1960s and limited the instrument's use to the second stage of labor. To minimize neonatal morbidity, it was recommended that vacuum application to the fetal head should not exceed 15 minutes. Using the Bird modification of the Malmstrom device and comparing vacuum with forceps and cesarean delivery, Greis and colleagues demonstrated that neither perinatal mortality nor serious neonatal injury were more likely with vacuum extraction when the procedure time was limited to 15 minutes and/or two sudden disengagements (“pop-offs”). Preferential use of vacuum over forceps was reported for managing challenging deliveries. In that retrospective study, it was noted that 60% of vacuum cases were initiated in the midpelvis compared with only 9% of forceps deliveries. Malpositioning of the fetal head as occiput posterior (OP) or occiput transverse (OT) was seen in 81% of vacuum cases as compared with only 9% of forceps cases. The utilization of the vacuum for operative vaginal delivery has surpassed the forceps in the United States, which traditionally has been considered a “forceps nation.” Findings from surveys undertaken in the mid 1990s revealed that vacuum delivery techniques were taught in most U.S. OBGYN residency training programs and frequently were practiced by U.S. obstetricians. Another survey found that residency program directors expected their OBGYN residents to be proficient with forceps and vacuum extraction for outlet and lowpelvic deliveries (with or without rotation). However, very challenging operative vaginal deliveries today probably reside more often in the vacuum domain since only 38% of the residency program directors expected their graduates to be proficient with midforceps procedures, while 69% expected proficiency with midpelvic vacuum extractions.

The age of the obstetrician is clearly important and relevant to choice of instrument for operative vaginal delivery. Recently trained obstetricians more commonly choose vacuum extraction over forceps, especially for the challenging case. Geography plays a role as well, since data from the National Center for Health Statistics and the National Hospital Discharge Survey demonstrated that the frequency of vacuum extractor use surpassed that of the forceps in the western United States in 1988, in the Northeast in 1990, and in the Midwest in 1991. Forceps procedures continued to outpace vacuum procedures in the southern United States during the study period until there was near parity between the two instruments in 1994, which was the last year of the study. With increasing use of operative vacuum delivery, there also was a significant increase in the number of reported neonatal complications. On May 21, 1998, the U.S. Food and Drug Administration (FDA) distributed a public health advisory entitled Need for Caution When using Vacuum-Assisted Delivery Devices. The advisory included reports of 12 neonatal deaths and 9 serious injuries that were received during the preceding 4 years (about 5 events per year) in newborns for whom vacuum devices were used to accomplish delivery. The FDA was concerned that some health care professionals who were using vacuum devices for delivery might not be fully aware of the possibility of life-threatening neonatal complications such as subgaleal hematoma or intracranial hemorrhage. The FDA's main points were as follows: The vacuum extractor should be used only when a specific indication exists. The operator should be versed in its use and aware of indications, contraindications, and precautions. The operator should follow manufacturer recommendations regarding cup placement, vacuum strength, cumulative duration of applications, and number of extraction attempts. Rocking movements or torque should not be applied to the device, and only steady traction in the axis line of the birth canal should be used. Neonatal staff should be educated about the specific complications that can occur in association with the use of vacuum devices to accomplish delivery. Adverse events and complications associated with vacuum-assisting devices should be reported to the FDA under the auspices of the Safe Medical Devices Act of 1990. The American College of Obstetricians and Gynecologists (ACOG) responded to the release of the FDA advisory with a committee opinion, which noted that an average of 228,354 vacuum deliveries occurred annually during the period of time covered by the FDA advisory —the equivalent of one adverse event for every 45,455 vacuum deliveries. Despite the infrequent occurrence of fetal injury, the ACOG committee recommended that all clinicians using vacuum devices for delivery should be familiar with the indications for the use of these devices and be properly educated in their use. This committee strongly recommended the continued use of vacuum-assisted vaginal delivery devices in appropriate clinical settings. In the first 6 months following release of the FDA advisory,

Ross and colleagues observed a 22-fold increase in the reporting of adverse events associated with vacuum delivery, including 10 neonatal deaths, 30 life-threatening events, 12 nonlife-threatening events, and 3 equipment failures. The increase in reports was ascribed to better compliance with reporting, increased awareness of the potential for fetal injury with vacuum extraction, and increased use of the vacuum device. In response to four neonatal deaths secondary to subgaleal hemorrhage, the Health Protection Branch of Canada issued their own warning on February 23, 1999. The recommendations issued were directly in line with those of the FDA.

Types of Vacuum Extractors: Stainless Steel Devices Stainless steel devices are mentioned primarily for their historical significance and because they have served as prototypes for plastic devices in use today. Early in 2000, the labor and delivery unit utilized by the authors attempted to buy new Malmstrom and Bird cups in order to teach our OBGYN residents the proper use of these devices. However, the European manufacturers declined to sell these devices to buyers in the United States. Their stated reservation was due to U.S. product liability laws and their wish to avoid any potential medicolegal entanglements. The Malmstrom vacuum extractor (Fig. 26.2) is a shallow, mushroom-shaped stainless steel cup, with two vacuum hoses, a traction chain and attached metallic disk, a traction handle, and a vacuum source. The center of the cup has a metallic suction port through which the traction chain passes. The traction chain is attached to the cup by a metallic disk that is inserted within the cup to prevent the fetal scalp from being pulled into the vacuum port. The margin of the metallic disk is scalloped at regular intervals such that the vacuum may be developed beyond the underside of the disk and onto the fetal scalp. The Malmstrom vacuum extractor can be assembled in seconds. After its use the device is easily disassembled, and the components are washed, autoclaved, and packaged for future use. The Malmstrom cup has an inverted lip such that the diameter of the opening is smaller than the internal diameter of the cup. When the cup is placed on the fetal scalp and vacuum is established, a small artificial caput forms, termed the chignon. When the fetal scalp fills the internal dimensions of the cup, the scalp underlies the opening of the cup in a “key-in-lock” fashion. This allows a considerable traction force to be applied before cup detachment occurs.

Figure 26.2 The original Malmstrom device with the bicycle-style pump.

The utility of the Malmstrom cup is limited by a combined vacuum port and traction apparatus in the dome of the cup, which makes appropriate application somewhat difficult in positions of the fetal head other than occiput anterior (OA). In 1969, Bird developed two modifications (anterior and posterior) of the Malmstrom cup to increase the versatility of the vacuum extractor for proper placement with difficult positioning of the fetal head. Bird separated the vacuum port and the traction apparatus (Fig. 26.2). The traction chain remained anchored to the center of the cup, while the vacuum port was attached eccentrically to the dome of the anterior cup. The vacuum port was attached laterally for the posterior cup. With these modifications, the vacuum tubing exited in the same plane as the cup, a change which enabled the physician to better maneuver the cup into its proper location within the maternal pelvis. In even later versions of the Bird cups, the central traction chain was replaced by a nylon cord anchored to the edges of the cup and to a traction bar for physician convenience.

Types of Vacuum Extractors: Soft-Cup Devices There are several types of plastic or silicone vacuum cups currently in use in the United States (Fig. 26.3). The cups are separated into three groups, depending on the shape of the vacuum cup: funnel, bell, or mushroom. Of these, the funnel-shaped cups are the least used. The prototype for this vacuum extractor was based on the original Kobayashi silastic cup, introduced in 1973. The diameter of this device (65 mm) is the largest of any of the commercially available cups, and therefore its size obviates the need for a chignon to form in order to achieve appropriate traction. This device also has a vacuum release valve on the stem, which allows the operator to reduce vacuum pressure between contractions, if desired. Variations on the original Kobayashi design are available from several vendors. A much lower rate of neonatal scalp trauma was reported with the Kobayashi cup in contrast to experiences with stainless steel cups, a finding that was corroborated by five randomized studies of the silastic cup versus the stainless steel cups. Although the

Kobayashi vacuum extractor was noted to effect delivery in less time than stainless steel devices, a higher failure rate occurred, especially when the fetal head was in the OP presentation.

Figure 26.3 Vacuum extractor cup designs. A: Typical bell-shaped cup with a hand pump. B: Disposable plastic version of the Bird cup with combined pump and traction bar. C: Bird OA cup.D: Typical disposable mushroom-shaped cup.

Bell-shaped vacuum cups are widely available from several vendors in the United States. One example is the Mityvac device (Cooper Surgical, Trumbull, CT), which was compared with a silastic funnel-shaped cup and Tucker-McLane forceps in a prospective, randomized study of 118 delivered patients by Dell in 1985. Trauma to the maternal genital tract trauma was noted in 48.9% of the women delivered by forceps as compared with 36.1% and 21.6% of the women delivered by the silastic and bell-shaped cups, respectively. This represented a statistically significant reduction in maternal genital tract trauma with use of the bell-shaped vacuum device. Success rates using the bell-shaped cup (89.2%) versus forceps (93.3%) were not significantly different. However, there was a significantly higher rate of cephalohematoma formation in the neonates delivered with vacuum devices (funnel-shaped cup, 13.9%; bell-shaped cup, 16.2%) than with forceps (2%). Caput and scalp discoloration was more apparent with the bell-shaped cup than with the funnelshaped cup. With regard to the utility of the soft-cup vacuum devices, Dell's group concluded that “the dramatic usefulness of these instruments to quickly deliver multiparas whose infants experienced fetal distress in late labor was far more impressive than their

performance as outlet instruments in nulliparas.” The first generation of mushroom-shaped cups represented an apparent attempt to produce a plastic version of the Malmstrom stainless steel cup. Several vendors offer disposable mushroom-shaped vacuum cup devices made of semirigid plastic; one of the more popular devices has been the M-cup (Mityvac). The efficacy of this cup was tested prospectively against the obstetric forceps in a large randomized clinical trial by Bofill in 1996. Both devices were comparably effective as tools to accomplish vaginal delivery, but deliveries with the M-cup were accomplished in less time and with less maternal genital tract trauma. As with nearly all other studies of vacuum and forceps, the clinical diagnosis of neonatal cephalohematoma was made significantly more often after vacuum delivery. The first generation of mushroom-shaped vacuum cups faced the same problems as the original Malmstrom stainless steel device—limited maneuverability. They were, however, more easily maneuvered than funnel- or bell-shaped cups within the maternal introitus because the traction stem could be bent at a 90-degree angle with respect to the cup. Nevertheless, the combined and centrally located vacuum port and traction stem limited the ability of the physician to place the vacuum cup on the median flexing point, especially in cases of difficult positioning of the fetal head such as OP or OT positions or in the presence of significant asynclitism. Past experience with improvements to the stainless steel cups afforded a design solution to this shortcoming as a plastic equivalent of the Bird posterior cup. In 2001, Vacca tested the OmniCup (Clinical Innovations Inc., Murray, UT) and found that it was quite useful for both nonrotational and rotational vacuum-assisted vaginal deliveries (Fig. 26.3). Vacca was able to achieve a median flexing application in 90% of applications, which resulted in “autorotation” in 32 of 33 cases in which rotation was expected.

Vacuum Pressure and Traction Forces The disposable plastic or silicone vacuum cups currently in use in the United States are marketed with a pistol grip hand pump that is connected to the cup by vacuum tubing (Fig. 26.3). A filter in the vacuum tubing prevents the suctioning of liquids or other debris into the pump. While it is possible to sterilize this pump, it is most commonly managed by a nurse or other attendant while the physician attends to the delivery. More recent versions of the mushroom vacuum cup are marketed with a disposable vacuum pump attached to the cup by a slender vacuum tube with an internal chain. This pump also contains a traction bar with a vacuum gauge and a vacuum release button. This allows the physician to better control the appropriate timing of vacuum pressure and traction. The recommended operating vacuum pressures for the majority of cups, whether stainless steel or plastic, is from 0.6 kg/cm2 to 0.8 kg/cm2 (about 500 to 600 mm Hg). The original stainless steel devices used a device that resembled a bicycle hand pump to achieve the required vacuum strength. The vacuum tubing was attached to a stoppered vacuum bottle that had ports for the vacuum pump and a vacuum gauge (Fig. 26.2). Alternatively, a portable electric vacuum pump or the hospital's wall suction system could be used to generate vacuum pressure. These systems are used rarely, if at all, in the United States for vacuum-assisted delivery.

Newer vacuum devices permit the rapid achievement of required vacuum pressure as a single step over several seconds, much faster than the slow and stepwise increase in pressure required with the original Malmstrom device. There is no difference between the final recommended vacuum pressure to achieve for plastic or silicone cups compared with the original stainless steel cups. With steel, the vacuum pressure is slowly brought to 600 mm Hg and is maintained at that level until delivery is accomplished—there is no reduction between uterine contractions and traction efforts. However, with the plastic cups, some authorities have recommended that the level of vacuum pressure should be reduced from 600 mm Hg during traction and contractions to 100 mm Hg during rest. The rationale for this recommended reduction in vacuum pressure is to expose the fetal scalp to the least amount of time at high vacuum pressures. A randomized trial of the intermittent versus continuous techniques of vacuum pressures during delivery with a mushroom-shaped cup failed to demonstrate any difference in neonatal outcomes. Regardless of the technique, however, the longer a vacuum cup resides on the fetal scalp, the greater is the likelihood of cephalohematoma formation and other cosmetic scalp lesions.

Vacuum Extraction Delivery: Recommended Practice The following list summarizes the recommended steps for use of a mushroom-shaped cup to accomplish vacuum-assisted vaginal delivery, analogous to the check-offs that a pilot undertakes while readying a plane for flight: CHECK—Specify the Indication: An indication should exist for the procedure. CHECK—Get Informed Consent: Obtain either verbally or as a written document. CHECK—Gestational Age ≥34 Weeks: The pregnancy is at term or near term—in the authors' practice, vacuum delivery generally is not used at a gestational age 10 minutes), duration of the second stage of labor, and a paramedian cup application. It is difficult, if not impossible, to compare the incidence of scalp trauma in studies of forceps and vacuum deliveries.

Cephalohematoma A cephalohematoma is a self-limited injury that is caused by the rupture and bleeding of an emissary vein into the potential space just beneath the periosteum of the neonatal parietal bone (Fig. 26.7). The periosteum of the parietal bone is firmly attached at the periphery, and only a limited amount of fetal blood can collect in this potential space. Cephalohematomas are diagnosed more commonly after vacuum extraction as opposed to forceps delivery. They typically resolve spontaneously over the course of a few days without long-term sequelae, although neonatal hyperbilirubinemia can develop. Most often, a cephalohematoma will not cross the suture lines of the skull, but edematous scalp can render the examination difficult and make the diagnosis challenging. Illustrative of this is the ultrasound confirmation of only three cephalohematomas in 12 neonates thought to have the condition. The other 9 infants had edematous scalps and not cephalohematomas.

Figure 26.7 Normal caput, cephalohematoma, subgaleal (subaponeurotic) hemorrhage, and intracranial hemorrhage.

Factors associated with cephalohematoma formation were studied in a Mississippi series of

322 vacuum extraction procedures performed with the semirigid mushroom-shaped cup. The rate of cephalohematoma formation in this study was 11%. Significant contributors to the diagnosis of neonatal cephalohematoma included the duration of the vacuum procedure and the amount of asynclitism at the time of cup placement. Asynclitism easily leads to a paramedian cup application that is productive of the chignon over one parietal bone more so than the other, which enhances the possibility of a false diagnosis of cephalohematoma.

Subgaleal (Subaponeurotic) Hemorrhage A much more serious and potentially fatal complication of vacuum extraction is a subgaleal (subaponeurotic) hemorrhage, in which a scalp vessel ruptures distal to the level of the periosteum where blood can accumulate in the layer of loose connective tissue known as the subgaleal or subaponeurotic space (Fig. 26.7). This potential space is very large and extends from the orbital ridges anteriorly, to the nape of the neck posteriorly, and to the zygomatic arches laterally. This space can easily accommodate the entire blood volume of a term newborn, even if filled only to a 1 cm depth. The most common physical finding with a subgaleal hemorrhage is a fluctuant mass that extends over the cranial sutures and fontanelles. This usually is accompanied by edema and bruising that extends posteriorly into the neck and laterally around the ears. The fluctuant mass can reach the upper eyelids and the root of the nose. The infant will commonly have evidence of hypovolemic shock. Shock may manifest hours after delivery or even later in the nursery. Subgaleal hemorrhage also has been associated with midforceps delivery, leading at least one investigator to conclude that instrumental delivery is the principal predisposing factor for this lesion. The incidence of subgaleal hemorrhage is estimated to occur in 4 of 10,000 spontaneous vaginal deliveries and in 59 of 10,000 vacuum-assisted deliveries. The 1998 FDA public health advisory primarily was directed at alerting all physicians who practice vacuum-assisted vaginal delivery to be very aware of subgaleal hemorrhage as a potential complication. Advising nursery personnel that a vacuum-assisted vaginal delivery has been performed also is key to facilitating the early diagnosis of a subgaleal hemorrhage.

Intracranial Hemorrhage Although intracranial hemorrhage in the term infant often is associated with traumatic operative vaginal delivery, it can occur after spontaneous delivery as well and have profound neonatal consequences (Fig. 26.7). In 1990, Hannigan and coworkers reported three cases of tentorial hemorrhage that were associated with soft-cup vacuum extraction deliveries. They reasoned that vacuum delivery could produce vertical stress in the occipitofrontal diameter, thereby causing tentorial venous hemorrhage. Nine other cases of tentorial subdural hemorrhage in term newborns were reported by another group, with five cases following delivery using the vacuum extractor. Seven of the nine infants were neurologically normal at 13 months of age. One infant delivered by vacuum extraction required a ventriculoperitoneal shunt for progressive hydrocephalus. Vacuum extraction typically is avoided in the fetus that is very preterm because of the

increased risk for intracranial hemorrhage at earlier gestational ages. There is no evidence-based gestational age threshold on which to base practice, but most clinicians avoid vacuum extraction altogether at 90 degrees) of the fetal head using classical forceps with a significant pelvic curvature mandates that the handles of the forceps circumscribe a wide arc so that the toe of the blade will circumscribe a small arc and remain in the center of the pelvis. This type of procedure likely is rare in current obstetric practice in the United States.

Relevant Maternal Anatomy Clinical assessment of the maternal pelvis is receiving less and less emphasis in current obstetric practice. Probably the best test of the cephalopelvic relationship in a patient is her conduct of labor. On occasion, careful and accurately undertaken clinical pelvimetry will demonstrate obvious abnormalities in a patient that possibly prevent a difficult labor due to obvious cephalopelvic disproportion.

Figure 26.10 The pure types of maternal pelves and the convergence and divergence of their sidewalls.

Knowledge that the female pelvis has different configurations is important (Fig. 26.10). Four basic shapes of the maternal pelvis are described in the 1933 Caldwell-Moloy classification, although subsequent study demonstrated that intermediate types of pelvic shapes are more common than the pure versions. Table 26.1 lists the important measurements of the maternal pelvis. Clinical knowledge of the type and relative dimensions of a given pelvis form the basis of any decision to perform a forceps delivery. Familiarity with the type of pelvis in a laboring patient will enable the obstetrician to better understand the mechanism of labor and also foster a more intelligent management of her labor.

TABLE 26.1 Diameters of the Maternal Pelvis Region of the Pelvis Measurement (Centimeters) Brim (Inlet) AP

11.5

Transverse

13.0

Midpelvis AP

12.0

Transverse

10.5

Outlet AP

12.5

Transverse

11.0

AP, anteroposterior.

Clinical Pelvimetry The pelvis usually is assessed in terms of the inlet, midpelvis, and outlet (Table 26.1).

Pelvic Inlet The pelvic inlet is best evaluated well before labor and engagement of the fetal head occurs with occupancy of the midpelvis and the posterior inlet. The examiner first assesses the anteroposterior (AP) diameter of the inlet by measuring the diagonal conjugate; namely, the distance from the undersurface of the symphysis pubis to the sacral promontory. Often, this causes discomfort for the patient being examined secondary to significant exerted pressure. The obstetric conjugate (the narrowest AP diameter of the inlet) is estimated by subtracting 2 cm from the diagonal conjugate measurement. The transverse diameter of the inlet cannot be measured directly by the obstetrician—a sense

of the shape and the extent of the circumference of the inlet can be gained by palpating laterally along the pelvic brim. If more than two thirds of the brim can be easily palpated, and especially if the posterior portions of the brim can be felt, it is likely that the patient has a contracted inlet.

Midpelvis The midpelvis is evaluated by palpating the shape of the sacrum (curved or straight) and the width of the sacrosciatic notch. Additionally, the shape and prominence of the ischial spines and the distance between them is very important. A contracted midpelvis typically has a flat and forward projecting sacrum, prominent ischial spines, and a narrow interspinous distance. The sacrospinous ligament is short and is less than two fingerbreadths long.

Pelvic Outlet The pelvic outlet is evaluated sequentially by (a) estimating the distance between the ischial tuberosities (usually about 10 cm), (b) palpating the coccyx to determine its orientation (not into the pelvis) and mobility, (c) assessing the subpubic angle to be greater than 90 degrees, (d) checking to ascertain that the retropubic angle is either flattened (platypelloid pelvis) or sharply angulated (android pelvis), and (e) the convergence or divergence of the pelvic sidewalls is assessed (Fig. 26.10). Clinical assessment of a patient's labor and her pelvis is mandatory (ideally with documentation) prior to an operative vaginal delivery. To denote that a pelvis is “adequate” is vague and open to question in cases of a less than optimal outcome. The art of intrapartum care demands that clinical pelvimetry be combined with fetal information such as head position, attitude, molding, caput, asynclitism, presence of meconium, parameters to construct a labor curve describing descent and dilatation, and fetal heart rate response with contractions or pushing.

Fetal Information Relative to Clinical Pelvimetry Fetal Lie The fetal lie describes the relationship of the long axis of the fetal body to the long axis of the maternal body. The fetal lie typically is described as a longitudinal lie (with a pure cephalic or breech presentations), oblique lie (with one fetal pole, the head or the breech, in the maternal iliac fossa), or a transverse lie (with the long axis of the fetal body at a 90degree angle to that of the long axis of the maternal body).

Fetal Presentation Fetal presentation is determined according to the lowermost portion of the fetus that encounters the pelvic inlet. Most commonly, it is either cephalic, breech, or a shoulder presentation. Less common are footling breech and funic (cord) presentations.

Fetal Engagement In a cephalic presentation, engagement is considered to occur when the largest part of the fetal head enters the pelvic inlet and/or when the leading edge of the fetal skull has reached the level of the ischial spines.

Fetal Attitude In a cephalic presentation, the attitude refers to the degree of flexion of the fetal head, ranging from fully flexed (vertex presentation) to fully extended (face presentation). Midway between these two is the neutral position of the fetal head, the so-called “military” or sincipital presentation.

Fetal Station The station of the fetal presenting part (fetal skull in a cephalic presentation, fetal sacrum in a complete breech presentation) describes its relationship in centimeters above, below, or exactly at the level (zero station) of the ischial spines within the maternal pelvis. Distance in centimeters of the presenting part above the ischial spines are considered as negative numbers, while those more deeply engaged (beyond the ischial spines) are positive numbers.

Fetal Position The fetal position is defined by the relationship of the fetal presenting part to the maternal pelvis. The position of the fetal occiput (in a cephalic presentation) or the fetal sacrum (in a breech presentation) is described in relation to the maternal pelvis as left or right as well as anterior or posterior. Examples are “left occiput anterior” and “right sacrum posterior.”

Fetal Molding Molding describes the degree of abutment or overlapping of the fetal skull plates as the fetal head progresses through the maternal pelvis. Generally, the occipital and frontal bones will slide under the parietal bones during labor. The extent of this overlapping of cranial bones can be clinically quantified (Fig. 26.5).

American College of Obstetricians and Gynecologists' Classification of Station In 1988, forceps operations were redefined by the ACOG with a classification system that emphasizes the station of the fetal head for stratification of the procedure. The leading part of the fetal skull is now described in numbers of centimeters above (0 to -5) or below the ischial spines (0 to +5). Minor degrees of rotation (45 degrees. Midforceps/Vacuum Station is >2cm but fetal head is engaged. Rotation is ≤45 degrees. Rotation is >45 degrees. High forceps/Vacuum Not included in 1988 classification AP, anteroposterior; OP, occiput posterior. Adapted from American College of Obstetricians and Gynecologists. Obstetrics forceps. Committee Opinion No. 71, 1988.

Figure 26.11 Bony anatomy, sutures, and fontanelles of the human fetal skull.

Applied Fetal Cephalic Anatomy Knowledge of term fetal skull anatomy is essential to excellent labor and delivery patient management, especially if the physician is performing forceps or vacuum extractor deliveries. Different positions of the fetal head will present the pelvis with different diameters that significantly impact the success rate of delivery. Figures 26.6 and 26.11 demonstrate important anatomic landmarks and depict the relevant diameters of the fetal skull. Tables 26.3 and 26.4 demonstrate the diameters and circumferences of the fetal head that are required to negotiate the maternal pelvis in specific fetal head positions. A number of terms are applied to swellings seen on the neonate's head. Caput succedaneum is seen in nearly all spontaneous deliveries and does not pose a risk to the neonate. Similarly, molding is seen to some extent in nearly all term vaginal deliveries and is considered normal. Figure 26.7 illustrates several examples of these normal lesions. In contrast, a cephalohematoma does involve a small subperiosteal bleed, and a subgaleal (subaponeurotic) hemorrhage can be a life-threatening condition for the newborn. The latter two conditions are most closely linked to vacuum delivery and were discussed in that section.

Caput Succedaneum and Molding Commonly referred to as caput, caput succedaneum denotes scalp edema, which is a

serous effusion between the aponeurosis and the periosteum that typically overlies the leading part of the skull. This is considered normal and develops in response to cervical pressure on the scalp, which interferes with its venous and lymphatic drainage during labor. There are varying degrees of caput; the edema usually will disappear within hours after birth.

TABLE 26.3 Diameters of the Fetal Head Diameter

Measurement (Centimeters)

Suboccipital–Bregmatic Nape of neck to center of bregma

9.5

Submental–Bregmatic Below chin to center of bregma

9.5

Mentum–Vertical Point of chin to above posterior fontanelle

14.0

Basal–Vertical Base of skull to most distant point of vertex

9.0

Occipital–Frontal Root of nose to occipital protuberance

11.5

Biparietal Between the two parietal eminences

9.5

Bitemporal Greatest distance between two halves of coronal suture

8.5

Molding is a normal deformation of the fetal head that occurs during labor. Some occipitoparietal molding is normally detected during the second stage of labor, but

excessive molding (particularly parietoparietal molding) is abnormal during the first stage of labor. Molding can be described by using the method of Stewart (Fig. 26.5) as follows: 0+ = suture easily felt between the two bones 1+ = no suture felt, but the bones can be separated easily with minimal digital pressure 2+ = overlap of bones, but they can be separated with digital pressure 3+ = overlap of bones that cannot be separated with digital pressure.

TABLE 26.4 Circumferences of Fetal Head in Specific Positions Circumference

Measurement (Centimeters)

Suboccipital–Bregmatic × Biparietal

28.0

Well-flexed vertex Occipital–Frontal × Biparietal

33.0

Deflexed vertex, OP position Mentum–Vertical × Biparietal

35.5

Brow presentation OP, occiput posterior.

Accurately Determining Fetal Head Position Precise knowledge of the position of the fetal head is essential in order to safely perform a forceps or vacuum delivery. The obstetrician should be able to delineate the positions of the fontanelles and fetal cranial bones and, and using this information, plan and perform the procedure. The true position of the fetal head can sometimes be difficult to determine, as caput succedaneum, molding, asynclitism, and maternal and fetal soft tissue edema can all combine to obfuscate the true fetal head position. Ascertainment of fetal head position is an important skill and practice for residents in training as well as in trained providers.

The authors stress to their house officers that it should become a routine practice during a vaginal examination in any laboring patient. In unusually difficult cases, translabial or transabdominal ultrasound can be used to ascertain the position of the fetal head. Neither forceps nor vacuum delivery should be attempted if the position of the fetal head cannot be ascertained.

Abdominal Examination Prior to Operative Vaginal Delivery Examination of the maternal abdomen should be included in the assessment prior to vaginal examination and any attempt at operative vaginal delivery. This evaluation will help in a number of ways. First, an experienced clinician's estimated fetal weight is probably as accurate as an ultrasound estimate. Second, it will reveal the fetal lie and give an idea of the position of the fetal spine. If the fetal back is not palpated laterally, there is an increased chance that the fetus is lying in an OP or OT position. Often, this knowledge will allow the obstetrician to understand an otherwise confusing vaginal examination. Finally, the amount of fetal head palpated above the pelvis brim can be assessed (Fig. 26.12). Although infrequently used in the United States, the Crichton method provides the examiner with an assessment of the level of the fetal head clinically in terms of “fifths of the fetal head palpable above the maternal pubic symphysis” and should be used only after ascertainment of an OA position. This measurement relies on the mean term fetal head diameter (basovertical) of 9 to 10 cm and the width of the obstetrician's finger being about 2 cm. No more than two fingerbreadths of the fetal skull should be palpable above the symphysis when the fetal skull is at zero station (the level of the ischial spines). If three fingerbreadths are palpable above the maternal symphysis, then the fetal head should not be considered engaged even if a portion of the fetal skull is palpable below the level of the ischial spines. Of course, an unengaged fetal head should preclude any attempt at operative vaginal delivery. In 1993, Knight and colleagues demonstrated that their abdominal assessment of engagement was superior and correctly predicted successful vaginal delivery as opposed to their vaginal assessment.

Figure 26.12 Abdominal palpation and the determination of the amount of the fetal head palpable above the pelvic brim.

Indications for Operative Vaginal Delivery Indications for operative vaginal delivery vary according to regional, national, and international practice. No indication is absolute. However, for obstetric practice generally in the United States, the ACOG has summarized these indications as follows:

Prolonged second stage of labor. In nulliparous women, a prolonged second stage of labor has been defined as lack of continuing progress for 2 hours without regional anesthesia or 3 hours with regional anesthesia. Suspicion of immediate or potential fetal compromise. Most obstetricians would rather use the term nonreassuring fetal status or fetal compromise with additional descriptive terminology instead of the formerly used but vague term fetal distress. Shortening the second stage of labor for maternal benefit. A common clinical scenario is maternal exhaustion, which is a poorly defined term. However, women with ocular, neuromuscular, cerebrovascular, or cardiovascular diseases in which vigorous or prolonged expulsive efforts are to be avoided are included in this group.

Contraindications to Operative Vaginal Delivery There are several obvious contraindications to operative vaginal delivery with forceps or vacuum and several more subtle ones. In today's practice, neither forceps nor vacuum should be considered if there is an unengaged fetal head or if there is obvious cephalopelvic disproportion. An operative vaginal delivery should not be attempted in a patient who does not consent or is unable to cooperate with the obstetrician. It also is not attempted if it is known that the fetus has a known bleeding diathesis such as hemophilia, alloimmune thrombocytopenia, or a disease of osseous fragility such as osteogenesis imperfecta.

Choice of Instrument: Obstetric Forceps Within the scope of current obstetric practice are a number of types of forceps that fall into one of two categories: the classical forceps and the specialized forceps. Resident physicians training in hospital systems within the United States typically are introduced to the art of forceps deliveries by using classical forceps such as the Simpson, Elliot, or Tucker-McLane instruments. These instruments are well suited for low- and outlet-forceps deliveries without the requirement for major rotations. Specialized forceps such as the Kielland (Fig. 26.8) forceps were designed and are utilized for specific requirements such as deliveries that require major rotational maneuvers or correction of asynclitism. Another example of a specialized forceps are the Piper forceps, which are designed to assist delivery of the after-coming head in a breech vaginal birth (Fig. 26.8). The Salinas forceps is a unique instrument that has been imported from Mexico and has two identically shaped, nonfenestrated blades with minimal pelvic curvature (Fig. 26.8). The lock of the Salinas forceps (Fig. 26.9) actually is part of the handle, which is used for traction. The convergent blades are maintained in place by maternal tissue, and the forceps produce no independent compression of the fetal head. The lack of pelvic curvature allows the instrument to be used for the purposes of rotation. The operator holds the locked handle of the forceps in

both hands and applies gentle traction to produce delivery. The blades will slip off if excessive force is applied. The choice of forceps typically will depend on the clinical situation, the training of the obstetrician, and the instruments available. For instance, a nulliparous patient with a prolonged second stage of labor with a molded fetal head but without a requirement for rotation is a candidate for forceps with an elongated cephalic curve that will allow significant traction such as the Simpson forceps. On the other hand, if a low pelvic forceps delivery with some rotation is required in a multiparous patient with an unmolded fetal head, the physician may use the Tucker-McLane instrument, whose more rounded cephalic curvature and nonfenestrated blades will allow for a better fit for the fetal head and safer rotation, respectively. Some obstetricians would rather use a nonfenestrated instrument when there is significant maternal genital tract edema in order to minimize the likelihood of a laceration; some would choose an instrument with overlapping instead of parallel shanks for a patient with a narrow introitus. Obstetricians in the United States who continue to perform major rotational forceps maneuvers usually will reach for the Kielland forceps, whose sliding lock also will allow for the correction of asynclitism; in Mexico, the choice likely would be the Salinas forceps in similar circumstances. The Barton forceps have been abandoned for rotational maneuvers.

Positioning of the Patient Typically, the patient is placed in the modified lithotomy position prior to undertaking an operative vaginal delivery. The maternal legs should be abducted, but there should not be excessive tension placed on the adductor muscles or on the soft tissues of the perineum. The patient's hips should not be overly flexed. The patient should not lie flat on her back— she should have at least a 30-degree upward tilt relative to the floor. To prevent pressure or stretching of any nerves, the patient should be maintained in this position only as long as is required for operative vaginal delivery and repair of any lacerations. The patient's hands typically are placed on handles that are near her hips on each side of the delivery table so that she can brace herself during any expulsive efforts.

Analgesia/Anesthesia Considerations More effective anesthesia is required to undertake a forceps delivery than a vacuumassisted delivery. The gold standard for anesthesia is a functioning epidural or spinal block. If the patient does not already have a regional anesthetic in place at the time of delivery, a pudendal block using 1% lidocaine will usually suffice for a low- or outlet-forceps procedure. Additional anesthetic can be infiltrated into the tissues of the perineum.

Prerequisites for Operative Vaginal Delivery Prior to any operative vaginal delivery, the patient and spouse/support person/family member(s) should be counseled regarding the rationale for undertaking the procedure. It is important that the physician remain calm and project a sense of confidence, maturity, and composure. Either verbal or written informed consent should be obtained. With

understanding and acceptance, the patient is likely to be less apprehensive and more cooperative. Ideally, the process taken for informed consent should be recorded in the physician's chart notes just before or just after the delivery is undertaken. The prerequisites for an operative vaginal delivery should be systematically checked off mentally by the physician. The cervix should be fully dilated and the membranes ruptured. The pelvic architecture and capacity should be evaluated if this was not done earlier during labor. If the fetal head is in an OA position, there should be no more than two fingerbreadths of the fetal head palpable above the maternal symphysis to indicate engagement (preferably deep engagement) of the presenting part. The position of the fetal head should be verified and the amount of caput, molding, and asynclitism should be known. The maternal urinary bladder should be empty. Anesthesia should be adequate. Proper patient positioning in the modified lithotomy position should be ascertained with care to prevent hyperflexion and avoid pressure points. The forceps should be examined to verify that they are from a matched set and appear symmetric. Since the position of the fetal head is known, the forceps are held in front of the perineum in the position that they are expected to assume after appropriate application. This practice is termed ghosting and is vitally important for young obstetricians in training. In this environment, an experienced obstetrician should be at hand in a supervisory role to perform the procedure if needed.

Application of Forceps The importance of the correct placement of the forceps into the vaginal canal and application to the fetal head cannot be overemphasized. It is best to introduce the forceps between contractions, when the patient is calm and resting. The application of the forceps blades should be gentle, smooth, and with minimal pressure. With correct insertion and positioning, gravity usually is sufficient to allow the forceps branch to fall into place. During residency training, it is recommended that the obstetrician learns to apply the forceps by using only the index finger, middle finger, and thumb to grasp the handle (Fig. 26.13) so that excessive force cannot be exerted. The blade should be positioned by using the thumb, index, and middle fingers placed on the edges. Minimal force should be required, and if there is resistance, the blade should be removed and reapplied. In this way, maternal and fetal injury will be minimized. A lubricant such as betadine soap or K-Y jelly placed on the blade may reduce friction and facilitate placement. Sudden vaginal bleeding after or during forceps placement suggests that the vaginal sidewall has been traumatized, for which immediate assessment is warranted.

Figure 26.13 Gentle grasp of the handle and proper positioning of the right hand for the direct application of classical forceps for outlet or low-pelvic delivery.

Direct Placement of the Forceps Direct placement of the obstetric forceps predominates, as most forceps operations performed with classical instruments will use this method. Most skilled operators will insert the posterior branch first in order to prevent loss of station of the fetal head. When there is a right OA position of the fetal head, the right or posterior branch will be placed first. With the fetal head in a left OP position or with a position that is directly OP, the left branch (i.e., the blade that lies on the maternal left) usually is placed first, by convention. The operator holds the handle above the level of the lock, and the blade is introduced into the vagina in the approximate position that it will ultimately lie. The right middle finger is used to support the edge of the blade at the introitus, and the right index finger is used to gently apply the upper border of the blade around the fetal head. Some operators will place the fingers or hand into the vagina to “protect” the vaginal sidewall, but this is not required and is frequently not possible in the nulliparous patient. Once the left blade is correctly positioned, minimal force with the left hand will be required to slide it further into the vagina and into its correct final position. The index and middle fingers of the right hand will slide along the upper and lower borders of the blade as it enters the vagina, gently guiding and adjusting its position. When correctly placed, the left branch should be in the approximate position that was expected earlier by ghosting, snugly maintained by the pressure between the fetal head and maternal vaginal sidewall. If the anticipated shank and handle positions are judged to be incorrect, any attempt to place the right branch and forcing the branches together is absolutely contraindicated, as this may result in maternal and/or fetal injury. If the correct placement of the left branch cannot be obtained by gentle manipulation of the

middle and index fingers of the operator's hand, then the branch should be removed by reversing the movements used for its insertion. Following placement of the left branch of the forceps, a “mirror image” procedure will introduce the right branch of forceps into the vagina. The handle of the right branch is then held with the right index finger, middle finger, and thumb, and the right branch is placed into the vagina in the approximate position that is expected according to the earlier ghosting application. The right branch should be above the left for appropriate locking. The left middle finger is used to support the edge of the blade at the introitus, and the left index finger is used to apply slight pressure onto the fetal head. Once the right blade is correctly inserted, a minimal force with the right hand is required to slide it farther into the vagina and into its correct final position. The index and middle fingers of the left hand will slide along the upper and lower borders of the blade as it enters the vagina, gently guiding and adjusting its position to complement that of the left branch. Force should not be used to lock the instrument. The shank and handle positions should be the same as that expected from the ghosting application. Once both branches of the forceps are placed, the fetal head position and the application of the forceps should be reviewed carefully prior to any traction efforts.

Wandering Placement Technique The wandering placement technique is used less commonly than the direct technique because it is usually performed as part of a major rotational forceps maneuver. A common clinical scenario for wandering placement is encountered with OT positioning of the fetal head. For rotation of the fetal head, the most common forceps utilized is the Kielland forceps. As noted previously, most obstetricians in the United States have ceased performing major forceps rotational maneuvers. When undertaken with Kielland forceps, a rotational maneuver usually is initiated by either the “inversion” application or the wandering application. The inversion application is mentioned only for historical reasons, as it is no longer recommended secondary to a high incidence of trauma to the lower uterine segment and urinary bladder. Instead, a wandering placement method is typically utilized for Kielland forceps rotation. After ghosting, the left branch is inserted first, especially with a left OT positioning of the fetal head. The Keilland forceps have “buttons” on the handles (Fig. 26.9), and when the forceps are applied correctly, these buttons should be oriented toward the fetal occiput. The operator holds the handle above the level of the lock, and the vertically held blade is introduced into the vagina with the toe of the blade at the posterior fourchette. The right index and middle fingers are used to support the edge of the blade at the introitus and to apply slight pressure onto the fetal head. Once the left blade is placed correctly, only minimal pressure is required to slide it farther into the vagina, because gravity and the weight of the handle are sufficient. The handle will move in an arc from the vertical to a horizontal position. To move the blade to the correct position with a left OT fetal head position, the right index and middle fingers gently guide the blade and “wander” it into a posterior position by using successive small finger movements (Fig. 26.14). The position of this branch is then compared with the expected ghosting application. After correct

placement of the left (posterior) branch, an assistant may hold the branch in position while the right branch is placed. Holding the right branch with the right index finger, middle finger, and thumb, the right blade is placed into the vagina in the same way as was the left branch. Again, only minimum pressure with the right hand will cause the blade to slide into the vagina, after which the left index and middle fingers gently guide the blade laterally. Repetitive finger movements help to “wander” the blade into an anterior position in the same way as was done with the left blade. The right branch should be maintained above the left branch to enable correct locking. Force should not be used to lock the instrument— the final shank and handle position should be the same as that expected from the ghosting application.

Checking the Position of the Blades In any forceps operation, after the blades are introduced, their positioning should be examined. The blades are appropriately positioned when they are against the sides of the fetal head in the spaces between the orbits and the ears (Fig. 26.15). This typically is called the biparietal or bimalar application. The toe of the blade should extend just beyond the malar eminences in order to allow even pressure distribution and to concentrate traction and compression forces on the less vulnerable regions of the fetal head. Before any traction or rotation can be performed, the operator should examine for the following: The sagittal suture in its entire length should be symmetric and perpendicular to the plane of the shanks. The posterior fontanelle should be about 2 cm from the plane of the shanks. The posterior fontanelle should be equidistant from the upper surface of each blade. The handles should not require any more than minimal pressure to close completely and should be pointing directly out. The amount of fenestration distal to the fetal head should allow only one fingertip to be inserted into this space.

Figure 26.14 Wandering placement of specialized (Kielland) forceps in right OT position.

Figure 26.15 The correct biparietal bimalar application of the forceps to the fetal

head.

Forceps Traction After the operator's examination demonstrates that the forceps have been correctly applied, traction usually is coordinated with maternal contractions and expulsive efforts. The maternal pelvis is curved, and this is important to remember when traction is initiated. In order to minimize friction, the traction forces on the fetal head should be maintained perpendicular to the axis of the pelvis by following the curve of Carus. It also is important to remember that the higher the forceps are applied, the greater is the initial downward pull that is required to negotiate the pelvic curve. As the head descends in the birth canal, the angle of traction moves forward (in the supine patient) so that it is ultimately turning upward at the outlet as delivery is accomplished. In order to facilitate forceps traction, the operator usually will stand slightly off center with respect to the patient. It is recommended that a right-handed individual stand to the maternal right with the right hand facing upward and the shanks of the locked forceps between the index and middle fingers (Fig. 26.16). The index and middle fingers are curled around the flange of the handle, which is held loosely when employing a forceps with crossed shanks or a sliding lock. With the classical forceps such as Simpsons with parallel shanks, the operator's middle finger can be placed in the space between the shanks with the index and ring fingers being placed on the handle flange. This hand (the operator's right hand) will apply the outward traction force. Because the traction occurs at the level of the lock (as opposed to the end of the handles), compression of the fetal head will be limited. The operator's left hand is placed palm down on the shanks of the forceps to exert a downward force known as the Pajot maneuver. The combined outward (right hand) and downward force (left hand) is continuously adjusted by the operator to produce force vectors as axis traction that follows the curve of Carus (Fig. 26.16).

Figure 26.16 Methods of hand placement and physician stance for standard operative vaginal delivery.

Axis traction similar to the Pajot maneuver can be accomplished by using the Saxtorph maneuver, in which the operator is seated and uses the fingers of the left hand to pull the locked shanks downward (Fig. 26.16). If, while sitting, the operator pulls in a direct line with the classical forceps, the fetal head will be pulled under the symphysis. The pelvic curvature of the classical instruments results in the handles being in a plane anterior to that of the handles. Many operators prefer to sit on a stool as they perform a simple forceps delivery, reasoning that in the sitting position much less force can be applied since the operator cannot use his or her weight to produce the traction force as can happen while standing. No longer is it permissible for the operator to brace his or her feet on the underside of the delivery table in order to achieve maximal axis traction. When the fetal

head is noted to crown, the handles of the classical forceps can be elevated until they are nearly perpendicular to the floor. At this point, the delivery can be completed with the forceps or the branches can be disarticulated so that delivery can be completed by using a modified Ritgen maneuver. Lastly, when the operator uses a specialized instrument with no pelvic curve or a reverse pelvic curve, it is important not to elevate the handles to more than 45 degrees above the horizontal at the outlet. Exceeding this limit invites an increased likelihood for sulcal tears to occur due to pressure from the toe of the blade. Delivery of the fetal head in an OP position, with its larger presenting diameters compared with the OP presenting head, has been associated with increased traction and compression forces. Axis traction for a persisting OP forceps delivery should be discontinued between contractions in order to reduce the intracranial pressure to which the fetus is exposed. Additionally, by releasing the pressure between contractions, any fetal bradycardia that often accompanies axis traction efforts can be ameliorated. Because of the potential for fetal heart rate abnormalities during delivery, the fetal heart rate should be monitored during operative vaginal deliveries.

Occiput Transverse Positions of the Fetal Head The OT head position frequently results in a deep transverse arrest and dystocia. In order to accomplish vaginal delivery, these fetuses usually will require rotation of the fetal head to the OA or OP position. Occasionally, patients with a platypelloid pelvis characterized by a flat sacrum and a short AP diameter will spontaneously deliver a baby with the head in a persistent OT position. In today's obstetric practice, the options for delivery of a patient with a deep transverse arrest include the following: Digital or manual rotation to OA or OP Rotation to OA or OP with forceps Cesarean delivery. A mid-1990s survey of ACOG Fellows revealed that most had stopped performing major rotational maneuvers with the obstetric forceps. The cohort of ACOG Fellows who had been in practice for fewer than 10 years did not use forceps for rotation at all. When sufficient training and clinical experience with rotational forceps delivery is lacking, cesarean delivery is the most prudent choice.

Occiput Posterior Positions of the Fetal Head An experienced obstetrician will recognize that OP presentations commonly are associated with deflexion attitudes of the fetal head. An OP position can be managed by spontaneous delivery as a direct OP, a forceps delivery as an OP, digital or manual rotation to OA, instrumental forceps rotation to OA, or a combination of these methods. Typically, if the fetal head is well flexed in the OP position, delivery can be accomplished by maternal exertion or assisted with forceps in the direct OP position. If the head is extended or only minimally flexed, an attempt at a direct OP forceps delivery may result in an increased risk

of maternal and fetal trauma due to the greater amount of axis traction required and the larger diameter of the presenting part. Traction on a deflexed head likely will exaggerate the extension and worsen the situation. If the delivering physician is not well versed in using the forceps for flexion and rotation of the fetal head from OP to OA, a cesarean delivery likely is the safest choice.

Digital or Manual Rotation If the operator has a small hand, digital or manual rotation often can be performed to rotate the fetal head from an OP or OT position to an OA position. Digital rotation entails placing the tips of the index and middle fingers onto the edge of the anterior parietal bone that overlaps the occipital bone near the posterior fontanelle. Thereafter, pressure is exerted upward with the tips of the fingers to rotate the posterior fontanelle toward the symphysis pubis (Fig. 26.17). This can be performed between contractions or even while the patient is pushing. With manual rotation, the whole hand is placed into the vagina, and the fingers are placed under the posterior parietal bone. The thumb is positioned on the anterior parietal bone and the head is rotated (Fig. 26.17). Care should be taken to not completely disengage the fetal head, as this could precipitate a prolapse of the umbilical cord. Manual rotation will not be possible for operators with large hands. If digital or manual rotation is successful, the patient should be encouraged to push in order to stabilize the new position of the fetal head. Alternatively, if the position now achieved is within 45 degrees of OA or OP, the forceps can be used to complete the delivery.

Postdelivery Management Following operative vaginal delivery by using forceps or vacuum, the vagina and cervix is meticulously inspected for lacerations or other injuries. If an episiotomy was performed, this is carefully examined for the possibility of extension into the muscular anal sphincter and then repaired without delay to minimize blood loss. Minor lacerations of the genital tract or cervix (first degree, some second degree) that are not bleeding usually do not require repair, because rapid healing is expected. The inspection and repair of the maternal genital tract is accomplished without delay, and the patient is taken out of the modified lithotomy position as quickly as possible—this is done to lessen the risk of nerve injury from prolonged pressure or stretching. An indwelling Foley catheter is advised if extensive repairs are required in the periurethral areas. The periurethral and perianal/rectal areas are carefully inspected after any repairs to exclude perforating sutures. If a patient complains of severe anal pain after a forceps delivery, a prompt examination should be undertaken to exclude the possibility of a vaginal or vulvar hematoma. Any evidence of hemorrhage such as maternal tachycardia, hypotension, or a sudden drop in hematocrit should initiate a search for continued bleeding either obvious (vaginal or vulvar) or occult (retroperitoneal hemorrhage).

Figure 26.17 Digital (A) and manual (B) rotation of the fetal head.

Complications of Operative Vaginal Delivery It is emphasized that many complications typically associated with operative vaginal delivery also are encountered with spontaneous delivery. Two of the major complications that may be found, especially in association with operative vaginal deliveries, are (a) an inappropriate evaluation of dystocia and (b) misuse of an instrument to accomplish delivery. Risk to the mother and the fetus–neonate can develop secondary to these two major complications. Maternal issues are considered first.

Lacerations Third-degree and fourth-degree lacerations are encountered more commonly with forceps delivery than with vacuum extraction delivery. In most studies, the incidence of severe lacerations (or episiotomy extension) ranges between 10% and 30% with vacuum in contrast to between 40% and 50% with forceps delivery.

Stress Urinary and Anal Incontinence The appeal of elective cesarean delivery for patients includes patient and physician convenience; the avoidance of labor with a possible concomitant reduction in the risk of hypoxic ischemic metabolic acidosis in the fetus; and the reduction of potential damage to the maternal genital tract and pelvic structures and thus less likely subsequent pelvic floor

dysfunction. The long-term effect of operative vaginal delivery on rectal or urinary incontinence is complex, and the literature remains unclear. Pregnancy itself and delivery via the vagina may contribute to persistent pelvic dysfunction. The greater the degree of perineal trauma consequent to vaginal delivery, the greater may be the likelihood that there will be residual sphincter abnormalities with resultant incontinence. For instance, anal incontinence has been reported to follow 20% to 54% of deliveries complicated by anal sphincter rupture with fourth-degree laceration. About half of women who sustained anal sphincter tears were reported to have associated anal, urinary, or perineal symptoms at a mean follow-up of 2.6 years after the injury. In 2001, Arya and colleagues retrospectively compared the incidence of new-onset urinary incontinence after forceps and vacuum delivery with that occurring in a cohort of primiparous women who had spontaneous vaginal deliveries. Although urinary incontinence was similar among the three groups during the first 2 weeks postpartum, the proportion of women developing new-onset urinary incontinence decreased significantly over time in the spontaneous vaginal (P = .003) and vacuum delivery groups (P = .009) but not in the forceps group (P = .2). Thus, in primiparous women, the authors concluded that urinary incontinence appears to be more likely to persist following forceps delivery compared with spontaneous vaginal or vacuum delivery. Farrell's group queried 690 Canadian primiparas by questionnaire regarding urinary incontinence during and 6 months after their first pregnancy. The rate of postpartum urinary incontinence 6 months after delivery was 26%, with more patients in the vaginal than the cesarean delivery groups (22% vs. 10%; odds ratio [OR] 2.1 [range 1.1 to –3.7]). Analysis of the impact of operative vaginal delivery revealed that 33% of patients who had a forceps delivery reported postpartum incontinence (forceps vs. spontaneous vaginal delivery, OR 1.5 [range 1.0 to 2.3]); forceps vs. cesarean, OR 3.1 [range 1.7 to 5.9]). Interestingly, vacuum delivery appeared not to be associated with a higher incidence of postpartum urinary incontinence when compared with spontaneous delivery, but when compared with cesarean delivery, there was a significantly higher rate of postpartum urinary incontinence (vacuum vs. cesarean, OR 3.5 [range 1.3 to 9.1]). These authors concluded that cesarean delivery performed before or during labor appeared to reduce the likelihood of postpartum urinary incontinence. Meyer and coworkers prospectively studied a cohort of Swiss primiparas during pregnancy, at 10 weeks postpartum, and again 10 months following delivery. The data included questionnaire, clinical examination, assessment of bladder neck and urethral sphincter function, and intravaginal/intra-anal pressures measured during pelvic floor contractions. No significant differences in urinary incontinence (20% vs. 15%) and fecal incontinence (4% vs. 5%) were observed at 10 months between the women who were delivered by forceps versus those who delivered spontaneously. However, more women in the forceps group were noted to have a weakened pelvic floor (20% vs. 6%; P = .05) and low intra-anal pressure (P = .04). MacArthur and colleagues questioned more than 5,000 postpartum women and found evidence to suggest that forceps deliveries are associated with a higher risk of fecal

incontinence than vacuum (OR 1.94; 95% confidence interval [CI] 1.30 to 2.89), while cesarean appears to offer some protection (OR 0.58; 95% CI 0.35 to 0.97). These findings were corroborated by the prospective randomized trial of Fitzpatrick and colleagues. This group used a symptom questionnaire, anal manometry, and endoanal ultrasound at 3 months postpartum. Using “intent to treat” analysis, they found that symptoms of altered fecal continence were significantly more common following forceps as opposed to vacuum delivery. However, in this study, 16 of 69 deliveries that randomized to vacuum were completed by the forceps. As is discussed later, this practice of “sequential” use of instruments should be discouraged. By no means should it be assumed that the vacuum will spare the patient the possibility of pelvic floor damage. Liebling and associates performed a prospective cohort study of 393 patients who either had a “difficult” operative vaginal delivery or a cesarean delivery in the second stage of labor. Of the operative vaginal deliveries, only 25% were delivered via the forceps while 51% were via the vacuum. In 24% of cases, the instruments were used sequentially. When compared with second-stage cesarean, a difficult instrumental delivery was associated with a greater risk of urinary incontinence at 6 weeks postdelivery (OR 7.8; 95% CI 2.6 to 23.6) and at 1 year (OR 3.1; 95% CI 1.3 to 7.6). While second-stage cesarean delivery did not completely protect women from pelvic floor morbidity, those with a difficult operative vaginal delivery had a significantly greater prevalence of urinary symptoms and dyspareunia. It is anticipated that vaginal delivery with or without instrumental assistance via vacuum or forceps will continue to be the principal route of delivery in the United States for the foreseeable future. Patients should be counseled that significant perineal trauma may be related to urinary and/or anal sphincter dysfunction and incontinence but that a fairly simple operative vaginal delivery without third- or fourth-degree laceration is not expected to cause sequelae that are significantly different from those following spontaneous delivery. Longer-term epidemiologic studies of pelvic function, preferably of a prospective type, should be performed before significant changes in modern obstetric practice are considered or recommended.

Nerve Injuries Rarely, a maternal nerve injury can result as a consequence of vaginal delivery (spontaneous or operative). This usually is caused by incorrect patient positioning and/or undue compression or traction on a nerve. When these injuries occur, most often they are temporary and the patient recovers completely. However, occasionally a nerve injury will result in long-term disability. Prolonged hyperflexion of the maternal hips at the time of delivery and genital tract repair usually is the culprit. Thus, if repair of genital tract lacerations is expected to be lengthy, it is recommended that the operator adjusts the patient's position so that there is minimal flexion of the hips. Additionally, attention should be directed to pressure points on the patient's legs to avoid nerve compression injuries; adequate padding and positioning are essential in this regard. The most common nerve injuries with their causes and presentations are shown in Table 26.5.

Neonatal Injuries Associated with Forceps As mentioned previously, neonatal injuries occur more commonly in association with vacuum delivery than with forceps. Potential injury includes retinal hemorrhage, cephalohematoma, and subgaleal (subaponeurotic) hemorrhage. Neonatal injury that is directly attributable to a forceps delivery itself is difficult to assign accurately, as the conditions that led to the intervention, such as a protracted labor or a compromised fetal situation, can be important contributors to a poor neonatal outcome.

Superficial Scalp and Facial Markings Forceps marks on the scalp and fetal face are nearly universal and inconsequential. A correct biparietal/bimalar application of the forceps blades will prevent tissue damage to sensitive regions such as the eyelids and face. An incorrect forceps application can be indicated by off-line forceps marks and/or bruising on the baby's face during the neonatal period. It should be explained to the parents that forceps marks usually are normal, expected, temporary, and not indicative of significant fetal injury. Significant abrasions or lacerations are outside the norm, usually prompting a review of the technique of forceps application utilized and the circumstances of the labor and delivery so that a second adverse outcome can be averted. Excessive pressure on the fetal face can result in vesicle formation, lipoid necrosis, and edema. Excessive compression of the fetal skull can result in fracture and intracranial trauma (see below). Most superficial injuries are short lived, recovery is uncomplicated, and lasting sequelae are absent.

TABLE 26.5 Nerve Injuries, Presentation, and Etiologies Femoral nerve (L2–4) Presentation: Quadriceps paralysis and impaired knee extension, loss of patellar reflex, hypoesthesia over the front of the thigh and medial aspect of calf, numbness of the anterolateral area of thigh. Etiology: Hyperflexion of the hips with traction or compression injury of the nerve, prolonged lithotomy position with kinking at Poupart ligament, midforceps delivery, retractors at cesarean, epidural anesthesia. Lateral femoral cutaneous nerve (L2–3) Presentation: Numbness over lateral thigh. Etiology: Compression of nerve under the inguinal ligament

from prolonged or incorrect lithotomy position, retractors at cesarean. Common peroneal nerve (L4–5, S1–2) Presentation: Foot drop; hypoesthesia over anterolateral aspect of lower calf, foot, and toes. Etiology: Compression of the nerve at the lateral aspect of the knee by a lithotomy pole, also reported after epidural anesthesia. Lumbosacral trunk (L4–5) Presentation: Paralysis of the dorsiflexors of the ankle with foot drop, hypoesthesia over the lateral aspect of calf and foot, slight weakness of the quadriceps (L4), slight weakness of the hip adductors (L4–5) Etiology: Compression of fetal head against sacrum, more common in midpelvic operative vaginal delivery, has been reported after epidural anesthesia. Sciatic nerve (L4–5, S1–3) Presentation: Inability to flex leg, pain from gluteal region down to the foot. Etiology: Traction injury from lithotomy position, midforceps, incorrect intramuscular injection. Obturator nerve (L2–4) Presentation: Inability to adduct leg, hypoesthesia medial thigh. Etiology: Lithotomy position, acute flexion of hip, hematoma, trauma from forceps blades. Saphenous nerve (L2–4) Presentation: Hypoesthesia medial foot and anterolateral lower leg. Etiology: Lithotomy position.

Facial Nerve Injury Injury to the facial nerve can occur, usually as the result of facial nerve compression by a forceps blade at a place where the nerve runs superficially in the mastoid region. This is

almost always a transient injury.

Corneal Abrasions and External Ocular Trauma Compared with nonoperative vaginal delivery, forceps delivery is associated with a higher incidence of fetal eyelid edema and minor external ocular trauma. Long-term sequelae are rare, and referral for ophthalmologic examination is individualized.

Intracranial Hemorrhage/Other Severe Injury Operative vaginal delivery is a contentious topic within the obstetric medicolegal arena. The authors speculate that this is due in part to the observation that the patient who requires operative vaginal delivery may have experienced a long or difficult labor. The fetus–neonate in such a pregnancy may be injured. It usually is difficult to ascertain with assurance and with certainty assign cause and effect, the etiology of injury. This is especially true when a fetus–neonate has a significant physical problem, such as a cerebrovascular injury that may be related indirectly to the underlying circumstances contributing to the decision for operative vaginal delivery or if the injury was directly related only to the forceps. In the situation of nonreassuring fetal status with a potential for developing fetal compromise, the decision to perform a cesarean or to attempt an operative vaginal delivery is frequently quite difficult in complex circumstances with time pressures that heightens the sense of trepidation. These situations will test the mettle of even the most experienced obstetrician. If the experienced operator is confident that a timely operative vaginal delivery can be performed and it is in the best interests of the mother and fetus, then this option is clearly a viable one and the forceps may be used while simultaneously preparing for a cesarean if the forceps procedure proves problematic. An operative vaginal delivery frequently will be the quickest and safest way to deliver the infant with nonreassuring status in the second stage of labor. Performance of a cesarean delivery in these circumstances will not repel the specter of litigation. Major fetal injuries have been reported following delivery with obstetric forceps. Standard obstetric teaching considers there to be approximately a 1% likelihood of neonatal skull fracture when a fetus is rotated by forceps from an OP to OA position with subsequent axis traction to effect delivery. This type of major rotational procedure is rarely encountered in today's practice of obstetrics. Yet, in 1995, a case series of 15 neonates with high cervical spinal cord injury and dismal outcome was published. The common feature in all cases was a forceps delivery that almost always was associated with rotation of the fetal head in excess of 90 degrees. In 1999, Towner and colleagues undertook a population-based study that examined the rates of neonatal intracranial hemorrhage associated with various modes of delivery. With this large cohort of 583,340 nulliparous women, the investigators determined that fetal– neonatal intracranial hemorrhage occurs with the following frequencies in selected circumstances: 1 in 334 in association with failed vacuum or forceps followed by cesarean

1 in 664 in association with a forceps delivery 1 in 860 in association with vacuum extractor delivery 1 in 907 in association with cesarean delivery during labor 1 in 2750 in association with cesarean before labor 1 in 1900 in association with normal spontaneous delivery. Also noted by Towner and colleagues in this data analysis was the finding that in comparison to spontaneous delivery, vacuum extraction (OR 2.7 [range 1.9, 3.9]), forceps delivery (OR 3.4 [range 1.9, 5.9]), and cesarean after abnormal labor (OR 2.5 [range 1.8, 3.4]) were each associated with an increased incidence of intracranial hemorrhage. Interestingly, there were no statistically significant differences among the rates of intracranial hemorrhage when vacuum, forceps, or cesarean after abnormal labor were compared with each other. Towner's group also made the observation that there appear to be risks associated with the “sequential” use (unsuccessful vacuum, then forceps) of instruments to accomplish operative vaginal delivery inasmuch as the risk of intracranial hemorrhage was significantly higher in this circumstance than with either vacuum or forceps alone. Intracranial hemorrhage occurred in 1 in 256 infants delivered by the sequential use of instruments (vacuum, then forceps), which was 3.4 times the rate associated with vacuum delivery alone. Finally, the study findings point toward abnormal labor as the common risk factor for fetal–neonatal intracranial hemorrhage, not the instrument(s) chosen to resolve the difficult labor and accomplish delivery.

Instrument of Choice: Vacuum or Forceps? Based on the variety of personal experiences and preferences among authorities, there is no uniformity of opinion with regard to which of the instruments for operative vaginal delivery is preferred over the other—the vacuum extractor or the obstetric forceps. Metaanalyses of forceps and vacuum trials have been problematic for several reasons. First, the published trials comparing vacuum with forceps have serious methodologic differences, and this has made the pooling of data difficult if not impossible. In addition, these investigations were undertaken over a 30-year span of time, during which the practice of obstetrics has undergone constant change. Finally, many different types of vacuum extractors and forceps have been employed in these investigations, and each of these different instruments have unique profiles of efficacy and complication that impedes the pooling of data for gross comparisons. Despite these hurdles, in 2000, Johanson and Menon performed a meta-analysis of trials of vacuum and forceps as part of the Cochrane Database of Systematic Reviews. These researchers combined the results from 10 prospective and randomized trials published in the obstetric literature and derived some important observations. First, the forceps appear to be significantly more likely to result in a successful delivery as opposed to the vacuum extractor. However, the women who randomized to the vacuum extractor in these studies actually had a lower cesarean delivery rate because a vacuum failure was frequently followed by a forceps delivery, whereas an unsuccessful forceps delivery most often was accomplished by cesarean. Of course, in current obstetric practice, it is rare to combine

the use of instruments in a single delivery. Second, in nearly all of the studies, maternal genital tract injury was significantly higher in the forceps group, and women who were delivered by the vacuum extractor had less pain at delivery and at 24 hours postpartum, even with a lower rate of usage of regional and general anesthesia. Third, neonatal cephalohematoma and retinal hemorrhage occur more frequently with the vacuum extractor, but there reportedly is no significant difference in the need to use phototherapy for neonatal jaundice between forceps or vacuum-delivered infants. In 2001, Wen and colleagues published a historical cohort study involving 31,015 women delivered by vacuum and 18,727 delivered by forceps in which it was concluded that vacuum delivery was associated with less maternal trauma but their use “may increase the risk of cephalohematoma and certain types of intracranial hemorrhage (eg, subarachnoid hemorrhage).” Generally, neonatal injuries with operative vaginal delivery are expected to occur more often with vacuum application, while maternal injuries occur more often with forceps use. It would be ideal if every graduate of every U.S. residency training program were equally adept with the forceps and the vacuum extractor. However, in modern practice, the obstetrician's choice of vacuum or forceps typically depends on local tradition and the influence of the instruction that he or she received during residency training. In everyday practice, the decision to use the vacuum or the forceps probably will not be based on the results of published studies but more likely will reflect the individual provider's preferences and proficiencies.

Summary Points In 2004, the total rate of operative vaginal delivery in the United States was 5.2%, obstetric forceps in 1.1% of all deliveries, and vacuum extractor in 4.1%. Adequate assessment of “the pelvis and passenger” is essential prior to attempting any operative vaginal delivery. Sequential operative vaginal delivery attempts with different instruments significantly increase the risk of neonatal intracranial complications. Both forceps and vacuum extractor are acceptable and safe instruments for operative vaginal delivery. Operator experience should determine which instrument should be used in a particular situation. Recommended steps for use of vacuum-assisted vaginal delivery include gestational age ≥34 weeks, full cervical dilation and fetal head well engaged, correct knowledge of the position of the fetal head, absence of contraindications (such as malpresentations), correct application of the vacuum cup, assurance that no maternal tissue is trapped under the cup, and traction undertaken in the direction of the pelvic axis and perpendicular to the cup. In

addition, the procedure should be terminated if there are 3 “popoffs” or if the delivery has not occurred within 20 minutes, or if there is no descent with correct application and appropriate traction. Further, intentional torsion of the cup or rocking of the cup is to be decried. In the United States, indications for operative vaginal delivery include prolonged second stage of labor, suspicion of immediate or potential fetal compromise, and shortening second stage of labor for maternal benefit. Contraindications to operative vaginal delivery include an unengaged fetal head or suspected cephalopelvic disproportion, lack of patient consent, known fetal bleeding diathesis, or fetal diseases of osseous fragility such as osteogenesis imperfecta. The importance of correct placement of the forceps in the vaginal canal and application to the fetal head is essential. The operator must be knowledgeable in the use of forceps and facile at checking the position of the forceps blades. Forceps appear to be significantly more likely to result in a successful vaginal delivery as opposed to the vacuum extractor. Maternal genital tract injury is higher in women having forceps deliveries, but neonatal cephalohematoma and retinal hemorrhage occur more frequently in women having delivery by vacuum extractor. Effort should be made to train resident obstetricians in the use of operative vaginal delivery techniques, as appropriate and safe deployment of forceps- and vacuum-assisted delivery remain an important part of modern-day obstetrics.

Suggested Readings Aguero O, Alvarez H. Fetal injuries due to the vacuum extractor. Obstet Gynecol 1962;19:212. Ahuja GL, Willoughby MLN, Kerr MM, et al. Massive subaponeurotic hemorrhage in infants born by vacuum extraction. Br J Med 1969;3:743. American College of Obstetricians and Gynecologists. Committee on Obstetrics, Maternal and Fetal Medicine. Obstetric forceps. Technical Bulletin No. 59, February 1988. American College of Obstetricians and Gynecologists. Delivery by vacuum extraction. Committee Opinion No. 208, 1998.

American College of Obstetricians and Gynecologists. Macrosomia. Practice Bulletin No. 22, November 2000. American College of Obstetricians and Gynecologists. Operative vaginal delivery. ACOG Practice Bulletin No. 17, 2000. Arnott N. Elements of physics or natural philosophy. London: Publisher, 1829. Arya LA, Jackson ND, Myers DL, et al. Risk of new-onset urinary incontinence after forceps and vacuum delivery in primiparous women. Am J Obstet Gynecol 2001;185:1318. Berkus MD, Rammurthy RS, O'Connor PS, et al. Cohort study of silastic obstetric vacuum cup deliveries: I. Safety of the instrument. Obstet Gynecol 1985;66:503. Berkus MD, Rammurthy RS, O'Connor PS, et al. Cohort study of silastic obstetric vacuum cup deliveries: II. Unsuccessful vacuum extraction. Obstet Gynecol 1986;68:662. Bird GC. Modification of Malmstrom's vacuum extractor. Br J Med 1969;3:526. Bofill JA. Guest editorial. Operative obstetrics: a lost art?. Obstet Gynecol Surv 2000;55:405–406. Bofill JA. Operative delivery by vacuum. In: Gilstrap LC, Cunningham FG, Van Dorsten JP, eds. Operative obstetrics, 2nd ed. New York: McGraw-Hill, 2002. Bofill JA, Rust OA, Devidas M, et al. Neonatal cephalohematoma from vacuum extraction. J Repro Medicine 1997;42:565–569. Bofill JA, Rust OA, Devidas M, et al. Prognostic factors for moderate and severe maternal genital tract laceration with operative vaginal delivery in a residency training program. J Pelvic Surg 1996;2:293–297. Bofill JA, Rust OA, Perry KG, et al. Forceps and vacuum delivery: a survey of North American residency programs. Obstet Gynecol 1996;88:622. Bofill JA, Rust OA, Perry KG, et al. Operative vaginal delivery: a survey of Fellows of ACOG. Obstet Gynecol 1996;88:1007. Bofill JA, Rust OA, Schorr SJ, et al. A randomized prospective trial of the obstetric

forceps versus the M-cup. Am J Obstet Gynecol 1996;175:1325–1330. Bofill JA, Rust OA, Schorr SJ, et al. A randomized trial of two vacuum extraction techniques. Obstet Gynecol 1997;89:758–762. Broekhuizen FF, Washington JM, Johnson F, et al. Vacuum extraction versus forceps delivery: indications and complications, 1979 to 1984. Obstet Gynecol 1987;69:338. Chalmers JA. James Young Simpson and the “suction-tractor”. J Obstet Gynaecol Br Commonw 1963;70:94. Chenoy R, Johanson R. A randomized prospective study comparing delivery with metal and silicone vacuum extractor cups. Br J Obstet Gynaecol 1992;99:360. Cohn M, Barclay C, Fraser R, et al. A multicentre randomized trial comparing delivery with a silicone rubber cup and rigid metal vacuum extractor cups. Br. J Obstet Gynaecol 1989;96:545. Crichton D. A reliable method of establishing the level of the fetal head in obstetrics. S Afr Med J 1974;48:784. DeLee JB. The prophylactic forceps operation. Am J Obstet Gynecol 1920;1:34. Dell DL, Sightler SE, Plauche WC. Soft cup vacuum extraction: a comparison of outlet delivery. Obstet Gynecol 1985;66:624. Ehlers N, Jensen IK, Hansen KB. Retinal haemorrhage in the new forceps and by vacuum extractor. Acta Ophthalmol 1974;52:73. Ezenagu LC, Kakaria R, Bofill JA. Sequential use of instruments at operative vaginal delivery: is it safe? Am J Obstet Gynecol 1999;180:1446. Farrell SA, Allen VM, Baskett TF. Parturition and urinary incontinence in primiparas. Obstet Gyncol 2001;97:350.

Fitzpatrick M, Behan M, O'Connell PR, et al. Randomized clinical trial to assess anal sphincter function following forceps or vacuum assisted delivery. Br J Obstet Gynaecol 2003;110:424. Food and Drug Administration. FDA public health advisory: need for caution when using

vacuum-assisted delivery devices. Rockville, MD: Author, May 21, 1998. Gardella C, Taylor M, Benedetti T, et al. The effect of sequential use of vacuum and forceps for assisted vaginal delivery on neonatal and maternal outcomes. Am J Obstet Gynecol 2001;185:896. Govaert P, Vanhaesebrouk P, De Praeter C, et al. Vacuum extraction, bone injury and neonatal subgaleal bleeding. Eur J Pediatr 1992;151:532. Greis JB, Bieniarz J, Scommengna A. Comparison of maternal and fetal effects of vacuum extraction with forceps or cesarean section. Obstet Gynecol 1981;57:571. Hagadorn-Freathy AS, Yeomans ER, Hankins GDV. Validation of the 1988 ACOG forceps classification system. Obstet Gynecol 1991;77:356. Hammarstrom M, Csemiczky G, Belfrage P. Comparison between the conventional Malmstrom extractor and a new extractor with silastic cup. Acta Obstet Gynaecol Scand 1986;65:791. Hankins GDV, Uckan E, Rowe TF, et al. Forceps and vacuum delivery: expectations of residency and fellowship training program directors. Am J Perinatol 1999;16:23. Hannigan W, Morgan A, Kokinski L, et al. Tentorial hemorrhage associated with vacuum extraction. Pediatrics 1990;85:534. Hofmeyer GJ, Gobetz L, Sonnendecker EWW, et al. New design rigid and soft vacuum extractor cups: a preliminary comparison of traction forces. Br J Obstet Gynaecol 1990;97:681. Holden R, Morsman DG, Davidek GMB, et al. External ocular trauma in instrumental and normal deliveries. Br J Obstet Gynaecol 1992;99:132. Holland E. The Princess Charlotte of Wales. A triple obstetric tragedy. Obstet Gynecol 1951;58:905. Huang CC, Shen EY. Tentorial subdural hemorrhage in term newborns: ultrasonographic diagnosis and clinical correlates. Pediatr Neurol 1991;7:171. Johanson RB, Heycock E, Carter J, et al. Maternal and child health after assisted vaginal delivery: five-year follow up of a randomized controlled study comparing forceps and ventouse. Br J Obset Gynaecol 1999;106:544.

Johanson RB, Menon BVK. Soft versus rigid vacuum extractor cups for assisted vaginal delivery. Cochrane Database Syst Rev 2000;2:CD000446. Johanson RB, Menon BKV. Vacuum extraction versus forceps for assisted vaginal delivery. Cochrane Database Syst Rev 2000;2:CD000224. Knight D, Newnham JP, McKenna M, et al. A comparison of abdominal and vaginal examinations for diagnosis of engagement of the fetal head. Aust N Z J Obstet Gynaecol 1993;33:154. Kuit JA, Eppinga HG, Wallenburg HC, et al. A randomized comparison of vacuum extractor delivery with a rigid and a pliable cup. Obstet Gynecol 1993;82:280. Learman LA. Regional differences in operative obstetrics: a look to the South. Obstet Gynecol 1998;92:514. Liebling RE, Swinigler R, Patel RR, et al. Pelvic floor morbidity up to one year after difficult instrumental delivery and cesarean section in the second stage of labor: a cohort study. Am J Obstet Gynecol 2004;191:4. MacArthur C, Bick DE, Keightly MRB. Faecal incontinence after childbirth. Br J Obstet Gynaecol 1997;104:46. Malmstrom T. The vacuum extractor—an obstetrical instrument. Acta Obstet Gynecol Scand 1954;33(Suppl 4):4. Martin JA, Hamilton BE, Sutton PD, et al. Births: final data for 2004 (National Vital Statistics Reports, Vol. 55, No. 1). Hyattsville, MD: National Center for Health Statistics, 2006. Maryniak G, Frank J. Clinical assessment of the Kobayashi vacuum extractor. Obstet Gynecol 1984;64:431. Menticoglu SM, Perlman M, Manning FA. High cervical spinal cord injury in neonates delivered with forceps: report of 15 cases. Obstet Gyncol 1995;86:589. Meyer S, Hohlfield P, Achtari C, et al. Birth trauma: short and long term effects of forceps delivery compared with spontaneous delivery on various pelvic floor parameters. Br J Obstet Gynaecol 2000;107:1360. Morales R, Adair CD, Sanchez-Ramos L, et al. Vacuum extraction of preterm infants with

birth weights of 1500—2499 grams. J Repro Med 1995;40:127. Ott WJ. Vacuum extraction. Obstet Gynecol Surv 1975;30:643. Plauche WC. Fetal cranial injuries related to delivery with the Malmstrom vacuum extractor. Obstet Gynecol 1979;53:750. Plauche WC. Subgaleal hematoma: a complication of instrumental delivery. JAMA 1980;244:1597. Pritchard J, McDonald PC, Gant NF. Williams obstetrics, 17th ed. Norwalk, CT: Appleton Century Crofts, 1985: 851. Revah A, Ezra Y, Farine D, et al. Failed trial of vacuum or forceps—maternal and fetal outcome. Am J Obstet Gynecol 1997;176:200. Ross MG, Fresquez M, El-Haddad MA. Impact of FDA advisory on reported vacuumassisted delivery and morbidity. J Matern Fetal Med 2000;9:321. Stewart KS. In: Myerscough PR, ed. Munro Kerr's operative obstetrics, 10th ed. London: Bailliere Tindall, 1980. Sultan AH. Anal incontinence after childbirth. Curr Opin Obstet Gynecol 1997;9:320. Teng FY, Sayre JW. Vacuum extraction: does duration predict scalp injury?. Obstet Gynecol 1997;89:281. Thomas SJ, Morgan MA, Asrat T, et al. The risk of periventricular—intraventricular hemorrhage with vacuum extraction of neonates weighing 2000 grams or less. J Perinatol 1997;17:37. Towner D, Castro MA, Eby-Wilkens E, et al. Effect of mode of delivery in nulliparous women on neonatal intracranial injury. N Engl J Med 1999;341:1709. The use of vacuum assisted delivery devices and fetal subgaleal haemorrhage. Medical Devices Alert No. 110. Ottawa: Health Protection Branch, February 23, 1999. Uchil D, Arulkumaran S. Neonatal subgaleal hemorrhage and its relationship to delivery by vacuum extraction. Obstet Gynecol Surv 2003;58:687. Vacca A. Handbook of vacuum extraction in obstetric practice. London: Edward Arnold,

1992. Vacca A. Operative vaginal delivery: clinical appraisal of a new vacuum extraction device. Aust N Z J Obstet Gynaecol 2001;41:2:156. Wen SW, Liu S, Kramer MS, et al. Comparison of maternal and infant outcomes between vacuum extraction and forceps deliveries.Am J Epidemiol 2001;153:103. Wider JA, Erez S, Steer CM. An evaluation of the vacuum extractor in a series of 201 cases. Am J Obstet Gynecol 1967;98:24. Williams MC, Knuppel RA, O'Brien WF, et al. Obstetric correlates of neonatal retinal hemorrhage. Obstet Gynecol 1993;81:688. Wood J, Amos L, Rieger N. Third degree anal sphincter tears: risk factors and outcome. Aust N Z J Obstet Gynaecol 1998;38:414. Yeomans E, Hankins GDV. Operative vaginal delivery in the 1990s. Clin Obstet Gynecol 1992;35:487–493. Zetterstrom J, Lopez A, Anzen B, et al. Anal sphincter tears at vaginal delivery: risk factors and clinical outcome of primary repair. Obstet Gynecol 1999;94:21.

27 Cesarean Delivery James R. Scott T. Flint Porter Cesarean section is the term commonly used to describe the delivery of an infant through an abdominal uterine incision. Since the words cesarean and section used together are redundant because both imply incision, cesarean delivery is preferable and is used in this chapter. Cesarean delivery has played a major role in lowering both maternal and perinatal morbidity and mortality rates during the past century. The initial purpose of the operation was to preserve the life of the mother with obstructed labor, but indications expanded over the years to include delivery for a variety of more subtle dangers to the mother or fetus. Contributing to its more frequent use is increased safety that is largely due to better surgical technique, improved anesthesia, effective antibiotics, and availability of blood transfusions. The cesarean rates during the past decade, both in the United States and worldwide, have increased dramatically. The percentage of women in the United States delivering by cesarean increased from 30%. While the rate of cesarean delivery has been rising, the rate of cerebral palsy remains unchanged. The incidence of placenta previa or placenta accreta progressively increases and is 3%, 11%, 40%, 61%, and 67% for the first, second, third, fourth, and fifth cesarean deliveries, respectively. The ACOG considers it ethical to perform a patient-choice cesarean if the physician believes that the overall health of the patient and fetus is greater with cesarean than with vaginal birth.

Suggested Readings American College of Obstetricians and Gynecologists. Assessment of fetal lung maturity. ACOG Educational Bulletin No. 230. 1996; issue 1. American College of Obstetricians and Gynecologists. Induction of labor. ACOG Practice Bulletin No. 10, November, 1999. American College of Obstetricians and Gynecologists. Surgery and patient choice. In: Ethics in obstetrics and gynecology, 2nd ed. Washington, DC: Author, 2004;21–25. American College of Obstetricians and Gynecologists. Task Force on Cesarean Delivery Rates. Evaluation of cesarean delivery. Washington, DC: Author, 2006. Baskett TF. Emergency obstetric hysterectomy. J Obstet Gynecol 2003;23:353–355. Cahill AG, Macones GA. Vaginal birth after cesarean: evidence-based practice. Clin Obstet Gynecol 2007;50(2):518–525.

Centers for Disease Control and Prevention. Births: preliminary data for 2004 (National Vital Statistics Reports, Vol. 54, No. 4). Atlanta, GA: Author, 2005. Flamm BL, Goings JR, Liu Y, et al. Elective repeat cesarean versus trial of labor: a prospective multicenter study. Obstet Gynecol 1994;83:927. Flamm BL, Quilligan EJ. Cearean section. Guidelines for appropriate utilization. New York: Springer-Verlag, 1995. Hankins GDV, Clark SL, Cunningham FG, et al. Cesarean section. In: Operative obstetrics. Norwalk, CT: Appleton & Lange, 1995: 301–332. Hawkins JL, Gibbs CP, Orleans M, et al. Obstetric anesthesia work force survey, 1981 versus 1992. Anesthesiology 1997;87:135. Hayman RC, Arulkumarian S, Steer PJ. Uterine compression sutures: surgical management of postpartum hemorrhage. Obstet Gynecol 2002;99:502–506. Hong TM, Tseng HS, Lee RC, et al. Uterine artery embolization: an effective treatment for intractable obstetrical hemorrhage. Clin Radiol 2004;59:96–101. Landon MB, Hauth JC, Leveno KJ, et al. Maternal and perinatal outcomes associated with a trial of labor after prior cesarean delivery. N Engl J Med 2004;351:2581–2589. Macones GA, Hausman N, Edelstein R, et al. Predicting outcomes of trials of labor in women attempting vaginal birth after cesarean section. Am J Obstet Gynecol 2001;184:409–413. National Institutes of Health. Cesarean delivery on maternal request. State-of-theScience Conference Statement, March 27—29, 2006. Obstet Gynecol 2006;107:1386–1397. Phelan JR, Clark SL, eds. Cesarean delivery. New York: Elsevier Science Publishing, 1988. Reyes-Ceja L, Cabrera R, Insfran E, et al. Pregnancy following previous uterine rupture. Obstet Gynecol 1969;34:387. Ritchie EH. Pregnancy after uterine rupture of the pregnant uterus.J Obstet Gynaecol Br Commonw 1971;78:642. Scott JR. Avoiding labor problems during vaginal birth after cesarean delivery. Clin

Obstet Gynecol 1997;40:533. Scott JR. Mandatory trial of labor after cesarean delivery: an alternative viewpoint. Obstet Gynecol 1991;77:811. Silver RM, Landon MB, Rouse DJ, et al. Maternal morbidity associated with multiple repeat cesarean deliveries. Obstet Gynecol 2006;107:1226–1232. Villar J, Valladares E, Wojdyla D, et al. Caesarean delivery rates and pregnancy outcomes: the 2005 WHO global survey on maternal and perinatal health in Latin America. Lancet 2006;367:1819–1829. Weber A. Elective cesarean delivery: the pelvic perspective. Clin Obstet Gynecol 2007;50(2):510–517. Zupancic Salek S, Sokolic V, Sanjug J, et al. Successful use of recombinant factor VIIa for massive bleeding after caesarean section due to HELLP syndrome. Acta Haematol 2002;108:162–163.

28 Psychologic Disorders of Pregnancy and the Postpartum Period Michael W. O'Hara Lisa S. Segre Depressive and anxiety disorders are common during pregnancy and the postpartum period. These disorders may impair the woman's self-care during pregnancy and negatively affect her parenting after delivery. The patterns of presentation vary widely. Depressive and anxiety disorders may exist before the pregnancy, or they may develop during pregnancy or after delivery. Sometimes, they are quite apparent to the obstetrician examining an obviously sad or anxious woman. Often, they are not obvious because women may conceal emotional disturbance for reasons that include stigma, fear of the baby being taken away, not recognizing that she has a psychiatric disorder, or simply not wanting to bother the doctor. Women with severe mental illness who become pregnant usually are already under the care of a psychiatrist. However, some women develop a “postpartum psychosis” within a few weeks of delivery. Although a previous history of psychosis is the most significant risk factor, the majority of women experiencing a psychotic episode after delivery have no significant history of psychiatric illness. Thus, the tasks of the obstetrician with respect to these disorders are to (a) understand their nature, risk factors, and consequences for the mother and fetus or child; (b) detect and assess for them during clinical visits; (c) educate patients and families; and (d) make effective referrals and/or manage clinical care of these disorders. In the first part of this chapter, perinatal psychiatric disorders are described, including their clinical presentation, prevalence, effects, and management in an obstetric setting. Because the detection of these disorders is not reliably accomplished by direct observation alone, the second part of this chapter will describe patient education and screening approaches feasible for an obstetrics office setting.

Postpartum Blues Description In the early postpartum period, many women experience a mild mood disturbance referred

to as “postpartum blues.” Symptoms often are most noticeable between days 3 and 5 postpartum and typically last anywhere from several hours to several days. Figure 28.1 illustrates this pattern. It shows daily mood ratings of a sample of pregnant and postpartum women at several time points in late pregnancy and the early postpartum period. By day 2 after delivery, women experience negative mood at about the same level as comparable women who have not recently delivered a child. Negative mood increases, peaking at day 6 postpartum. It is interesting to note that mood is, on average, more negative late in pregnancy than at the time in the postpartum period during which the blues peaks in intensity. Finally, although the term blues primarily connotes sadness, it is not a form of mild depression. It might best be considered a problem in affect regulation. Prominent symptoms include mood lability, irritability, interpersonal hypersensitivity, insomnia, anxiety, tearfulness, and even elation. Because the blues is common and almost always occurs in close proximity to childbirth, the phenomenon is considered normal and probably hormonally driven, though research is inconclusive in this respect. The literature does suggest that women with a history of depression are at increased risk for the blues and that the blues is itself a risk factor for later depression. These and other findings suggest that the blues may lie within the spectrum of affective disorders.

Figure 28.1 Visual Analogue Scale negative mood scale scores for childbearing and nonchildbearing subjects during pregnancy and after delivery. (VAS, Visual Analog Scale.) (From O'Hara MW, Zekoski EM, Philipps LH et al. Controlled prospective study of postpartum mood disorders: comparison of childbearing and nonchildbearing women. J Abnorm Psychol 1990;99:3–15.)

Prevalence and Effects Because there is no single accepted definition of the blues, estimates of its prevalence have varied considerably, ranging from 26% to 84%. Table 28.1 includes two definitions of the blues, the Pitt and the Handley criteria. The Pitt criteria will identify about half of

postpartum women as experiencing the blues, while the Handley criteria will identify about a quarter of women as experiencing the blues. Generally, the blues lasts no more than a few days, requires no treatment, and is not associated with negative sequelae. However, in some cases, what appears to be the postpartum blues is actually the beginning of a depressive episode, which is discussed in the section on Perinatal Depression.

TABLE 28.1 Definitions of Blues Based on Pitt and Handley Criteria Pitt Criteria for the Blues Period lasting at least part of day (in the first week to 10 days postpartum) when woman felt very depressed and tearful. Handley Criteria for the Blues At least four of the following seven symptoms in the first week to 10 days postpartum: 1. Dysphoric mood for at least part of 1 day 2. Mood lability (easily changing mood) that definitely is noticeable to the woman 3. Crying frequently over at least 1 day 4. Anxiety that definitely is noticeable to the woman 5. Insomnia with at least a 1-hour delay over 3 days 6. Appetite decrease that definitely is noticeable to the woman 7. Irritability increase that definitely is noticeable to the woman

Clinical Management Prenatal education about the frequency, normality, and the symptoms of this mild mood disturbance will help new mothers and their families keep the blues in proper perspective (i.e., recognize that the blues is a common phenomenon, that it passes quickly, and that there are no consequences). It is especially important to provide this type of normalizing information to women who experience the blues to relieve any guilt feelings or fears they may have because they are unexpectedly experiencing negative feelings about the new baby. This education can occur in childbirth preparation classes, by nurses or physicians during prenatal visits, and on the maternity ward. Patients should be instructed that if their “blues” continues beyond a week's period and they do not seem to be feeling better by the end of the second week postpartum, they should contact their obstetrician or primary care physician. The patient actually may be in the early stages of a major depression, which requires prompt treatment.

Perinatal Depression Depression may preexist the pregnancy or begin at any time during pregnancy or the postpartum period. It is a devastating disorder that robs women of their joy and energy and creates impairment in self-care and parenting. There often is confusion surrounding this term. Major depression that occurs in the postpartum period usually is referred to as “postpartum depression.” The term postpartum depression does not exist in the diagnostic nomenclature and, in fact, often is erroneously used to refer to cases of the postpartum blues and postpartum psychosis as well as any other mood disturbance (including anxiety) that are prevalent in the postpartum period. The Diagnostic and Statistical Manual of the American Psychiatric Association (DSM-IV-TR) includes “postpartum onset” as a “course specifier” if the episode of major depression begins in the first 4 weeks after delivery. In clinical practice, however, the diagnosis is applied to a major depressive episode within the first year of childbirth. The adjective postpartum before depression also is misleading, implying that there is something about childbirth or the early postpartum period that causes or contributes to the onset of a depressive episode. Although this may be true for postpartum psychosis (see later discussion), the empirical evidence linking childbirth per se to the onset of depression is at best equivocal. Several studies (admittedly with relatively small sample sizes) comparing rates of depression in postpartum and nonpostpartum women have found little evidence of elevated rates of depression associated with childbirth. Nevertheless, depression is common in the postpartum period (and pregnancy) and should be treated. Epidemiologic research confirms that the period of highest risk for depression among women is in the age range of 18 to 45 years, the years during which most women will bear children. These data also suggest that the obstetrician–gynecologist should be alert to depression even in the context of yearly exams.

Description The diagnosis of major depression requires the presence of either sad mood or the loss of interest and pleasure in usual activities along with four additional symptoms (Table 28.2). These symptoms must be present for more days than not over a 2-week period, must represent a change from previous functioning, and must cause significant distress or impairment in social or occupational functioning. Minor depression refers to an episode of at least 2-weeks duration in which there are two or more but less than five symptoms, (including sad mood or loss of interest). Other requirements are the same as for major depression except that the requirement for impairment in functioning is somewhat less than that for major depression.

Prevalence Estimates based on recent meta-analyses suggest that 18.4% of women will experience a major or minor depression at some point during pregnancy, and for major depression it is 12.7%. The period prevalence for major and minor depression during the first 3 months

postpartum is 19.2%, and for major depression it is 7.1%. The rates for incident episodes in pregnancy and the postpartum period are similar, 14.5% and 6.5%, respectively. Rates of depression are higher in populations that have significant risk factors, such as women with history of depression or women living in poverty.

TABLE 28.2 Criteria for Major Depressive Episode 1. A total of five symptoms that includes depressed mood and/or loss of interest or pleasure that have been present every day or nearly every day for at least 2 weeks and represents a change in usual functioning 1. Depressed mood 2. Markedly diminished interest or pleasure in all or nearly all activities 3. Significant weight loss or weight gain or significant decrease or increase in appetite 4. Insomnia or hypersomnia 5. Psychomotor agitation or retardation 6. Fatigue or loss of energy 7. Feelings of worthlessness or inappropriate guilt 8. Diminished ability to think or concentrate 9. Recurrent thoughts of death or suicide 2. Significant distress or impairment in functioning 3. Symptoms not due to direct effects of a substance or a general medical condition 4. Symptoms not due to normal bereavement

Effects Depressed women relative to nondepressed women during pregnancy use more alcohol, tobacco, and drugs of abuse, and they have poorer nutrition. Depressed pregnant women also are more likely to experience nausea and vomiting, prolonged sick leave during pregnancy, and increased visits to the obstetrician. There is evidence that depressed and anxious women have higher rates of operative deliveries and are at increased risk for preterm delivery and low birth weight. Finally, infants of depressed mothers are more likely to be admitted to a neonatal care unit and have lower scores on neurologic development scales. After the infant's birth, depressed mothers are less likely to engage in positive maternal safety practices such as using electrical outlet coverings or placing the child in a car seat. Depressed mothers interact with their infants in ways that are less sensitive, more

negative, and less stimulating than nondepressed mothers. These suboptimal parental practices have a negative effect on child development—toddlers of depressed mothers have poorer social and emotional development as demonstrated by increased likelihood of insecure attachments, unfavorable self-concepts, and delays in intellectual development. Maternal depression also is associated with increased risk of child abuse. Because women may experience depression chronically, these deleterious consequences for children persist over time and include internalizing and externalizing behavior problems as well as depression during adolescence and young adulthood.

Risk Factors Depression and its risk factors can be best understood within a biopsychosocial framework. Some women inherit a susceptibility to depression that is manifest in emotion or affect regulation. Indicators of a basic vulnerability to depression include a personal and family history of depression and related disorders. Other risk factors are more social in nature (Table 28.3). Determination of the presence of these factors early in pregnancy will alert the clinician to the need to develop plans to follow “at-risk” patients more carefully than normally would be the case (i.e., using key interview questions or using simple screening tools). Although there is no simple algorithm linking the number of risk factors to likelihood of depression, it is the case that the greater the number of risk factors (particularly those reflecting biologic vulnerability), the greater the likelihood that an episode of depression will develop.

TABLE 28.3 Risk Factors for Perinatal Depression Risk Factors

Comments

Previous perinatal depression

Critical risk factor

Personal history of depression or anxiety outside of perinatal period

Critical risk factor

Depression during pregnancy

Depression often will continue or reemerge after delivery

Family history of depression

Note serious depression, particularly if there has been treatment

History of premenstrual dysphoric disorder

—

Young maternal age

Adolescents are at high risk

Low income/poverty

—

Poor marital relationship

—

Poor relationship with mother

—

Poor social support, particularly that provided by the partner

May be important for women who live at a great distance from their family

Stressful life events over the past 6 to 12 months

Examples include relocation, loss of income, death of family member

Trauma related to pregnancy or birth

Examples include emergency cesarean section, significant tearing

Severe postpartum fatigue

Sleep deprivation can play a role

Interpersonal violence in past or present

Domestic violence will continue during pregnancy

Special Populations Immigrant women represent an at-risk group. These women face several issues relevant to their risk for depression. In some cases, they are cut off from their normal sources of support, both in terms of cultural supports and family supports. Moreover, these women may experience conflicts between typical American practices and norms reflecting their native culture. Complicating this picture is the fact that Western concepts of psychologic depression do not always map on well to non-Western understandings of depression. For example, in some cultures, only the most seriously mentally ill individuals are identified

and receive care. As a consequence, women may be reluctant to acknowledge that they might be unwell because of the associated stigma. The key for the clinician is to understand as well as possible the patient's expectations about pregnancy, childbirth, and the early postpartum period. Asking questions that illuminate possible gaps between expectations and likely reality will be helpful in preparing patients and identifying those at risk for depression. Also, the clinician should be prepared to provide education about depression and other disorders to increase the likelihood that a patient will accept help if required. Poverty is a marker for both personal and environmental characteristics that put women at risk for depression. Poor women are likely to experience environmental stressors such as substandard housing, unsafe neighborhoods, unreliable transportation, unstable employment or unemployment, and lack of adequate child care. All of these circumstances increase the likelihood that a woman will become depressed during pregnancy or after delivery. These risk factors are exacerbated if the woman does not have a good social support network of family and friends and if she already has young children living at home. There are many other groups that have special circumstances that put them at risk for depression. Women in lesbian relationships who have children may face social disapproval in some communities. Women with disabilities will face special challenges in parenting that if not successfully negotiated will increase their risk for depression. Finally, women who have experienced miscarriages, have lost children at a young age, or who have finally succeeded in conceiving after a long period of infertility may have unrealistic expectations about their life after the birth of the child. The larger the gap between personal expectations and the reality of parenting, the greater the likelihood that a woman will experience depression.

Treatment Antidepressant medication often is used to treat depression during pregnancy and the postpartum period. The most commonly used medicines are selective serotonin reuptake inhibitors (SSRIs) and tricyclic antidepressants (TCAs). Relatively few controlled trials have evaluated antidepressants for use during the postpartum period, and there have been no controlled trials of antidepressants during pregnancy. The little research that has been done suggests that antidepressants are efficacious during pregnancy and the postpartum period—conclusions that also are supported by open trials and case reports. There is considerable controversy regarding the safety of antidepressant medications for use during pregnancy and breast-feeding. Although there is no evidence of significant teratogenic effects of SSRIs and TCAs, there is some evidence of minor anomalies associated with some of the SSRIs as well as some evidence of withdrawal or toxicity symptoms in infants after delivery associated with maternal use of SSRIs. With regard to breast-feeding, there is increasing evidence that SSRIs and TCAs are relatively safe, particularly for older infants. Decisions regarding use of medication during pregnancy and breast-feeding should be made in consultation with the patient, recognizing that untreated depression carries its own risks for the mother

and fetus or infant that may be more significant than risks associated with medication use. Psychologic interventions are effective for depression during pregnancy and the postpartum period. Interpersonal Psychotherapy (IPT), which has been validated for the treatment of major depression in the general population, is efficacious for depression during pregnancy and the postpartum period. Cognitive-behavioral therapy, which has been widely disseminated and is effective for major depression, also is likely to be efficacious for postpartum depression. Brief supportive counseling delivered by nonmental health professionals (usually nurses) has been validated in several European studies. This approach has particular merit because it is much less costly to deliver than conventional psychotherapies, and it is more likely to be acceptable to women who may resist treatment by mental health professionals. Brief supportive counseling and other interventions that are implemented by individuals who are not professional therapists should only be used with women who are suffering from mild to moderate depression. These women should be followed by their obstetrician as well.

Postpartum Psychosis Description Recognized since the time of Hippocrates, psychosis in the early postpartum period is dramatic and unsettling. Postpartum psychosis is believed to be a variant of bipolar disorder. Because postpartum psychosis significantly impairs a woman's ability to function normally, it requires prompt identification and inpatient treatment. Typically, the symptoms of postpartum psychosis emerge rapidly within the first 2 to 4 postpartum weeks and often are evident on the maternity ward. Figure 28.2 displays data regarding hospitalizations for psychosis for a cohort of 54,087 women using a 4-year window (2 years before to 2 years after childbirth). The peaking of admissions in the period immediately following delivery is highly significant and dramatically reflects the fact that the first 90 days after childbirth represents the period of highest risk in a woman's life to have a psychotic episode.

Figure 28.2 Risk for hospitalization for psychosis associated with childbirth. (From Kendell R, Chalmers J, Platz C. Epidemiology of puerperal psychoses. Br J Psychiatry.

1987;150:662–673.)

Clinical presentation of postpartum psychosis includes severely depressed mood; disorganized thinking; psychotic thoughts (e.g., delusions of reference, persecution, jealousy, and grandiosity); and visual, tactile, or olfactory hallucinations. Reflecting hypomania or frank mania that is common in bipolar disorder, many women with postpartum psychosis will show evidence of sleeplessness and high activity levels. The vast majority of these psychoses reflect bipolar disorder or psychotic depression. Postpartum psychosis has a rapid onset and can be associated with tragic outcome. Tragically, suicide is a leading cause of death among women in the postpartum period. A large proportion of these women will have experienced a postpartum psychosis.

Prevalence and Risk Factors Postpartum psychosis is relatively rare, with estimates in the general population ranging between 1 and 4 women in 1,000 births. The major risk factors for postpartum psychosis are past history of postpartum psychosis, bipolar disorder, or schizoaffective disorder, which is associated with an increase in risk from 1 episode of postpartum psychosis in 500 deliveries to approximately 1 episode in 2 to 5 deliveries. Women with a history of bipolar disorder who have a first-degree relative who has had postpartum psychosis have a greater than 50% risk of experiencing a postpartum psychosis.

Treatment Postpartum psychoses typically have a rapid onset, with the afflicted woman often being a danger to herself and her child. As a consequence, immediate inpatient hospitalization usually is indicated. Because postpartum psychoses generally present as bipolar disorder, the most common treatment is a mood stabilizer such as lithium or valproic acid or an atypical antipsychotic agent such as olanzapine or risperidone. Adjunctive psychotherapy may be indicated after the patient has stabilized. Goals for psychotherapy in the context of postpartum psychosis include assisting the patient in regulating her mood and activity; developing or restoring her confidence in parenting; and developing skills to manage life stressors, including problematic relationships (e.g., those with the husband and/or extended family).

Perinatal Anxiety Worry and anxiety are normal during pregnancy and the postpartum period. Women, particularly first-time mothers, face many uncertainties. Common worries of pregnant women include fears of fetal abnormality or death of the infant, being inadequate as a mother, and the physical pain of childbirth. After childbirth, new mothers commonly worry about their infant's health and safety, about being criticized in their new role as a mother, and about not having enough support.

Anxiety disorders represent clear departures from these normal concerns, are highly comorbid with depressive disorders, and are frequent in women of childbearing age. Relative to depression, there has been little research on puerperal anxiety disorders. The prevalence of generalized anxiety disorder (GAD) in the first 2 months of the postpartum period is about 8%. Comparable estimates for obsessive-compulsive disorder (OCD) and panic disorder (PD) are 3% and about 1.5%, respectively. The prevalence rate for GAD is higher than typical rates found in the community. The rates for OCD and PD are comparable to community rates.

Effects Because anxiety and depressive disorders are highly comorbid both at the diagnostic and symptom levels, it has been difficult to tease apart the effects of anxiety and depression. Almost all of the effects on pregnancy outcomes and most of the effects associated with depression in the postpartum period are found with anxiety as well. In addition, there is evidence that independent of depression, children exposed to prenatal maternal stress display significantly more behavioral and emotional problems at 4 years of age, even after statistically controlling for postpartum maternal anxiety; antenatal, obstetric, and socioeconomic risks; and antenatal and postpartum depression. Moreover, these negative effects of exposure to maternal anxiety extend into adolescence and may affect the functioning of the hypothalamic–pituitary–adrenal (HPA) axis long term, resulting in poor affect regulation in these young adults.

Specific Anxiety Disorders GAD is a chronic disorder characterized by uncontrollable excessive worry or anxiety (Table 28.4). It is sometimes difficult to distinguish from normal worries during pregnancy. Three diagnostic features help to make this distinction. First, in GAD, worrying is not limited to a single domain; second, it interferes with daily functioning; and, third, it is not triggered by a specific event.

TABLE 28.4 Generalized Anxiety Disorder 1. Excessive anxiety or worry about a variety of events or activities over at least 6 months occurring on most days. 2. Patient finds it difficult to control worry 3. At least three of the following six symptoms that occur on most days: 1. Restlessness, feeling keyed up 2. Fatigue 3. Difficulty concentrating, mind going blank 4. Irritability

5. Muscle tension 6. Sleep disturbance 4. Anxiety not primarily focused on features of another psychiatric disorder, such as panic attack 5. Significant distress or impairment in functioning 6. Symptoms not due to direct effects of a substance or a general medical condition 7. Does not occur exclusively in context of another disorder such as major depression OCD is characterized by recurrent obsessions or compulsions that are either time consuming or cause marked distress or significant impairment and are recognized by the afflicted as unreasonable. Puerperal OCD is specifically characterized by the preponderance of intrusive aggressive obsessional thoughts (e.g., stabbing the infant, putting the infant in the microwave, throwing the infant down the stairs or out of the window, or sexually abusing the infant). As opposed to women suffering from puerperal psychosis, women with OCD consider these intrusive thoughts to be frightening and unwelcome (ego dystonic). Although obsessive thoughts generally lead to compulsive rituals outside of the postpartum period, this link is weaker in postpartum OCD. New mothers who suffer from OCD tend to simply avoid their infant (e.g., returning prematurely to work, spending large amounts of time out of the home, and avoiding giving the child a bath). One exception, however, is among new mothers who experience worry about their infant's health or safety that goes beyond ordinary worries and concerns. They often report excessive checking of the infant at night and during the day. This obsessionality also can result in the woman frequently contacting the infant's primary care provider with concerns about the baby. OCD is likely to be underreported out of fear that their infant will be removed from the home. However, once identified and treated with psychotropic medication, the symptoms typically diminish or resolve. Cognitive-behavioral therapy also appears to be effective for OCD; however, there are no treatment trials of OCD during the postpartum period. PD is characterized by the experience of at least one unexpected panic attack (a period of intense fear) and somatic symptoms (at least four) such as palpitations, sweating, and trembling or shaking. Because some of the associated somatic symptoms (e.g., feeling of choking or chest pain) are so distressing, women with PD often will harbor fears of having an undetected and life-threatening illness. Patients with PD often overutilize health care services and typically are not reassured by negative clinical results.

Treatment The management of anxiety disorders during pregnancy and the postpartum period is similar to that for depression. Antidepressant medication commonly is used for anxiety disorders It sometimes is supplemented with benzodiazepines in cases of severe anxiety.

Patient Education and Screening The effective management of perinatal emotional health can be feasibly accomplished in an obstetric office setting by introducing four routine procedures. First, women should be provided educational information about their emotional health and the symptoms of perinatal mood disorders during early prenatal visits. There are many educational resources on the Internet in the form of brochures and educational materials for women and their families, including a brochure developed by the American College of Obstetrics and Gynecology (ACOG), which can be used for clinician–patient and family discussion and can be given to patients and family members (refer to the Suggested Readings section). Although the primary goal of education is to inform patients of the common symptoms of these disorders, a secondary purpose is to make the discussion of emotional health a routine and acceptable part of the prenatal visit. Second, routine risk assessment will help to identify patients who will require subsequent monitoring. Most women without a personal or family history of psychologic disorders will successfully navigate pregnancy and the birth of their child, leaving only a few who require special attention. To identify women at risk, it is important to ask questions during early prenatal visits regarding a woman's personal and family psychiatric history and other psychosocial risk factors (Table 28.5). These questions are designed to identify women who may need to be followed more closely than the average patient or women who need to be referred to a psychiatrist for additional support and monitoring during pregnancy and the postpartum period. The major risk factors are previous personal or family history of depression, anxiety, bipolar illness, and any psychotic illness including postpartum psychosis. These women may increase their risk further by discontinuing medication (either unilaterally or in consultation with their physician) because of concern about the effects of medication on the fetus. Routine risk assessment of all women early in the antenatal period and the development of protocols for women at risk can therefore help to detect risk in these unsuspecting cases and avert tragic consequences. Third, all patients should be screened for depression at least once during pregnancy and once in the postpartum period. The postpartum follow-up visit usually is a good time to do a screen for depression. Consistent with this standard, the U.S. Preventive Services Task Force recommends screening adults for depression in clinical practices that have systems in place to assure accurate diagnosis, effective treatment, and follow-up. Further supporting regular screening during pregnancy and the postpartum period is a 2006 New Jersey state law mandating depression screening during pregnancy, on the maternity ward, and at a postpartum visit. Despite these recommendations, many postpartum depressions will be missed because they begin after the woman's last visit to the obstetrician. Women should therefore be encouraged to contact the obstetrician if emotional problems develop later in the postpartum period. Women who have already been educated about perinatal mood disorders in an early prenatal visit usually will be accepting of depression screening later in pregnancy and at the postpartum visit. Depression screening can be feasibly accomplished by utilizing one of the widely used screening tools. The Edinburgh Postnatal Depression Scale (EPDS) and the Postpartum Depression Screening Scale (PDSS) were both developed and validated as

screens for perinatal depression. The Patient Health Questionnaire (PHQ-9) was designed to screen for depression in general primary care settings, but it is also appropriate for depression screening during pregnancy and in the postpartum period. The procedures for routine depression screening utilizing the EPDS are described in Figures 28.3 and 28.4. In addition to the implementation of these simple procedures, routine depression screening also requires the development of a network of mental health professionals (both psychiatrists and psychotherapists such as psychologists and social workers) for referral and follow-up. This referral network is especially important for the obstetrician who prefers not to personally manage the treatment of depression or other mental health problems and for those cases that are more complicated, reflect severe symptoms, or do not respond to first-line treatment with an antidepressant. Finally, along with assessing risk and doing screening, it is important for the physician to evaluate and rule out potential physical causes of depression or anxiety symptoms, notably hypo- or hyperthyroidism or other medical conditions that lead to symptoms that mimic depression or anxiety. Prescribed medications and drugs of abuse also may be responsible for producing depression and anxiety symptoms.

TABLE 28.5 Risk Assessment Interview Target Risk Examples of Questions Factor

History of depression or anxiety

Have you ever been treated (as an outpatient or an inpatient) for depression or anxiety with medication or counseling or psychotherapy? Have you ever had a period lasting 2 weeks or more when you were depressed or sad or during which you lost interest in your usual activities? Did you find it hard to function normally during this period?

Comments

If the episode is ongoing, you will want to inquire about current treatment. A referral to a psychiatrist or counselor may be indicated.

These questions may already have been answered by

History of bipolar disorder or psychosis

Have you ever been treated for bipolar disorder or what is sometimes called manic-depressive disorder? Have you ever had a period during which you were seeing or hearing things that other people could not see or hear? Have you ever believed things that other people found unusual?

Family history of psychiatric illness

Have your parents or siblings: … ever been treated for a psychiatric disorder? … ever been treated for bipolar disorder or what is sometimes called manicdepressive disorder? … ever had a period during which they were seeing or hearing things that other people could not see or hear? … or ever believed things that other people found unusual?

Here you are interested in serious psychiatric illness in family members. Be sure to inquire about postpartum episodes in mothers or sisters.

Do you have concerns about the support that you will receive after the baby comes from your husband (partner) or from your other family members or your friends?

Be alert to significant marital conflict or domestic abuse. Be alert to circumstances in which a woman has very little local support from family and friends.

Social support

asking about depression and anxiety. Here you are asking about indications of hallucinations or delusions in the past. Be sure to inquire if these disorders occurred during pregnancy or the postpartum period.

Stressful life events

Other risk factors

Are you anticipating or have you experienced any significant events such as death or serious illness of a family member, loss of income, or the need to move your household?

Negative life events can overwhelm the coping abilities of women who are already struggling to manage their current life responsibilities.

You might ask about any of the factors described in Table 28.3 if you believe that they might be relevant for your patient.

Figure 28.3 Routine depression screening procedures for the Edinburgh Postnatal Depression Scale.

Figure 28.4 Edinburgh Postnatal Depression Scale. © 1987 The Royal College of Psychiatrists. The Edinburgh Postnatal Depression Scale may be photocopied by individual researchers or clinicians for their own use without seeking permission from the publishers. The scale must be copied in full and all copies must acknowledge the following source: Cox JL, Holden JM, and Sagovsky R. (1987). Detection of postnatal depression. Development of the 10-item Edinburgh Postnatal Depression Scale. British Journal of Psychiatry, 150, 782–786. Written permission must be obtained from the Royal College of Psychiatrists for copying and distribution to others or for republication (in print, online or by any other medium.) Note: Questions 1, 2, and 4 are scored 0–3, remaining questions are scored 3–0.

Women often develop a significant trust in their obstetrician during this rather vulnerable

and important time in their lives. Because of this trust, obstetricians are well situated to implement these practices of risk assessment, formal screening, clinical management, and clinical referral to ensure the emotional health of their patients.

Summary Points Depressive and anxiety disorders are common during pregnancy and the postpartum period. The obstetrician has a significant role in the detection and treatment of these disorders. Postpartum blues, common in the first week after delivery, often is experienced as a dysregulation of mood that usually diminishes within a few days. There are no significant sequelae, and it does not require treatment. Depressions during pregnancy and the postpartum period range from mild to severe and are diagnosed based on DSM-IV criteria for major and minor depression. The period prevalence for minor and major depression during pregnancy is 18.4%, and for the first 3 months postpartum it is 19.2%. Personal history of depression or anxiety, significant social stress, and poorly functioning social networks are major risk factors for depression during pregnancy and the postpartum period. Medical and psychologic interventions are effective for postpartum depression. Postpartum psychosis is a rare and extremely serious disorder characterized by psychotic symptoms such as hallucinations and delusions. It usually presents as bipolar disorder and typically requires inpatient treatment. Past history of psychosis or bipolar disorder increases the risk. Anxiety disorders often occur with depression in pregnant and postpartum women. Significant anxiety during pregnancy can have deleterious long-term consequences for the infant. Obstetrical providers should educate patients about emotional health during pregnancy and the postpartum period. All patients should be screened for depression at least once during pregnancy and once during the postpartum period.

Suggested Readings Patient Education American College of Obstetrics and Gynecology. Postpartum depression. Available at: http://www.acog.org/publications/patient_education/bp091.cfm.

American Psychiatric Association. Let's talk facts about depression. Available at: http://www.healthyminds.org/multimedia/depression.pdf. Health Resources and Services Administration. Depression during and after pregnancy. Available at: http://www.mchb.hrsa.gov/pregnancyandbeyond/depression/. This booklet is an excellent resource for women and their families, and print copies can be ordered from the HRSA Information Center 1-888-275-4772. Minnesota Department of Health. Postpartum depression educational materials. Available at: http://156.98.150.11/divs/fh/mch/fhv/strategies/ppd/index.html. New Jersey Department of Health and Senior Services. Brochures. Available at: http://www.state.nj.us/health/fhs/ppd/brochure.shtml. Postpartum Support International. Available at: http://www.postpartum.net/.

Perinatal Mood Disorders Gavin NI, Gaynes BN, Lohr KN, et al. Perinatal depression: a systematic review of prevalence and incidence. Obstet Gynecol 2005;106:1071–1083. Henshaw C. Mood disturbance in the early puerperium: a review. Arch Wom Men Health 2003;6(Suppl 2):s33–s42. Levey L, Ragan K, Hower-Hartley A, et al. Psychiatric disorders in pregnancy. Neurol Clin 2004;22:863–893. Munk-Olsen T, Laursen TM, Pedersen CB, et al. New parents and mental disorders: a population-based register study. JAMA 2006;296:2582–2589. Ross LE, McLean LM. Anxiety disorders during pregnancy and the postpartum period: a systematic review. J Clin Psychiatry 2006;67:1285–1298. Wisner KL, Parry BL, Piontek CM. Postpartum depression. N Engl J Med 2002;347:194–199.

Postpartum Psychosis/Bipolar Disorder Cohen LS, Altshuler LL, Harlow BL, et al. Relapse of major depression during pregnancy in women who maintain or discontinue antidepressant treatment. JAMA 2006;295:499– 507.

Lewis G. (ed.) Why Mothers Die. 2000–2002: The Sixth Report of Confidential Enquiries into Maternal Deaths in the United Kingdom, London: RCOG Press (2004) (http://www.cemach.org.uk/publications/saving_mothers_Lives_Report_2000– 2002.aspx). Sit D, Rothschild AJ, Wisner KL. A review of postpartum psychosis. J Womens Health 2006;15:352–368.

Screening American College of Obstetrics and Gynecology. Psychosocial risk factors: perinatal screening and intervention. ACOG Committee Opinion No. 343. Obstet Gynecol YEAR;108:469–477. Cox J, Holden J. Perinatal mental health: a guide to the Edinburgh Postnatal Depression Scale. London: Gaskell, 2003. Gordon TEJ, Cardone IA, Kim JJ, et al. Universal screening in an academic medical center. Obstet Gynecol 2006;107:342–347. Jones I, Craddock N. Bipolar disorder and childbirth: the importance of recognising risk. Br J Psychiatry 2005;186:453–454. Lang AJ, Stein MB. Screening for anxiety in primary care: why bother? Gen Hosp Psychiatry 2002;24:365–366. U.S. Preventive Services Task Force. Screening for depression, 2002. Available at: http://www.ahrq.gov/clinic/uspstf/uspsdepr.htm#related.

Treatment of Perinatal Mood Disorders: Medication American College of Obstetrics and Gynecology. Treatment with selective serotonin reuptake inhibitors during pregnancy. ACOG Committee Opinion No. 354. Obstet Gynecol 2006;108:1601–1603. Gentile S. The safety of newer antidepressants in pregnancy and breastfeeding. Drug Saf 2005;28:137–152. Henry AL, Beach AJ, Stowe ZN, et al. The fetus and maternal depression: implications for antenatal treatment guidelines. Clin Obstet Gynecol 2004;47:535–546.

Rubinow DR. Antidepressant treatment during pregnancy: between Scylla and Charybdis. Am J Psychiatry 2006;163:954–956.

Yonkers KA, Wisner KL, Stowe Z, et al. Management of bipolar disorder during pregnancy and the postpartum period. Am J Psychiatry 2004;161:608–620.

Treatment of Perinatal Mood Disorders: Psychotherapy Cooper PJ, Murray L, Wilson A, et al. Controlled trial of the short- and long-term effect of psychological treatment of post-partum depression I. Impact on maternal mood. Br J Psychiatry 2003;182:412–419. O'Hara MW, Stuart S, Gorman L, et al. Efficacy of Interpersonal Psychotherapy for postpartum depression. Arch Gen Psychiatry 2000;57:1039–1045. Segre LS, Stuart S, O'Hara MW Interpersonal Psychotherapy for antenatal and postpartum depression. Prim Psychiatry 2004;11:52–56. Stuart S, O'Hara MW, Gorman LL. The prevention and psychotherapeutic treatment of postpartum depression. Arch Wom Men Health 2003;6(Suppl 2):S57–S69. Zlotnick C, Miller IW, Pearlstein T, et al. A preventive intervention for pregnant women on public assistance at risk for postpartum depression. Am J Psychiatry 2006;163:1443– 1445.

Reference Books Nonacs R. A deeper shade of blue: a woman's guide to recognizing and treating depression in her childbearing years. New York: Simon & Schuster, 2006. A self-help book for women explaining the issues associated with perinatal depression and providing practical techniques of managing stress as well as describing treatment options. Steiner M, Yonkers KA, Eriksson E, eds. Mood disorders in women. London: Martin Dunitz, 2000. This book provides a description of the broad range of perinatal mood disorders and includes chapters on neurochemistry, epidemiology, and treatment.

29 Office Gynecology and Surgical Procedures Marian D. Damewood William R. Keye Jr. Charles C. Coddington III The number of women in the United States is approximately 153 million and increasing. Women in their reproductive years represent 49% of the total, with those under age 15 at 20% and those over 50 at 31%. The number of postmenopausal women is projected to increase to 52 million in 2010 and 62 million in 2020. The entire female population is estimated to grow over 17% in the next 20 years. Gynecologists have a major role in the provision of health care for women, with changes in technology, patient expectations, office procedures, and health care delivery formats providing new challenges. The number, percentage, and characteristics of patients who receive care exclusively from gynecologists are increasing. Thus, the complexity and details of the gynecologic history and examination are of great importance in women's health care. Gynecologic procedures that primarily were performed in the hospital setting can now be performed in the office, such as transvaginal ultrasound with saline infusion sonography (SIS), decreasing the number of hospital-based diagnostic procedures. These changes in the specialty of gynecology coupled with recent demands on the medical community for cost control has stimulated the trend for more outpatient care and officebased surgery. The technology to perform minor gynecologic surgical procedures in an office setting or procedure room is readily available. This chapter will discuss the gynecologic history and examination and review a number of procedures that may, with the appropriate facilities and patient selection, be performed in an office surgical setting.

Preventive Care A great deal of gynecologic care is preventative and depends on population characteristics, risk profiles, epidemiology, and statistics for screening programs. Annual examinations may be recorded on data sheets containing “check-off” lists for preventive services. An example of this type of form is available at the American College of Obstetricians and Gynecologists (ACOG) website (http:// www.acog.com). Reminder systems for follow-up visits for Papanicolaou (Pap) smears and mammograms can help to integrate disease prevention and health maintenance into gynecologic practice. In addition, gynecologists play a major role

in screening for domestic violence, depression, injury, and other psychosocial concerns as well as sexual dysfunction. Counseling practices for sexually transmitted diseases (STDs) human immunodeficiency virus (HIV), and human papillomavirus (HPV) infection has changed markedly over the past 2 decades. In June 2006, the Food and Drug Administration (FDA) licensed the first HPV vaccine developed to prevent cervical cancer and other diseases in females caused by HPV infection. The quadrivalent vaccine labeled as Gardasil® protects against four HPV subtypes (6, 11, 16, 18). These types are responsible for approximately 70% of cervical cancers and 90% of genital warts. Indications at this time include the use of this vaccine in females ages 9 to 26 years. Ideally, it should be administered before the onset of sexual activity but may be useful afterward as well. The vaccine has been tested in over 11,000 women worldwide, with studies noting that there are no serious side effects. Clinical trials have demonstrated close to 100% efficacy in preventing cervical, vulvar, and vaginal precancers as well as genital warts caused by the four HPV types. If the patient is already infected by one of the HPV types, the vaccine will not prevent disease from that type but will prevent against the remainder. Current studies suggest that the vaccine is effective for at least 5 years. Additional preventative measures include genetic screening for some forms of breast and ovarian cancer, which could result in the assimilation of routine genetics into gynecologic office practice. In addition, postmenopausal women have a variety of preventive health needs including breast and cervical cancer screening and primary care such as cholesterol screening and smoking cessation. This health care interaction begins with the gynecologic history and follows up with physical examination, along with office diagnostic procedures.

Medical History Women who want to be actively involved in decisions regarding their gynecologic care usually expect physicians to use the history to obtain information concerning not only medical issues but also concerns regarding family history, cancer risk, sexual partners, or significant personal and social issues. The quality of the medical care provided by a physician, as well as the type of the relationship between the physician and patient, may be determined largely by the depth of the gynecologic history. A comprehensive history and physical examination should be performed on each new patient. It is important to establish a database on each patient, along with a physician– patient relationship based on good communication. Scheduling should permit dedicated time for new patient bookings to allow sufficient time to obtain the information, perform an examination, provide the management plan, and allow for health education. Many preprinted history and physical examination forms exist, some of which may be obtained at the ACOG website, including the Women's Health Record for initial and long-term follow up office care. Some physicians prefer to use patient-directed history forms, others use an assistant or nurse, and still others prefer to take the history personally. Multiple studies have documented that personally directed questioning is more productive than the use of

patient questionnaires. Understanding the preventive medicine needs based on family history, patient history and lifestyle, and integrated functional medical investigations is important. The development of personal preventive programs impacts the ongoing health and wellness relationship. Once a good database has been established, updates should include any changes in gynecologic or pregnancy history. Additional surgery, accidents, hospitalizations, new medications, or allergies should be added. Any changes in family history should be noted. This type of history taking, both for new and established patients, results in a wellorganized, problem-oriented medical record. Besides obtaining the historical details, it is important to understand why the patient is seeking care in the gynecologist's office. In addition to understanding and meeting patients' needs, physicians must be prepared to do a medical evaluation in a physically and emotionally comfortable setting, making the visit as comfortable and informative as possible so that women leave the office calm and with their questions answered. This is achieved by an understanding attitude and an ability to listen. Several things can be done when obtaining a history to reduce patients' anxiety. The history should be obtained in as comfortable and private a setting as possible. Many patients prefer to be clothed and seated at the same level as the physician, especially if they are meeting for the first time. Other patients may choose to change into an examination robe before seeing the physician if the visit is for a follow-up examination. Under most circumstances, patients should be interviewed alone. Exceptions may be made for children, adolescents, and mentally impaired women or at the specific request to have an attendant or a family member present. Even in these situations, it usually is a good idea to give patients the opportunity of speaking privately. The initial portion of the interview should be designed to put patients at ease. This often can be accomplished by discussing neutral and nonmedical subjects, such as recent recreational activities, employment, and family. The discussion should be viewed not merely as a means of relaxing patients but also as an opportunity for gathering information about their psychologic and social backgrounds. Physicians should not make assumptions about patients' backgrounds. For example, a clinician usually assumes that all adult female patients are sexually active and heterosexual. Either assumption or both may be incorrect. By asking neutral, open-ended questions (e.g., “Are you sexually active?” and “Are you having sex with men?”), physicians let patients know that these assumptions have not been made. An appropriate length of time should be scheduled to allow a patient to tell her story without being hurried or interrupted. Interruptions from phone calls or office staff should be avoided, if at all possible, so that the patient has the physician's undivided attention. Patients should be made to feel that they have the respect of the physician. This means that they will have the opportunity of sharing in the decision-making process, will not be forced to endure unwanted pain, will have what they tell the physician held in strict confidence, and are free to ask questions. Patient satisfaction is related to the

time required to get an appointment, the patient mix in the reception area, the length of waiting time in the reception or examination room, the attitude of the office staff, and the billing procedures. In this age of rapidly expanding medical knowledge and an emphasis on preventive health care, it is ironic that there is widespread dissatisfaction in physician–patient relationships. There is increasing evidence that a physician's attitude influences not only patient compliance but also the ultimate effect of therapy. The first step in effective communication is establishing a good physician–patient relationship. Research in human relations has demonstrated that a rapport is most readily established if physicians possess and display certain qualities including empathy, respect, non-possessive warmth, genuineness, non-judgmental acceptance, kindness, and interest. These qualities are common to all effective counselors and can be learned by most clinicians. They reinforce these qualities by summarizing their understanding of patients' problems in terms that patients can understand. The communication of warmth, kindness, and interest is, for the most part, non-verbal. Examples of nonverbal communication that convey these qualities include maintaining eye contact, having a relaxed open posture, facing the patient, leaning toward the patient, showing a facial expression consistent with the patient's predominant emotion, and having a modulated, nonmechanical tone of voice. The history provides information about the total patient and is perhaps the most important part of the gynecologic evaluation. In most cases, it provides the data to establish a tentative diagnosis before the physical examination. If the gynecologic history is sufficiently comprehensive, it should in many cases permit a physician to narrow the likely diagnoses. Like a hospital chart, the office chart is a legal and medical record. As such, it is subject to subpoena, and whatever is recorded in it may someday need to be defended in court. It should not contain extraneous or casually entered material, and the notes should be sufficiently complete that the case can be reconstructed readily. The gynecologic history should include the following information: I. Chief complaint A. Primary problem B. Duration C. Severity D. Precipitating and ameliorating factors E. Occurrence in relation to other events (e.g., menstrual cycle, coital activity, gastrointestinal activity, voiding, other pertinent functions) F. History of similar symptom G. Outcome of previous therapies H. Impact on the patient's quality of life, self-image, relationship with family, and daily activities I. Role of other stresses in the chief complaint

II. Menstrual history A. Age at menarche B. Date of onset of last normal menstrual period C. Timing of menstrual periods D. Duration and quantity (i.e., number of pads used per day) of flow E. Degree of discomfort F. Premenstrual symptoms G. Contraception (i.e., current and past methods)

II. Obstetric history A. Number of pregnancies B. Number of living children C. Number of abortions, spontaneous or induced D. History of previous pregnancies (i.e., duration of pregnancy, antepartum complications, duration of labor, type of delivery, anesthesia used, intrapartum complications, postpartum complications, hospital, physician) E. Perinatal status of fetuses (i.e., birth weights, early growth and development of children, including feeding habits, growth, overall well-being, current status) F. History of infertility (evaluation, diagnosis, treatment, outcome)

V. Medical historys A. Allergies B. Medications currently used C. Past and current medical problems D. Hospitalizations (reason, date, outcome) E. Vaccinations (type, date), including HPV vaccine

V. Surgical history A. Operative procedures (i.e., outcome, complications)

VI. Review of systems A. Pulmonary B. Cardiovascular C. Gastrointestinal D. Urinary E. Vascular

F. Neurologic G. Endocrinologic H. Immunologic

II. Breast symptoms A. Masses B. Galactorrhea C. Pain D. Family history

II. Social history A. Exercise B. Dietary habits (including calcium or folic acid supplementation) C. Drug use D. Alcohol use E. Smoking habits F. Marital status G. Number of years married H. Sexual history (partners, contraception, protection from STDs) I. Occupational history (i.e., exposure to environmental toxins, ionizing radiation, infectious agents) J. Emotional, physical, or sexual abuse

X. Family history A. Significant medical and surgical disorders in family members

Chief Complaint It often is effective to begin the history with an open-ended question concerning the symptoms that patients may have. This gives them the opportunity to describe their symptoms and concerns in their own words. Less information will be obtained if the interviewer asks only focused, closed-ended questions to which patients can answer only yes or no. Some clinicians find it helpful to have an outline of questions about the gynecologic history to obtain all the necessary information. The following questions are typical of a gynecologic history: What were the circumstances at the time the problem began (i.e., time, place, activity, cycles)?

What has been the sequence of events? (Having a calendar to refer to is often helpful.) Have you had this problem before? Can you describe the previous occurrence and what led to its disappearance? To what extent is the problem interfering with your daily life and the life of your family? Have you had previous evaluations or treatments? (Records from previous physicians may be helpful.) Why did you seek evaluation for the problem now? What questions do you want answered today? What do you expect and want from today's visit?

Menstrual History The cycle interval is counted from the first day of menstrual flow of one cycle to the first day of next menstrual flow. There is a wide range of normal, and a recent change in the usual pattern may be a more reliable sign of a problem than the absolute interval. Although 28-day cycles are the median, only a small percentage of women have cycles of that length. The normal range for ovulatory cycles is between 24 and 35 days. Duration of flow is usually 4 to 6 days. Estimating the amount of menstrual flow by history is difficult. The average blood loss is 30 mL (range 10 to 80 mL). The need to frequently change saturated tampons or pads (i.e., more often than one per hour for 6 or more hours) and the passage of many or large blood clots usually are signs of excessive blood flow. Some degree of dysmenorrhea is common. It usually begins just before or soon after the onset of bleeding and subsides by day 2 or 3 of flow. The discomfort is characteristically lower midline and often is associated with backache and, in primary dysmenorrhea, with systemic symptoms such as lightheadedness, diarrhea, nausea, and headache. Mittelschmerz, or midcycle unilateral pelvic pain at the time of ovulation, usually is mild and seldom lasts for more than 1 or 2 days. It is important to ask whether or not there is bleeding between menstrual periods and whether this occurs after coitus. Intermenstrual bleeding is a characteristic sign of cervical cancer, although it also is present with benign lesions such as cervical polyps and fibroids or infection. Finally, physicians should inquire about the presence of premenstrual syndrome (PMS). The symptoms experienced by women with PMS may be physical, emotional, and behavioral. The most common of the physical symptoms are fatigue, headache, abdominal bloating, breast tenderness and swelling, acne, joint pain, constipation, and recurring herpetic or yeast infections. Although these physical symptoms often are uncomfortable, most women with moderate to severe PMS complain most about their premenstrual emotional symptoms, especially depression, anxiety, hostility, irritability, rapid mood changes, altered libido, and sensitivity to rejection. Women with PMS also may experience changes in behavior, including physical or verbal abuse of others, suicide attempts, withdrawal, craving for or intolerance of alcohol, craving for sugar or chocolate, and binge eating. Many women report that long-standing or severe PMS causes psychologic or social problems

that may be as disruptive as the premenstrual symptoms themselves.

Sexual History The screening for sexual history is designed to determine whether major sexual problems exist that need in-depth evaluation and therapy and whether the patient should be referred elsewhere for more intensive evaluation. In an attempt to put patients at ease, physicians can begin the sexual history by prefacing questions with statements such as “Most people experience….” or “Because sexual problems can develop as part of other gynecologic problems….” If physicians can convey a willingness to help, patients are more likely to discuss problems. In addition, the screening history should begin with a discussion of topics that are unlikely to provoke anxiety. For example, questions about the occurrence of pain during intercourse are less likely to cause anxiety than questions about orgasmic function or noncoital sexual practices. With these principles in mind, physicians can begin with a general question, such as “Are you having any sexual problems?” If the response is non-committal, a more specific question, for example, “Are you satisfied with the frequency of sexual relations?” can be posed. If a problem is identified, physicians can proceed to the problem-oriented sexual history and ask about the date of onset, severity, previous evaluation and treatment, the results of such treatment, conditions that diminish or exacerbate the problem, the patient's response to the problem, and the effect of the problem on the patient's relationship with her partner. To conclude the screening history, physicians should invite patients to discuss concerns that have not been covered by the screening history. Even if a patient denies having any problems, the screening history is of value because it demonstrates the physician's willingness to discuss sexual problems. The problem-oriented history is designed to differentiate organic from psychogenic sexual problems, determine the complexity of the problem, determine the need for referral of the patient to a more sophisticated sexual counselor, and provide information for the formulation of a treatment program if the physician elects to treat the patient. The problem-oriented sexual history should include onset, severity, course, conditions increasing the severity of the problem, prior evaluation and treatment if any, and the impact on the patient and her sexual or marital relationship. A treatment or referral can be formulated on the basis of discussion of these and related questions. It is important to obtain a history of STDs. Physicians should tactfully question patients about past episodes of STDs, sexual practices, number of sexual partners, background of sexual partners, use of barrier forms of contraception, intravenous drug use, previous blood transfusions, genital lesions, persistent vaginal discharge, and pelvic pain. The discussion of STDs provides an opportunity to discuss modes of prevention, including the safe sex practice and the use of barrier methods of contraception when the sexual history of a partner is unknown.

Psychosocial History

Health care providers can play a vital role in identifying women who are victims of psychologic, physical, or sexual abuse. Unfortunately, women who are abused are often hesitant to acknowledge it. Questions should include the following: Are you or have ever been in a relationship in which you have been physically hurt or threatened by a partner? Have you ever been forced to have sex against your will? Has your partner ever destroyed things that you care about? Are you or have you ever been in a relationship in which you were treated badly? If the answer to any of these questions is yes, the physical examination may reveal signs of physical abuse. In addition, many abused women may report chronic pain, sleep or appetite disorders, and frequent vaginal and urinary infections. One may suspect an abusive relationship if the patient's partner is present at every office visit, insists on staying close to the patient, and answers questions directed to her. Once abuse is recognized, the physician must acknowledge the problem and direct the woman to an appropriate community resource. Inquiry about the woman's safety should be made before she leaves the office. Some physicians obtain wallet-sized cards or brochures from local agencies that provide support and protection for battered women and place them in the restrooms. This provides an option for those women who would not acknowledge abuse when asked by their health care providers. Depression is another very common condition that may be detected during an annual gynecologic examination. The potential life-threatening nature of depression and the availability of effective antidepressant medications with few side effects make it even more important to diagnose depression. To aid in diagnosing depression, physicians can ask the following questions: Have you lost interest in the things you used to enjoy? Do you feel sad, “blue,” or “down in the dumps”? Do you have feelings of guilt or worthlessness? Do you have thoughts of death or suicide? Are you sleeping too much, or do you have difficulty falling or staying asleep? Do you have a loss of energy and feel tired all the time? An affirmative answer to one or more of these questions may indicate the patient is depressed and a candidate for psychotherapy or drug therapy. More than 50% of depressed individuals will respond to antidepressant therapy.

Adolescent History As the percentage of adolescents increases, gynecologists find themselves dealing with problems unique to the 13- to 19-year-old age group. These include menstrual and breast disorders, pubertal development problems, and the challenges presented by sexually active

adolescents. Over 50% of high school students, male and female, have had sexual intercourse, and less than half have reported that they used contraception the last time they had intercourse. The frequency of adolescent sexual activity and its consequences mean that gynecologists caring for adolescents certainly will encounter gynecologic problems such as STDs and pregnancy among their young patients. Gynecologists who provide such care to adolescents, particularly with respect to history taking, need to know their specific needs, with particular importance placed on confidentiality. The gynecologist must be prepared to handle multiple issues related to pubertal development, sexuality, self-esteem, and body image and approach the adolescent patient in a somewhat different manner than that used for adults. This includes having the parent present with young women, 14 years of age or less, during history taking and speaking to the adolescent first when she is fully clothed. If the adolescent refuses to have the parent or mother present, the physician may ask the young woman's permission to speak to her mother or guardian with respect to important issues, especially those requiring treatment. A detailed educational pamphlet on the first gynecologic visit is available at the ACOG website.

Gynecologic Examination The pelvic examination is one of the most commonly performed medical procedures and is considered a highly unpleasant experience by most women. Aspects of the pelvic examination, such as genital exposure, make it likely that women will have feelings of anxiety, vulnerability, apprehension, or fear. It is important that the gynecologist observes a woman's behavior, which will communicate her feelings and possibly anxieties. A complete physical examination most commonly is performed at the first visit. In order to reduce anxiety, patients should be encouraged to give feedback to the physician during the examination, especially when the examination causes pain. Description of the examination, including which portions may include mild to moderate discomfort (such as the rectal examination), should be given to the patient beforehand. When the physician enters the room, the patient should be sitting up on the examination table with the examination gown completely covering her. During the physical examination, a female chaperone, either a nurse or medical assistant, must be present. This woman can assist the physician and also lend psychologic support to the patient. The patient should be asked to lie down and place her feet in the stirrups, and the physician should be at the level of the patient's head, speaking to her when her position is changed. This dialog may include the physician asking the patient about her symptoms, location of any pain, or other pertinent questions. Studies evaluating anxiety in women with respect to pelvic examinations have found those who have had a less positive first experience have higher anxiety levels with their gynecologists. A general impression should be recorded of patient's nutritional state, distribution and proportion of body fat, texture and condition of skin and hair, presence of facial or excessive body hair, acne, abnormal nevi (>5 mm, asymmetric outline, variable pigmentation, and indistinct borders), and any specific physical features. The patient's hair is examined for cleanliness, texture, and scalp health. The eye examination may include

ophthalmoscopy to detect retinal aberrations. The patient's nose, throat, and teeth also can be checked. Finally, the anterior cervical, posterior cervical, and supraclavicular nodes, as well as the thyroid gland, should be palpated. Hypertension is the most common chronic disease in women over 50 years of age. Therefore, every woman, especially one over 50, should have her blood pressure measured with her annual gynecologic examination. Careful cardiac auscultation may be performed as part of the gynecologic examination. Mitral valve prolapse (MVP), the most common cardiac condition diagnosed by auscultation in asymptomatic women, can be problematic during surgery or pregnancy. From the back, a curvature of the vertebral column can be assessed by observation and palpation.

Examination of the Breasts The breast examination begins with a breast-oriented history. Patients are asked whether they have noted any lumps, pain, discharge, or other changes in their breasts. They also should be asked about breast surgery, date and results of the last mammogram, current and past hormone use, and family history of breast cancer. The axillary and supraclavicular nodes are then palpated. The breasts should be examined with patients both sitting or standing and lying supine. In the vertical position, the nipples and inframammary folds are evaluated for asymmetry. The examiner looks for elevation of one nipple, flattening of one breast, dimpling of the skin, or asymmetry by having patients raise both arms above the head and lean forward and then contract the pectoral muscles with hands on hips. Then, with patients in the supine position with one arm above the head, all quadrants of each breast are felt with the flat part of the distal phalanges of the fingers. The subareolar area also should be palpated, because up to 15% of carcinomas occur under the areola. The axillary and supraclavicular areas should be palpated for enlarged or tender lymph nodes. The nipples and adjacent areolar tissue are then compressed in an effort to express fluid from the nipple. The examination of the breasts should conclude with a description of the examination results and a recommendation for follow-up physical or imaging examinations. Gynecologists as primary care physicians have the responsibility for screening mammography. A diagnostic approach to the breast, including clinical breast examination, possible fine-needle aspiration, and mammography, may be implemented by the gynecologist and performed with findings of a breast mass or suspicious area. Ongoing discussion has addressed the value of screening mammography with respect to breast cancer mortality. Studies have noted that mammograms can be lifesaving and that recommendations for gynecologists based on all available information are to urge all women to follow the advice of their physicians and obtain mammograms per current clinical guidelines.

Examination of the Abdomen Patients should be positioned supine, with arms against the body to relax the abdominal musculature. If necessary to obtain adequate relaxation, the knees can be elevated and flexed. In a methodical and consistent manner, all quadrants of the abdomen should be palpated. Relaxation of the abdomen to evaluate a suspected mass can be assisted by

having patients breathe deeply and then exhale. After all quadrants have been examined, the inguinal nodes should be palpated. Asking about the origin of abdominal scars may provide information that was not elicited during the history. Bulging of the flanks suggests free abdominal fluid, but thin-walled ovarian cysts and irregularly shaped uterine leiomyomata may have a similar clinical picture. Although large ovarian cysts and leiomyomata most commonly cause protrusion of the anterior abdominal wall, there are many confusing exceptions. Percussion for areas of flatness or tympany and for shifting dullness may aid in determining whether the distension is caused by intraperitoneal fluid or by intestinal gas. Auscultation is useful in differentiating among a large tumor and distended bowel.

Examination of the Extremities Examination of the lower extremities supplies important information regarding the cardiovascular system. Any edema or varicosities should be noted. In a patient with congenital absence of the vagina, evidence of muscle atrophy in the extremities should be sought because such patients may have nerve root compression secondary to congenital vertebral anomalies. The peripheral pulses and reflexes also may be evaluated at this time. Examination of the calves and ankles for melanomas or dysplastic nevi is advisable.

Pelvic Examination The first examination of the female genitourinary system often takes place in the neonatal period. An examination is indicated at any age when abnormal bleeding or pelvic symptoms are present, there are questions about primary or secondary sexual development, or sexual activity is being initiated. For teenagers, the first pelvic examination should probably occur at 18 years of age or at the initiation of sexual activity, whichever comes first. Examinations usually are repeated at yearly intervals, at which time a Pap smear should be performed in addition to a pelvic examination and a screening for breast cancer and hypertension in the later reproductive years. The pelvic examination provides physicians with an opportunity to answer questions and to educate with respect to pelvic anatomy, physical development, and sexual function. Patients often are reassured if the physician carries on a running dialogue, describing the findings, asking and answering questions, and demonstrating on occasion the physical findings with the aid of a handheld mirror. To maximize the educational aspects of an examination, clinicians can (a) describe all procedures in advance; (b) maintain eye contact with patients during the examination, whenever possible; and (c) explain all findings clearly. The pelvic examination is performed with the patient lying on her back with both knees flexed. The buttocks are positioned at the edge of the examining table, and the feet are supported by stirrups. This position allows the necessary exposure of the pelvic organs. Traditionally, patients have been placed with the head and body in a horizontal position. This position does not allow maintaining eye contact and increases a patient's sense of

vulnerability. The alternative, assuming the availability of an adjustable examination table, is to elevate the head of the table at an angle between 30 and 90 degrees. There are no apparent technical disadvantages to this alternative position, and many patients find it easier to relax, actually making the bimanual part of the examination more accurate. The patient should empty her bladder just before the examination. The minimal equipment needed to perform a pelvic examination includes a good light source, a speculum of the correct size, a nonsterile glove, and a water-soluble lubricant. Additional supplies that should be available in the examination room include a variety of speculum sizes, materials to obtain cytologic samples including fixatives, various culture media, large cotton-tipped swabs, pH indicator paper, and screening tests for fecal occult blood. Specialized examinations require other specific equipment. The pelvic examination begins with inspection of the vulva. Physicians should note and record evidence of developmental abnormalities as well as the general state of cleanliness, discharge, hair growth and distribution, and abnormalities of the skin, including tumors, ulcerations, scratch marks, rashes, and minor lacerations or bruises. Vulvar varicosities or hemorrhoids also should be noted. A careful inspection of the skin folds, vulva, and pubic hair may reveal occult lesions or infection. The vulva should be palpated for subcutaneous lesions. The labia are then spread, and the condition of the hymen and vulvovaginal skin and the size of the clitoris are noted. The examination should be performed in a systematic manner and include the labia majora, labia minora, vestibule, urethral opening, periurethral glands, Bartholin glands, perineum, anus, and perianal areas. With an index finger in the outer vagina and the thumb on the perineum, the labia and urethra are palpated for masses or tenderness. Patients are asked to contract the muscles of the vaginal opening to assess the tone of the levator muscles and the degree of perineal support and then to strain to reveal the presence of a urethrocele, cystocele, rectocele, enterocele, or vaginal or cervical prolapse. The vagina should first be inspected with the aid of a speculum. Specula come in various sizes, and an appropriate size should be selected, using the largest size that is comfortable and provides the best visualization. Painless insertion of the speculum may be aided by several techniques. First, the muscles at the opening of the vagina may be relaxed by gentle downward pressure with one or two fingers. The speculum may be moistened with warm water before insertion, but other types of lubricants should be avoided if cultures or cytologic samples are to be collected. The speculum blades should be inserted obliquely, not vertically, through the introitus; immediately rotated to the horizontal plane; and then slowly opened after the vaginal apex is reached. The vaginal walls and cervix should be inspected for lesions. Any vaginal discharge should be assessed for volume, color, consistency, and odor. The endocervical mucus also should be examined. Samples for cervical or vaginal cytologic examination and cultures and direct microscopic examination of the vaginal or cervical discharge should be obtained as indicated. Before the speculum is removed, the cervix should be evaluated for ectropion, erosion, infection, discharge, lacerations, polyps, ulcerations, and tumors. As the speculum is removed, with the patient bearing down, the degree of vaginal wall relaxation and uterine prolapse can be assessed. With the speculum removed and the patient still bearing down, they physician can screen

for stress incontinence. The technique for the bimanual examination is shown in Figures 29.1,29.2,29.3,29.4,29.5. After the speculum has been withdrawn, the physician should gently insert the index and middle fingers along the posterior wall of the vagina. At the same time, the other hand is placed on the patient's abdomen in the midline. The first palpable structure is the cervix. Next is the uterine fundus. The bimanual technique can outline its position, size, shape, consistency, and degree of mobility. Uterine or cervical mobility can be assessed further by placing the fingers on one side of the uterus and moving them to the contralateral side. This can be done on both the right and left sides to detect chronic or acute inflammatory changes and fixation. The other hand is then placed on one lower quadrant of the abdomen and slowly moved inferiorly and medially to meet the fingers of the hand examining the vagina. In this way, adnexal structures on that side can be appreciated. The degree of adherence of an adnexal structure to the uterus often can be ascertained. Enlargement, consistency, and position of ovaries and tubes can be noted. The ovary is a sensitive structure, and patients differ in tolerance to palpation. The contralateral side should be examined similarly. Finally, the vaginal walls and adjacent structures (bladder and rectum) are palpated. The glove of the hand used for vaginal examination is then replaced with a clean glove for the rectovaginal or rectal examination.

Figure 29.1 Bimanual examination, first step. The fingers that are placed in the vagina to feel the consistency and symmetry of the cervix and its axis in relation to the axis of the vagina. They then elevate the uterus toward the abdominal wall so that the total length of the uterus can be determined. (From Duncan AS. In: Bourne A, ed. British gynaecological practice. Philadelphia: FA Davis Co, 1955; drawn by G. McHugh, with permission.)

Figure 29.2 Bimanual examination, second step. The fingers examining the vagina are moved into the anterior fornix to permit palpation of the uterine corpus. If the abdominal wall is thin and well relaxed, it is possible to define even minor irregularities in the contour or consistency of the uterus. Third step: With the fingers still in the anterior fornix and with the aid of the hand palpating the abdomen, the uterus is moved gently toward a retroverted position and then from side to side to determine its mobility and the presence or absence of pain on movement of the uterus. (From Duncan AS. In: Bourne A, ed. British gynaecological practice. Philadelphia: FA Davis Co, 1955; drawn by G. McHugh, with permission.)

The rectal examination is uncomfortable, but it can be made less so if the physician gently places a finger into the anal opening, requests that the patient valsalva and wait for the anal sphincter to relax before proceeding. The middle finger is inserted into the rectum and the index finger into the vagina. The tone and symmetry of the sphincter are determined. The parametrial tissue is then palpated between the index finger in the vagina and the middle finger in the rectum. Finally, the posterior uterine surface, adnexal areas, uterosacral ligaments, and pouch of Douglas, along with the ano-rectal area, are palpated. The rectovaginal examination enhances the evaluation of cul-de-sac or ovarian pathology. Particles of hard fecal material may interfere with an accurate examination. Additional important information can be gathered from a separate rectal examination. Exerting pressure against the perineum allows introduction of the index finger. Hemorrhoids, polyps, and tumors of the rectum may be felt. The rectal examination can be assisted by placing one hand on the lower abdomen to make it a bimanual procedure. This examination is useful when a vaginal examination is impossible, such as in infants and children. The rectal wall is palpated throughout its circumference and as far as the finger permits. Almost one half of all rectosigmoid cancers can be detected by this palpation. The finger also can explore the surface of each pelvic

wall, feeling for enlarged nodes or other abnormalities. Any fecal material can be tested for occult blood. Following the rectal examination, the patient is instructed to slide up on the table while the lower one third of the table is replaced. The examiner can answer any questions about the examination and then step out of the room while the patient dresses. Physicians should always wash their hands after examining a patient.

Figure 29.3 If the fingertips of both hands come together when carrying out the second step of the bimanual examination, it can be concluded that the uterus is retroverted; the fingers in the vagina are then moved to the posterior fornix to outline symmetry, consistency, and mobility of the retroverted corpus. (From Duncan AS. In: Bourne A, ed. British gynaecological practice. Philadelphia: FA Davis Co, 1955; drawn by G. McHugh, with permission.)

Figure 29.4 Bimanual examination, fourth step. To outline the adnexa, the fingers examining the vagina are moved to the right fornix, and the examiner attempts to bring the fingers of both hands together at a point presumed to be superior to the fallopian tube and ovary. (From Duncan AS. In: Bourne A, ed. British gynaecological practice. Philadelphia: FA Davis Co, 1955; drawn by G. McHugh, with permission.)

Figure 29.5 Bimanual examination, fifth step. When the fingers of both hands are quite close together (it is desirable but not always possible to approximate these fingers), they are then moved gently toward the examiner so that the adnexa slip between the fingers and can be outlined. (From Duncan AS. In: Bourne A, ed. British gynaecological practice. Philadelphia: FA Davis Co, 1955; drawn by G. McHugh, with permission.)

Physical examination can be recorded electronically or on preprinted forms as shown on the ACOG website and should be organized according to the following elements: I. Perineum—lacerations, scarring

II. External genitalia—stage of development, color, lesions, Bartholin glands

II. Vestibule—Skene glands, urethral orifice, hymenal ring

V. Vagina—color, lesions, leucorrhea, tone, rugae

V. Cervix—shape, consistency, mobility, parity, lesions

VI. Uterus—position, mobility, size, shape, consistency

II. Adnexa—position, mobility, masses, tenderness

II. Rectovaginal examination—confirmation of pelvic findings

X. Rectal examination—additional findings, occult blood Back in the consultation room, the findings, diagnoses, and plans for therapy are explained to the patient in terms that she can understand. This is especially important when surgery is contemplated, because the nuances of an operation may be unclear to patients. The physician should explain carefully what the patient may expect if any special diagnostic or therapeutic procedures were performed, such as bleeding after cervical biopsy. In some situations, patients may be instructed to abstain from sexual activity for a specific length of time. The importance of a follow-up examination should be stressed. Prescriptions for medications should be detailed adequately and restrictions on refills stated explicitly.

Diagnostic Procedures Pap Smear The diagnosis of precancerous lesions of the cervix is based on periodic cytologic screening of the cervix. Despite extensive debates regarding the optimal frequency and accuracy of the Pap smear, it has become the standard method of screening. In addition to cancer screening, the Pap smear also can be used to assess hormonal status and to assist in identifying sexually transmitted pathogens, such as herpes simplex, HPV, Chlamydia trachomatis, and Trichomonas vaginalis as well as benign conditions. Pap smears should be obtained at periodic intervals in women after they reach the age of 18 or become sexually active, whichever comes first. They should be obtained yearly, especially in women who have had coitus with more than one sexual partner, began to have coitus as an adolescent, or have a history of an STD. A Pap smear should be performed annually in women who have had a hysterectomy for pelvic cancer or in situ disease, although it may not be necessary in women who have had a hysterectomy for benign disease. After visualizing the cervix, a plastic or wooden spatula is used to scrape the squamocolumnar junction and any areas on the cervix or vagina that look suspicious (Fig. 29.6). In premenopausal women, the squamocolumnar junction is likely to be within the endocervical canal. The spatula is wiped on a clean glass slide, and the slide is sprayed immediately with a fixative (i.e., alcohol and ether) before the cells dry. A second specimen is taken from the endocervix with a cotton-tipped applicator or cytobrush that is placed into the endocervical canal and rotated 360 degrees three to five times. The cytobrush is more effective than a cotton swab in obtaining endocervical cells. The cells are then transferred to the slide, and a fixative is used to preserve the cellular material. The slide, previously labeled to identify its source, is then sent for cytologic evaluation.

Figure 29.6 Pap smear. A: Cells obtained from transformation zone using an Ayers spatula. B: Cells obtained from the cervix by using a cytobrush.

Studies evaluating automated preparation systems versus conventional cervical cytologic preparation have shown excellent cellular presentation and superior sensitivity for automated systems compared with conventional techniques. Thin-layer cytology for Pap smears has become widely accepted during the last decade, addressing some of the imperfections with traditional Pap smear screening. In traditional Pap smear screening, there is a 5% to 10% false-negative result rate. Yearly testing decreases the possibility of a false-negative result for any particular woman. The thin-layer liquid-based cytology, or “thin prep,” appears to decrease the false-negative rate by picking up more potentially precancerous changes. Thin-layer cytologic preparation is made by submerging the sample in a vial of liquid fixative and mixing the cells in the solution. This avoids difficulties with the fixative, piled up cells, and air drying common to smears on glass. The thin prep also appears to decrease the false-positive rate from inflammatory conditions. The atypical squamous cells of undetermined significance to squamous:intraepithelial cell ratio was reduced by 54% in a thin-prep group. Controversy still exists as to the optimal cytologic screening approach.

Testing for Vaginitis Although normal vaginal secretions are clear or white, homogenous, and odorless, with vaginitis there may be an abnormal discharge, vulvar irritation, dysuria, and vaginal odor. The majority of cases of vaginitis are due to bacterial vaginosis, vaginal candidiasis, T. vaginalis, or atrophic vaginitis. Additionally, STDs such as gonorrhea and chlamydia may cause an abnormal vaginal discharge. Detailed history should include the description of the discharge, presence or absence of odor, duration of symptoms, sexual history, and history of infections. Standard office procedures include preparation of a wet mount, with material

from the swab or the speculum placed on each end of a plain microscope slide, and microscopic examination to assess for bacterial vaginosis. Patients with bacterial vaginosis complain of thin white, yellow, or gray vaginal discharge, commonly with a musty or fishy odor. The pH of the vaginal fluid is usually 5.0 or 6.0. Clue cells on the microscope slide on saline wet mount are described as vaginal squamous epithelial cells that have bacteria adhering to the membrane, giving them a speckled appearance as the focus shifts. Treatment of symptomatic patients and pregnant patients is routinely recommended. T. vaginalis may be diagnosed by a saline wet mount showing polymorphonuclear leukocytes and motile flagellating organisms. The female partner complains of copious frothy yellow to green vaginal discharge. The patient and sexual partner should be treated simultaneously. Atrophic vaginitis is seen often in postmenopausal women and may be associated with a blood-tinged discharge. Evidence of atrophy on the vulvar vaginal examination may be present. The saline wet mount shows numerous leukocytes with small, round epithelial cells. Topical therapy usually is prescribed, although oral therapy can be utilized. Patients who have vulvar itching and a thick, white, curdlike discharge usually have vaginal candidiasis. The diagnosis is confirmed by examining a slide treated with 10% potassium hydroxide, with a sample of the discharge showing filaments, hyphae, or spores. Topical therapy usually is undertaken with oral antifungals saved for resistant infections or immunocompromised women.

Colposcopy Colposcopy aids in examining the visible portion of the female reproductive tract (i.e., vulva, vagina, cervix) once a cytologic abnormality has been identified. This technique complements cytologic evaluation and localizes the source of abnormal cells seen on cytologic examination guiding selective biopsy. Vulvar diseases amenable to colposcopic evaluation include HPV infections, Herpes genitalis, and preinvasive cancers. The magnification afforded by the colposcope may aid in the selection of areas for biopsy. The application of 3% acetic acid for 3 to 5 minutes also may help to highlight abnormal areas, which typically turn white and display sharp borders (i.e., acetowhite epithelium). The colposcope may aid in the recognition of clinically inapparent vaginal intraepithelial neoplasia or HPV infection. These lesions also are characterized by acetowhite epithelium. Colposcopy is used most commonly for evaluating the cervix in a patient with abnormal Pap smear results. After it is visualized and excess mucus is gently removed with a dry cotton ball, the cervix is treated with 3% to 5% acetic acid. As noted, flat condylomata or dysplastic areas turn white or develop a vascular pattern with a mosaic appearance or punctuation. The squamocolumnar junction and transformation zone are then inspected thoroughly, and biopsy of suspicious areas is performed. In addition, a nonpregnant patient with an abnormal Pap smear result should have an endocervical biopsy. Bleeding occurring as a result of the biopsy can be controlled easily with ferric subsulfate (Monsel solution).

Endometrial Sampling Advances in the technique used for endometrial sampling have simplified the evaluation of abnormal uterine bleeding. Endometrial sampling is of greatest value in the evaluation of

abnormal bleeding when diffuse rather than focal endometrial changes are suspected. Before obtaining an endometrial sample for biopsy, the physician should have the patient's informed consent. The physician should then rule out intrauterine pregnancy, cervical or endometrial infection, and cervical stenosis. The size and position of the uterus are determined by a pelvic examination or by ultrasonography, and a speculum is placed in the vagina. If the patient is sensitive to cervical manipulation, a paracervical block can be administered. When endometrial cancer is suspected, an endocervical biopsy sample can be obtained before endometrial sampling. The cervix and upper vagina are then cleansed with an antiseptic such as povidone-iodine. If the uterus is not anteflexed or retroflexed, a biopsy sample often can be obtained without placing a tenaculum on the cervix. If the degree of flexion is marked, a tenaculum aids in straightening the uterus. It is necessary in some women to anesthetize the anterior cervix with 1% lidocaine to avoid discomfort when the tenaculum is applied. The instrument used to collect the sample is inserted to the top of the fundus and the length of the uterine cavity noted (Fig. 29.7). It is not necessary to dilate the cervix with sounds before obtaining the biopsy sample in most situations. Several samples are then obtained from the endometrial cavity and submitted for histologic evaluation. If cervical stenosis is present, instruments as narrow as 2 to 3 mm in diameter can be used or the cervical os dilated. There are several instruments available for sampling the endometrium. The most commonly used is the Unimar Pipelle endometrial suction curette (Cooper Surgical, Shelton, CT). Others include the Novak endometrial suction biopsy curette (Miltex Instrument Company, Lake Success, NY) and Tis-U-Trap uterine suction curette set (Milex Products, Chicago, IL). Patients may experience vasovagal syncope during the procedure and cramps or bleeding afterward. When sampling the endometrium, it is important to consider that the device used can adjust to the shape and curvature of the uterus, which minimizes pressure on the uterine wall, reducing the likelihood of pain and cramping. Bleeding usually stops within 1 to 2 days after the biopsy.

Figure 29.7 Endometrial biopsy.

Vulvar Biopsy Due to the high rate of false-positive and false-negative results associated with tolidine blue staining, colposcopy has been shown to be a very sensitive tool for diagnosing vulvar lesions such as HPV infections. The only definitive way to exclude invasion is to perform a biopsy of, and to examine microscopically, suspicious areas of the vulva. Vulvar biopsy samples usually are simple to obtain in the office. The area under suspicion is cleansed with an antiseptic solution and then infiltrated with 1% lidocaine by using a 25-gauge needle. Then, a 3- to 6-mm Keyes punch is used to obtain a sample (Fig. 29.8). Any bleeding that occurs can be controlled with silver nitrate or Monsel solution and gentle pressure. For larger areas, a single interrupted suture usually is all that is required to achieve hemostasis.

Ovulation Detection and Prediction The confirmation of ovulation is always an important part of the evaluation of patients with infertility or abnormal uterine bleeding. It also is useful in timing donor and homologous artificial insemination. Methods used to detect ovulation reflect a preovulatory follicle or progesterone secretion by the corpus luteum. The simplest among these is the determination of a biphasic temperature pattern by recording the basal body temperature (BBT). Serial ultrasonographic studies of follicular growth and disappearance and subsequent formation of a corpus luteum is another method of detecting and timing ovulation. The serial sonographic changes associated with ovulation include a preovulatory follicle of 20 mm or more, a change in the shape of the follicle, thickening of the follicular wall, disappearance of the follicle, and the appearance of fluid in the cul-de-sac. However, these changes can occur without actual ovulation, and ovulation can occur without these

characteristic changes. The introduction of home test kits for detecting the midcycle surge of luteinizing hormone (LH) in urine has made it possible for patients to predict when ovulation will occur. A peak in urinary LH typically occurs between 8 a.m. and 3 p.m., and ovulation usually occurs 12 to 36 hours later. This makes it possible for infertile couples to time coitus or insemination more accurately than ever before. False-positive results may occur in women with polycystic ovary syndrome, whose LH levels may be elevated in the range of an LH surge and in those taking ovulation-inducing drugs.

Figure 29.8 Vulvar biopsy by using a Keyes punch.

Testing for Bone Mineral Density Osteoporosis is a major health threat in the United States, which is particularly prevalent in the postmenopausal woman. The gynecologist often is called on to assess risk factors for osteoporosis in the menopausal population and in those women who are hypoestrogenic. Although the dual energy x-ray absorptiometry (DEXA) scan of the spine and hip is the gold standard for evaluation of osteopenia and osteoporosis, newer screening measures of bone strength, such as heel ultrasonography, have been introduced and used in a gynecology office setting. Measurements of bone mineral density are determined as a T score in the heel, as with the spine and hip density measurements. This additional service in the

gynecology office will help in screening women for osteoporosis, with appropriate referral for a spine and hip study. In addition, a combination of risk factor evaluation and the bone mineral density measurement in the office may increase the ability to predict the development of osteoporosis and fracture risk and improve evaluation and treatment decisions in the menopausal patient.

Transvaginal Ultrasonography Although there is no substitute for a bimanual pelvic examination, transvaginal ultrasonography may enhance and extend the pelvic examination. Ultrasonographic examination cannot replace the physician's physical determination of the mobility and texture of tissues or the presence of tenderness, but it can provide objective confirmation of the size, shape, and location of pelvic organs. The introduction of lightweight, mobile machines with 5- and 7.5-MHz probes has made office-based ultrasonography a valuable diagnostic technique. Compared with other methods of imaging, ultrasonography is unsurpassed in safety and in providing inexpensive images. Several advantages of ultrasonography available in the gynecology office include picture clarity, ease of operation, and dynamic use of the probe. Officebased ultrasonography can be helpful in the following situations, including evaluating pelvic masses, abscesses, cysts, leiomyomata, monitoring follicular growth, differentiating intrauterine from ectopic pregnancies, and evaluation of the endometrium. Another important area in which ultrasonographic evaluation is valuable is in the postmenopausal woman. In evaluating endometrial abnormalities, endometrial thickness of 5 mm is used to determine whether further evaluation is needed. Women whose endometrium measures ≤5 mm are considered to have normal results, and those women whose endometrium measures >5 mm are subjected to endometrial biopsy in a screening study performed in a private office setting. However, a suboptimal examination may have serious consequences. The ultrasonographic image is only as good and as useful as the clinical skills used to relate the sonographic findings to the situation under evaluation.

Saline Infusion Sonography Since the development of high-resolution ultrasound, SIS has been gaining in popularity. Numerous studies have looked at the benefit of ultrasound in establishing the diagnosis in women with abnormal uterine bleeding. The use of fluid instillation into the uterine cavity coupled with ultrasound has become a useful diagnostic tool. SIS is easily performed in the clinical setting and is remarkably well tolerated in most patients. The clinical use of SIS is not in its use to replace surgery but to identify those patients who need surgical intervention. Principles of SIS are listed in Table 29.1. The minimum supplies required to perform SIS include a SIS catheter, instillation medium, a 20-cc syringe, povidone-iodine solution, scopettes, an open-sided speculum, and an ultrasound that preferably has transvaginal capabilities. The most widely used medium for instillation into the uterine cavity is saline; however, other echolucent contrast media can be used but do not appear to perform better than normal saline and are more costly. SIS

can be performed during any time of the cycle; however, performing SIS during the follicular phase will avoid the potential disruption of an early pregnancy. In addition, there is a thinner endometrium during the follicular phase, which may aid in better evaluation of the uterine lining. Instilling saline during menses may lead to poor uterine distention, so avoiding the procedure during the menstrual cycle is preferred. There are several SIS catheters on the market, and pediatric Foley catheters, insemination catheters, and pediatric feeding tubes can be used. The choice of the catheter will depend on the patient, and therefore several catheter types should be available to the physician performing the SIS. In particular, one should have a thin, stiff catheter available for the nulliparous cervix to occlude the os.

TABLE 29.1 Saline Infusion Sonography Useful for evaluation of bleeding in pre-, peri-, and postmenopausal women SIS or transvaginal ultrasound alone: 94.1% vs. 23.5% detection of focal pathology SIS and biopsy: 96.2% sensitivity and 98.0% specificity Advantage: can determine fibroid penetration depth Disadvantage: small irregularities may be misinterpreted as polyps After performing a bimanual exam or baseline ultrasound to determine uterine position, a speculum is inserted and the cervix is identified. The cervix may be cleansed with povidone-iodine or similar antiseptic solution. The catheter is primed with saline and then inserted through the cervical os. The exact placement will depend on the catheter used. For a balloon-type catheter, the balloon should be positioned in the cervical canal or lower uterine segment and inflated. However, the Goldstein SIS cone-type catheter is inserted to 7 cm, or near the uterine fundus, with the white acorn cone occluding the cervical os (Fig. 29.9). A ring forceps may be needed to assist in placing the SIS catheter. Once the catheter is in place, the speculum is removed with special care taken so that the catheter is not dislodged. The vaginal ultrasound probe is inserted into the vagina, and the uterus is imaged as the saline is infused slowly. Usually, about 5 to 10 cc of saline is used in order to get good distention. It is important to remember that the seal will not be watertight. Although a watertight seal may produce better images, this will result in significantly more cramping with the procedure. When there is a large efflux of saline out of the cervix, more saline may be needed to get good images. Visualization in both the longitudinal and transverse axis should be performed. The entire uterine cavity should be visualized from left to right broad ligaments longitudinally and from the cervix to the fundus in the coronal plane (Fig.

29.10). It is important to realize that full distention of the uterus is not necessary to get a good-quality evaluation. Most patients have minimal discomfort after a SIS procedure. Patients usually do well by using nonsteroidal anti-inflammatory drugs (NSAIDs) or similar analgesics for pain control. Patients should be advised to call if they are experiencing heavy bleeding that is not associated with menses that continues for more than 4 days. Additionally, patients should be evaluated if they have a fever >100.5°F or develop a vaginal discharge.

Figure 29.9 Placement of the Goldstein catheter for SIS by using a cone to occlude the cervical os. (Reprinted with permission from Cook Ob/Gyn, Spencer, IN.)

Figure 29.10 SIS evaluation of the uterine cavity. A: SIS demonstrating a normal uterine cavity. B: SIS demonstrating an intrauterine mass. C: SIS demonstrating a localized posterior wall thickening. D: Bicornuate or septate uterus visualized prior to instillation of saline.

Contraceptive Procedures As part of residency training, most obstetrician–gynecologists will obtain the clinical training needed to perform insertion and removal of an intrauterine device (IUD) in the office. Two IUDs are available in the United States: Mirena and ParaGard. IUDs are generally recommended as a contraceptive method to women in a stable monogamous relationship who are not at risk for pelvic inflammatory disease, STDs, or ectopic pregnancies. IUDs are contraindicated in the following situations: Suspicion of pregnancy Congenital uterine anomaly Fibroid uterus that severely distorts the uterine cavity Pelvic infections

Unresolved abnormal Pap smear Untreated cervicitis or vaginitis Genital bleeding of unknown etiology Women with multiple sexual partners Leukemia AIDS Breast cancer Ectopic pregnancy or history of ectopic pregnancy. The Mirena IUD consists of a T-shaped polyethylene frame with a steroid reservoir around the vertical stem (Fig. 29.11). The reservoir consists of a cylinder made up of a mixture of the progestin widely used in contraception, levonorgestrel, and silicone. The levonorgestrel within the stem provides release of levonorgestrel at a rate of 20 mcg per day initially. This level declines to half the 52-mcg level at 5 years, so it is approved for 5 years of contraception. There is a stable blood level of 150 to 200 pg/mL 3 weeks after insertion of the Mirena device. The T-shaped system is 32 mm in length and width. The Tshaped body also has barium embedded, which makes it radiopaque. There is a monofilament string attached to the bottom of T-shaped stem. Although the exact mechanism for contraception is not clearly identified, it appears that the Mirena IUD has mostly local effects within the uterine cavity. Additionally, it may have an effect on ovulation. In a 1-year study of the system, only 45% of cycles were ovulatory; however, in a 4-year study, 75% of cycles were noted to be ovulatory. Contraceptive effectiveness is quoted to be 0.2 pregnancies per 100 women, and the cumulative 5-year pregnancy rate is 0.7 per 100 women. Half of the pregnancies that occur while using the Mirena IUD are ectopic gestations, at a rate of 1 ectopic pregnancy per 1,000 users per year. It is important to inform patients that the Mirena IUD can alter the menstrual bleeding pattern. During the first 3 to 6 months of use, there may be an increase in vaginal spotting. Additionally, it has been noted that approximately 20% of users will be amenorrheic after 1 year of use. The ParaGard IUD has a T-shaped polyethylene body. The vertical portion of the T is wound with 176 mg of copper wire along with a copper collar of 68.7 mg on each of the transverse arms. The exposed areas of copper are approximately 380 mm2. ParaGard has a monofilament thread attached to the bulb end of the base of the T-shaped device. The available data indicate that the copper is released continuously into the uterine cavity. The additional copper load to the body from a copper IUD may precipitate symptoms in patients with Wilson's disease. The exact mechanism in which the copper provides contraception is unclear; however, it is thought that there is interference with sperm transport, fertilization, and embryo implantation. ParaGard is approved for 10 years of contraceptive use, twice the interval of the Mirena. Women who use the copper IUD should be advised that blood loss at the time of menses might increase. There is an approximately 35% increase in menstrual blood loss among copper IUD users.

Figure 29.11 The Mirena IUD. A: Insertion of the Mirena into the uterine cavity. B: The arms of the Mirena are released. C: The Mirena is positioned near the uterine fundus. D: Releasing the Mirena IUD and withdrawing the inserter. E: The Mirena IUD.

If a woman becomes pregnant while an IUD is in place, the manufacturers recommend removing the IUD if the string is visible. It is important to confirm the location and viability of the pregnancy prior to removal of the IUD. Patients in whom the IUD cannot be removed or in those who choose not to have the IUD removed should be informed that there is an increased risk of septic abortion and preterm labor and delivery and should be monitored accordingly if they choose not to terminate the pregnancy after understanding the risks.

Intrauterine Device Insertion Technique An IUD should be inserted, managed, and removed only by clinicians trained in IUD use. The Mirena and ParaGard have different techniques for preparing the IUD insertion, so clinicians should refer to the package inserts for guidance. IUDs can be inserted at any time during the menstrual cycle. Traditionally, physicians have preferred to insert an IUD at the time of menses to insure that the patient is not pregnant. However, insertion at the time of menses increases the risk of expulsion of the IUD during the first 2 months of use. It is best to give patients an NSAID 1 hour prior to IUD insertion. After loading the IUD into its insertion device, the uterus should be examined by bimanual examination and a speculum inserted into the vagina and the uterus sounded. With both IUDs, there is an adjustable flange that should be set to the length to which the IUD should be inserted. A single tooth tenaculum is applied to the anterior lip of the cervix to aid in cervical and uterine straightening. Benzocaine spray or local infiltration of lidocaine may be used prior to tenaculum placement. The IUD must be inserted within 5 minutes of loading so that the arms will spring back open after insertion. The IUD is then passed through the cervical canal to the fundus. The plastic flange should be at the level of the internal os if the IUD is inserted correctly. Once correct placement is confirmed, the insertion device is used to release the arms of the IUD. The insertion device is then removed gently so as not to disturb the placement of the IUD. The monofilament thread should be cut approximately 2 cm from the external os. The risk of uterine perforation is 1 in 1,360 insertions. Insertion immediately in the postpartum period, particularly during lactation, has been associated with an increased risk of uterine perforation. However, there is no increased risk of perforation if the IUD is inserted immediately after expulsion of the placenta. It is preferred, however, to delay insertion of an IUD until the second postpartum month. After insertion of an IUD, the patient should be taught how to palpate the strings monthly. Patients should be seen in 3 months to review bleeding patterns and concerns with the IUD. At that time, a speculum examination should be performed to rule out partial expulsion of the IUD. It is important to note the type of IUD prior to removal. The strings are grasped with a ring forceps and pulled outward through the vagina until the IUD is expelled. If the strings break off during removal or the strings are not visible, removal under ultrasound guidance is advisable. Under ultrasound guidance, while using packing forceps, the lower stem is located. Using gentle traction, it is removed through the internal then external os. If gentle force does not produce the IUD, then the IUD may be embedded and, in such cases, hysteroscopic removal in the operating room may be needed. It is important to note that some IUDs that are used outside the United States do not have strings and are designed for permanent placement. These should not be removed in the office setting.

Implantable Contraception The levonorgestrel implant (Norplant) is no longer marketed in the United States due to difficulties encountered in insertion and removal. A long-lasting single rod etonogestrel (ENG) implant is highly effective and was approved by the FDA in July 2006. Marketed as Implanon, this device has been used in over 30 countries worldwide and in more than 2.5

million women. This progestin-only implant consists of a single sterile rod (4 cm by 2 mm) implanted subcutaneously and provides up to 3 years of continuous contraception. It also is very useful for those patients who cannot tolerate estrogen. The ENG implant is designed for rapid, simple insertion and removal. However, a physician should be trained in the specific technique in an appropriate training program. The average insertion time for Implanon is approximately 1 to 2 minutes, and the disposable applicator comes preloaded, including a needle tip that has two cutting edges (Fig. 29.12). The implant is placed subdermally on the inner aspect of the nondominant arm, 6 to 8 cm above the elbow under local anesthesia. Removal of the implant requires a 2- to 3-mm incision at the distal tip of the implant and pushing the other end of the rod until it pops out. If that technique does not work, a small tissue forceps may be used to remove the implant, with removal time usually Table of Contents > 30 - Gynecologic Ultrasound

30 Gynecologic Ultrasound Mika Thomas Bradley J. Van Voorhis The use of sonography has become widespread in gynecology. Its accessibility, relatively low cost, and high patient acceptance make it applicable as an initial step in assessing many gynecologic disorders. This chapter discusses and illustrates the common uses of ultrasound (US) in the evaluation and treatment of a variety of gynecologic disorders. The subsections are divided according to the most common indications for gynecologic US, and a list of suggested readings is available at the end of the chapter for further in-depth reading on the subject.

Sonographic Instrumentation and Technique US uses high frequency sound waves at various frequencies to allow imaging of internal organs and vessels. The waves emitted by the transducer pass through the soft tissue, and a portion of the wave reflects off perpendicular tissue/fluid interfaces. This reflection, or return echo (much like a sonar), is detected by the transducer, while the remaining portion continues through until the waves encounter another perpendicular tissue/fluid interface, sending back another reflected echo delayed in time. The US machine collates the information from the reflected echoes, based on the time required for their return and intensity, and reconstructs a two-dimensional (2D) sonographic image. Both the origin of the signal, the transducer, and the receiver are contained in the same unit. Threedimensional ultrasonography (3D-US) characterizes an entire soft tissue volume by storing multiple 2D images, and the computer software rapidly collates the multiple 2D images thus yielding a 3D image. Once the information is electronically stored, this computerized storage system allows reconstruction of images within the defined volume in any plane and provides the opportunity to reorient the scan relative to internal soft tissue landmarks, which enhances the usefulness of the technology. US is particularly useful in defining the internal acoustic characteristics of a soft tissue structure, thus distinguishing fluid-filled structures from solid structures. This makes US the imaging modality of choice in evaluating the ovary for cysts or neoplasms. This imaging technique is not as well adapted to distinguish solid structures from other adjacent, or surrounding, solid structures. A perfect example of this is the ease at which an intrauterine gestational sac can be visualized, while a comparably sized intracavitary uterine polyp or

fibroid may be quite difficult to distinguish from the adjacent endometrium or myometrium with a similar acoustic appearance. Diagnostic US of the pelvic organs can be performed by using the transabdominal sonography (TAS) approach, in which the uterus and adnexa are imaged through a distended urinary bladder, or transvaginal ultrasound (TVUS), where the probe is inserted into the vagina for imaging with an empty bladder. In general, the lower the frequency emitted by the US transducer, the further the penetration and the deeper the window of visibility but the smaller the amount of discrimination between soft tissues. Therefore, TAS uses lower frequency sound waves (3.5 to 5.0 MHz) to allow for the deeper penetration required to visualize intra-abdominal structures beneath the subcutaneous tissue, which can be quite variable in depth between patients. A TAS is most useful in fully assessing large masses that extend out of the pelvis or in situations where TVUS cannot be performed, such as in pediatric or adolescent patients. Due to problems visualizing the pelvic organs through intervening tissues such as the small and large bowel or the anterior abdominal wall, the transabdominal approach is best performed with a fully distended urinary bladder, enabling a better acoustic window without interfaces to reflect echoes to visualize the uterus and adnexa. However, TAS remains limited by body habitus and any intervening bowel or preperitoneal fat, which can increase artifacts and scatter the incident US beam. TVUS uses higher frequency sound waves (5 to 8 MHz), which allow higher image resolution but with less tissue penetration, thus limiting the ability to “see” objects more distant than 10 cm clearly but images the closer tissues much better. TVUS is a better modality with which to image obese women because the US transducer can be positioned immediately adjacent to the uterus and ovaries without the hindrance of subcutaneous tissue. For most applications, a slightly curved transducer probe that has high line density affords the most detailed image (Fig. 30.1). It becomes increasingly difficult to see the uterine fundal region if it extends above the pelvis, as in the case of a large fibroid uterus or the pregnant uterus in the second and third trimesters. By contrast, the transvaginal component of an examination of the uterus typically can better visualize the proximity of fibroids to the endometrial cavity than can TAS. Image clarity with TVUS usually is superior when evaluating ovarian abnormalities as compared with TAS and also can be helpful as a means of distinguishing between ovarian and uterine masses. In addition, TVUS with Doppler sonography affords assessment of the flow of blood within vessels adjacent to and within the uterus and ovaries.

Figure 30.1 Transvaginal ultrasound. A: Diagram showing a transvaginal probe adjacent to the cervix in a retroflexed uterus. (Drawing by Paul Gross, MS.) B: Picture of a tightly curved curvilinear array transvaginal transducer probe. C: Flat-faced transvaginal probe with a needle guide attached to the shaft.

TVUS is best performed in patients placed in the lithotomy position with an empty bladder. The vaginal probe should be disinfected and covered with a sheath prior to insertion. For optimal patient comfort, the probe should be inserted into the vagina while the operator's finger gently depresses the posterior introitus. Alternatively, the patient may insert the probe herself. A US examination must be thorough and reproducible; for this reason, most would suggest performing each US in a proscribed fashion, following the same routine with every scan. A complete pelvic US examination begins with images of the uterus as the central pelvic landmark both in the sagittal and coronal axes. The probe can be withdrawn into the midvagina and directed anteriorly to provide views of an anteflexed uterus. The retroflexed uterus is imaged easily without major manipulation of the probe because it is closer to the plane of the vagina, though some vaginal probes angle the US beam superiorly, making this somewhat more difficult or uncomfortable for the patient. The operator can then orient the probe for imaging the adnexal regions by using the internal iliac artery and vein as landmarks for delineation of the ovarian fossa. The normal ovary usually can be found just medial to the internal iliac artery and vein, but there is substantial variation in the location of the ovaries, particularly in women who have undergone pelvic surgery or hysterectomy or who have enlarged ovaries that may extend upward out of the pelvis. Typically, enlarged ovaries or ovaries containing cysts are relatively easy to identify, while the normal postmenopausal ovary might be more difficult to visualize. The operator can

use one hand to mildly compress the abdominal wall and evaluate the mobility of these organs. If there are no adhesions, the uterus and ovaries should move smoothly away from each other as the probe is advanced. This has been termed the sliding organ sign and, if absent, may suggest the presence of agglutinating pelvic adhesions. To evaluate the vascularity of an organ, US machines make use of the physics principle known as the Doppler effect. This principle states that sound or light waves reflected by a moving object will undergo a change in frequency proportional to the relative velocity of that object, toward or away from the transducer (e.g., like the difference in sound made by an approaching and departing train). Detecting these frequency changes can help to determine the blood flow to a structure being imaged. Transvaginal color Doppler sonography (TV-CDS) combines the anatomic information provided by TVUS with blood flow information provided by CDS (Fig. 30.2). TV-CDS assesses blood flow and resistance to blood flow in larger vessels supplying pelvic organs. The flow within a vessel can be characterized in several different ways by TV-CDS. First, the flow waveform recorded by the Doppler can be described (e.g., the presence or absence of diastolic flow through the vessel). Alternatively, the waveform can be analyzed by measuring resistive indices that indicate the downstream impedance to blood flow within a vessel. These resistive indices are only indirect measures of the actual blood flow to an organ. Commonly measured indices are the resistive index (peak systolic velocity minus minimum end diastolic velocity divided by peak systolic velocity) or the pulsatility index (peak systolic velocity minus end diastolic velocity divided by the mean velocity over the cardiac cycle.) These parameters are unitless values and are measures of relative impedance to forward flow. One must obtain signals from between 30 and 60 degrees to the longitudinal axis of the vessel in order to provide optimal waveforms. Actual blood flow volume and velocity can be determined in larger vessels, but these measurements are not accurate in the smaller vessels. Standard, frequency-based color Doppler is assigned red colors for flow toward the transducer and blue colors for flow away from the transducer.

Figure 30.2 Transvaginal color Doppler sonography. A: TV-CDS showing low-impedance flow (resistive index = 0.45; pulsatile index = 0.60) within the wall of a corpus luteum. B: Amplitude color Doppler image of hemorrhagic corpus luteum showing no flow within the center of the mass, which contained an organized clot. C: Complex mass with low-impedance arterial and increased venous flow within an irregular solid area, which is highly indicative of ovarian cancer. (See Color Plate)

A new type of processing known as power Doppler has been developed for the detection of flow within much smaller vessels. This technique is more sensitive, which allows for the detection of areas of low blood flow, and the information is independent of the angle of insonation of the vessel. The main disadvantages are that there is no information about speed or direction of flow, and there is high motion sensitivity leading to false readings. The principal aim of power Doppler is to determine the simple presence or absence of flow, although computer analysis of images allows for quantification of blood flow for research purposes. Clearly, the accuracy of TVUS is operator dependent, and significant clinical experience with anatomic correlation is required for effective use. For those who do not routinely perform pelvic sonograms as part of their practice but rather order them, it is crucial that they have a working understanding of not only the lexicon of US but also at least a rudimentary ability to interpret the images that are collected. US images and reports must also be saved for medicolegal reasons. US, to some extent, is subjective and documentation of results is incomplete without a narrative description of the overall impression by the operator. While becoming more widely available and used in obstetric practice, the clinical value of 3D-US in gynecology over the standard 2D technique has yet to be demonstrated. With 3DUS, data is captured and stored during a “sweep” of the pelvis with the vaginal probe. This allows for the rapid acquisition of data and the ability to subsequently display the images in three dimensions. Since data from the entire volume of the pelvis has been stored, any 2D plane can be recreated that is oriented toward the internal organs and thus display the optimal section through the region of interest. For example, the true coronal image of the uterus can be displayed, which cannot be viewed in standard 2D images from an external orientation. 3D-US has been shown to be efficient and accurate in characterizing Müllerian abnormalities and in measuring ovarian and fibroid volumes and shows promise in some urogynecologic applications. Whether or not the improved imagery actually improves the detection rate of pathology has not been demonstrated for most gynecologic applications. An even more recent advance is the ability to display 3D images live on the screen (sometimes called live 3D- or “4D”-US). The true clinical advantage of these newer techniques currently is under investigation.

Abnormal Uterine Bleeding

Irregular uterine bleeding is a common presenting complaint for the gynecologist, and it is necessary to differentiate abnormal uterine bleeding (AUB) from dysfunctional uterine bleeding (DUB), as their management approaches differ greatly. DUB, which may only be diagnosed once organic or anatomic sources have been ruled out, is most commonly caused by anovulation due to estrogenized anovulation, or polycystic ovary syndrome (PCOS). Ultrasonic diagnostic criteria for PCOS is discussed later in the Infertility section. AUB, on the other hand, may be caused by a variety of conditions including uterine fibroids, endometrial polyps, endometrial hyperplasia or carcinoma, and endometritis. TVUS plays an important role in evaluating these women. Because of the proximity of the transvaginal probe to the uterus, the endometrial and myometrial architecture can be accurately depicted in detail in most patients. One of the most important structures to image in the evaluation of a woman with AUB is the endometrial stripe. It becomes very clear when measuring the endometrial stripe that proper imaging technique is critical, as the endometrium is not a precise geometric shape and operator error can account for over- or underestimation of its thickness. Thus, it is of utmost importance to properly orient the scan of the endometrium in its greatest long-axis plane and maximal thickness in the fundal region, which optimizes its bilayer measurement (Fig. 30.3). Normal endometrial thickness varies depending on both the patient's reproductive endocrine status and the use of hormones. In women of childbearing age, the endometrial thickness changes according to the stage of the menstrual cycle. During menses, the normal endometrium is 3- to 5-mm thick with a mildly echogenic texture. As the endometrium proliferates in the periovulatory period, a multilayered texture can be seen with thicknesses ranging from 5 to 8 mm. The outer echogenic layer represents the basalis, whereas the inner layer is the enlarging functionalis. In the secretory phase, the endometrium becomes diffusely echogenic and enlarges up to 12 to 14 mm in thickness. This is in contrast to the thin endometrial stripe of the postmenopausal patient, which typically measures 10 mL) in the absence of other follicular development. Peripheral follicular distribution and an increased ovarian stromal volume commonly are seen in PCOS, but these findings are subjective and are not included in the diagnostic criteria. The diagnosis of PCOS cannot be made on US findings alone, however, as evidenced by the fact that many other conditions are associated with “polycystic ovary– appearing” or “polyfollicular” ovaries on TVUS. In fact, up to 25% of normally ovulatory women may have a polycystic ovarian appearance on US exam. More recently, various investigators have used TVUS in conjunction with uterine cannulation as a screening tool for assessing the endometrial cavity and tubal patency. At this time, this newer mode of tubal assessment should not replace the gold standard method of hysterosalpingography. Using various contrast media (including saline, as in SIS), the endometrial cavity can be evaluated for the presence of fibroids or polyps that may result in subfertility as well as for Müllerian abnormalities such as a uterine septum, which often is associated with recurrent miscarriage. In conjunction with SIS, the escape of saline out of the fimbriated end of the tube is readily apparent in women with patent fallopian tubes as the cul-de-sac fills rapidly with fluid. The presence of cul-de-sac fluid during or after SIS confirms that at least one fallopian tube is patent. Attempts have been made to use CDS to assess in real time the efflux of echogenic contrast from each fallopian tube, with varying degrees of success.

Sonographically Guided Procedures US can be very useful in assisting difficult gynecologic procedures, particularly those

involving the uterus. In cases in which dilation of the uterine cervix has been unsuccessful or more difficult than usual, simultaneous TVUS or TAS can decrease the risk of uterine perforation and creation of a false tract. If perforation of the uterus is suspected, the path that the dilator or curette has followed as well as its tip can be readily visualized by using sonography, as long as the instrument has not been moved once perforation is suspected. Traditionally, the internal US transducer was placed in the rectum or the abdominal transducer, with the aid of a distended bladder, was used to assist in directing the dilator as it traversed the cervix or confirmed the correct path to take. With the smaller transducers found on most vaginal US probes today, the transducer usually can be placed next to the cervix through an open speculum, particularly in patients whose cervix is flush with the vagina, as in postmenopausal patients, or in those who have undergone cervical conization. Once the dilator is through the internal cervical os, TVUS or TAS can localize the dilator or curette within the uterine cavity. Real-time monitoring of the procedure can greatly reduce the risk of uterine perforation. US also can be helpful in monitoring a curettage being performed for the surgical management of either an incomplete miscarriage or early pregnancy termination. A US done at the end of the procedure can decrease the likelihood of the patient needing a second procedure at a later date by identifying those with an inadequate curettage. TAS also can be used to ensure correct placement of a uterine tandem being used for local radiation treatment of cervical or uterine cancer. TVUS can provide real-time delineation of the location of a needle relative to an area of interest within the ovary or adjacent structures. For this purpose, a needle guide with an internal opening can be attached to the shaft of the vaginal transducer, which confines the course of the needle to a prescribed path in the exact plane of the 2D scan. The most common use of this technique is transvaginal oocyte retrieval during an in vitro fertilization or in vitro maturation cycle, which is accomplished by aspirating individual follicles under direct US guidance. Cystic ovarian or adnexal masses may be drained in this manner as well. Ovarian or adnexal masses that are amenable to transvaginal drainage include endometriomas (at the start of a COH cycle or when needed for the short-term relief of acute pain), symptomatic yet relatively small simple ovarian cysts (where there is no concern for malignancy), or hydrosalpinges (at the time of transvaginal oocyte retrieval for an in vitro fertilization cycle, particularly for those in whom surgical intervention is relatively contraindicated). Likewise, tuboovarian abscesses may be drained by using the TVUS-guided approach. In the case of endometriomas or hydrosalpinges, it is unlikely that transvaginal drainage will be curative, as they typically reaccumulate over time. If an ovarian cyst is drained and subsequently reaccumulates, two options are available— surgical excision and transvaginal needle aspiration followed by instillation of a sclerosing agent such as alcohol or tetracycline. In postmenopausal patients and patients who are poor surgical candidates, the latter offers conservative management of a simple ovarian cyst as an outpatient without the need for general anesthesia. Very similar to TVUS-guided oocyte retrieval, a needle is directed under US guidance through the vaginal mucosa into the cyst. The cyst contents are then drained, and the sclerosing agent is infused and left in place for 20 minutes, after which time it is aspirated. This conservative treatment method also has been used for the treatment of ovarian remnant syndrome.

Summary Points Transabdominal and transvaginal scanning are both useful in establishing the source of AUB, characterizing pelvic masses found on physical examination, evaluating acute pelvic pain, diagnosing ectopic pregnancies, and assessing and treating infertility. Advances in technology such as higher transducer frequencies for improved resolution, rapid computerized assembly of 2D images to yield virtual 3D images, and smaller equipment have fostered wider clinical applications and made office use routine. US guidance during gynecologic surgical procedures has proved very useful in making difficult intrauterine procedures safer and diagnosing and treating selective pelvic masses by needle aspiration. It is the single most important advance in collecting oocytes for in vitro fertilization. SIS has improved the diagnostic capability of TVS in circumstances of AUB. Pelvic US is the initial diagnostic modality of choice in most circumstances, whereas secondary tests such as CDS, MRI, and computed tomographic scanning provide a means to further enhance diagnostic specificity in difficult or nondiagnostic US studies.

Suggested Readings General Callen PW. Ultrasonography in obstetrics and gynecology, 4th ed. New York: Elsevier, 2000.

Sonographic Instrumentation and Technique Babinszki A, Nyari T, Jordan S, et al. Three-dimensional measurement of gestational and yolk sac volumes as predictors of pregnancy outcome in the first trimester. Am J Perinatol 2001;18:203–211. Jokubkiene L, Sladkevicius P, Rovas L, et al. Assessment of changes in volume and vascularity of the ovaries during the normal menstrual cycle using three-dimensional power Doppler ultrasound. Hum Reprod 2006;21(10):2661–2668. Jurkovic D. Three-dimensional ultrasound in gynecology: a critical evaluation.

Ultrasound Obstet Gynecol 2002;19:109–117.

Abnormal Uterine Bleeding Breitkopf DM, Frederickson RA, Snyder RR. Detection of benign endometrial masses by endometrial stripe measurement in premenopausal women. Obstet Gynecol 2004;104:120–125. DeWaay DJ, Syrop CH, Nygaard IE, et al. Natural history of uterine polyps and leiomyomata. Obstet Gynecol 2002;100:3–7. Dueholm M, Lundorf E, Hansen ES, et al. Evaluation of the uterine cavity with magnetic resonance imaging, transvaginal sonography, hysterosonographic examination, and diagnostic hysteroscopy. Fertil Steril 2001;76:350–357. Goldstein RB, Bree RL, Benson CB, et al. Evaluation of the woman with postmenopausal bleeding: Society of Radiologists in Ultrasound-sponsored consensus conference statement. J Ultrasound Med 2001;10:1025–1036. Soares SR, Barbosa dos Ries MMB, Camargos AG. Diagnostic accuracy of sonohysterography, transvaginal sonography and hysterosalpingography in patients with uterine cavity diseases. Fertil Steril 2000;73:406–411. Tabor A, Watt HC, Wald NJ. Endometrial thickness as a test for endometrial cancer in women with postmenopausal bleeding. Obstet Gynecol 2002;99:663–670. Tur-Kaspa I, Gal M, Hartman M, et al. A prospective evaluation of uterine abnormalities by saline infusion sonohysterography in 1,009 women with infertility or abnormal uterine bleeding. Fertil Steril 2006;86:1731–1735.

Pelvic Mass Ekerhofd E, Wienerroith H, Staudach A, et al. Preoperative assessment of unilocular adnexal cysts by transvaginal ultrasonography: a comparison between ultrasonographic morphologic imaging and histopathologic diagnosis. Am J Obstet Gynecol 2001;184:48–54. Geomini PMAJ, Kluivers KB, Moret E, et al. Evaluation of adnexal masses with threedimensional ultrasonography. Obstet Gynecol 2006;108:1167–1175. Paley, PJ. Screening for the major malignancies affecting women: current guidelines. Am J Obstet Gynecol 2001;184:1021–1030.

Soper JT. Radiographic imaging in gynecologic oncology. Clin Obstet Gynecol 2001;44:485–494.

Pelvic Pain Eskenazi B, Warner M, Bonsignore L, et al. Validation study of nonsurgical diagnosis of endometriosis. Fertil Steril 2001;76:929–935. Lone FW, Balogun M, Khan KS. Adenomyosis: not such an elusive diagnosis any longer. J Obstet Gynaecol 2006;26(3):225–228. Molander P, Paavonen J, Sjoberg J, et al. Transvaginal sonography in the diagnosis of acute appendicitis. Ultrasound Obstet Gynecol 2002;20:496–501.

Ectopic Pregnancy Gamzu RI, Almog B, Levin Y, et al. The ultrasonographic appearance of tubal pregnancy in patients treated with methotrexate. Hum Reprod 2002;17:2585–2587. Rogers RG, Kammerer-Doak D, Miller M, et al. A comparison of ultrasound and surgical findings in suspected ectopic pregnancy. J Diagn Med Sonogr 2000;16:60–64.

Müllerian Anomalies Kupesic S. Clinical implications of sonographic detection of uterine anomalies for reproductive outcome. Ultrasound Obstet Gynecol 2001;18(4):387–400. Makris N, Kalmantis K, Skartados N, et al. Three-dimensional hysterosonography versus hysteroscopy for the detection of intracavitary uterine abnormalities. Int J Gynaecol Obstet 2007;97(1):6–9. Patton PE, Novy MJ, Lee DM, et al. The diagnosis and reproductive outcome after surgical treatment of the complete septate uterus, duplicated cervix and vaginal septum. Am J Obstet Gynecol 2004;190(6):1669–1678.

Infertility Balen AH, Laven JSE, Tan S-L, et al. Ultrasound assessment of the polycystic ovary: international consensus definitions. Hum Reprod Update 2003;9(6):505–514. Brown SE, Coddington CC, Schnorr J, et al. Evaluation of outpatient hysteroscopy, saline

infusion hysterosonography, and hysterosalpingography in infertile women: a prospective, randomized study. Fertil Steril 2000;74:1029–1034. Flisser E, Grifo JA. Is what we clearly see really so obvious? Ultrasonography and transcervical embryo transfer—a review. Fertil Steril 2007;87:1–5.

Hendriks DJ, Mol B-WJ, Bancsi LFHMM, et al. Antral follicle count in the prediction of poor ovarian response and pregnancy after in vitro fertilization: a meta-analysis and comparison with basal follicle-stimulating hormone level. Fertil Steril 2005;83:291–301. Järvelä IY, Sladkevicius P, Kelly S, et al. Evaluation of endometrial receptivity during invitro fertilization using three-dimensional power Doppler ultrasound. Ultrasound Obstet Gynecol 2005;26:765–769. Kosmas IP, Janssens R, De Munck L, et al. Ultrasound-guided embryo transfer does not offer any benefit in clinical outcome: a randomized controlled trial. Hum Reprod 2007;22(5):1327–1334. Kupesic S, Kurjak A. Predictors of IVF outcome by three-dimensional ultrasound. Hum Reprod 2002;17(4):950–955. Palomba S, Russo T, Falbo A, et al. Clinical use of the perifollicular vascularity assessment in IVF cycles: a pilot study. Hum Reprod 2006;21(4):1055–1061. Prefume F, Serafini G, Martinoli C, et al. The sonographic evaluation of tubal patency with stimulated acoustic emission imaging. Ultrasound Obstet Gynecol 2002;20:386–389. Rotterdam ESHRE/ASRM-sponsored PCOS Consensus Workshop Group. Revised 2003 consensus on diagnostic criteria and long-term health risks related to polycystic ovary syndrome. Hum Reprod 2004;19(1):41–47.

31 Pediatric and Adolescent Gynecology Ann J. Davis Pediatric and adolescent gynecology is frequently viewed as a single focused aspect of gynecology. In fact, these two areas are reasonably distinct, with a logical division being at the onset of puberty and the activation of the hypothalamic–pituitary–ovarian (HPO) axis. Prepubertal girls differ from postpubertal girls in anatomy, etiologies of similar symptoms, and the spectrum of likely and common syndromes. However, both groups require specific and different communication skills. Psychosocial and developmental milestones and characteristics help to guide the obstetrician and gynecologist in how to communicate with each age group in an effective manner. Involvement of the family or adult caretaker also is critical in achieving the goals of providing excellence in gynecologic care. This chapter will discuss topics in both of these age groups, with an emphasis on the differences in children and teens as compared with those of mature reproductive women.

Examination The Prepubertal Child The genital examination of the prepubertal child should be approached quite differently from the gynecologic examination of an adolescent or adult. However, the complete exam may include all of the same elements as the examination of the more mature reproductive female: examination of the external genitalia, examination of the vagina, and palpation of the uterus and adnexal structures.

External Genitalia It is often helpful to examine a toddler on her mother's lap while the mother elevates or abducts the child's hips for the so-called “frog-leg position.” It is important to place the child on a towel or chuck pad in case urination occurs. An older child can sit straddling her mother's lap fully clothed while the mother places the child's legs in the stirrups. Usually, children between the ages of 4 and 6, and sometimes as young as 3, can position themselves in classic lithotomy with use of the stirrups. Clinicians can use their hands to provide lateral and downward traction on the area of the labia majora (Fig. 31.1). This will allow full visualization of the hymen and vaginal orifice.

Care should be taken to inform the child of the necessary steps of the exam. Continuously conversing with the child during the exam will allow her to relax. Children should never be forced or held down in order to perform a genital exam.

Vagina Various positions have been described to visualize the vagina. In the very young infant or toddler, a Valsalva maneuver can be helpful in the exam; the child can be asked to pretend that she is blowing up a balloon or blowing out her birthday candles. This will often allow visualization of the distal 1 to 2 cm of the vagina. The knee–chest position is very helpful; children 3 years of age and older can typically cooperate and hold the knee–chest position. The child places her buttocks in the air with knees placed apart and allows her abdomen to sag. The examining physician and one assistant provide lateral and upward traction on the labia and buttocks. An otoscope can be used as a magnification instrument and light source to shine into the vagina, allowing visualization to the level of the cervix even without inserting the instrument. A vaginal speculum is neither appropriate nor indicated in the examination of the prepubertal child in the office (Fig. 31.2).

Figure 31.1 Diagram of the genital anatomy of a prepubertal girl. This drawing shows a crescent hymen. (From Pokorny SF. Pediatric and adolescent gynecology. New York: Chapman and Hall, 1996.)

Uterus and Adnexa Examination of the uterus and adnexa requires a rectal examination and should be reserved for the pediatric gynecology patient when information regarding the uterus or adnexa is necessary in the evaluation. Rectal bimanual examination should not be done routinely in every child requiring gynecologic examination.

In prepubertal children, the adnexa should not be palpable. In children, the ovaries lie at the level of the pelvic brim and drop into the pelvis with the onset of puberty. If an adnexa is palpable, there is, by definition, an adnexal enlargement that will require swift and careful evaluation of a possible ovarian neoplasm. In the normal prepubertal child, the uterus should be easily palpable on rectal examination. Prior to puberty, two thirds of the uterine volume is cervical in contrast to the one third proportion in adults. The cervix, therefore, is a relatively easy structure to palpate on rectal examination in prepubertal children.

Figure 31.2 The knee–chest position can be used to examine the vagina of a prepubertal child: the otoscope is used for a light source and magnification and is not inserted into the vagina.

The Newborn The obstetrician–gynecologist should be encouraged to observe the normal genitalia of the female infants that he or she delivers. Under the influence of maternal estrogens, the labia are generous in size, and the estrogenized hymen is prominent, turgid, and fimbriated or redundant in appearance. The female infant will sometimes experience an estrogenwithdrawal spotting episode within several days after birth. Parents should be informed of this normal phenomenon in an effort to preclude maternal anxiety and even unnecessary visits to the pediatric emergency department (ED). In a series of pediatric patients seen in the ED of Cleveland's Children's Hospital for vaginal bleeding, the vast majority of those under the age of 2 were seen for this reason. These ED visits are completely avoidable through parental education. Previously, before early obstetrical discharge, this estrogenwithdrawal spotting occurred in the hospital nursery. Observation of the genitalia of female infants at birth allows the detection of various developmental and congenital abnormalities, some of which may be life threatening. If ambiguous genitalia are observed, the obstetrician must use excellent communication skills in the delivery room to help set the stage for the evaluation of the infant and to assist in decreasing parental anxiety. The parents should be informed that the baby's genitals are not fully developed and a simple examination of the external genitalia cannot determine

the actual sex. The parents should be told that they definitely have either a girl or a boy; but because development is not complete, data will have to be collected before they are told what sex the baby is and what treatment is required. Guesses must be avoided. It is critical to wait until all the information allows that the initial sex assignment given to the parents is the final and correct assignment. The problem of ambiguous genitalia represents a social and potential medical emergency that is best handled by a team of specialists, which may include urologists, neonatologists, endocrinologists, and pediatric gynecologists. The differential diagnosis of ambiguous genitalia includes chromosomal abnormalities, enzyme deficiencies (such as 21-hydroxylase deficiency, which is a form of congenital adrenal hyperplasia [CAH]), and prenatal masculinization of a female fetus resulting from maternal androgen-secreting ovarian tumors or, rarely, drug exposures. The etiology of these problems as well as intersex disorders that may be discovered in an older child can be complex. The possibility of CAH is especially critical to exclude. With the salt-wasting form of this disease, death can occur in the neonatal period, so electrolytes should be obtained immediately. Often overlooked is one simple physical exam finding that rules out CAH; the presence of gonads in the labial scrotal folds in the infant with ambiguous genitalia eliminates the diagnosis. One additional benefit of an observation of the genitalia of female infants at the time of birth is that some genital anomalies such as an imperforate hymen, vaginal agenesis, or other hymeneal anomalies may be diagnosed. Hymeneal abnormalities occur in Table of Contents > 32 - Contraception

32 Contraception Lisa Memmel Melissa Gilliam Reproductive rights embrace certain human rights that are already recognized in national laws, international human rights documents, and other relevant consensus documents. These rights rest on the recognition of the basic right of all couples and individuals to decide freely and responsibly the number and spacing and timing of their children and to have the information and means to do so, and the right to attain the highest standard of sexual and reproductive health. —Beijing Platform for Action, 1995 All women have a basic human right to determine whether and when they will become pregnant. Sexually active women and men have a wide variety of contraceptive choices for implementing this right, ranging from temporary to permanent methods. Most women have the potential to become pregnant over at least 3 decades of their lives, and most men are fertile for virtually their entire adulthood. Thus, a series of different contraceptive decisions may be made over a person's reproductive life span. Since 2000, the range of contraceptive choices in the United States has increased with a wide range of new contraceptive methods, including a vaginal ring, a contraceptive patch, a progestinreleasing intrauterine device (IUD), an implantable contraceptive device, and a transcervical method of tubal occlusion. This chapter focuses on information with which the health professional can counsel women and men to make the contraceptive choices that best address their needs and circumstances.

Contraceptive Use in the United States and around the World Data from the U.S. National Survey of Family Growth indicate that in 2002, 61.9% of women between the ages of 15 and 44 used some method of contraception. Among women who used contraception, permanent methods were the most popular; 16.7% had undergone tubal sterilization, and 6.3% had partners who had undergone vasectomy. Oral contraceptives were the most popular temporary method, but the proportion of pill users decreased from

27% of contraceptive users in 1995 to 19% in 2002. In addition, the proportion of condom users decreased from 20.0% in 1995 to 11.1% in 2002. Only 3.3% and 1.0%, respectively, used the injectable depot medroxyprogesterone acetate (DMPA) and the IUD. Despite this level of reported contraceptive use, 49% of pregnancies concluding in 2002 were unintended, with 42% of those ending in elective abortion. Globally, according to the Demographic and Health Surveys, tubal sterilization is the most common method of contraception (in 1997, 20% of couples in which the woman was of reproductive age and who used a contraceptive method used tubal sterilization), followed by IUDs (15%), oral contraceptives (8%), and condoms (5%).

Choosing a Method of Contraception Although sterilization is the most widely used method of contraception in the United States and in much of the rest of the world, it is appropriate only for women and couples who have made a decision to permanently prevent pregnancy. Thus, many couples will choose reversible contraceptive methods. Factors that influence the appropriateness of any contraceptive choice include the relative safety and effectiveness of the method for that individual, the frequency and acceptability of side effects, the willingness and ability to use the method consistently and correctly, cost, and the importance of personal factors such as societal attitudes as well as religious or cultural beliefs regarding method acceptability. Other factors include the frequency of coitus, the length of time that intended pregnancy is to be delayed, the impact on lactation and the breast-fed infant, and any potential impact of the method on future fecundity. In addition, many women are at risk for sexually transmitted infections, including HIV infection, and must consider dual goals of protection against pregnancy and prevention of sexually transmitted infections. Doing both entails the correct and consistent use of condoms or use of another contraceptive method in conjunction with condoms. The need for such dual protection produces special challenges, as there is some evidence that the use of a highly effective method of contraception other than condoms may affect a person's willingness or ability to use condoms for disease prevention.

Contraceptive Effectiveness Contraceptive effectiveness is measured as reduction in the probability of conception with use of a contraceptive method over a defined period; it cannot be measured directly, largely because studies cannot determine the proportion of women in a given population who would have become pregnant during that time had they not been using contraception. By contrast, contraceptive failure rates can be directly determined and are the most clinically useful measures of effectiveness. Yet, it is important to note the limitations of the widely used Pearl Index method in which contraceptive failures occur per 100 womanyears of use, which limits the comparability of the new method being studied to an older regimen. Instead, the life-table method, which considers failures over time, may be preferable. Widely used estimates of contraceptive failure rates are shown in Table 32.1. These rates

are provided in two categories: “typical use” and “perfect use.” The former is similar to “use effectiveness” and is characteristic of a typical couple starting to use a method (some use the method properly and others do not); the latter is similar to “method effectiveness,” which is the result of consistent and correct use of the method. For some methods, the typical and perfect use rates are substantially different, which indicates that the user's willingness and ability to use these methods consistently and correctly are more important than they are for those methods that have similar typical and perfect use rates. For example, according to Trussell and colleagues (Table 32.1), although women who take a combined oral contraceptive (COC) pill each day should have a near-zero probability of pregnancy, 8% of couples in which the woman initiates use of oral contraceptives experience an unintended pregnancy during the first year if they do not discontinue pill use for any other reason. By contrast, the typical and perfect use failure rates are virtually the same for IUD users and for users of etonorgestrel implants. Published estimates of contraceptive failure rates apply to groups and may vary substantially among individuals within those groups, particularly among those who use methods with major differences in estimates between typical and perfect use. Most failure rates address the risk of pregnancy within 12 months of starting to use the method. The risk of pregnancy for some methods, particularly those that depend on proper use, is likely to decline over time.

Oral Contraception Combined Oral Contraceptives COCs, which contain both estrogen and a progestin, have been available in the United States since 1960, have been used by millions of women worldwide, and have been extensively studied. Formulations for oral contraceptives have changed over time from higher to lower doses of the synthetic components. Today, COCs prescribed in the United States contain between 20 and 35 mcg of ethinyl estradiol. The progestin component of COCs varies and may include a first-generation progestin (estranes) such as norethindrone, norethindrone acetate, ethynodiol diacetate, and norethynodrel; a second-generation progesti, (gonanes), including levonorgestrel and norgestrel; or a third-generation progestin such as desogestrel, norgestimate, and gestodene (gestodene is not available in the United States). A recently developed contraceptive uses drospirenone, a spironolactone derivative, as its progestin. Monophasic pills have constant doses of estrogen and progestin, whereas multiphasic pills vary the doses of estrogen, progestin, or both throughout the cycle. The primary mechanism of progestins is inhibition of ovulation by suppressing folliclestimulating hormone and luteinizing hormone. In addition, the pharmaceutical progestin thickens the cervical mucus, impeding the ascent of sperm into the upper genital tract, lowers embryo receptivity of the endometrium, and may also act by altering tubal transport. Although COCs are highly effective in preventing pregnancy when used consistently and correctly, 29% of COC users reported missing one or more pills or not starting on time in the last 3 months in the 1995 National Survey of Family Growth. COCs are substantially less effective when used inconsistently (i.e., as seen with many typical users) (Table 32.1).

Metabolic Effects The estrogen and progestin components of COCs induce some metabolic changes, but for most healthy women, the changes associated with the current low-dose COCs have little or no clinical significance. Estrogens generally alter lipid metabolism in a fashion that is considered beneficial, including slightly increasing levels of high-density lipoprotein (HDL) and decreasing lowdensity lipoprotein (LDL). Depending on their level of androgenicity, progestins can counteract these effects, decreasing HDL and increasing LDL. Therefore, the net effect depends on the doses of both estrogen and progestin as well as the type of progestin; however, most changes are within the normal range and not clinically relevant.

TABLE 32.1 Percentage of Women Experiencing an Unintended Pregnancy during the First Year of Typical Use and the First Year of Perfect Use of Contraception and the Percentage Continuing Use at the End of the First Year in the United States % of women experiencing an unintended pregnancy within the first year of use Typical usea

Perfect useb

% of Women continuing use at one yearc

No methodd

—

Spermicidese

Withdrawal

Periodic abstinence

—

Calendar

—

Method

Ovulation method

—

Symptothermalf

—

Postovulation

—

Capg

Parous women

Nulliparous women

Sponge

Parous women

Nulliparous women

Diaphragmg

Condomh

Female (Reality®)

Male

Combined pill and minipill

0.3

Evra® patch

0.3

NuvaRing®

0.3

Depo-Provera®

0.3

Lunelle®

0.05

Intrauterine devices (lUDs)

Progestasert® (progesterone T)

2.0

1.5

ParaGard® (copper T)

0.8

0.6

Mirena® (levonorgestrel 20)

0.1

Norplant® and Jadelle

0.05

Female sterilization

0.5

100

Male sterilization

0.15

0.10

100

Emergency contraceptive pills: Treatment initiated within 72 h after unprotected intercourse reduces the risk of pregnancy by at least 75%i. Lactational amenorrhea method: LAM is a highly effective, temporary method of contraceptionj aAmong typical couples who initiate use of a method (not

necessarily for the first time), the percentage who

experience an accidental pregnancy during the first year if they do not stop use for any other reason. bAmong couples who initiate use of method (not necessarily for the first time) and who use it perfectly (both consistently and correctly), the percentage who experience an accidental pregnancy during the first year if they do not stop use for any other reason. cAmong couples attempting to avoid pregnancy, the percentage who continue to use a method for 1 year. d The percentages becoming pregnant in columns two and three are based on data from populations where contraception is not used and from women who cease using contraception in order to become pregnant. Among such populations, about 89% become pregnant within 1 year. This estimate was lowered slightly (to 85%) to represent the percentage who would become pregnant within 1 year among women now relying on reversible methods of contraception if they abandoned contraception altogether. eFoams. creams, gels, vaginal suppositories, and vaginal film. fCervical mucous (ovulation) method supplemented by calendar in the pre-ovulatory and basal body temperature in the post-ovulatory phases. g With spermicidal cream or jelly. hWithout spermicides. iThe treatment schedule is one dose within 72 h after unprotected intercourse, and a second dose 12 h after the first dose. Plan B (1 dose is 1 white pill) and Preven (1 dose is 2 blue pills) are the only dedicated products specifically marketed in the United States for emergency contraception.The Food and Drug Administration has, in addition, declared the following 13 brands of oral contraceptives to be safe and effective for emergency contraception: Ovral or Ogestrel (1 dose is 2 white pills), Alesse or Levlite(1 dose is 5 pink pills), Aviane (1 dose is 5 orange pills). Nordette or Levlen (1 dose is 4 light-orange pills), Lo/Ovral, Levora or Low-Ogestrel (1 dose is 4 white pills), Triphasil orTri-Levlen (1 dose is 4 yellow pills), and Trivora (1 dose is 4 pink pills), jHowever, to maintain effective protection against pregnancy, another method of contraception must be used as soon as menstruation resumes, the frequency or duration of breastfeeds is reduced, bottle feeds are introduced, or the baby

reaches 6 months of age. Adapted from Trussell J. In Hatcher RA, Trussll J, Stewart F, et al, eds. Contraceptive technology, 18th ed. New York: Ardent Media, 2003.

Although some studies of older formulations of high-dose COCs reported progestinassociated elevated glucose and insulin levels and higher rates of relative peripheral insulin resistance, clinical studies of low-dose COCs have not found clinically significant effects on glucose metabolism. A large, cross-sectional study of U.S. women found no elevation in hemoglobin A1C, fasting glucose, insulin, and C-peptide levels among current COC users compared with those who never used COCs. Large, prospective studies have not found increased risks of diabetes mellitus among COC users with either high-dose or lowdose pills.

Cardiovascular Diseases Epidemiologic research confirms that the overall risk of serious cardiovascular complications attributable to COC use is extremely low for the vast majority of users of the current low-dose ethinyl estradiol preparations (≤35 mcg). However, individual user characteristics and the type of COC modify the risk. Cardiovascular complications associated with COC use occur while the pill is being used; once pills are discontinued, risk levels return to baseline.

Hypertension COC use may slightly increase blood pressure among normotensive women, but studies suggest that this increase is reversible when COC use is discontinued. Among women with mild hypertension, COC use also has been associated with increased blood pressure. In a cross-sectional study of 94 women with mild hypertension, COC users had significantly increased daytime and nighttime ambulatory systolic blood pressure values (mean 8.3 mm Hg increase for daytime and mean 6.1 mm Hg increase for nighttime). No significant differences in diastolic blood pressure values were found.

Venous Thromboembolism The incidence rate of venous thromboembolism (VTE) in healthy nonpregnant white women is estimated to be between 10 and 30 per 100,000 woman-years. When such women use COCs, the incidence increases to between 30 and 120 per 100,000 woman-years, or three to four times higher than non-COC users, depending on personal characteristics and the type of pill. By comparison, the risk of thrombosis associated with pregnancy is about 200 per 100,000 pregnant women. The case fatality rate of VTE is 1 to 2 per 100 and the risk of death from thromboembolism attributable to COC use is extremely low, at 1 to 5 per million per year of use. The most important risk factor for thromboembolism is family

history of the disease, which often is related to genetic thrombophilia. The most common genetic cause of thrombophilia is resistance to activated protein C (factor V Leiden mutation), which occurs in about 5% of whites but is rare in non-whites. The presence of the factor V Leiden mutation substantially increases the risk of COC-associated venous thrombosis; screening for the condition before starting pill use has been considered. However, cost–benefit considerations lead most authorities to recommend against screening before starting COCs unless women have a family history of thrombosis. The third-generation low-dose pills with the progestins desogestrel or gestodene have been associated with a nearly two-fold increased risk of thrombosis relative to secondgeneration or first-generation pills, which contain levonorgestrel or norethindrone. Although these elevated risks are noteworthy, they are nonetheless very low in absolute terms—an estimated excess of 4 deaths per 1 million woman-years of use.

Stroke and Myocardial Infarction Older age, smoking, diabetes, and hypertension are major risk factors for arterial diseases such as stroke and myocardial infarction. For women with these risk factors, COC use increases their already elevated baseline risk; thus, women with multiple major risk factors for cardiovascular disease generally should not use COCs. The annual incidence rates of hemorrhagic and ischemic stroke in healthy, nonsmoking women between 20 and 24 years of age are estimated to be 2.0 and 0.5 per 100,000, respectively. In women between 40 and 44 years of age, these annual rates are 5 and 1 per 100,000, respectively. Non-smoking women younger than 35 years with normal blood pressure who use COCs have no extra risk of hemorrhagic stroke and only a marginally increased risk of ischemic stroke. Among such women 35 years or older, the risk of hemorrhagic or ischemic stroke is increased 1.5- to 2-fold during use of COCs. Smoking and hypertension increase the COC-associated risk of hemorrhagic and ischemic stroke. Use of COCs by women with classic migraine further elevates their moderately increased risk of ischemic stroke. In healthy, non-smoking women of reproductive age with normal blood pressure, the risk of myocardial infarction is extremely low, and the use of COCs causes little if any increase in risk. On the other hand, women who smoke, have hypertension, or have hyperlipidemia elevate their baseline risk of myocardial substantially by COC use. Myocardial infarction is rare in women younger than 35 years, even if they have risk factors; for women 30 to 34 years old who use COCs and smoke, the risk is estimated to be 2 per 100,000 woman-years. By contrast, women 40 to 44 years old who use COCs and smoke have an estimated risk of 25 per 100,000 woman-years. Some studies suggest that women who take pills containing the progestins desogestrel or gestodene may have an even lower risk of myocardial infarction than that associated with the very low risk of pills containing levonorgestrel or norethindrone, but findings are inconsistent.

Malignant Neoplasia COCs clearly reduce the risk of some cancers and may increase the risk of some others.

Most data are based on COCs with higher doses of estrogens and progestins than in the currently available pills; studies suggest that lower-dose preparations are likely to have similar effects on cancer risk.

Breast Cancer A pooled analysis of 54 studies found a small increased risk of breast cancer (relative risk = 1.24) while COCs were being used or recently discontinued. The excess risk was among women with localized disease, and there was a corresponding decrease in metastatic disease. These findings argue that women who use COCs are: Simply more likely to have existing breast cancers diagnosed because they are more likely to have clinical exams or mammograms More likely to have late-stage promotion of tumors that subsequently are more likely to remain localized to the breast. The observation that the duration of COC use does not increase breast cancer risk argues for the former explanation. The excess risk of breast cancer disappears 10 years after cessation of pill use. Thus, women who use the pill from age 15 to age 35 years have the same breast cancer risk at age 50 as comparable women who never took COCs. Because the incidence of breast cancer is low at ages when COC use is most common, any effect would affect a relatively small number of women. For example, among women who stop using COCs at 25 years of age, the cumulative risk from ages 25 through 34 years is estimated to be 1 excess cancer diagnosed per 10,000 women. In women who stop COC use at age 40, when incidence rates are higher, an estimated 19 excess cancers will be diagnosed from ages 40 through 49 years. As noted, even these excess cancers may represent only an earlier detection of existing disease; at worst, they represent a small absolute excess occurrence of localized disease.

Cervical Cancer In the past, several studies suggested that COC use of 5 years or longer increased the risk of cervical cancer 1.3- to 1.8-fold, but the causality of this association was uncertain. Persistence of genital human papillomavirus (HPV), particularly HPV 16 and 18, cause cervical cancer, and oral contraceptive users may be more likely to have sexual intercourse and less likely to use a barrier method of contraception. Exposure to COCs does cause eversion of the columnar epithelial cells of the cervix exposing these metaplastic cells to sexually transmitted HPV virus. A meta-analysis has shown that the relative risk of cervical cancer with COC use is 1.1 after 5 years and 2.2 for women who have used COCs for 10 or more years. Available data suggest that the increased risk decreases over time after stopping pill use. Questions remain about whether the risk is related to pill use per se; to other characteristics of pill users, such as sexual behavior; or to other factors associated with pill use, such as cytologic screening. Regardless, where screening services are available, COC users should avail themselves of these services as advised for other women. COC users do not require special screening procedures or recommendations.

Ovarian Cancer Use of COCs reduces the risk of epithelial ovarian cancer, the most common type of cancer of the ovary. Risk reduction is positively correlated with the duration of use. Using COCs for 5 years or longer confers at least a 50% reduced risk that persists for up to 15 years after cessation of use.

Endometrial Cancer COC use reduces the risk of cancer of the endometrium. As with ovarian cancer, the risk reduction is related to duration of use. After 5 years of use, the risk of endometrial cancer is at least 50% lower than in women who never used COCs. Furthermore, the risk reduction persists for 15 to 20 years after stopping pill use.

Liver Tumors Long-term use of high-dose oral contraceptives has been associated with the development of benign liver tumors such as focal nodular hyperplasia and adenomas. Though benign, adenomas of the liver can lead to significant problems related to rupture of the liver capsule. In COC users who have an enlarged liver or tenderness to palpation on physical examination, the COC should be stopped and evaluation is warranted. Primary cancer of the liver is rare in populations where hepatitis B or C is not endemic. Some studies in the 1980s pointed to a substantially increased risk of primary liver cancer after long-term use of COCs. In populations where chronic hepatitis is common, pill use has not been associated with primary liver cancer. Liver cancer is rare and usually fatal within 1 year of diagnosis; thus, the fact that there has been no increase in liver cancer deaths in the United States in the 4 decades that COCs have been in widespread use argues against any substantial risk.

Other Cancers Some studies have found a lower incidence of colon cancer among women who have used COCs, but it is unclear whether the association is causal. Previous speculation of an increased risk of tumors of the pituitary and the skin in users of COCs have not been confirmed.

Medical Eligibility Criteria for Combined Oral Contraceptive Use Most women can safely use COCs. There are, however, some conditions under which COCs should not be used. These conditions include the following: Age >35 years and smoking >15 cigarettes per day Multiple risk factors for arterial cardiovascular disease (e.g., older age, smoking, diabetes, hypertension)

Elevated blood pressure of 160 mm Hg systolic or 100 mm Hg diastolic hypertension with vascular disease Current or history of deep vein thrombosis or pulmonary embolism Major surgery with prolonged immobilization Current or history of ischemic heart disease Stroke Complicated valvular heart disease Migraine with focal neurologic symptoms (migraine with aura) Migraine without focal neurologic symptoms and age >35 years Current breast cancer Diabetes with nephropathy, retinopathy, neuropathy, vascular disease, or diabetes of >20 years duration Severe cirrhosis Liver tumors. In addition, there are several other conditions in which women generally should not use COCs (Table 32.2).

Noncontraceptive Benefits of Combined Oral Contraceptive Use In addition to protecting against pregnancy, including ectopic pregnancy, and the noted protection against endometrial and ovarian cancers, COC use provides other health benefits including preventing and treating menstrual abnormalities (bleeding problems and pelvic pain), reduced risk of symptomatic pelvic inflammatory disease (PID) (although there is no protection against lower genital tract infections and HIV infection), reduced risk of benign breast cysts, reduced risk of iron deficiency anemia, and treatment of acne. While low-dose contraceptives have not been shown to affect the size of preexisting leiomyomata or lead to new ones, they can be effective in controlling menstrual bleeding due to leiomyomata. The protection against ovarian cysts, seen with higher dose COCs, is reduced in low-dose monophasic COCs and may not be present for triphasic COCs.

Return to Fertility after Discontinuing Combined Oral Contraceptives Women who discontinue COCs have no overall reduction in fertility. There may be a very short delay in time to conception compared with women not using COCs based on the time required to begin ovulating. This delay is temporary, and by 3 to 12 months after discontinuation, there are no differences in fertility rates.

Side Effects Nausea and breakthrough bleeding are the most common side effects of COC use, although they often diminish or disappear after the first few months of use. Breakthrough bleeding may relate to the specific pill formulation, but it also may be caused by missed pills. If breakthrough bleeding lasts beyond the first 3 months of use, is a problem for the woman, and other gynecologic causes have been ruled out, it may be beneficial to switch to a different COC formulation, typically containing a higher ethinyl estradiol dose. Other approaches to managing breakthrough bleeding include adding concurrent oral estrogen (1.25 mg conjugated equine estrogen or its equivalent, daily for 1 week at the time the breakthrough bleeding occurs), doubling up on active pills for 2 or 3 days until the breakthrough bleeding stops, doubling up on active pills through the end of the cycle, or using active pills in a continuous regimen. Nonsteroidal anti-inflammatory drugs (NSAIDs) may also help alleviate breakthrough bleeding. Other common side effects associated with COCs are breast tenderness and headaches. Weight changes are reported frequently, but most recent studies suggest that little, if any, weight gain can be attributed to COC use.

Choices for Pill Initiation Standard regimens for pill initiation include the following: Sunday Start: In this commonly used regimen, the woman is counseled to begin the active pills on the first Sunday after her menses begins. If her menses begins on a Sunday, she should start her pills that day. The advantage to this approach is that the woman will likely not be on her menses over the weekend. Alternatively, disadvantages include not being able to get prescriptions filled on weekends. Thursday Start: With the newly approved 24-day active pill/4-day placebo regimens, a Thursday start will accomplish the same goal of no menses on the weekend. First-day Start: This approach has the woman start her active pills on the first day of her menses, as long as she has a normal cycle and has no concern of being pregnant. Quick Start: With the quick-start method, the patient begins taking the pills on the first day of her office visit, as long as she is not pregnant. She should be counseled to use a back-up method for the first 7 days and be informed that her menses will be delayed until she completes the active pills in the pack. This method does not lead to increased spotting or bleeding. In addition, this method helps women to start and continue the pill as they avoid complex counseling regarding pill initiation. In one study, 25% of women counseled for Sunday or menstrual start did not initiate their COCs as prescribed for reasons such as an interim pregnancy, failing to fill the prescription, or misunderstanding instructions.

TABLE 32.2 World Health Organization Medical eligibility Crite

Contraceptive Use

WHO Categories for Temporary Methods WHO 1 Can use the method. No restriction on use. WHO 2 Can use the method. Advantages generally outweig theoretical or proven risks. Category 2 conditions could be cons in choosing a method. If the client chooses the method, more usual follow-up may be needed. WHO 3 Should not use the method unless a doctor or nurse ma clinical judgment that the client can safely use it. Theoretica proven risks usually outweigh the advantages of the method. M of last choice, for which careful follow-up will be needed WHO 4 Should not use the method. Condition represents a unacceptable health risk if method is used. Condition Pregnant

Combined Progestin- DMPA/NET Norplan OCs only OCs EN implants NA

Less than 18( Table of Contents > 33 - Induced Abortion

33 Induced Abortion Sabrina Holmquist Melissa Gilliam Recent estimates find that approximately 1.29 million abortions were performed in the United States in 2003, a 2% decrease from 1.31 million in 2000. Each year in the United States, 2% of women of reproductive age (15 to 44 years) terminate a pregnancy legally. Given the current rate, it is estimated that over one third of women in the United States will have had an abortion by age 45. The abortion rate in 2000 was about 21.3 per 1,000 women. This rate has decreased from 27.4 abortions per 1,000 women in 1990 (Fig. 33.1). While nearly all women in the United States have used some form of contraceptive at some point in their lives and contraceptive use has increased considerably since the legalization of abortion, about half of the 6 million pregnancies occurring each year are reportedly unplanned. Roughly half of these unplanned pregnancies, one in five pregnancies overall, are terminated by induced abortion. Women who opt for abortion tend to be never married, in their 20s, live below the federal poverty level, and are mothers of at least one child. Over half of women who have had an abortion used some form of contraception during the month that they became pregnant. Since legalization in 1973, abortion in the United States has become very safe (Fig. 33.2). Yet, worldwide, 19 of the 46 million abortions performed annually are done so illegally. Illegal abortion remains very unsafe and account for some 68,000 deaths globally each year.

Legalization The landmark 1973 Supreme Court decision in Roe v. Wade effectively legalized abortion in the United States. Since that time, federal and state legislators have proposed or enacted hundreds of pieces of legislation aimed at restricting access to abortion or challenging the Court's Roe decision, making induced abortion the most actively litigated and highly publicized area in medicine. As early as 1976, the Hyde Amendment prohibited the use of federal Medicaid funding for abortions. In 1992, the Supreme Court's decision in Planned Parenthood v. Casey reaffirmed a woman's right to an abortion “before viability” but at the same time opened the door for states to impose additional restrictions that would not impose an “undue burden” on the woman. Antiabortion legislation seeks to chip away at access to abortion through a variety of means. The federal so-called “partial-birth abortion” ban of 2003 attempted to abolish

certain late-second-trimester abortion procedures, but due to its vague language, it could have further reaching effects; at the time of this writing, a Supreme Court case challenging the ban awaits a decision. A number of states have mandated parental notification or consent before a minor is able to obtain an abortion. In some states, women seeking abortions must undergo a waiting period of at least 24 hours or receive state-sanctioned counseling beforehand; in some cases, this counseling contains ideologically charged or scientifically disputed information that is meant to discourage women from ultimately choosing abortion. A handful of states, most notably South Dakota in 2006, have attempted to pass bans on almost all abortions with the express purpose of challenging Roe.

Abortion Counseling Pregnancy options counseling is an essential element of abortion provision, whether in a dedicated abortion clinic, a private office, or an inpatient setting. This type of counseling has three primary goals: helping the patient make an informed decision about her pregnancy, increasing the patient's knowledge and comfort with the abortion procedure, and alleviating anxiety and pain during the procedure while providing emotional support for her decision. Pregnancy options counseling can be performed by nursing staff, physicians, or dedicated counselors but is most effective when performed by an experienced options counselor with knowledge of local laws governing consent procedures and state-mandated counseling requirements.

Figure 33.1 Number of abortions per 1,000 women ages 15 to 44, by year. (From Guttmacher Institute. Facts on Induced Abortion in the United States. New York: Guttmacher, 2006. Available at: http://guttmacher.org/pubs/fb_induced_abortion.html. Accessed August 29, 2007.)

Preprocedure counseling has two primary components: pregnancy options counseling and decision making and preprocedure counseling and informed consent for women who choose to have an abortion. The initial part of the counseling session should center on exploring

feelings about the pregnancy, including when and under what circumstances the patient became pregnant, how she feels about that pregnancy, and what options she has considered regarding its outcome. Women choose to have an abortion for a variety of reasons (Fig. 33.3) and have a wide variety of emotional responses to unplanned pregnancy, ranging from acceptance to ambivalence to anger, shame, and fear. Maintaining an open, nonjudgmental atmosphere is essential in allowing women to explore their feelings regarding their pregnancy and options that are open to them. The full range of pregnancy options should be discussed, including parenting, adoption, and abortion. Women should be encouraged to consider how each of these options would impact her life personally, financially, and emotionally as well as how they mesh with her values and those of her partner and family, if applicable. Any misconceptions regarding pregnancy options should be corrected, and the provider should assure that she is not being coerced into a decision.

Figure 33.2 The number of deaths from abortion has declined dramatically since Roe v. Wade. (From Alan Guttmacher Institute, Trends in Abortion in the United States, 1973–2002. New York: Author, 2005.)

For women who choose abortion as their best option, the next step is helping them select an appropriate procedure. Before 9 weeks gestation, women can choose a medication or surgical abortion. Medication abortion is a process by which a pregnancy is terminated by use of medication without surgical intervention. It generally requires two visits, and patients must be willing to administer medication at home and be prepared for cramping, bleeding, and passage of tissue outside of a medical setting. For women without contraindications to medication abortion (allergy to mifepristone or misoprostol, bleeding dyscrasias, severe anemia) who are able to come for one follow-up visit, medication abortion provides a nonsurgical alternative to traditional dilation and curettage (D&C). For women who choose a surgical procedure, there are two options for first-trimester abortion: manual vacuum aspiration (MVA) and suction D&C. The characteristics of each of these modalities are listed in Table 33.1. Acceptability studies reveal that patients are highly satisfied with any of these procedures as long as they are able to make their own choice. The specifics of each procedure are covered in subsequent sections of this chapter as well

as informed consent for each. Women presenting after the first trimester also have the option of undergoing a medication or surgical procedure; these procedures are discussed in subsequent sections.

Figure 33.3 Most important reasons given for terminating an unwanted pregnancy. (From Guttmacher Institute, An Overview of Abortion in the United States. New York, Author, 2006.)

Preprocedure Assessment Prior to providing an abortion procedure, whether medication or surgical, each patient requires a preoperative assessment. Obstetric, medical, and surgical history should be recorded, emphasizing sexually transmitted disease history, contraception, menstrual history, the outcomes of previous pregnancies, previous uterine or cervical surgery, and any medication allergies. Previous anesthetic complications, bleeding problems, or transfusions also should be noted. Special attention should be paid to any conditions that may affect minor surgical procedures, including asthma, current medications, alcohol or drug abuse, chronic steroid use, HIV disease, coagulopathies, heart disease, or seizure disorders. Vital signs as well as a brief heart, lung, abdominal and thorough pelvic exam should be performed, including ascertainment of uterine size and position and abnormal or mucopurulent cervicovaginal discharge. Screening for cervical gonorrhea and chlamydial organisms prior to performing an abortion procedure can be employed universally, in atrisk patients only (based on clinical history and risk factors), or not at all depending on the practice setting. Because untreated chlamydial infection at the time of a transcervical procedure is associated with a 19% rate of postoperative salpingitis, prophylactic periabortal antibiotics should be administered to all patients regardless of preprocedure cervical screening. While Pap testing can be done for women who are due for their annual screening, it is not a necessary part of abortion care.

TABLE 33.1 Characteristics of Medication and Surgical Abortion in the First Trimester Medication Abortion

Dilation and Curettage

May be used up to 9 weeks gestation

May be used up to 14 weeks gestation

High success rate (95% – 99%)

High success rate (99%)

Requires at least two visits

May be done in a single visit

Avoids instrumentation of the uterus

Requires instrumentation of the uterus

Abortion occurs within 24 hours in most cases

Procedure takes 5–10 min

Some of the process will occur at home

Procedure is done in a clinic/medical office

Oral pain medications can be used

Oral or intravenous sedating medications can be used

Patient will have to administer some medications at home

Procedure performed by a health care provider

Medications will induce cramping and bleeding, with passage of tissue akin to a miscarriage

Minimal pain or bleeding following the procedure in most cases

Accurate estimation of gestational age is key to both procedure selection and ascertainment of surgical risk; incorrect estimation of gestational age is an important cause of abortion complications. In the absence of a certain last menstrual period and

clinical correlation of uterine size by an experienced provider, ultrasound examination is a highly accurate way of confirming and dating an intrauterine pregnancy as well as a means for ruling out an ectopic or anembryonic gestation. In the absence of an intrauterine gestation, comprehensive pelvic ultrasound and serum human chorionic gonadotropin (hCG) testing should be employed to locate the pregnancy prior to attempted termination either by medication or surgical means. If the patient is too early in gestation to detect a gestational sac, the procedure should be delayed until a sac is visible. Absolute hCG levels at which an intrauterine gestation should be visible vary depending on ultrasound resolution and the skill of the sonographer; however, a hCG discriminatory threshold of 1,500 mIU/mL typically is accompanied by a gestational sac detectable by transvaginal ultrasound. Laboratory tests should include Rh(D) typing, with administration of Rh immune globulin to Rh-negative patients immediately after their procedure as well as hemoglobin/hematocrit to assess for anemia. Most generally healthy women can safely obtain abortion procedures in the outpatient setting. Patients with severe medical or psychiatric conditions requiring intraoperative monitoring as well as those with pregnancy complications requiring pre- or postoperative monitoring or administration of intravenous antibiotics are best served in the inpatient operative setting. Induction termination procedures generally are performed in a hospital setting.

Surgical Abortion in the First Trimester Surgical abortion in the first trimester can be performed between approximately 5 and 13 completed weeks gestation (depending on when an intrauterine sac is visible). Considered the gold standard for pregnancy termination, a first-trimester surgical procedure is very effective (99.0% efficacy rate), very safe (major complication rate of 0.5%), and very common—89.0% of abortions provided in the United States occur before 13 completed weeks gestation; more than half occur before 8 weeks (Fig. 33.4). The D&C procedure includes both dilation of the cervix, which can be achieved chemically, mechanically, or a combination of the two, and emptying of the uterine contents, which is most commonly achieved by suction curettage either by using a traditional electric suction aspirator or via MVA.

Figure 33.4 Abortions in the United States by gestational age. (From Strauss et al. MMWR, 2004).

Anesthesia for first-trimester procedures typically is achieved by using deep paracervical infiltration with lidocaine—6 cc at the 4 o'clock and 8 o'clock positions, respectively, in tandem with oral analgesics such as ibuprofen (400 to 800 mg) and an oral anxiolytic, usually a benzodiazepine such as lorazepam 1 to 2 mg. A support person to calm and help focus the patient during the procedure is another vital component to providing comfortable procedures under local anesthesia. Approximately 58% of women receive only local anesthesia for early surgical abortion. Many providers also offer the option of light to moderate intravenous sedation, typically employing a short-acting anxiolytic such as midazolam and a short-acting narcotic such as fentanyl. Preoperative nonsteroidal antiinflammatory drugs (NSAIDs) are often employed as well. Satisfaction surveys reveal that patients are highly satisfied with either anesthesia option as long as they are given a choice. Providers who wish to offer conscious sedation must have appropriate perioperative monitoring equipment available, including pulse oximetry, a continuous supply of oxygen, reversing medications, and resuscitation equipment, as well as adequate staff to provide postoperative monitoring.

Cervical Dilation Cervical dilation is one of the most important aspects of abortion care, as it confers safety to the procedure. Inadequate or forced dilation is the primary cause of surgical complications in the first trimester. Dilation can be achieved chemically with the use of cervical ripening agents such as misoprostol or mechanically by using rigid cervical dilators. A mixed approach is employed most often, particularly after 10 weeks gestation. Mechanical dilation is accomplished with progressive use of graduated cervical dilators to serially enlarge the cervical canal; tapered dilators such as the Pratt (Fig. 33.5) or Denniston (Fig. 33.6) are easiest to pass through the internal cervical os. After administration of local anesthetic, the provider should don sterile gloves; grasp the anterior lip of the cervix with a single-tooth tenaculum, ring forceps or similar stabilizing

instrument; and gently and progressively dilate the cervix to a diameter roughly equal to the gestational age in weeks (i.e., an 8-week pregnancy should be dilated to 8 mm, or 23 to 25 French. To decrease the risk of infection, particularly in a nonsterile environment, a “no-touch” technique is employed by which no part of an instrument that enters the uterine cavity is touched by the provider during the dilation process. This includes both mechanical dilator tips and the suction cannula. Use of a uterine sound to measure uterine size prior to dilation is discouraged, as uterine size can be estimated in other ways and the uterine sound is the most common instrument responsible for uterine perforation.

Figure 33.5 Pratt dilators. (From MedGyn website. Available at: http://www.medgyn.com/picprattdilator.htm.)

Figure 33.6 Denniston dilators. (From Ipas website. Available at: http://www.ipas.org/products/Ipas_Denniston_Dilators.aspx.)

Mechanical dilation should never be forced. If a dilator does not pass easily, allow the dilator that is one size smaller to remain in the cervix for a few minutes before advancing the next. Forcing mechanical dilation can lead to cervical fracture, uterine perforation, or creation of a false passage within the cervix. Ultrasound guidance can be employed in patients with a tortuous cervical canal or other anatomic abnormality. For nulliparous patients or those with cervical stenosis or higher gestational ages, preoperative misoprostol can be used from 20 minutes to 24 hours prior to the procedure. Patients can be given a low (200 to 400 mcg) dose orally the night before the procedure; alternately, 400 to 800 mcg of misoprostol can be administered vaginally 40- to 90-minutes preprocedure or 400 mcg buccally or sublingually 20 to 40 minutes prior. Some providers use premedication with misoprostol with all patients regardless of gestational age to aid with speed and comfort of dilation. Many patients at 8–9 weeks, many providers prefer electric suction aspiration, which has the advantage of providing continuous suction without reloading of the collection chamber and more commonly employs rigid suction cannulas (Fig. 33.8). Larger tubing and cannulas that are up to 16 mm in diameter also can be employed. Rigid suction cannulas may be straight or curved; a curved cannula will conform more anatomically with the position of the uterus and consequently may be easier to pass to the fundus. The technique for electric suction aspiration is identical to MVA; signs of complete uterine evacuation include bubbles in the suction tubing and the characteristic gritty texture of the empty uterine cavity.

Figure 33.7 MVA Plus mechanical vacuum aspirator. (From Ipas website: Available at: http://www.ipas.org/products/Ipas_MVA_Plus_Aspirator.aspx?ht)

Figure 33.8 Rigid suction cannula.

Meticulous examination of the uterine aspirate is essential in confirming complete uterine emptying. The uterine aspirate can be washed with water or saline and examined with backlighting though a clear receptacle (such as a glass pie plate and a light box) (Fig. 33.9). Identification of the gestational sac in early pregnancy is essential in preventing an incomplete or failed procedure. At later gestational ages, all fetal parts should be identified. If there is any question regarding completeness of the procedure, transvaginal ultrasound can be performed to confirm and document complete uterine emptying (Fig. 33.10). Pathologic examination of tissue is indicated for suspected abnormal pregnancies (i.e., hydatidiform mole), and cytogenetic examination can be employed in the cases of miscarriage or known or suspected genetic abnormality. Otherwise, pathologic confirmation is not mandatory, provided all products of conception are examined and villi identified. Blood loss should be minimal, at 15 to 30 cc. Aftercare should include perioperative antibiotic prophylaxis as detailed previously, NSAIDs for analgesia, and commencement of a contraceptive method before resuming sexual activity. Placement of an intrauterine device (IUD) immediately after first-trimester surgical termination is safe and convenient and has not been associated with an increased rate of expulsion. Cervical cultures should be obtained in all patients who are planning to receive a postabortal IUD.

Figure 33.9 Transillumination of villi floating in saline allows visualization for placental tissue confirmation after pregnancy termination.

Figure 33.10 A: Longitudinal view of the uterine cavity within minutes after a surgical abortion showing the endometrial stripe and constricted endocervical canal. B: Transvaginal ultrasound image taken in a longitudinal view of an 11-week gestation 1 hour after uterine evacuation shows evidence of procedure completion, but the endometrial stripe is less prominent due to the natural accumulation of blood within the endometrial cavity. C: Two weeks after suction curettage, transvaginal endometrium shows 16 mm of endometrial tissue, likely to be decidua and a few chorionic villi consistent with the normal involution process, and warrants observation if clinically stable.

Second-trimester Abortion Approximately 12% of abortions performed in the United States occur after 12 completed weeks gestation. More than 95% of these are performed surgically by D&E. More secondtrimester abortion procedures are performed in the United States than in any other country worldwide, which likely is due to the higher abortion numbers in the United States overall, better record keeping, and the relative delay in accessing services in the United States in comparison to countries with socialized medicine where abortion care is widely available and provided under national health care policies (Table 33.2). Abortion after the first trimester is a riskier procedure than earlier procedures; while the major complication rate is still 80 µU/mL) or glucose-stimulated (>300 to 500 µU/mL) levels, although exact diagnostic criteria are lacking, in part due to the heterogeneity of the syndrome. Patients can be severely hyperandrogenemic, with testosterone levels reminiscent of patients with androgen-secreting neoplasms, resulting in the development of severe hirsutism and even virilization. In addition to significant hirsutism, patients also develop the characteristic dermatologic finding of acanthosis nigricans (Fig. 39.7). Because of their high androgen levels, gonadotropin levels in these patients may be somewhat suppressed, resulting in persistent endometrial atrophy and amenorrhea despite the administration of a cyclic progestogen or an oral contraceptive. Because of the mitogenic effect of insulin on ovarian theca cells, the ovaries of many patients with HAIR-AN syndrome will become hyperthecotic. On ultrasound and histology, the ovaries morphologically have a paucity of cortical cysts and demonstrate a thickened and enlarged theca/stroma compartment. In addition, these patients are at significant risk for dyslipidemia, type 2 DM, hypertension, and CVD. These patients can be particularly difficult to treat, although the selected use of long-acting GnRH analogs has been promising. Some patients may necessitate surgery, either ovarian wedge resection or oophorectomy. Concomitant insulin sensitizer use may lower both androgen and insulin levels.

Nonclassic Adrenal Hyperplasia NCAH, also referred to as late-onset congenital adrenal hyperplasia, is a homozygous recessive disorder due to mutations in the CYP21 gene, resulting in an abnormal (or absent) cytochrome P450c21 with relatively deficient 21-OH activity. Overall, between 1% and 8% of women with androgen excess have 21-OH deficient NCAH depending on ethnicity, with the highest rates reported in Ashkenazi Jewish populations. Due to the lack of 21-

hydroxylation, the progestogenic precursors to cortisol, 17α-hydroxyprogesterone (17-HP), and to a certain degree 17-hydroxypregnenolone accumulate in excess. These steroids are then metabolized to C19 products, principally androstenedione and testosterone (Figs. 39.1, 39.2). However, clinically and biochemically, these patients are very difficult to distinguish from other hyperandrogenic patients, particularly patients with PCOS. Patients with NCAH may present only with persistent acne or may have moderate degrees of hirsutism and oligoamenorrhea, although frank virilization or even severe hirsutism is relatively rare. The levels of the exclusive adrenal androgen metabolite DHEAS are not any higher than those of other hyperandrogenic women. Although the frequency is relatively low, all patients with unexplained androgen excess should be screened for NCAH due to CYP21 mutations, as this diagnosis has a different prognosis, a different treatment regimen, and requires genetic counseling regarding the risks of congenital transmission. The measurement of a basal 17-HP in the follicular phase and in the morning can be used to screen for this disorder, with a level of 10 ng/mL, the diagnosis of 21-OH–deficient NCAH is established. As noted previously, hirsute women claiming to have regular menstrual cycles should be evaluated for ovulatory dysfunction, most simply by obtaining a serum progesterone in the luteal phase (days 20 to 24) of the menstrual cycle. If the patient has ovulatory dysfunction, as evidenced by either a luteal phase progesterone level 30% normal forms

No significant sperm agglutination

No significant pyospermia

No hyperviscosity

Although normal ovulation usually is assumed in women with regular menses and premenstrual moliminal symptoms, ovulation should be objectively confirmed. Only a single documented ovulation is required; there is no demonstrated value and significant frustration associated with months of repeat ovulation testing. There are three methods to evaluate ovulation. The classic method is a basal body temperature (BBT) chart. This method has a low cost, is fairly reliable, and documents the timing of ovulation. The daily BBT is obtained throughout the menstrual cycle, and the temperature should be taken first thing in the morning at the same time each day. Most women will have a temperature drop at the time ovulation, followed by a sustained temperature elevation of at least 0.4°F that coincides with the luteal phase of the menstrual cycle. It is important for the provider to evaluate this chart with the couple, as it often is difficult for them to interpret. A simpler but more costly method is the luteinizing hormone (LH) or ovulation predictor kit. Unlike the BBT chart, this method identifies the time of ovulation by identifying the LH surge 24 to 36 hours prior to release of the oocyte. This may be of value to patients whose lifestyles limit midcycle coitus. Finally, a midluteal (days 18 to 24) serum progesterone of >3 ng/mL indicates that ovulation has occurred. Although the timing of ovulation and the length of the follicular and luteal phases are not identified, this simple test unequivocally documents ovulation. Serial ultrasounds, cervical mucus examination, and endometrial biopsy also can suggest or confirm ovulation, although these tests are less frequently used because of reliability, discomfort, and cost. For women over the age of 30, testing for decreased ovarian reserve should be added to the assessment of ovulation. The effect of advancing maternal age on fertility will be fully discussed later in the chapter, but there is no doubt that fertility begins to decrease in the mid-30s. Although the method of testing may change as our understanding of the menopausal transition increases, the classic test is a day 3 follicle-stimulating hormone (FSH) level. A normal value for a day 3 FSH varies between laboratories, with current assays identifying decreased ovarian function with a level >10 to 15 IU/L. Although pregnancy can occur with elevated day 3 FSH levels, the chance of pregnancy is markedly reduced. Alternatively, a normal day 3 FSH should not falsely reassure women of the success of infertility treatment. This test primarily measures the number of oocytes remaining (i.e., ovarian reserve), not oocyte quality. The chance of pregnancy in the late 30s and 40s is reduced, compared with younger women, even with a normal day 3 FSH level. Other forms of ovarian reserve testing such as the clomiphene citrate challenge test and antral follicle counts are used by some infertility specialists. The clomiphene challenge test involves measuring a day 3 FSH and estradiol level, followed by 100 mg per day of clomiphene citrate on cycle days 5 to 9 and a day 10 FSH. The clomiphene challenge test

may be a better predictor of decreased ovarian reserve for older women and those with unexplained infertility. An antral follicle count utilizes a high-resolution transvaginal ultrasound on day 3 of the menstrual cycle to count the number of follicles measuring between 2 and 10 mm in diameter. A count of 70 years, MI within the preceding 12 months, and evidence of congestive heart failure on physical examination significantly increase postoperative cardiac complications in patients undergoing gastrointestinal, urologic, and gynecologic surgery.

Concurrently, the pelvic surgeon should attempt to determine the patient's “functional capacity.” The simple inability to walk three blocks or climb two flights of stairs portends a poor functional status and increased operative risk. Physical examination evaluating the patient's overall status is mandatory. This evaluation, coupled with pertinent laboratory and radiologic information and an electrocardiogram (ECG), provides a baseline estimate as to actual perioperative cardiac risk. Numerous schema from Goldman and others intended to quantify cardiac risks have been designed, reported, and verified in an attempt to quantitate perioperative cardiac risk. The American College of Cardiology–American Heart Association (ACC-AHA) published revised practice guidelines based on qualitative analysis. The guidelines define clinical risk stratification for noncardiac surgical procedures. Noncardiac procedures with high (>5%), intermediate (1% to 5%), and low (5%) Emergent major operations, particularly in the elderly Aortic and other major vascular Peripheral vascular Anticipated prolonged surgical procedures associated with large fluid shifts or blood loss or both Intermediate (Reported Cardiac Risk Generally 70% stenosis, easily induced myocardial ischemia on preoperative stress testing, and left ventricular systolic dysfunction at rest.

TABLE 45.5 Cardiac Conditions Associated with Endocarditis Endocarditis Prophylaxis Recommended High-risk category Prosthetic cardiac valves, including bioprosthetic and homograft valves Previous bacterial endocarditis Complex cyanotic congenital heart disease (e.g., singleventricle states, transposition of the great arteries, tetralogy of Fallot) Surgically constructed systemic pulmonary shunts or conduits Moderate-risk category Most other genital cardiac malformations (other than those listed above and below) Acquired valve dysfunction (e.g., rheumatic heart disease) Hypertrophic cardiomyopathy Mitral valve prolapse with valvular regurgitation, thickened leaflets, or both Endocarditis Prophylaxis Not Recommended Negligible-risk category (risk no greater than that of the general population) Isolated secundum atrial septum defect Surgical repair of atrial septal defect, ventricular septal defect, or patent ductus arteriosus (without residual beyond 6 months) Previous coronary artery bypass graft surgery Mitral valve prolapse without valve regurgitation Physiologic, functional, or innocent heart murmurs Previous Kawasaki syndrome without valve dysfunction Previous rheumatic fever without valve dysfunction Cardiac pacemakers (intravascular and epicardial) and

implanted defibrillators Dajani AS, Taubert KA, Wilson W, et al. Prevention of bacterial endocarditis: recommendations by the American Heart Association. JAMA 1997;277:1795, with permission.

Cardiac Disease–Specific Approach Coronary Artery Disease CAD commonly occurs at a lower incidence in females than in males; however, diabetic women are risk equivalent to men. The mortality of an acute MI is greater for women and increases dramatically in the aged patient. Importantly, MIs occurring during the perioperative period carry a higher mortality risk than those occurring otherwise. Many surgical patients have diagnosed CAD or risk factors for CAD. Women who are potential candidates for attempts at preoperative myocardial revascularization may benefit from noninvasive cardiac testing performed to determine the amount of myocardium in jeopardy, the patient's ischemic threshold, and the objective determination of ventricular function. Test results should be used to assist in stratifying prognostic information and determining the extent and benefit of perioperative surgical or medical intervention and postoperative monitoring.

Hypertension As the training and practice of obstetricians–gynecologists increasingly stresses the importance of primary care, the preoperative evaluation and the management of hypertension have become a major focus on the gynecologic patient's problem list. Although the identification of early-stage hypertension should lead to the institution of appropriate medical therapy, the ACC-AHA guidelines suggest that those with stage II or milder hypertension (systolic blood pressure below 180 mm Hg and diastolic blood pressure below 110 mm Hg) are not at increased risk for perioperative cardiovascular complications. Surgical delay for medical treatment of women with stage I or II hypertension is not necessary or beneficial. However, elevated blood pressure in patients with stage III hypertension (systolic blood pressure 180 mm Hg or higher and a diastolic blood pressure 110 mm Hg or higher) should be controlled prior to surgery. The administration of βadrenergic blockers in this clinical situation results in rapid, effective control of severe blood pressure elevation. β-adrenergic blockade also prevents perioperative hypo- or hypertension, either of which is associated with an increased risk of coronary ischemia. Regardless of actual measured systemic pressures, the ACC-AHA guidelines suggest that the blood pressure of patients with significant hypertension who require urgent surgery be controlled. The goal is to avoid the ischemic complications associated with perioperative blood pressure fluctuations that commonly occur in the surgical patient who has uncontrolled hypertension.

Heart Failure Ventricular failure is an important predictor of and prognostic factor for perioperative cardiac morbidity. The initial attempt to identify women with ventricular dysfunction begins with a detailed history and organ-specific physical examination. Determination of ventricular status is mandatory in those with evidence or history of congestive heart failure, because the physiology of perioperative ventricular failure portends an ominous situation. Perioperative subspecialty consultation, pharmacologic manipulation to maximize cardiac oxygen supply–demand ratio, careful administration of intravenous fluids, and cardiac monitoring may benefit these patients. During preoperative investigation, gynecologic surgeons should not exclude the possibility of rare causes of cardiomyopathy, including hypertrophic obstructive cardiomyopathy, because their appropriate medical management decreases morbidity. Echocardiography, to obtain an estimate of ventricular function and to rule out anatomic abnormalities, should be considered and may be necessary for the perioperative assessment for those women with suspected, known, or history of heart failure or cardiomyopathy.

Valvular Heart Disease Although interpretation of the physical findings can be challenging, the gynecologic surgeon should attempt to identify significant heart murmurs. Echocardiography aids in defining the anatomic abnormality and in detailing the need and benefit of antibiotic endocarditis prophylaxis (Table 45.4). Failure to diagnose any significant valvular dysfunction or to administer appropriate antimicrobial prophylaxis increases the risk of a catastrophic perioperative consequence. Aortic stenosis poses the greatest valvular risk for poor postoperative cardiac outcome. Cardiac morbidity in women with untreated aortic stenosis undergoing noncardiac surgery approaches 10%, sufficient to persuade every pelvic surgeon to diagnose this condition. ACC-AHA practice guidelines advise postponement of elective surgery in women with severe or symptomatic aortic stenosis until valve replacement (the accepted standard intervention) can be performed. In emergent situations, aortic valvuloplasty may be employed but has less certain success. In general, surgical correction of mitral stenosis is not indicated prior to noncardiac surgery unless the severity would warrant treatment in a nonsurgical setting. If deemed necessary, balloon valvuloplasty is an appropriate corrective option for those with severe mitral stenosis. Mild to moderate mitral stenosis requires control of perioperative heart rate to reduce the risk of heart failure. Significant aortic regurgitation requires attention to intravascular volume control and attempts at medical afterload reduction. In contrast to mitral stenosis, bradycardia should be avoided or aggressively treated to avoid left ventricular backfill. Mitral regurgitation most commonly is associated with papillary muscle dysfunction and

mitral valve prolapse. Prior to surgical procedures, antimicrobial prophylaxis may be indicated for those with mitral valve prolapse and demonstrable clinical evidence of regurgitation or echocardiographic evidence of anatomic mitral valve leaflet abnormalities. Women with significant mitral regurgitation murmurs require careful monitoring of the left ventricular ejection fraction, because the low-resistance regurgitant valve predisposes perioperative patients to retrograde cardiac flow, resulting in pulmonary edema and high pulmonary artery pressures. Invasive perioperative cardiac monitoring may be necessary, as echocardiography tends to overestimate ejection fraction in patients with mitral regurgitation. Patients with prosthetic mitral valves receiving systemic anticoagulants require intervention to lessen the risk of endocarditis and intracardiac coagulation. For patients at low, intermediate, and high risk of thromboembolism, the Seventh Consensus Conference on anticoagulation suggests that warfarin therapy should be stopped approximately 4 days before surgery, allowing the international normalized ratio (INR) to return to near-normal values. More specific recommendations based on an individual patient's category of risk were also outlined by the conference and are as follows:

1. For patients with a low risk of thromboembolism who are undergoing an intervention that increases the risk of thrombosis, postoperative prophylaxis should be used consisting of low-dose unfractionated heparin (UFH) or a prophylactic dose of low-molecular-weight heparin (LMWH). Warfarin therapy should be restarted simultaneously. Alternatively, a low dose of UFH or a prophylactic dose of LMWH also can be used preoperatively.

2. Patients with an intermediate risk of thromboembolism should be covered preoperatively with a low dose of UFH or a prophylactic dose of LMWH while the INR is returning to normal. Postoperatively, therapy should be commenced with low-dose UFH or LMWH and concurrent warfarin therapy.

3. For patients with a high risk of thromboembolism, therapy with full-dose UFH or full-dose LMWH should be instituted approximately 2 days preoperatively. UFH can be administered as a subcutaneous injection as an outpatient or as a continuous intravenous infusion after hospital admission in preparation for surgery and can be discontinued approximately 5 hours before surgery with the expectation that the anticoagulant effect will have worn off at the time of surgery. Alternatively, subcutaneous UFH or LMWH can be used preoperatively, discontinuing therapy 12 to 24 hours before surgery with the expectation that the anticoagulant effect will be very low or have worn off at the time of surgery. In these patients, therapy with low-dose UFH or LMWH should be commenced postoperatively.

Arrhythmias Every gynecologic surgeon will encounter perioperative cardiac arrhythmias. The majority are considered benign, but their underlying etiology should be sought aggressively because undiagnosed cardiac ischemia may initially become clinically evident as a perioperative arrhythmia. Perioperative arrhythmias may worsen existing ischemia by increasing myocardial demand or decreasing cardiac efficiency. Pulmonary disease, metabolic

derangements, or drug toxicities are common causes. Monitoring and treatment is important, because an unstable arrhythmia such as atrial fibrillation occasionally may deteriorate into a life-threatening rhythm (i.e., ventricular fibrillation). In addition to conferring a therapeutic cardiac morbidity risk reduction in patients with CAD, β-blockers may reduce arrhythmia-related perioperative morbidity and mortality. Premature ventricular contractions occurring at a rate of fewer than 6 per minute are presumably “benign.” Even short and spontaneously converting runs of ventricular tachycardia may not predispose patients to perioperative death from MI. However, underlying coronary ischemia may be unmasked by the occurrence of these rhythms, making it imperative that the underlying etiology of a perioperative arrhythmia be ascertained, even if these are not treated by antiarrhythmic agents other than β-blockade. Atrioventricular (AV) block, especially Mobitz type II or third-degree heart block, may increase operative risk. Patients with type I second-degree AV block, first-degree AV block, and left and right bundle branch blocks are usually asymptomatic, and their arrhythmias rarely contribute to postoperative morbidity and mortality. It is reasonable to consider early subspecialty consultation to diagnose and treat women who develop perioperative cardiac arrhythmias. Patients with known or previously treated or untreated congenital heart disease or pulmonary vascular disease deserve close evaluation. Individuals with previous surgical correction of a ventricular septal defect, patent ductus arteriosis, or tetralogy of Fallot may be at increased operative cardiac risk, possibly due to decreased pulmonary vasculature reactivity to hypoxia.

Risk Stratification According to Type of Surgery Although individually weighted, existing patient risk factors, the type and extent of operation, and the operative circumstances are important to delineate the risk of perioperative cardiac morbidity. Intuitively, the decision to operate and the choice of operation or operative approach should be made in an attempt to offer the most effective treatment while minimizing patient cardiac risk. Other medical conditions should be addressed to lessen any indirect impact on perioperative cardiac outcome. Every surgical intervention should be based on acute or chronic patient-specific factors. Although emergent surgical indications lessen available evaluation time, urgency does not absolve the responsibility to search diligently for significant risk factors. The young woman in shock with a ruptured ectopic pregnancy may provide the physician with only a brief opportunity for cardiac evaluation; however, cardiac risk factors are uncommon in this population, minimizing the necessity for or benefit of an extensive evaluation. The elderly patient with acute intestinal obstruction and strangulated bowel related to ovarian carcinoma may harbor significant cardiac risk factors but may require lifesaving surgery despite significant coronary risk and a high potential for morbidity. Perhaps more problematic is evaluation of those patients who require diagnostic or therapeutic surgery for pelvic malignant neoplasms and who are discovered to have

cardiac disease during the presurgical evaluation. The clinical situation surrounding this or semiurgent gynecologic procedures may preclude the benefit of extensive intervention (i.e., coronary artery bypass grafting [CABG]). In this situation, consultation and maximal medical therapy can improve the patient's perioperative cardiac condition and lessen risks. Perioperative evaluation of women undergoing elective pelvic surgery should consider the risk of an adverse cardiac event in relation to the extent of the necessary surgical procedure. The benefit of medical management of the gynecologic condition should always be considered carefully. A minimally invasive or a vaginal surgical approach carries less physiologic stress and less risk of associated cardiac morbidity when compared with more extensive intervention (e.g., an abdominal approach). Although it requires planning and technical flexibility, matching the patient's gynecologic and medical conditions to a proper surgical approach should be every surgeon's goal.

Risk Assessment and Treatment The ultimate objective of preoperative cardiac risk assessment is to rule out serious CAD that requires cardiac intervention separate from the need for noncardiac surgery. Preoperative evaluation should be designed to recognize existing disease, expose occult underlying heart disease, and provide an opportunity for appropriate cardiac assessment.

Noninvasive Testing ACC-AHA recommendations for those undergoing noncardiac surgery provide a short-cut to the appropriate application of noninvasive cardiac testing, which is indicated by two of three listed risk factors (Table 45.6). This testing schema assumes that the identification of a high-risk patient will identify those who would benefit from preoperative coronary revascularization or maximization of medical therapy. Either would contribute to improving the patient's long-term quantity and quality of life. Noninvasive studies include the 12-lead ECG, echocardiography, contrast ventriculography, radionuclide angiography, exercise stress testing, nonexercise stress testing, myocardial perfusion imaging, and dobutamine stress echocardiography. The ACC-AHA evaluation guidelines algorithm can be applied to all patients.

TABLE 45.6 Shortcut to Noninvasive Testing in Preoperative Patients If Any Two Factors Are Present 1. Intermediate clinical predictors are present (Canadian class 1 or 2 angina, prior MI based on history or pathologic Q waves, compensated or prior heart failure, or diabetes) 2. Poor functional capacity (70 y

Study

Wightman,

Obesity

Unselected

BrooksBrunn

1.3

Thoracic or abdominal

Garibaldi et al., Moulton et al., Dales et al.

19–36

17–27

0.8–1.7

COPD

Unselected

Wightman, Pedersen et al., Tarhan et al.

6–26

2–8

2.7–3.6

Thoracic or abdominal

Kroenke et al.

4.7

ASA, American Society of Anesthesiologists; COPD, chronic obstructive pulmonary disease. From Smetana GW. Preoperative pulmonary evaluation. N Engl J Med 1999;340:937–944, with permission. A patient who is unable to exercise is at increased risk for PPC following abdominal surgery. The inability to climb a flight of stairs or blow out a match at 6 inches (equals a forced expiratory volume [FEV] 80% of predicted value, may minimize pulmonary risk in these patients. A short course of oral steroids may assist in achieving this preoperative goal. Even though history and physical examination may detect those at risk for PPC, no spirometric or other test detects those patients whose abdominal surgery should be canceled. Most patients can undergo surgery, even if at high risk.

Although the optimal reduction regimen is unknown, the realization that postoperative pneumonia is extremely morbid and occasionally lethal in even a healthy patient demands adequate attention to perioperative pulmonary management.

Procedure-Related Pulmonary Risk Factors Limitation of surgery to the lower abdomen greatly reduces the extent of pulmonary dysfunction and the risk of developing PPC. Upper abdominal incisions increase this risk by as much as 40% in general surgery patients. A laparoscopic approach significantly reduces the risk of PPC by as much as 33%. The type of anesthesia, anesthetic pharmaceutical agent, and length of surgery play important roles in patient risk. Although reports have shown mixed results, spinal conduction anesthesia (spinal or epidural anesthesia) offers pain relief, improves pulmonary mechanics, and may significantly reduce the chance of PPC when compared with general endotracheal anesthesia.

Preoperative Evaluation Using findings from the history and physical examination, one can select the majority of patients who are at risk for developing PPC. It has been suggested previously that preoperative pulmonary function testing should be used in patients who have significant pulmonary risk factors or in those undergoing high-risk surgical procedures, particularly if requiring abdominal or thoracic incisions. Preoperative spirometry neither identifies highrisk patients who would escape clinical detection or those patients whose risk of proceeding to surgery is prohibitive. Pulmonary function testing (PFT) should not be used to deny surgery if the reason for the surgery is compelling. Although not considered a standard part of routine preoperative evaluation, preoperative PFT may be indicated in specific patient subsets. PFT can be helpful in cases when the history and physical examination does not explain a patient's exercise intolerance or dyspnea. PFT may also be useful if it is unclear whether a patient with severe asthma or COPD is at her best baseline function. Some have recommended that perioperative PaCO2 monitoring can assist in the management of those who are chronic CO2 retainers. Although hypercarbia is a significant risk for PPC, no validated published studies suggest a CO2 threshold that prohibits surgery. Baseline CO2 determination may be useful for postoperative ventilator management.

Risk-Reduction Strategies The inability to quantify pulmonary risk highlights the importance for the gynecologist to develop clinical acumen in an effort to reduce pulmonary complications. Several riskreduction strategies have been proposed (Table 45.9). Attention to maneuvers that enhance postsurgical lung expansion combined with adequate pain control to reduce splinting and subsequent atelectasis are the vital components of good postoperative

pulmonary care. Preoperative education engages the patient in her care, increases her willingness and active participation, and assists in overcoming a major psychologic obstacle to postoperative pulmonary health. The potential benefits of incentive spirometry, chest physiotherapy, and inhalational nebulizer treatments should be explained and understood preoperatively.

TABLE 45.9 Postoperative Pulmonary Complication Riskreduction Strategies Preoperative Encourage cessation of cigarette smoking for at least 8 weeks prior to surgery. Treat airflow obstruction in patients with chronic obstructive pulmonary disease or asthma. Administer antibiotics and delay surgery if respiratory infection is present. Begin patient education regarding lung expansion maneuvers. Intraoperative Limit duration of surgery to 0.3 mg/dL per day) should raise suspicion for a unilateral ureteral injury. Although overt oliguric renal failure rapidly becomes clinically obvious, lesser degrees of renal insufficiency may occur silently. Although all patients are at risk, the geriatric patient is at particular risk of perioperative renal insufficiency secondary to an age-related decrease in glomerular filtration rate; a decrease in urinary concentrating ability; and narrowed limits for sodium, potassium, and acid excretion. This population should be monitored carefully to maintain euvolemia and minimize the electrolyte load found in many medications. Research has detailed the predominant biochemical and physiologic changes occurring in the patient with acute renal failure. Recognizing the important effects of medullary hypoxia, tubular cell injury, and alterations associated with diuretics and electrolytes assists in understanding the mechanisms of disease; however, the clinical usefulness of this new information has yet to make a significant impact on daily practice. Thus, the classic approach of evaluating intrinsic renal, prerenal, or postrenal etiologies of perioperative renal failure remains useful. Prerenal azotemia results from any condition that prevents adequate blood flow to the renal unit. Hypovolemia, renal artery atherosclerotic disease, and pharmacologic etiologies (e.g., a combination of angiotensinconverting enzymes [ACE] inhibitors and diuretics) interfere with normal renal perfusion. Hypovolemia may occur as a result of intrinsic cardiac failure; general anesthesia; excessive blood loss; pre-, intra-, or postoperative volume contraction; or physiologic vasodilation (e.g., as in septic shock). Most postoperative causes of prerenal azotemia are reversible with the correction of intravascular volume deficits, minimizing the effect of left ventricular dysfunction or the reversal of anesthesia. Postrenal failure, which can be related to outflow tract obstruction at any level of the renal collecting system, carries significant importance following pelvic surgery. Functional obstruction due to a neurogenic bladder or the inability to void spontaneously may be related to existing deficits or postsurgical changes. Urethral catheterization typically reverses this problem. Postobstructive oliguria related to causes proximal to the bladder

requires significant ureteral obstruction. Although this situation can occur with bilateral renal calculi, bilateral or unilateral obstruction can occur after prolapse surgery and is most frequently encountered with advanced carcinoma of the cervix or in idiopathic retroperitoneal fibrosis. Renal ultrasonography is an easily obtained and low-risk diagnostic study. Acute management of most causes of postrenal failure involve appropriate diversion of the urinary units, either by transvesical ureteral stenting or percutaneous nephrostomy, to preserve existing renal function. Lastly, intrinsic renal dysfunction may be due to acute tubular necrosis, interstitial nephritis, and acute glomerulonephritis. Intrinsic renal failure most often is due to renal parenchymal ischemia or the effects of nephrotoxic agents, including aminoglycoside antibiotics, vancomycin, amphotericin B, and cisplatin. Radiocontrast agents and heme pigments are two agents commonly associated with acute tubular necrosis. The former may have intrinsic parenchymal effects and create a diuresis that aggravates existing volume deficits. Interstitial nephritis associated with an allergic drug reaction, autoimmune diseases, infiltrative diseases, and infectious agents represents another form of intrinsic renal failure. When present, withdrawal of the offending agent usually results in reversal; however, glucocorticoid administration may hasten recovery. Finally, acute glomerular nephritis, rare in the gynecologic patient, may also be responsible for intrinsic renal failure and should be entertained in the differential diagnosis of postoperative renal insufficiency, particularly in the absence of other causes.

Diagnosis, Morbidity, and Mortality The initial diagnostic evaluation of women with perioperative renal insufficiency requires a systematic method of investigation. Intraoperative suspicion and assessment with cystoscopy (or cystotomy) and methylene blue or indigo carmine dye injection is an important initial step. Postoperative hypovolemia may be obvious. However, volume status determination may be difficult when based on history, physical examination, and quantitation of perioperative input and output data. The urinalysis in those with prerenal azotemia shows a high osmolality (>500 mOsm/kg), a fractional sodium excretion of 20to-1 ratio) is strongly indicative of prerenal azotemia. Renal azotemia often is associated with minimal proteinuria; however, urine osmolality will be 1%. The surgeon's degree of suspicion based on operative findings and events is an important aspect of assessment to exclude postrenal azotemia, particularly when the procedure required a difficult pelvic dissection, repair of prolapsed pelvic organs, or treatment of a malignancy. Renal ultrasonography can quickly determine the extent of unilateral or bilateral hydronephrosis and eliminate the possibility of clinically significant ureteral ligation or kinking. If an ultrasonograph is not diagnostic, an IVP may answer important questions, although the administration of contrast may worsen the clinical condition of a patient with intrinsic renal insufficiency. Nonoliguric and oliguric renal insufficiency can occur in the postoperative patient, and physicians should not assume that “adequate” urine production indicates intact renal function. Importantly, oliguric renal failure portends a worse prognosis than nonoliguric

renal failure. Using low-dose dopamine to increase renal perfusion (and convert an oliguric problem to a nonoliguric situation) has no proven efficacy and thus should not be utilized, as it creates a propensity for cardiac arrhythmias and alters blood supply to other vital organs. The morbidity and mortality of renal failure in the postoperative patient is five times higher than that of individuals treated medically. These adverse outcomes are probably related to many factors, from perioperative ischemic insults to the volume depletion and other changes associated with contrast used for preoperative testing (i.e., IVP, CT) or mechanical bowel preparation. Common predisposing comorbid illnesses, including diabetes mellitus, hypertension, and cardiopulmonary insufficiency, carry their own inherent risks for causing renal insufficiency. Medications such as ACE inhibitors and nonsteroidal anti-inflammatory drugs, used frequently in the perioperative patient, also increase risk. Methods to promote perioperative renal protection include practicing good surgical technique, limiting the use of nephrotoxic agents, maximizing cardiopulmonary function by paying attention to intraoperative blood and volume losses, and replacing intravascular losses. Although invasive monitoring to guide fluid replacement may be helpful, its use and the administration of pharmacologic agents (dopamine, mannitol, furosemide) or other interventions has not been conclusively proven beneficial. Women with chronic renal insufficiency are at risk for acute renal insufficiency during the perioperative period. Preoperative internal medicine or nephrology consultation should be considered in an attempt to optimize volume, use dialysis strategically, and manage coexisting morbidities.

Management Dialysis is the cornerstone of perioperative management of renal insufficiency once postrenal obstructions are relieved. Specialists should be consulted to treat acidemia, recalcitrant hyperkalemia, symptomatic volume overload, or impending cardiovascular failure. All medication dosages and schedules should be reviewed regularly to maximize efficacy and minimize toxicity. In conclusion, although perioperative renal failure represents a significant danger to the operative patient, insufficient scientific data exist to identify patients at risk and to develop guidelines for postoperative renal surveillance and management. The surgical community awaits a more specific definition of renal failure; additional research regarding renal protection strategies; and better, less invasive treatments for patients with perioperative renal insufficiency.

Wounds and Incisions Once surgery has been deemed appropriate therapy, selecting the operative approach is possibly the most important initial surgical decision. Choice of approach is related primarily to physician bias and comfort, which is related to previous teaching and

experience. However, surgical indications, disease process, previous abdominal incision (and resultant adhesions), patient preference, and existing medical comorbidity should be considered carefully prior to solving this sometimes complex problem. Adequate intraoperative exposure must be a primary consideration. Although a vertical lower midline incision should be the first consideration, some, particularly those with a large body mass index, may be best managed with an upper abdominal incision, avoiding trauma to the infection-prone panniculus. A panniculectomy may be necessary or appropriate. It is evident that many, if not most, gynecologic (even oncologic) and obstetric procedures can be completed safely through a more cosmetic transverse lower abdominal approach. The transverse approach may offer the additional advantage of less pain and diminished postoperative pulmonary dysfunction. Although the Pfannenstiel incision, when combined with a table-stabilized self-retaining retractor, will often suffice, preoperative consideration of a Maylard (rectus muscle splitting) incision or intraoperative conversion to a Cherney (rectus splitting–incision at pubic insertion) may be necessary. To avoid increased risk of hernias, care should be taken to avoid placing the incision perpendicular to a previous incision. Placing the long axis of the incision in the direction of maximal skin tension creates the most aesthetically pleasing scar. A more contemporary approach to numerous gynecologic procedures involves laparoscopy. Many, if not most, routine procedures and a significant proportion of complex procedures used for the management of benign or malignant disease can be safely completed laparoscopically, with less physiologic stress, less pain, and a more rapid return to normal activity. Although there are many correct answers to surgical incision placement, performing an incomplete procedure because of a compromised incision is an unacceptable alternative and should be avoided by immediate conversion to a more accommodating approach (e.g., hand-assisted laparoscopy or an open operation). Operative laparoscopy and abdominal approach are associated with additional inherent surgical risks, so they should not replace vaginal surgery. Although laparoscopy may be complementary to “convert” abdominal procedures and to complete (extensive) operations, stand-alone vaginal surgery should remain an important arm of the obstetrician–gynecologist's surgical repertoire because it results in less morbidity. Vaginal surgery will suffice for many, if not most, gynecologic procedures. Although lesser invasive (laparoscopic or vaginal) surgical approaches are associated with diminished physiologic stress, their use does not negate the need for appropriate preoperative evaluation, preparation, and management.

Wound Preparation Although many rituals of preoperative skin preparation exist, only a few add documented value to patient care. Preoperative hair removal is not deemed necessary; however, if performed, clipper removal at a time close to surgery avoids microinjury and is associated with a lower risk of wound infection than is razor preparation. Routine preoperative skin antisepsis is necessary to minimize the infectious potential of normal flora as well as of pathogens. Bacterial concentrations in moist body areas (i.e., perineum) reach 106/cm2 of tissue and are greater than those in drier (abdomen) areas,

reaching 103/cm2 of tissue. These areas also harbor different ratios of aerobic to anaerobic bacteria. Preparation solutions differ significantly in the immediate or late (>3 hours) mean bacterial reduction. Manufacturer recommendations should be used to guide the length of time that the solution remains on the skin prior to the incision (i.e. ≥5 minutes for provodine iodine; ≥2 minutes for chlorhexidine).

Surgical Technique Creating an abdominal incision with a single bold knife stroke through the skin and subcutaneous tissue avoids a stair-step effect in the subcutaneous tissues. The use of multiple knife blades to create the incision offers little benefit and contributes to expense. Avoiding the creation of subcutaneous dead space is important, as dead space increases the risk of wound infection and poor wound outcome, even when closed. The use of electrical or laser coagulation techniques to create an incision saves little time and adds little value. Their use creates “devitalized” tissue, which may contribute to an adverse wound environment and increase the risk of surgical site infection, resulting in poor wound outcomes. Surgical technique may be of specific impact in those already at high risk because of thick (≥3.0 cm) subcutaneous tissues. The rationale for proper suture selection rests on the need for tensile strength, the duration of retained tensile strength, and the biologic effects on the involved tissue (Table 45.10). In general, the suture's chemical composition is more important than the physical configuration, although braided and multifilament sutures may potentiate infection. When compared with other absorbable materials, polyglycolic acid suture is associated with less inflammation and decreased pain, and in animal models, it lessens the risk of infection. The incorporation of permanent suture material creates an increased risk (approximately 10%) of chronic wound problems (i.e., pain, wound sinus); however, their use is associated with a lessened risk of developing a fascial hernia. Vascular pedicle ligation can be accomplished safely by using short-term absorbable sutures because the risk of bleeding is minimal 96 hours after ligation. Prior evidence suggested that there is little clinical benefit to be gained from peritoneal closure; however, newer studies regarding the closure of the peritoneum at the time of cesarean section suggests that there may be a benefit to closure with respect to decreased formation of significant intra-abdominal adhesions.

TABLE 45.10 Suture Material

Type

Tensile Knot Tissue Strength Security React

Nonabsorbable Natural Silk

Cotton

Linen

Steel

—

Polyamide (nylon)

Polyester (Dacron)

Polyolefin (Prolene)

Polybutester (Novafil)

—

Polytetrafluororoethlene (PTFE)

—

Catgut

Chromic

Polyglycolic acid

Polydioxanone sulfate (PDS)

Polygluconate (Maxon)

Glycolide caprolactine (Monocryl)

Manufactured

Absorbable

Polygalactin 910 (Rapid)

Glycolide/Dioxanone/Trimetheline carbonate (Brosyn)

4 = most, 1 = least. Suture size selection should be based on specific needs. Excluding fascial closure, there is little rationale for using suture larger than 2–0. Additional wound suture material increases the inflammatory response and may predispose to infection, and the tensile strength of a 2– 0 absorbable suture is adequate for nearly all pedicle ligations. Although it seems basic, correct suture-tying techniques can contribute to surgical outcome. Complex knots (e.g., surgeon's) impart greater tensile strength than multiple simple square knots. Avoiding excess knots minimizes the amount of suture material, lessens inflammatory response, and potentially decreases the risk of poor wound outcome. Although all knots should be secure, tightly tied fascial sutures strangulate the incorporated tissues, increase ischemia, and lessen wound strength. Although good surgical technique always has been tied to attempts to prevent adhesion formation, the development of hyaluronic acid products for adhesion prevention has opened new avenues. The astute surgeon recognizes the different tissue-related healing curves and selects a suture designed to promote good outcome. Although short-term wound results are important, the risk of late problems (e.g., hernia) can be minimized with appropriate closure technique. A suture length–to–wound length ratio of >4 decreases the risk of hernia formation and can be accomplished by placing sutures at least 1.5 cm from the fascial edge and 1.5 cm apart. Subcutaneous tissue closure is typically only recommended in patients in whom the subcutaneous tissue depth is >2 cm. If closure is required, small minimally reactive sutures should be chosen. Closed suction and subcutaneous drain placement are of little apparent benefit, and drains increase the risk of surgical site infection. The best method or material for epithelial approximation should be related to the potential time, cost, need for return visits, and cosmetic results.

Gastrointestinal Care Perioperative management of the gastrointestinal tract during pelvic surgery focuses on the following three aspects: (a) avoidance of operative injury and reduction of subsequent complications, (b) the role of early feeding, and (c) the appropriate diagnosis and management of patients with liver disease. Excluding the need to address important aspects of coexisting intestinal diseases (e.g., inflammatory bowel disease) and issues related to cancer screening, gastrointestinal

preparation values the decisions related to the incorporation of bowel preparation. Mechanical intestinal preparation offers a number of potential benefits (Table 45.11) and currently is a common practice before abdominal surgery in both gynecologic and general surgical procedures. Despite this trend, at present, no evidence exists to recommend its routine use in the prevention of perioperative infection or bowel injury. Suboptimal preparation may actually increase the risk of contamination, yet most pelvic surgeons are inclined to use a mechanical bowel preparation when the risk of manipulation or injury is substantial. If a preoperative bowel preparation is thought to be necessary, several regimens are available and choice of regimen should be tailored to the individual patient. Care should be taken when prescribing preparations with high electrolyte concentrations to patients with a history of or risk factors for renal insufficiency.

Early Oral Feeding and Nasogastric Suction Nasogastric suction often has been incorporated into the postoperative care of women who are undergoing difficult pelvic operations. Reports not only question its use but deny its benefit as it relates to symptomatic relief, lessened risk of ileus, need for reinsertion, and protection of intestinal anastomosis. Regardless of procedure, fewer than 10% of patients require nasogastric suction, and it appears to be of little benefit to the other 90%. Importantly, early oral feeding is well tolerated, does not increase the risk of ileus or symptoms, and may shorten hospital stay.

TABLE 45.11 Mechanical Bowel Preparation Potential Benefits Removes fecal material. Lowers bacterial load. Improves handling. Reduces spillage, contamination. Lessens risk of mechanical disruption. Facilitates intraoperative palpation. Allows intraoperative colonoscopy. Aids laparoscopic handling

Liver Disease The preoperative detection of liver disease may not be easy, because serum liver enzymes may not be elevated in patients with late-stage disease. However, the historical and physical findings of significant alcohol intake or exposure to hepatotoxins should raise suspicion. Physical evidence of malnutrition, signs of hepatic encephalopathy, or jaundice usually signify advanced disease. Laboratory evidence of hepatic dysfunction includes a 10fold increase in serum transaminase levels, abnormal coagulation study results, elevated

total bilirubin values, and low serum albumin levels. Classic surgical risk indices have been based on the Child classification, initially detailed in the 1960s to determine risks associated with surgical management of those with esophageal varices. These indices have been applied to the risks in those with liver disease who are undergoing abdominal surgery. Perioperative management of women with hepatic disease requires particular attention to drugs (and to their dosing and scheduling) that are metabolized by the liver. For example, patients receiving benzodiazepines and narcotics are at risk for drug accumulation and overdosage due to poor hepatic clearance. Patients with acute liver disease should not undergo elective surgery until stabilization of liver dysfunction has been secured. Those with chronic liver disease and hepatic encephalopathy may require subspecialty consultation in an attempt to stabilize liver function.

Infection Perioperative surgical site infection occurs in the practice of every gynecologic surgeon. Knowledge of prophylactic measures and the optimal treatment regimen for those with active or acquired infection are expected of every pelvic surgeon. Numerous factors including obesity, diabetes, use of steroids, excessive blood loss, and even length of preoperative hospitalization are all risk factors for infectious perioperative morbidity (Table 45.12). Although addressing each of them is beyond the scope of this chapter, numerous technical methods can modulate these risks. Proper use of prophylactic antibiotics lessens infectious risks in many pelvic procedures. Numerous antibiotics and regimens are efficacious. In most situations, a properly administered single dose is as effective as most multiple-dose regimens. However, in longer procedures (i.e., ≥3 hours) when the duration of the procedure is longer than the half-life of the chosen drug or if blood loss exceeds 1,500 mL, repeat dosing improves its benefit. The use of antibiotics prophylactically can result in patient hypersensitivity and the development of resistant strains of bacteria. Although careful thought is never to be discouraged, the potential benefit of controlling operative site infection with antibiotic prophylaxis usually outweighs other patient risks. A firstgeneration cephalosporin has been recommended for perioperative prophylaxis, recognizing the lack of enterococcus coverage. Patients allergic to penicillin have an 8% risk of cross reactivity with cephalosporins, but anaphylaxis risk is estimated at 0.0001% to 0.1% in non–penicillin-allergic patients to 0.02% in penicillin-allergic patients. Doxycycline or metronidazole represents an excellent alternative in patients undergoing abdominal or vaginal hysterectomy. Although the benefit of antibiotic prophylaxis has not been definitively demonstrated in patients undergoing laparoscopy-assisted hysterectomy, it would seem prudent to use these drugs, as recent American College of Obstetricians and Gynecologists (ACOG) guidelines recommend their use in vaginal hysterectomy. The recommendation of prophylaxis for other procedures varies (Table 45.13). Specific prophylaxis for those women at risk for endocarditis is imperative (Table 45.14).

TABLE 45.12 Infection Risk Factors Surgeon Related

Patient Related

Preoperative stay

Age

Preparation

Nutritional status

Patient

Diabetes

Staff

Renal insufficiency

Incision

Hepatic insufficiency

Placement

Radiation therapy

Method

Chemotherapy

Hemostasis

Hypoxemia

Suture material

Sepsis

Vasoconstrictors

Immunocompetence

Drains

Obesity

Closure technique

—

Dressing

—

Antibiotic prophylaxis

—

Experience

—

Excessive blood loss

—

TABLE 45.13 Antimicrobial Prophylactic Regimens by Procedure Procedure

Antibiotic

Dose

Vaginal/abdominal

Cefazolin

1 or 2 g single dose i.v.

Hysterectomya

Cefazolin

2 g single dose i.v.

Cefotetan

1 or 2 g single dose i.v.

Metronidazole

500 mg single dose i.v.

Laparoscopy

None

—

Laparotomy

None

—

Hysteroscopy

None

—

Hysterosalpingogram

Doxycyclineb

100 mg twice daily for 5 d orally

IUD insertion

None

—

Endometrial biopsy

None

—

Doxycycline

100 mg orally 1 h before procedure and 200 mg orally after procedure

Induced abortion/D&C

Metronidazole

Urodynamics

500 mg twice daily orally for 5 d None

—

IUD, intrauterine device; D&C, dilation and curettage. a A convenient time to administer antibiotic prophylaxis is just before induction of anesthesia. bIf hysterosalpingogram demonstrates dilated tubes. No prophylaxis is indicated for normal study. From ACOG Practice Bulletin No. 74. Antibiotic prophylaxis for gynecologic procedures. Obst Gyn 2006;108(1):225–234.

TABLE 45.14 Prophylactic Regimens for Prevention of Endocarditis in Susceptible Patients Undergoing Genitourinary or Gastrointestinal Procedures Situation

High-risk patients

High-risk patients allergic to ampicillin/amoxicillin

Agents

Regimena

Ampicillin plus gentamicin

Ampicillin, 2 g i.m. or i.v., plus gentamicin, 1.5 mg/kg (not to exceed 120 mg) within 30 min of starting the procedure; 6 h later, ampicillin, 1 g i.m/i.v, or amoxicillin, 1 g p.o.

Vancomycin plus gentamycin

Vancomycin, 1 g i.v. over 1–2 h, plus gentamicin, 1.5 mg/kg i.m./i.v. (not to exceed 120 mg); complete injection/infusion

within 30 min of starting the procedure.

Moderate-risk patients

Moderate-risk patients allergic to ampicillin/amoxicillin

Amoxicillin or ampicillin

Amoxicillin, 1 g p.o. 1 h before procedure, or ampicillin 2 g i.m./i.v. within 30 min of starting the procedure.

Vancomycin

Vancomycin, 1 g i.v. over 1–2 h; complete infusion within 30 min of starting the procedure

aNo second dose of vancomycin or gentamicin is

recommended. Adapted from Dajani AS, Taubert KA, Wilson W, et al. Prevention of bacterial endocarditis: recommendations by the American Heart Association. JAMA 1997;277:1799.

Treatment for Existing Infection Prophylactic drugs are administered to patients in the absence of preoperative evidence of active infection. However, gynecologic patients with an obvious infection prior to surgery should receive an antibiotic treatment regimen appropriate for the type of infection. For example, patients with tuboovarian abscess should be treated with a broad-spectrum antibiotic regimen covering gram-positive, gram-negative, and anaerobic bacteria. Postoperatively, antibiotics should be given for documented infection. It is clear that most postoperative febrile illness is not related to a documented infection. When postoperative fever, leukocytosis, and clinical picture suggest postoperative infection, an examination to identify potential sources should be performed. Source-directed therapy is appropriate. Adjunctive procedures, including CT or ultrasonographically guided drainage, may hasten recovery in patients with fluid collections or abscesses. In general, patients should receive adequate, broad-spectrum antibiotic treatment prior to surgical intervention.

Thromboembolism Thromboembolic phenomena, including deep venous thrombosis (DVT) and pulmonary embolism (PE), are inevitable following gynecologic surgery. A 1988 meta-analysis estimated a 6% to 7% proximal DVT risk and a 0.5% to 0.8% fatal PE risk in unprotected patients over 40 years of age undergoing abdominal surgery. This risk increases the level of

anxiety in most surgeons because of the difficulty of diagnosing venous thromboembolism (VTE) and the potential catastrophic outcome of PE. The impact and importance of postoperative thromboembolic prophylaxis is no longer a question. In a survey by the American College of Surgeons, approximately 96% of surgeons claimed that they regularly used antiembolic prophylaxis. However, patient poll and chart review suggest that only one third of patients received adequate prophylaxis. All gynecologic patients should be considered at risk for venous emboli. Approximately 50% of thromboembolic events following surgical procedures occur postdischarge, fostering a belief that such events are rare. Additionally, surgeons have been anxious about the potential side effects of prophylaxis, because low-dose UFH or LMWH administration has been associated with postoperative bleeding and wound hematomas. The infrequent occurrence of heparin-induced thrombocytopenia has also created some anxiety regarding prophylaxis. Finally, the initial or primary cost of thromboprophylaxis has deterred some from its use, although prophylaxis has been shown to be cost-effective. Thromboembolic phenomena can be clinically silent, whereas complications related to prophylaxis are not easily missed by the gynecologic surgeon or the patient. Furthermore, according to the Rochester Epidemiology Project and other studies, the incidence of PE and DVT is increasing as women age. The Agency for Healthcare Research and Quality recently published a report containing a systematic review ranking patient safety interventions based on the strength of the evidence supporting more widespread implementation of these procedures. The highestranked safety practice was the “appropriate use of prophylaxis to prevent VTE in patients at risk.” This recommendation was based on overwhelming evidence that thromboprophylaxis reduces adverse patient outcomes while, at the same time, decreasing overall costs. Despite these common misperceptions, principles of good gynecologic perioperative care demand careful attention to the role and benefit of thromboprophylaxis. The American College of Chest Physicians published guidelines regarding perioperative thromboprophylaxis. Risk factor stratification (Table 45.15) allows delineation of low-risk, moderate-risk, high-risk, and highest-risk categories, with coincident risk of developing DVT, clinical PE, and fatal PE. A report suggested that the frequency of DVT following gynecologic procedures was approximately 16% (a range of 4% to 38%). Fatal PE was reported in only 0.4% of the pooled sample. The cited risks for postoperative thromboembolic event included age >40, history of venous embolism, surgery for cancer, and an abdominal surgical procedure. It was suggested that gynecologic oncology patients were at particularly high risk, fulfilling Virchow's triad of advanced age, cancer, and the hypocoagulable state; venostasis related to pelvic mass compression; vascular injury due to lymph node dissection; postoperative immobility; and the thrombogenic effect of chemotherapy. Importantly, the authors noted a 75% reduction in fatal PE (from 0.4% to 0.1%) with the use of appropriate thromboprophylaxis. The strongest evidence presented for thromboprophylaxis was a relative risk reduction of 64% with use of low-dose UFH (reductive from 20% of patients to 7%). A dose response was suggested. Patients undergoing procedures for gynecologic cancers

derived less protection from the twice daily administration of low-dose UFH than patients undergoing other noncardiac procedures. It would appear that dosing three times a day is more appropriate. Although of concern, the potential risk of bleeding complications was not reproducible. Importantly, aspirin use was deemed insufficient for thromboprophylaxis. The Seventh American College of Chest Physicians Conference on Antithrombotic and Thrombolytic Therapy recently released evidence-based guidelines regarding the perioperative prevention of VTE. For gynecologic surgery patients undergoing brief procedures of lasting 3,400 U daily), or

LMWH (>3,400 U daily), fondaparin oral VKAs (INR, 2–3) IPC/GCS + LDUH/LMW

DVT, deep vein thrombosis; PE, pulmonary embolism; LDUH, low-d unfractionated heparin; LMWH, low-molecular-weight heparin; GC graduated compression stockings; IPC, intermittent pneumatic

compression; VTE, venous thromboembolism; VKAs, vitamin K antagonists; INR, international normalized ratio; HFS, hip fracture surgery; SCI, spinal cord injury. Modified from Geerts WH, Pineo GF, Heit JA, et al. Prevention of venous thromboembolism: the Seventh ACCP Conference on Antithrombotic and Thrombolytic Therapy. Chest 2004;126:338S–40 Thromboprophylaxis with one of the above agents should be used in all patients undergoing major gynecologic surgery. For those undergoing major gynecologic surgery for benign disease without additional risk factors, low-dose UFH, 5,000 U twice daily, is recommended. Alternatives to this regimen include once-daily prophylaxis with LMWH, ≤3,400 U per day, or IPC started just before surgery and used continuously until the patient is ambulating. For patients undergoing extensive surgery for malignancy, and for patients with additional VTE risk factors, routine prophylaxis with low-dose UFH, 5,000 U three times a day, or higher doses of LMWH (i.e., >3,400 U per day) is recommended. Alternative considerations include IPC alone continued until hospital discharge, or a combination of low-dose UFH or LMWH plus mechanical prophylaxis with GCS or IPC. For patients undergoing major gynecologic procedures, prophylaxis should be continued until discharge from the hospital. For patients who are at particularly high risk, including those who have undergone cancer surgery and are >60 years of age or have previously experienced VTE, continuing prophylaxis for 2 to 4 weeks after hospital discharge has been suggested.

Neurologic Complications Avoiding serious perioperative neurologic sequelae, including stroke, seizure, altered mental status, and operation-associated nerve injury, is a vital aspect of perioperative management. Most general anesthetics adversely affect central nervous system (CNS) function. Even short-term anesthetic use impairs psychomotor performance for 5 hours and sleep patterns for 24 hours or more. Women at risk for cerebrovascular disease (as evidenced by transient ischemic attacks, peripheral vascular disease, or other events) may require specific preoperative evaluation and neurologic consultation. Although an asymptomatic carotid bruit may signal the need for imaging studies or consultation, it does not, by itself, increase perioperative risk. Presurgical neurologic and radiologic evaluation, extracranial carotid endarterectomy, systemic anticoagulation, and platelet inhibition are some of the potential perioperative risk-sparing procedures to be considered. Particular attention should be paid to avoiding perioperative hypotension in patients with a history of arterial disease who are at increased risk for thrombolic events. The overall risk of recurrent stroke approaches 3.0%, but fortunately, the risk of stroke is 0.2% to 0.7% in those with no such history. Cerebral blood flow is unstable and brain metabolism is depressed for 6 to 8 weeks

following a completed stroke, making it prudent to avoid any significant elective operations during this interval. The risk of a second infarct may approach 20%, and the mortality rate is high (approximately 25%). Preoperative CNS scanning may assist in determining the time of resolution of the initial infarct, when operative procedures are less likely to result in repeated infarct. Emergency procedures in those at risk for CNS infarct should be completed in a perioperative environment that maintains an elevated blood pressure and avoids events that may increase the risk of CNS hypoperfusion. Vertebral basilar ischemic episodes are associated with a lower perioperative stroke risk than is carotid ischemia. Although perioperative neurologic evaluation may be appropriate, these patients usually are managed medically, with minimal surgical risks.

Operative Neurologic Deficits Nearly 2% of gynecologic procedures are associated with postoperative lower extremity neurologic deficits, regardless of attention paid to preoperative care or positioning. Multiple nerves are at risk, regardless of positioning, surgical duration, or approach. Mechanisms of nerve injury include prolonged compression (e.g., femoral nerve), excessive traction, stretch (e.g., sciatic nerve), or transection (e.g., lateral femoral cutaneous nerve). Regardless of the extent of injury, attention to positioning, or retractor placement, these problems occur and are managed by evaluation and rehabilitation. Fortunately, most resolve. Attention to minimizing hip flexion and external rotation potentially lessens the risk of traction injury. Ilioinguinal and iliohypogastric nerve injuries can be diagnosed with relief after local infiltration of nerve block or excision.

Summary Points The primary goal of the pelvic surgeon involves prospective preoperative recognition, evaluation, and management of existing medical comorbidities. Every pelvic surgeon should commit to the development of operative techniques that form a surgical skill set geared to the safe completion of indicated surgical procedures. Appropriate consultation should be sought if the level of qualification does not fit the necessary procedure. A thorough, multisystem physical examination is an essential part of the preoperative evaluation to detect important coexisting disease. The suspicion or diagnosis of coexistent morbidities that have not been diagnosed previously requires preoperative investigation. Laboratory and radiologic investigation should be conducted patiently and procedures directed in a safe, costeffective manner. Coexisting or occult cardiac disease represents a significant contributor to perioperative morbidity. Particular attention to the detection, evaluation, and management of cardiac risk factors including CAD, hypertension, congestive heart failure, valvular disease, arrhythmias, and hypercholesterolemia is imperative.

Particular attention to ACLS guidelines is important. Perioperative assistance by personnel experienced in cardiac care should be invoked when necessary. Perioperative pulmonary care is an important concern. The procedure should be designed to minimize pulmonary risks when possible. Preoperative and postoperative attention to pulmonary toilet may render the best possible outcome. Perioperative renal failure is associated with high morbidity and mortality. No intervention, including prophylactic low-dose dopamine, mannitol, or furosemide therapy, has been shown to be of any benefit in reducing the incidence of perioperative renal insufficiency. The optimal surgical incision is chosen according to the procedure done, existing comorbidity, disease process, and patient preference. Appropriate preoperative skin antisepsis is necessary and, in combination with intravenous antimicrobial agents, will decrease the incidence of wound infection. Good surgical technique is mandatory for wound health and maximizing patient outcome. Classically, bowel preparation (mechanical, with or without antibiotic) is undertaken prior to many gynecologic procedures, but this practice is not currently supported by evidence. Nasogastric suction has not been shown to lessen the risk of ileus, and only 10% of patients require insertion of a nasogastric tube postoperatively. Most patients can be managed without nasogastric suction. Proper use of prophylactic antibiotics lessens infectious risks in many pelvic procedures. Single-agent broad-spectrum antibiotic use, such as cephalosporin, doxycycline, or metronidazole, appears to be safe and effective for women who are undergoing abdominal or vaginal hysterectomy. The American College of Chest Physicians has published guidelines regarding perioperative thromboprophylaxis. Patients at low risk should be mobilized aggressively postoperatively. Those at moderate and high risk should use pneumatic compression hose or pharmaceutical methods. Patients at highest risk may also benefit from combined mechanical and pharmaceutical prophylaxis. Approximately 2% of gynecologic procedures are associated with postoperative lower extremity neurologic deficits. Special attention should be paid to patient positioning, surgical duration, proper use of surgical retractors to prevent excessive traction and stretch, and careful operative techniques.

Suggested Readings General Considerations Rutkow IM. Surgical operation in the United States. Then (1983) and now (1994). Arch Surg 1997;132:983–990.

Surgical Indications and Consent Birkmeyer JD, Siewers AE, Finlayson E, et al. Hospital volume and surgical mortality in the United States. N Engl J Med 2002;346:1128–1135. Guidelines for referral to a gynecologic oncologist: rationale and benefits. Gynecol Oncol 2000;78:S1–S13. Montz HG. “Curbside” consultations in gynecologic oncology: a close look at a common practice. Gynecol Oncol 1999;74:456–459.

Preoperative Evaluation and Testing American Heart Association. ACLS provider manual. Dallas: Author, 2001. Brooks-Brunn JA. Predicators of postoperative pulmonary complications following abdominal surgery. Chest 1997;111:564–571. Eagle KA, Brundage BH, Chaitman BR, et al. Guidelines for perioperative cardiovascular evaluation for noncardiac surgery: report of the American College of Cardiology (American Heart Association Task Force on Practice Guidelines (Committee on Perioperative Cardiovascular Evaluation for Noncardiac Surgery). Circulation 2002;105:1257. Eagle KA, Rihal CS, Mickel MC, et al. Cardiac risk of noncardiac surgery: influence of coronary disease and type of surgery in 3368 operations. CASS Investigators and University of Michigan Heart Care Program. Coronary Artery Surgery Study. Circulation 1997;96:1882–1887. Fischer SP. Cost-effective preoperative evaluation and testing. Chest 1999;115:96S–100S. Fleisher LA, Beckman JA, Freeman WK, et al. ACC(AHA 2006 guideline update on perioperative cardiovascular evaluation for noncardiac surgery: focused update on perioperative beta-blocker therapy. A report of the American College of Cardiology

(American Heart Association Task Force on practice guidelines (Writing Committee to update the 2002 guidelines on perioperative cardiovascular evaluation for noncardiac surgery). American Heart Association, American College of Cardiology website. Available at: http://www.americanheart.org/presenter.jhtml?identifier/3038250. Accessed January 13, 2007. Fleisher LA, Eagle KA. Lowering cardiac risk in noncardiac surgery. N Engl J Med 2001;345:1677–1682. Hodges PJ, Kam PC. The perioperative implications of herbal medicines. Anaesthesia 2000;57:889–899. Orr JW Jr. Preoperative care. In: Gershenson D, ed. Operative gynecology. Philadelphia: WB Saunders, 2001. Proceedings of the American College of Chest Physicians Seventh Consensus on Antithrombotic Therapy 1998. Chest 1998;114:439S–769S. Raymer K, Yang H. Patients with aortic stenosis: cardiac complications in non-cardiac surgery. Can J Anaesth 1998;45:855–859. Roizen MF. More preoperative assessment by physicians and less by laboratory tests. N Engl J Med 2002;342:204–206.

Perioperative Pulmonary Evaluation Smetana GW. Preoperative pulmonary evaluation. N Engl J Med 1999;340:937–944.

Renal Disease Gilmour DT, Dwyer PL, Cary MP. Lower urinary tract injury during gynecologic surgery and its detection by intraoperative cystoscopy. Obstet Gynecol 1999;94:883–889. Novis BK, Roizen MF, Aronson S, et al. Association of preoperative risk factors with postoperative acute renal failure. Anesth Analg 1994;78:143–149.

Wounds and Incisions Labib M, Palfrey S, Paniagua E, et al. The postoperative inflammatory response to injury following laparoscopic assisted vaginal hysterectomy versus abdominal hysterectomy. Ann Clin Biochem 1997;34:543–545.

Orr JW Jr, Orr PF, Bolen D, et al. Radical hysterectomy: does the type of incision matter? Am J Obstet Gynecol 1995;173:399–406. Orr JW Jr, Orr PF. Perioperative care. In: Greer BE, Montz FJ, eds. Atlas of clinical gynecology, Vol 4. New York: McGraw-Hill Professional, 1998. Soper DE, Bump RC, Hurt WG. Wound infection after abdominal hysterectomy: effect of the depth of subcutaneous tissue. Am J Obstet Gynecol 1995;173:465–469. Vrijland WW, Tseng LN, Eijkman JH, et al. Fewer intraperitoneal adhesions with use of hyaluronic acid-carboxymethylcellulose membrane: a randomized clinical trial. Ann Surg 2002;235:193–199.

Gastrointestinal Care Andrews FJ. Early postoperative feeding after major gynecologic surgery: evidencebased scientific medicine. Am J Obstet Gynecol 2001;185:1–4. Cheatham ML, Chapman WC, Key SP, et al. A meta-analysis of selective versus routine nasogastric decompression after elective laparotomy. Ann Surg 1995;221:469–478. Pearl ML, Frandina M, Mahler L, et al. A randomized controlled trial of a regular diet as the first meal in gynecologic oncology patients undergoing intraabdominal surgery. Obstet Gynecol 2002;100:230–234. Zamora O, Pikarsky AJ, Wexner SD. Bowel preparation for colorectal surgery. Dis Colon Rectum 2001;44:1537–1549.

Infection American College of Obstetricians and Gynecologists. Clinical management guidelines for obstetrician-gynecologists. ACOG Practice Bulletin. Washington, DC: Author, 2006. Cinat ME, Wilson SE, Din AM. Determinants for successful percutaneous image-guided drainage of intra-abdominal abscess. Arch Surg 2002;137:845–849. Scher KS. Studies on the duration of antibiotic administration for surgical prophylaxis. Am Surgeon 1997;63:59–62.

Thromboembolism

Geerts WH, Pineo GF, Heit JA, et al. Prevention of venous thromboembolism: the Seventh ACCP Conference on Antithrombotic and Thrombolytic Therapy. Chest 126:338S– 400S.

Maxwell GL, Synan I, Dodge R, et al. Pneumatic compression versus low molecular weight heparin in gynecologic oncology surgery: a randomized trial. Am Coll Obstet Gynecol 2001;98:989–995. Silverstein MD, Heigh JA, Mohr DV, et al. Trends in the incidence of deep vein thrombosis and pulmonary embolism: 1. 25-year population-based study. Arch Intern Med 1998;158:585–593.

Neurologic Warner MA, Warner DO, Harper CM, et al. Lower extremity neuropathies associated with lithotomy positions. Am Soc Anesth 2000;93:938–942. Wong GY, Warner DO, Schroeder DR, et al. Risk of surgery and anesthesia for ischemic stroke. Am Soc Anesth 2000;92:425–434.

46 Laparoscopic Surgery Joseph S. Sanfilippo Lisa M. Roberts Endoscopic (minimally invasive) surgery originated in 1847; the pioneering work of Sir James Y. Simpson of Edinburgh, Scotland, introduced chloroform narcosis. The first endoscopic evaluation of the abdominal cavity utilized a dog model in 1901 and was undertaken by Kelling. In 1911, Jacobaeus reported the first laparoscopic procedure in the human. Cold illumination fiber optics by Semm followed in 1963 and then the surgical area evolved rapidly. The first laparoscopic appendectomy was performed in 1980 and the first cholecystectomy in 1985. This relatively new aspect of endoscopic surgery has far-reaching and ever-increasing innovative aspects. Advances in hysteroscopic surgery have altered the approach to uterine leiomyomas. Currently, the spectrum of laparoscopy includes radical hysterectomies and node sampling. The technical advances, including new instrumentation, are within the scope of this chapter. There appears to be a continuous state of evolution and more far-reaching new and improved instrumentation within the discipline of minimally invasive surgery.

Laparoscopy Patient Positioning Proper patient positioning is paramount to avoid injuries. The surgeon should position the patient so as to prevent any excessive pressure on the lower extremities. Use of intermittent pneumatic compression devices is becoming more commonplace in order to prevent thromboembolic events. Surgeons must also be aware of nerve injuries that can result from improper placement of the lower extremities in stirrups. The lithotomy position with access to steep Trendelenburg is oftentimes utilized. The physician should discuss with the anesthesia team decisions regarding whether the arms should be extended or “tucked” along the sides of the patient. The latter requires particular attention to prevent any trauma to the hands and fingers when the table is maneuvered. Plastic “sleds” can be utilized to secure the upper extremities in obese patients. With the patient in the low lithotomy position and the legs supported in stirrups, the

buttocks should protrude slightly from the lower edge of the table. The lateral aspect of the knee should be protected with padding in the stirrup to prevent peroneal nerve injury. The knees should be kept in slight flexion to minimize stretching of the sciatic nerves and to provide increased stability in the Trendelenburg position. With respect to positioning of the arms, care should be taken not to stretch or traumatize the brachial plexus. It has been advocated that an angle of 145 degrees between the abdomen and the lower extremity (thigh) is ideal, providing the surgeon with adequate space for instrumentation. The typical patient positioning for endoscopic surgery is noted in Figure 46.1.

Equipment The array of instruments designed to facilitate operative laparoscopic procedures continues to evolve. This section describes a number of instruments.

Viewing System The video equipment should include a three-chip camera, a processor, a 300-watt xenon light source with fiber-optic cable, a high-resolution monitor, and a video recorder. The three-chip camera provides a sharper, brighter image with higher resolution than the older single-chip cameras (Fig. 46.2). Three-chip cameras can deliver over 600 lines of resolution; therefore, the video monitor's horizontal resolution should be greater to maximize image quality. Fiber light cables should be inspected for broken fibers and replaced if a significant number of fibers are broken, because damaged fibers will result in suboptimal light delivery.

Figure 46.1 Patient positioning for laparoscopic surgery.

Operating Table An operating room table that allows 30 degrees of flexion (Trendelenburg position) is ideal for visualization of the deep pelvis. Shoulder braces (Stierlen-Maquet Shoulder Braces, Siemens Medical Systems, Englewood, CO) placed at the acromioclavicular joints and the

arms placed at the patient's sides will minimize nerve injuries.

Insufflator For most procedures, the pneumoperitoneum may be maintained with an insufflator that flows at a rate of 2 to 7 L per minute. High-flow insufflators that achieve up to 30 L per minute are available and will maintain the pneumoperitoneum during procedures with frequent changes in instruments that allow escape of large amounts of carbon dioxide (CO2), such as during tissue morcellation.

Figure 46.2 Autoclavable Goldtip videolaparoscope with camera processor and xenon light source (Olympus, Melville, NY).

Figure 46.3 Five-millimeter laparoscopes (Karl Storz Endoscopy–America, Culver City, CA).

Carbon Dioxide Warmer There is evidence that warmed CO2 is less irritating to the peritoneal surface and,

therefore, may cause fewer postoperative adhesions. CO2 warmers are available commercially.

Laparoscopes Laparoscopes are telescopes that vary in size from 2 to 10 mm. Viewing angles are available in 0-, 30-, 45-, and 70-degree increments. The choice is operator dependent. Most diagnostic laparoscopes do not contain an operating channel. Operative laparoscopes, with a smaller fiber diameter, contain a channel through which instruments or a laser (Figs. 46.3, 46.4) can be used.

Trocars Trocars come in a variety of sizes, materials, and designs. Sizes range from 3 to 15 mm. Reusable metal trocars have the advantage of cost efficiency, but they may actually be more dangerous if the tips are not kept sharp (Figs. 46.5,46.6,46.7). Disposable trocars are utilized in most operating rooms; they decrease the risk of injury during insertion compared with reusuable instrumentation that may require increased force during insertion (Fig. 46.8). Some trocars are designed to stretch the fascia so that fascial closure is not necessary. Others have been designed to allow visualization of tissue layer separation with the laparoscope during insertion. Advocates assert that this type of trocar decreases bowel and vascular injuries. There are no objective data supportive of a reduction in risk for any trocar. The trocar chosen should be based on the surgeon's preference. Hasson-type trocars have a blunt end for placement in open laparoscopy (Figs. 46.9, 46.10).

Figure 46.4 Ten-millimeter laparoscope (Karl Storz Endoscopy–America, Culver City, CA).

Figure 46.5 Five- and ten-millimeter trocars (Karl Storz Endoscopy–America, Culver City, CA).

Operating Instruments A standard laparoscopy set should include the following: Trocars Bipolar forceps (Figs. 46.11, 46.12) Atraumatic grasping forceps (Figs. 46.13,46.14,46.15) Biopsy forceps (Fig. 46.16) Blunt probe Blunt sawtooth scissors (Fig. 46.17) Pointed Metzenbaum scissors (Fig. 46.18)

Figure 46.6 Autoclavable 5-mm slim trocar with duckbill (Olympus, Melville, NY).

Figure 46.7 Five- and ten-millimeter reusable trocars.

Figure 46.8 Ten-millimeter disposable trocars (Olympus, Melville, NY).

Figure 46.9 Ten-millimeter blunt trocar for open laparoscopy (Marlow Surgical Technologies Inc., Willoughby, OH).

Figure 46.10 Ten-millimeter blunt trocar for open laparoscopy (Apple Medical, Bolton, MA).

Figure 46.11 Five-millimeter bipolar forceps (Olympus, Melville, NY).

Figure 46.12 Five-millimeter bipolar forceps (Olympus, Melville, NY).

Figure 46.13 Atraumatic tissue grasper (Applied Medical, Rancho Santa Margarita, CA).

Figure 46.14 Atraumatic tissue grasper.

Figure 46.15 Atraumatic tissue grasper.

Figure 46.16 Biopsy forceps.

Figure 46.17 Blunt sawtooth scissors (Richard Wolf Medical Instruments, Vernon Hills, IL).

Figure 46.18 Metzenbaum scissors (Richard Wolf Medical Instruments, Vernon Hills, IL).

Cyst aspiration needle (Fig. 46.19) Suction and irrigator Uterine manipulator (Figs. 46.20, 46.21) An advanced laparoscopy set may include the following: Needle holders (Figs. 46.22,46.23,46.24) Knot pusher (Fig. 46.25)

Figure 46.19 Cyst aspiration needle.

Figure 46.20 RUMI uterine manipulator (Cooper Surgical, Shelton, CT).

Vaginal delineator (Fig. 46.26) Babcock atraumatic grasper (Fig. 46.27) Allis clamp Adson forceps (Fig. 46.28) Corkscrew Single-tooth tenaculum Atraumatic bowel grasper Monopolar spatula (Fig. 46.29) Endoscopic specimen retrieval bags (Figs. 46.30, 46.31) Endoscopic suture ligatures (Fig. 46.32) Microbipolar forceps

Morcellator Rectal probe

Figure 46.21 Hulka uterine manipulator tenaculum (Richard Wolf Medical Instruments, Vernon Hills, IL) and Cohen Uterine Cannula (Karl Storz Endoscopy–America, Culver City, CA).

Figure 46.22 Five-millimeter needle holder (Olympus, Melville, NY).

Figure 46.23 Five-millimeter needle holder (Olympus, Melville, NY).

Figure 46.24 Five-millimeter needle holder (Karl Storz Endoscopy–America, Culver City, CA).

Figure 46.25 Knot pusher for extracorporeal suturing (Marlow Surgical, Roebling, NJ).

Staplers Endoscopic staplers that simultaneously ligate and divide tissue are available. In gynecologic procedures, they are used most commonly on the infundibulopelvic ligament, round ligament, fallopian tubes, and utero-ovarian ligaments in laparoscopically assisted vaginal hysterectomies. They also may be used when excising endometriosis from the bowel (Fig. 46.33).

Harmonic Scalpel The active blade of the Harmonic Scalpel (Ethicon Endosurgery Inc., Cincinnati, OH) vibrates at a rate of 55,000 cycles per second, resulting in coagulation and

tissue separation. The scalpel is available as a 5- or 10-mm “hook,” “ball” dissector, spatula, or opposing jaws. Although electrical energy is not used, the tissue still becomes heated, and a 2-mm lateral energy spread that can cause thermal injury may be encountered.

Figure 46.26 Koh Cup Vaginal Fornices Delineator (Cooper Surgical, Shelton, CT).

Figure 46.27 Babcock atraumatic grasper.

Figure 46.28 Adson forceps.

Figure 46.29 Monopolar spatula for cutting and coagulation.

Figure 46.30 Endo Catch instrument with a specimen bag (U.S. Surgical, Norwalk, CT).

Figure 46.31 Specimen retrieval bag (Cook Ob/Gyn, Spencer, IN).

Figure 46.32 Surgitite endoscopic suture ligature (U.S. Surgical, Norwalk, CT).

Electrosurgery Unipolar electrosurgical instruments are used to cut and coagulate tissue. Cutting occurs when there is sufficient voltage (at least 200 V) between the electrode and the tissue to produce an electric arc. This arc concentrates the current to points along the tissue, resulting in a cutting effect. In contrast to cutting current, coagulation is produced through instrument contact with the tissue. Contact allows heating of the tissue followed by irreversible cellular damage, vaporization of intracellular water, coagulation, and contraction of blood vessels and surrounding tissue. Electrosurgical burns may occur due to insulation failure, direct coupling (activated electrode makes unintended contact with another metal object in the area of the surgical field), or capacitive coupling (induction of stray current to a surrounding conductor through the intact insulation of an active electrode). Bipolar electrosurgical instruments contain the electrical current between an active and return electrode, usually the two blades of forceps. The flow of alternating current is passed between the two electrodes rather than passing through the patient to a grounding pad. In comparison to monopolar current, bipolar elctectrocautery eliminates the risk of capacitive coupling and stray current.

Figure 46.33 Stapling device (U.S. Surgical, Norwalk, CT).

Laser Lasers offer an alternative method of cutting and vaporizing tissue. The CO2 laser with a depth of penetration of 1 mm allows the surgeon some security when working around bowel, ureters, and large blood vessels. In addition, a CO2 laser will not traverse through water, thus irrigation fluid may be used as a backstop. The Coherent 5000L (Coherent Laser, Palo Alto, CA) laser offers high-power density over a short period of time, minimizing thermal damage to surrounding tissue. This laser uses a 13C isotope of CO2 with an 11.1-mm wavelength beam. The wavelength of the CO2 purge gas in the operating channel of the laparoscope is 10.6 mm. Because the wavelengths are different, there is no absorption of the laser beam by the purge gas, keeping the power density ten times more than at similar settings with other standard laser beams with 10.6-mm wavelengths. The 1.5-mm spot size is maintained at all power settings, offering precision, minimal surrounding tissue damage, and less charring. Fiber lasers (potassium titanyl phosphate [KTP], argon, and neodymium-doped yttrium aluminium garnet [Nd:YAG]) are introduced through small channels of the operating laparoscope or through ancillary trocars. The KTP and argon lasers may be used for cutting and coagulating. As the tip of the fiber approaches the tissue, the power density increases and the laser is used for cutting. As the tip is moved away from the tissue, the spot size increases and power density decreases rapidly. The clinical applications for the YAG laser are more limited. The YAG laser coagulates well, but it does not cut well unless a sapphire tip is used to increase the power density.

Uterine Manipulators A comparative survey of uterine manipulators has been done, each of which has advantages and disadvantages. The Clermont-Ferrand manipulator (Storz Endoskope, Tuttlingen, Germany) allows movement +140 degrees, is reusable, and requires cervical dilation to a Hegar dilator no. 9. The Hohl manipulator movement ranges up to 130 degrees, and is minimally traumatic. (Endoworid Gyn, Karl Sturz, Ltd. Tuttlingen, Germany). The Endopath (Ethicon Ethosurgery Inc., Cincinnati, OH) allows movement range of +130 degrees and is disposable, and the pneumoperitoneum is maintained with difficulty. The RUMI System with the KOH Colpotomizer (Cooper Surgical, Shelton, CT) has a snap drum that rotates around a 140-degree arch, allows good delineation of the vaginal fornices, and can be used with the harmonic scalpel. The disadvantage is

that it is not always easy to place the device, especially with a narrow vagina. Elevation of the uterus is restricted. The Histerophore uterine manipulator levers the lateral fornices free, facilitating uterine pedicle formation, and is reusable and easy to assemble (Karl Sturz, Tuttlingen, Germany). The range of motion is less than other manipulators. The Vcare manipulator (ConMed Corporation, Utica, NY) provides for optimal exposure of the vaginal fornices, maintains the pneumoperitoneum, and allows for easy uterine manipulation. It is disposable and cannot be used as a laser backstop. The Total laparoscopic hysterectomy uterine manipulator allows for movement in the range of +130 degrees, is reusable, and provides for good presentation of the vaginal fornices. The one disadvantage is restricted movement of the external device over the internal rod.

Handoscopy Hand-assisted laparoscopy, or “handoscopy,” has received some attention, mainly in the field of solid organ and bowel surgery. This involves making a small incision that is large enough to squeeze a hand through with a seal to prevent loss of CO2. To date, the only gynecologic procedure where this device has been used is in rectal resection for deep fibrotic endometriosis. The main advantage of handoscopy is that it allows the surgeon to regain the tactile feel of tissues lost in standard laparoscopies. The disadvantage is that the incision needs to be carefully closed to prevent hernia, and it requires a longer recovery interval, albeit less than if the procedure were performed open.

Physiologic Effects of the Pneumoperitoneum The respiratory, hemodynamic, and renal consequences of the pneumoperitoneum are substantial but usually are well tolerated by the healthy patient. These changes may be severely problematic in the patient whose cardiopulmonary or renal system is compromised.

Respiratory Changes Ventilation during laparoscopic surgery is altered by the increased intra-abdominal pressure (IAP) of the pneumoperitoneum. The airway pressure required for adequate ventilation consequently is increased. Thoracic compliance, diaphragmatic excursion, and functional residual capacity are all decreased. Studies have shown that the increase in IAP alone reduces compliance by 30%; this may be decreased by another 20% when the patient is placed in a Trendelenburg position. In addition to mechanical changes, the CO2 pneumoperitoneum produces changes in acid– base balance. Because CO2 is absorbed rapidly from the peritoneal cavity, the minute volume must be increased as indicated by the end-tidal CO2 to prevent respiratory acidosis (Table 46.1).

TABLE 46.1 Ventilatory Effects of Carbon Dioxide Pneumoperitoneum

1. Hypercapnia with subsequent acidosis 2. Increased airway pressure 3. Decreased functional residual capacity 4. Decreased thoracic compliance 5. Decreased diaphragmatic excursion

Hemodynamic Changes Circulatory changes seen during laparoscopic surgery are the result of the mechanical compressive effects of the increased IAP and its associated hormonal changes (Table 46.2). Catecholamines, angiotensin, and vasopressin are all increased, resulting in increased systemic vascular resistance. An increase in systemic vascular resistance results in an increase in mean arterial pressure and a decrease in cardiac index. The increased IAP also causes increased intrathoracic pressure, with resultant increases in central venous pressure, pulmonary capillary wedge pressure, and pulmonary vascular resistance.

Renal Blood Flow Changes Animal studies have shown an increase in renal vascular resistance and a decrease in renal perfusion and glomerular filtration rate secondary to increased IAP. A subsequent decrease in urine output may be observed and may continue to remain low 1 hour after release of the pneumoperitoneum (Table 46.3).

Compromised Patient The multiple cardiopulmonary and renal changes observed during CO2 laparoscopy are well tolerated by the healthy patient. Extreme caution must be taken when performing gaseous laparoscopy in patients with compromised respiratory function, ischemic heart disease, congestive heart failure, and renal dysfunction. These compromised states may even be considered relative contraindications to pneumoperitoneum laparoscopy. The lowest IAP that allows adequate visualization should be used to minimize increases in intrathoracic pressure. An alternative consideration would be to use an abdominal wall lift method (elevating the ventral abdominal wall by an inflatable balloon or fan retractor), eliminating the

consequences of CO2 in the peritoneum. The use of alternative gases such as argon, nitrous oxide, helium, and room air for pneumoperitoneum has been considered. CO2's advantages over these gases include higher solubility and therefore possibly fewer deleterious effects in the event of gas embolism, the ability to use cautery in its presence, and its low cost. It is the surgeon's responsibility to take a careful history and perform appropriate preoperative diagnostic testing when determining a patient's candidacy for laparoscopic surgery.

TABLE 46.2 Hemodynamic Effects of Carbon Dioxide Pneumoperitoneum 1. Increased systemic vascular resistance 2. Increased mean arterial pressure 3. Decreased cardiac index 4. Increased central venous pressure 5. Increased pulmonary vascular resistance 6. Increased pulmonary capillary wedge pressure

TABLE 46.3 Renal Effects of Carbon Dioxide Pneumoperitoneum

1. Increased renal vascular resistance 2. Decreased renal blood flow 3. Decreased glomerular filtration rate 4. Decreased urine output

Anatomy of the Anterior Abdominal Wall Knowledge of the anterior abdominal wall vascular anatomy will reduce vascular complications associated with trocar placement. Of particular concern are the superior and

inferior epigastric vessels. The superior epigastric artery, one of the terminal branches of the internal thoracic artery, enters the rectus sheath first and then the rectus muscle coursing near its lateral border. This artery and its adjacent vein often can be visualized by transillumination of the abdominal wall with the laparoscope. Visualization of the ventral abdominal wall laparoscopically will often locate the deep inferior epigastric vessels. The artery, a branch of the external iliac, and its accompanying vein course along the abdominal wall peritoneum just lateral to the rectus muscle until midway between the symphysis pubis and umbilicus, where it blends into the body of the rectus muscle. These vessels may be seen medial to the insertion of the round ligament at the deep inguinal ring. Therefore, placement of the trocar lateral to the deep inguinal ring and lateral border of the rectus muscle will avoid injury to these vessels. If placement of the trocar is too far laterally, branches of the superficial circumflex iliac vessels may be injured. Again, transillumination of the anterior abdominal wall by using the laparoscope will assist in avoiding these vessels. As a general guideline, the superficial and inferior epigastric vessels are located approximately 5.5 cm from the midline. The superficial circumflex iliac vessels are approximately 7 cm from the midline. Theoretically, a “safe area” would be 8 cm above the symphysis pubis and 8 cm from the midline. If transillumination is not effective due to a thick abdominal wall, the surgeon may consider insertion of a spinal needle through the abdominal wall at the selected trocar insertion site. If no bleeding is observed after removal of the needle, the location is likely safe for trocar placement.

Obtaining Intra-Abdominal Access For most laparoscopic surgeons, obtaining access to the peritoneal cavity is the most anxiety-provoking step of the entire endoscopic procedure. There are a number of ways to obtain intra-abdominal access for trocar placement and establishment of a pneumoperitoneum. None of the available methods preclude the possibility of complications from trocar or needle insertion. In general, these methods of entry can be classified as either open or closed. An open entry uses the technique first described by Hasson. It remains a very popular method of entry into the abdominal cavity. An incision into the peritoneal cavity through all anterior abdominal wall layers at the umbilicus is made carefully. A blunt-tipped trocar is placed through the incision into the abdominal cavity. Insufflation is conducted through this trocar sleeve. This technique may reduce vascular injuries due to sharp trocar or needle placement, but the possibility of bowel injury still exits if there are abdominal wall adhesions. The closed entry may be performed with or without the use of a Veress needle to insufflate CO2. Placement of the sharp trocar through the umbilicus without prior insufflation in general has lost favor due to the higher risk of bowel and vascular injuries. Insufflation of CO2 through a Veress needle is the most common method of gas instillation, although some would argue that the open technique should become the method of choice.

One technique of access by using a Veress needle is performed in the following manner:

1. A vertical incision through the skin corresponding to the size of the trocar is made either within the umbilicus or at the base. This is because the distance between skin and peritoneum on the anterior abdominal wall is shortest at the base of the umbilicus. In addition, the peritoneum is firmly attached, which will prevent tracking through the subcutaneous tissue and subsequent retroperitoneal insufflation.

2. The Veress needle is inspected for sharpness and a functioning spring mechanism to extend the protective sheath in the absence of pressure.

3. The anterior abdominal wall inferior to the umbilicus is grasped with the non-dominant hand, and the umbilicus is moved in the caudad direction, further displacing it below the bifurcation of the aorta. Alternatively, the incision may be elevated by grasping the edges of the umbilical incision with two Alice clamps and lifting.

4. The tip of the Veress needle is held in the dominant hand between the thumb and forefinger while the ulnar palm rests on the patient's abdomen. The needle is inserted carefully at a 90-degree angle, through the base of the umbilicus, millimeter by millimeter, until a click is heard and resistance is no longer felt, identifying intraabdominal placement.

5. A saline-filled 10-cc syringe is attached to the Veress needle and aspirated, inspecting for blood or bowel contents. If only bubbles are visible, saline is injected and observed to fall from the trough on the needle into the peritoneal cavity.

6. The syringe is removed, the insufflation tubing (with CO2 turned on low flow) is attached, and the initial IAP is observed. If the pressure is >10 mm Hg, the needle should be removed quickly to avoid retroperitoneal insufflation, which further displaces the peritoneum from its attachment to the anterior abdominal wall. A second needle placement attempt is then made.

7. Once intraperitoneal placement is confirmed, a CO2 pneumoperitoneum is obtained. Insufflation up to an IAP of 20 to 25 mm Hg, as initially described by Reich and others, remains one accepted method. This temporary increase in IAP increases the distance between abdominal viscera and the anterior abdominal wall (in the absence of adhesions) during primary sharp trocar placement through the umbilicus. It is also extremely beneficial for surgeons with small hands, who may find it difficult to grasp and further elevate the abdominal wall if the initial pressure is 1,000), transvaginal ultrasonography can reliably visualize a normal gestational sac. The absence of an intrauterine sac above this level should alert the physician to a high likelihood of ectopic pregnancy. With the advent of methotrexate use, the total number of ectopic pregnancies treated surgically has decreased. Laparoscopy remains a standard for surgical management in the stable patient. While obtaining informed consent, the surgeon must discuss management alternatives. Should the pregnancy alone be removed, leaving the fallopian tube in place, or should a salpingectomy be performed? Assuming that the pregnancy can be aborted without significant bleeding from the fallopian tube, this decision should be based on the status of the contralateral ovary and tube. If the contralateral tube and ovary are normal in appearance, without adhesions, then a salpingectomy or salpingostomy may be performed with a subsequent intrauterine pregnancy rate of 85% and a repeat ectopic rate of 10%. If the contralateral tube is impaired, then the subsequent intrauterine pregnancy rate is 46% and repeat ectopic rate is 52%. In this situation, the affected fallopian tube should be removed.

Technique for Salpingostomy or Salpingectomy Laparoscopic access is obtained as described previously. In addition to the umbilical port, two 5-mm lower abdominal ports are indicated, left and right. A suction-irrigator is used to aspirate the hemoperitoneum, if present. The pregnancy is identified within the fallopian tube, usually within the ampullary portion. The tube is stabilized with a Babcock or atraumatic grasper. There is considerable debate regarding the use of dilute vasopressin prior to making the incision on the antimesenteric side of the tube overlying the

pregnancy. Clinicians must understand that the use of vasopressin has the potential for delayed bleeding postoperatively. An incision parallel to the axis of the tube is now made on the antimesenteric side. This may be performed by using a spoon, knife, or hook monopolar electrocautery, set at 50 to 80 W to minimize bleeding. An effort should be made to minimize tubal epithelium trauma. The suction-irrigator is used to “aquadissect” the attachments between the pregnancy and tube, thus aborting the pregnancy into the pelvis. Alternatively, the pregnancy may be grasped by using atraumatic graspers and pulled from its attachment. It is then removed from the abdomen.

TABLE 46.4 Ultrasonographic Criteria for Malignant Ovarian Tumors Size >5 cm High (solid) echogenicity Internal septations Irregular border Papillary intracystic formations Ascites

If significant bleeding is encountered or the pregnancy does not dissect freely, a salpingectomy may need to be performed. Again, the fallopian tube is grasped with an atraumatic grasper and lifted. Transection of the involved tube is performed. Transection should be done after complete desiccation by using cautery or may be performed after suture ligation (a window is created within the mesosalpinx inferior to the ligation site). The mesosalpinx, immediately inferior to the fallopian tube, is then desiccated by using bipolar cautery and transected, freeing the tube and pregnancy from its anatomic attachments.

Adnexal Mass Laparoscopic management of adnexal masses is gaining widespread acceptance, but some aspects still conjure considerable debate. The patient's age, transvaginal sonographic findings, and to some extent CA-125 level (if indicated based on patient's age) will determine if a laparoscopic approach rather than laparotomy is acceptable. Ultrasonographic criteria for malignant and benign tumors are presented in Tables 46.4 and 46.5. CA-125 levels are most useful in postmenopausal women; a level of 35 U/mL in postmenopausal women carries a sensitivity of 81% and specificity of 91% for malignancy. If

the level is >50, then the sensitivity remains essentially the same and the specificity increases to 97%. In premenopausal women, sensitivity remains 60% as the level increases, but specificity increases from 73% at a level of 35 to 95% at a level of 100. A primary concern for those advocating laparotomy over laparoscopy for management of suspicious adnexal masses is the potential increased risk of cyst rupture during laparoscopic surgery. Preoperative or intraoperative rupture changes a stage Ia ovarian carcinoma to a stage Ic. Studies have shown that intraoperative iatrogenic rupture of the tumor capsule does not adversely affect survival, but survival is negatively influenced by spontaneous or preoperative rupture. The American College of Obstetricians and Gynecologists (ACOG) guidelines for intraoperative management of adnexal masses are presented in Table 46.6. As a general rule, if malignancy is highly suspected, then complete surgical staging procedure should be performed. If a laparoscopy is performed initially and malignancy subsequently is identified histologically, the staging procedure should be completed within 1 week.

TABLE 46.5 Ultrasonographic Criteria for Benign Ovarian Tumors Size Table of Contents > 47 - Hysteroscopic Surgery

47 Hysteroscopic Surgery R. Stan Williams Although hysteroscopy has been described since the early 1800s, widespread use by practicing gynecologists did not occur until the 1980s. With improvements in optics, video systems, instrumentation, and distension media, there has been an increased acceptance of hysteroscopy as the gold standard in the evaluation of the uterine cavity and treatment of intracavitary pathology. Hysteroscopy is used most commonly for evaluation of abnormal uterine bleeding, but it also is used frequently for evaluation of the endometrial cavity in patients with recurrent pregnancy loss and infertility, particularly when intracavitary pathology is suspected. Many studies have shown that blind dilation and curettage may miss up to 60% of endometrial pathology, such as endometrial polyps and submucous leiomyoma, although with increasing expertise in ultrasonographic techniques such as the saline sonohysterogram, endometrial pathology often can be identified prior to performing diagnostic and therapeutic operative hysteroscopy. Alternatively, many practitioners perform office hysteroscopy with smalldiameter hysteroscopes, which do not require significant dilation of the cervix, can provide direct visualization of the endometrial cavity, and facilitate a directed biopsy of suspected endometrial lesions or better characterization of suspected intracavitary pathology. Operative hysteroscopy requires larger-diameter instrumentation and is best performed under anesthesia in the outpatient operating room because of the need for significant cervical dilation and more extensive instrumentation. Hysteroscopic surgery allows a variety of intrauterine surgical procedures such as myomectomy, polypectomy, resection of a uterine septum, endometrial ablation by a variety of techniques, correction of intrauterine synechiae, cannulation of proximal tubal occlusion, and placement of intraluminal coils to occlude the tube for permanent sterilization.

Instrumentation Hysteroscopy can be used both as a primary diagnostic tool and as a more definitive operative technique. Diagnostic hysteroscopy can be performed either in an office setting or in the outpatient operating room and requires only small 3.6-mm to 5-mm hysteroscopes. These hysteroscopes may be either flexible or rigid. A small channel often is provided for a biopsy instrument, but these are rather delicate, and significant surgical

procedures will require larger-diameter hysteroscopes. The flexible hysteroscope is used often for office hysteroscopy because it can be inserted through a narrow cervical os and can negotiate the cervical canal by using a deflecting lever to guide the instrument under direct vision. The flexible hysteroscope is available in two diameters, 3.6 mm and 4.9 mm, both with a zero-degree optical view. The largerdiameter endoscope also provides a 2.2-mm diameter instrument channel, which allows for directed biopsies of endometrial pathology. The larger instrument provides better optics than the smaller flexible hysteroscope but is still somewhat optically inferior to a 4-mm rigid scope. Small rigid diagnostic hysteroscopes are 4 to 5 mm in diameter and have only a single channel for installation of a distending medium. If a low-viscosity liquid distension medium is used, then a continuous flow sheath that is 5.5 mm in diameter is used, allowing for the continuous simultaneous inflow and outflow of the medium, thus flushing any blood or mucus from the cavity and providing an optimal view. Rigid hysteroscopes are available with 0-, 12-, 15-, 30-, and 70-degree optical views. For diagnostic procedures, 30-degree endoscopes are primarily used in order to easily see the entire endometrial cavity, which can be done simply by rotating the telescope 360 degrees. Operative procedures most commonly require the 12- or 15-degree telescopes so that the operative component of the instrumentation can be visualized fully during the procedure. The operative hysteroscope uses a 4-mm rigid telescope within a 7- to 8-mm operative sheath, which can be configured to either provide a port for the insertion of accessory instruments (scissors, biopsy forceps, catheters, etc.) or a resectoscope with a working element for the resectoscope electrodes. Older models of operative hysteroscopes included only a single channel for installation of distension medium. Adequate egress of fluid usually is not possible with these hysteroscopes, because the only available exits are the fallopian tubes or around the hysteroscope through a patulous or overdilated cervix. Use of these single-channel hysteroscopes should be limited to high-viscosity distension media. Most commonly, operative hysteroscopy is performed with a continuous flow sheath allowing for input of the distension medium through a middle channel and egress of a low-viscosity distension medium through an outer evacuation channel. This provides for constant inflowto-outflow exchange of media, washing of the uterine cavity, and removal of blood and debris. Infusion of low-viscosity fluids can be accomplished either by the force of gravity or with infusion pumps. Suction tubing attached to the outflow port can be directed to wall suction or allowed to drain by gravity. Low-viscosity fluid pumps have been designed to operate in pressure ranges of 0 to 80 mm Hg. They can deliver fluid at a rate necessary to maintain a preset pressure with a maximum flow rate of 300 mL per minute, although the upper limit of flow through the outflow ports for most hysteroscopes is 250 mL per minute. Outflow usually is adjusted to be significantly lower than the maximum to allow adequate visualization, free from blood and debris; maintain adequate uterine distension; and minimize the amount of fluid needed to complete the procedure. Fluid management

systems are available that not only control the inflow pressure but also continuously measure the fluid deficit. Alternatively, inflow of the distension medium can be controlled by gravity. The height of the infusion bag above the patient controls the maximum intrauterine pressure. Every 1 foot of height above the patient that the bag of distension medium is placed will deliver approximately 25 mm Hg of pressure to the endometrial cavity. This system is then regulated by the amount of outflow to maximize visualization while maintaining adequate uterine pressure. Because pressure of inflow is constant, changes in intrauterine pressure, and thus distension, are affected by alterations of the rate of the outflow. Use of standard suction containers to collect the outflow will make fluid measurement and calculation of any fluid deficit straightforward. Modern operative hysteroscopy requires a video camera and video monitor for adequate operative visualization. A halogen or xenon light source providing 150 to 300 W of incandescent light is used and attached to the hysteroscope by a fiber optic light cable. The light cable should be inspected frequently to ensure that a significant number of the internal fibers have not broken and that the light cable is capable of delivering an adequate amount of light through the hysteroscope. Most chip cameras have the capability to adjust gain and can be integrated with the light source for automatic light balance. For documentation of findings and recording of procedures, video capture units may be used. Most commonly, VCRs are used to videotape pertinent portions of the procedure. Also available are video capture units for taking still pictures or storing digital images on a computer hard disk or CD. DVD recorders also may be used to capture digital videos. Energy for operative hysteroscopy can be delivered either with the neodymium-doped yttrium aluminium garnet (Nd:YAG) laser or with electrosurgical generators with either unipolar or bipolar electrodes. Other lasers, such as the carbon dioxide (CO2) laser, are not used in hysteroscopy because of their failure to penetrate fluid and because of the generation of smoke if CO2 is used as the distension medium. The Nd:YAG laser can be delivered through a flexible quartz fiber passed through the instrument channel of the operating hysteroscope, and its wavelength penetrates through the liquid distension medium used in hysteroscopy. The extent of tissue necrosis can be up to a depth of 4 to 5 mm. Varying the distance of the fiber tip and incident angle can regulate the extent of thermal damage. It is rendered ineffective at distances >2 cm or as the incident angle deviates more than 90 degrees. This laser is often used to perform endometrial ablation, using power outputs of 50 W by dragging the fiber over endometrial surfaces. Electrosurgery through a standard resectoscope typically utilizes a monopolar electrode, with the electrical probe serving as the source electrode and the return plate on the patient as the return electrode. The resectoscope can be used with either cut or coagulation output settings on the electrosurgical generator or a blend of the two. When used in the cutting mode, a high-frequency sine wave is delivered that creates extremely high current density, instantly superheating cellular water to vaporization, causing cellular architecture to explode, and resulting in tissue cutting. In the coagulation mode, delivery of high-frequency energy is interrupted by periods of modulation. This alternation of frequency and interruption results in wider zones of tissue coagulation and damage,

resulting in coagulation and sealing of blood vessels. A variety of electrode tips are available, including a cutting loop for excision of tissue, a rollerball or bar for coagulation and ablation, and a knife electrode for incision. Bipolar electrical generators (Versapoint, Gynecare Inc., Somerville, NJ) have recently been developed. Electrodes have been designed in several configurations, producing variable tissue effects. A ball tip can be used for vaporization with limited tissue desiccation, a spring tip for vaporizing larger amounts of tissue, and a twizzle tip for resecting and morcellating tissue. These tips have both active and return electrodes and require an electrolyte-containing medium such as saline. In contrast, when using a monopolar resectoscope, a non-electrolyte distension medium such as glycine must be used.

Distension Media Four basic types of distension media are used for hysteroscopy. The first type, CO2, is used primarily for diagnostic hysteroscopy in an office setting. Secondly, a high-viscosity medium such as Hyskon is used primarily with inflow only–type hysteroscopes. The third and fourth types are both low-viscosity solutions that are used with continuous-flow hysteroscopes, electrolyte solutions, and non-electrolyte solutions. The choice between an electrolyte and non-electrolyte solution will depend on the use of monopolar versus bipolar electrocautery. For diagnostic procedures in the office, some physicians choose CO2 as the distension medium. CO2 use requires a hysteroflator that delivers the gas at preset intrauterine pressures and has regulated flow rates. CO2 may be used with either a small diagnostic rigid hysteroscope or a flexible hysteroscope and does not require a return channel for continuous flow, because the CO2 gas will escape from the cervix or through patent fallopian tubes into the peritoneal cavity, where it is absorbed. Starting pressures for CO2 are usually between 50 and 75 mm Hg. If adequate distension is not achieved, it may be necessary to increase the intrauterine pressure to a maximum of 100 mg Hg or a maximal flow of 100 mL per minute. Higher pressures or flow rates may produce a gas embolus, and rare fatalities have been reported. CO2 will give an ideal view of the endometrial cavity that is not bleeding, because light reflection is identical to that of room air. However, any blood or mucus within the endometrial cavity will require changing to a liquid medium. Many physicians are routinely using low-viscosity solutions for office-based diagnostic procedures by using a large syringe as the delivery system. Since these procedures only take a few minutes to perform, larger volumes are not needed. Distention of the uterus can be controlled by varying the pressure on the syringe. For many years, prior to the evolution of hysteroscopes that accommodate continuous flow, 32% high-molecular-weight dextran-70 (Hyskon) was commonly used as a liquid distension medium for operative hysteroscopy. Its nonmiscibility with blood allows its use when either blood or mucus is present in the endometrial cavity or bleeding is anticipated. Hyskon is compatible with either the Nd:YAG laser or electric cautery devices. When using Hyskon as the distension medium, its delivery requires significant constant pressure to

overcome the resistance of a high-viscosity fluid flowing through the tubing and a standard diagnostic sheath. The major disadvantage of Hyskon is the difficulty in cleaning the solution from the instruments and stopcocks. If the instrumentation is not thoroughly cleaned, the dextran crystallizes and results in clouding of the hysteroscope lens and freezing of stopcocks. Rarely, patients may have an anaphylactic reaction to the dextran. Intravascular absorption of Hyskon results in a proportional 10-fold increase of intravascular volume, and if the absorbed volume is large, there may be accompanying cardiovascular overload and pulmonary edema. Careful monitoring of the amount of Hyskon intravasated during the procedure is mandatory, and absorption of 100 to 200 mL of Hyskon should warrant termination of the procedure. Because the molecular weight of Hyskon exceeds that which can pass into the circulation from the peritoneal cavity, spill through the fallopian tubes is inconsequential. Operative hysteroscopy most commonly uses low-viscosity solutions, which can be either electrolyte solutions or non-electrolyte solutions. If monopolar resectoscopes are used, non-electrolyte solutions are required so that the flow of energy will be directed from the electrode tip into the tissue and not allowed to “short circuit” through an electrolytecontaining medium throughout the entire uterus. The electrolyte-free solutions that are used most often for operative hysteroscopy include 1.5% glycine, sorbitol, 5.0% mannitol, and dextrose in water. Significant intravasation of distension medium may occur with resectoscope use. As tissue is resected, venous channels within the endometrium and myometrium are opened, and the pressure of the distension medium will result in the absorption of these solutions. The primary complications associated with non-electrolyte low-viscosity solutions include fluid overload and hyponatremia. Fluid overload may result in pulmonary edema, and severe hyponatremia may result in neurologic sequelae such as confusion, seizures, and even death. Intraoperative monitoring of inflow and outflow must be performed every 5 to 10 minutes throughout the procedure, and a discrepancy between 500 and 1,000 mL with non-electrolyte solutions should warrant termination of the procedure. Glycine use has also been reported to cause hyperammonemia because of its conversion from glycine to ammonia by the liver. Electrolyte solutions such as normal saline or lactated Ringer's solution are used with bipolar electrical devices or for continuous-flow diagnostic hysteroscopy. Because bipolar devices contain both the active and return electrodes at the electrode tip, electrolytes are needed to complete the electrical circuit. The primary complication associated with electrolyte solutions is fluid overload, and a discrepancy of 1,500 to 2,000 mL during the procedure warrants termination of the procedure. During operative hysteroscopy with significant operating time and use of large amounts of distension medium, the anesthesiologist should keep intravascular fluid replacement to a minimum to avoid fluid overload. Anesthesia personnel should also monitor the patient carefully for electrolyte abnormalities when using non-electrolyte solutions and anaphylactic shock under anesthesia when using Hyskon.

General Technique

Hysteroscopy can be difficult to perform during the luteal phase because of the abundance of endometrial tissue. Performing hysteroscopy during the early to middle follicular phase should ensure adequate visualization of the uterine cavity. Alternatively, the endometrium can be suppressed with 2 to 4 weeks of progestin therapy, or hysteroscopy may be performed at any time in a patient taking oral contraceptives because of the dominant atrophy effect of progestin. Gonadotropin-releasing hormone (GnRH) analogues have most commonly been used to prepare the endometrium for endometrial ablation. At least 4 weeks of preoperative treatment are required for GnRH analogs such as leuprolide acetate (Depo-Lupron), because these medications are initially agonists and will actually increase estrogen output for the first 7 to 14 days before subsequent down-regulation of the pituitary ovarian axis and subsequent endometrial atrophy. The cervix should be dilated no larger than the outer diameter of the hysteroscope that will be used. With many of the larger operative hysteroscopes, this will require dilation of the cervix to at least the diameter of a 20-French Hank dilator or a 9/10-French Hegar dilator. Care should be taken to avoid cervical lacerations and uterine perforation during cervical dilation. Preoperative treatment with intravaginal misoprostol can soften the cervix for easier dilation and may prevent cervical lacerations. With insertion of the hysteroscope, the cervical canal can be visualized and the hysteroscope guided into the endometrial cavity under direct vision. If overdilation of the cervix has occurred and the distension medium cannot be retained within the endometrial cavity, an additional tenaculum may be placed on the posterior lip of the cervix or a special four-pronged tenaculum can be used to compress the cervix around the hysteroscope. The cervical canal and internal os will appear off center within the field of view when using offset-angle lenses. When the angle of the lens is oriented to look downward, the internal os will appear at the 12 o'clock position. If the telescope is inverted and the lens is pointed upward, the os will appear in the 6 o'clock position. The latter position is useful for viewing a retroverted uterus. The surgeon should always maintain the camera position in a straight up-and-down orientation so that the view on the screen corresponds anatomically to the patient's position. As the hysteroscope is rotated to visualize the entire endometrial cavity, one hand should be kept on the camera to prevent its rotation; otherwise, the view on the monitor will be oriented improperly. With insertion of the hysteroscope, the cervical canal should be visualized and the endometrial cavity entered carefully through the internal os. If adequate visualization is prevented by blood and mucus, continuous flow of the distension medium should be maintained for 30 to 60 seconds to wash out blood and debris. If the field of view still appears red, the hysteroscope should be pulled back 1 to 2 cm, as it is a common mistake to insert the hysteroscope too far, and the lens may be obscured by abutting the uterine fundus. Visualization can also be compromised by inadequate distension of the uterine cavity because of insufficient intrauterine pressure. The fluid delivery devices should be checked to ensure adequate pressure. If a gravity system is being used, the height of the bag above the patient should be extended. Careful adjustment of the outflow should be made to clear any ongoing bleeding and debris without decreasing intrauterine pressure or using extremely large volumes of distension medium.

The entire endometrial cavity should be inspected carefully, including the identification of both tubal ostia, the fundus, and the anterior and posterior portions of the uterine wall. Video documentation of the intraoperative findings is useful. If operative techniques are to be used during the hysteroscopy, inflow and outflow should be measured carefully and reported to the surgeon every 5 to 10 minutes. If significant bleeding or a long operative time is anticipated, vascular constriction through the paracervical injection of a dilute pitressin solution may be used. Care should be taken to avoid intravascular injection of pitressin because reports of fatalities have been reported when that occurs.

Endometrial Ablation Approximately 35% of gynecologic complaints concern menorrhagia, and it is estimated that 60% of these women ultimately will be treated with hysterectomy. Endometrial ablation originally was developed as an alternative treatment for patients who are medically too unstable for the surgical stress of hysterectomy. Since its original development in the 1980s, however, patient selection criteria have now expanded, and hysteroscopic endometrial ablation is viewed by many as an alternative to hysterectomy, even in healthy patients. Prior to consideration of hysteroscopic endometrial ablation, endometrial pathology needs to be excluded with either a combination of endometrial biopsy to rule out hyperplasia or carcinoma and transvaginal ultrasonography with saline infusion to rule out polyps or submucous myomas. Alternatively, office diagnostic hysteroscopy could be performed with directed biopsies. Because the goal of an endometrial ablation is destruction of the functional layer of endometrium with the artificial creation of intrauterine synechiae, many experts feel that preoperative preparation of the endometrium with a GnRH agonist or continuous progestin will maximize the chance of adequate scar formation within the endometrial cavity. As an alternative, some authors perform a mechanical preparation of the endometrium by using a sharp curette or suction curettage immediately prior to endometrial ablation. This technique has the advantage of being able to immediately perform the procedure without a lengthy preoperative medical suppression of the endometrium. The disadvantage of a mechanical preparation, however, is the possibility of inadequate visualization during the procedure because of bleeding and the possibility of a compromised outcome secondary to inadequate destruction of the endometrial basalis.

TABLE 47.1 Global Endometrial Ablation Devices Device

Method Thermal

Cervical Tim Cavity Limit Dilation T (centimeters) (millimeters) (mi

ThermaChoice

balloon

5.0

4.0–10.0

Hydro ThermAblator

Circulated hot water

8.0

50% of their volume projecting into the cavity and are Table of Contents > 48 - Epidemiology, Pathophysiology, and Evaluation of Pelvic Organ Support

48 Epidemiology, Pathophysiology, and Evaluation of Pelvic Organ Support John O. L. DeLancey Pelvic organ prolapse is a condition that has been known to affect women since the earliest medical records 4,500 years ago. Attempts to correct this condition helped to define the specialty of obstetrics and gynecology. Although it is often discussed as a purely mechanical phenomenon, prolapse is associated with significant functional problems. Stress urinary incontinence, micturition difficulties, and problems with defecation are all associated with prolapse. These functional derangements are not simply results of altered support of the bladder and rectum but have to do with the innervation and musculature of the urinary and intestinal tracts as well. This chapter reviews the structural and functional aspects of prolapse necessary to understand and manage these conditions and describes current clinical evaluation of women who have pelvic organ prolapse.

The Pelvic Floor and the Nature of Genital Prolapse The pelvis lies at the bottom of the abdominopelvic cavity, and the pelvic floor closes the canal within the bony pelvis (Fig. 48.1). If the body cavity were a box containing the abdominal and pelvic organs, the pelvic floor would form the bottom of the box. It is the structure that carries the load. Its structural role can best be appreciated by considering a surgeon's hand placed through an abdominal incision that pushes caudally on the pelvic organs. All of the elements that prevent this hand from passing through the pelvic canal constitute the pelvic floor. In addition to this supportive role, the pelvic floor must accommodate conception and parturition while also controlling storage and evacuation of urine and feces. To understand the pelvic floor and genital prolapse, it is necessary to understand the mechanical strategies that evolution has put in place to prevent downward descent of the pelvic organs as well as the process by which genital prolapse occurs. As Victory Bonney pointed out, the phenomenon of prolapse is similar to the maneuver that a scrub nurse uses to evert the in-turned finger of a surgical glove (Fig. 48.2). Compressing the air within the glove drives the invaginated finger outward in much the same way that increases in abdominal pressure force the vagina and the uterus to prolapse. It is not the weight of the uterus that is important in the development of prolapse but rather the forces placed on the pelvic floor by increases in abdominal pressure.

Two mechanical principles explain how the pelvic floor prevents prolapse (Fig. 48.2). First, the uterus and vagina are attached to the walls of the pelvis by a series of ligaments and fascial structures that suspend the organs from the pelvic sidewalls. Second, the levator ani muscles constrict the lumina of these organs, forming an occlusive layer on which the pelvic organs may rest. It is a combination of these two factors—suspension of the genital tract by the ligaments and fasciae and closure of the pelvic floor by the levator ani—that holds the vagina over the levator ani muscles and forms a flap-valve closure. This flap-valve mechanism is instrumental in keeping the posterior cul-de-sac closed and preventing the development of an enterocele. Failure of this mechanism is common in women. The following sections describe how often it occurs, what changes are involved, and how to evaluate women who present with complaints of prolapse.

Figure 48.1 Sagittal section of the abdomen and pelvis shows the relation of the pelvic floor to the abdominal cavity. (From Kelly HA. Gynecology. Baltimore: Appleton and Co, 1928:64, with permission.)

Figure 48.2 A: Diagrammatic representation of the vagina within the abdomen shows how increases in abdominal pressure (arrow) force the vagina to prolapse. B: This prolapse may be prevented by (C) constricting the lower portion of the vagina, (D) suspending the vagina from the pelvic walls, and (E) forming a flap-valve closure, wherein the vagina is pinned against surrounding structures.

Epidemiology of Surgically Managed Pelvic Organ Prolapse Prevalence and Age of Occurrence Pelvic organ prolapse is the pelvic floor disorder that most often requires surgery (Fig. 48.3), followed by surgeries for stress incontinence and fecal incontinence. Based on national hospital discharge data, it is known that approximately 200,000 American women undergo procedures for pelvic organ prolapse, while 80,000 operations per year are done for stress urinary incontinence and approximately 2,000 are for fecal incontinence. In 1997, the National Hospital Discharge Survey information indicated that this is approximately 22.7 operations per 10,000 women. The mean age of these women is in their mid-50s. The annual direct cost of treating pelvic organ prolapse is slightly in excess of $1 billion annually. The effect of age on pelvic organ prolapse surgery has been studied in health maintenance organization populations. Olsen found that among 149,554 women over the age of 25 who were members of Kaiser Permanente Northwest Health Maintenance Organization, 384 women had surgical treatment for either pelvic organ prolapse or urinary incontinence or both in 1 year. They documented that a woman's lifetime risk for needing a single operation by age 80 was 11.1%. Among this group of women, there was a great

variety in the types and sizes of prolapse (Table 48.1). Repeat operations were remarkably common occurring in 29.2% of patients.

Figure 48.3 Operations for pelvic floor dysfunction.

In contrast to these data concerning surgical procedures required for pelvic floor dysfunction, studies of symptomatic women in the population offer a somewhat different picture. In a study of members of a group health plan (Kaiser Permanente Southern California) where 4,458 women were selected to represent the population, the prevalence of pelvic floor symptoms was as follows: pelvic organ prolapse, 7%; stress urinary incontinence, 15%; overactive bladder, 13%; and anal incontinence (including flatal incontinence), 25%. Overall, 37% of these women had symptoms of pelvic floor disorder. The difference between the number of operations and the occurrence of symptoms relates to the severity of the problem. For example, many women have relatively mild symptoms of stress or fecal incontinence and may not consider it a particular problem and do not seek surgical correction, while more women with symptomatic prolapse have their problem addressed surgically.

TABLE 48.1 Preoperative Prolapse Severity according to Operative Site No prolapse

Anterior Posterior Compartment Compartment (n[%]) (n[%]) 36 (9.4%)

61 (15.9%)

Apex (n[%])

Worst grade (n[%])

80 (20.8%)

14 (3.6%)

Grade 1

81 (21.1%)

73 (19.0%)

20 (5.2%)

54 (14.1%)

Grade 2

124 (32.3%)

92 (24.0%)

63 (16.4%)

173 (45.1%)

Grade 3

41 (10.7%)

21 (5.5%)

26 (6.8%)

61 (15.9%)

Not assigned

34 (8.9%)

25 (6.5%)

27 (7.0%)

59 (15.4%)

Not documented

68 (17.7%)

112 (29.2%)

168 (43.8%)

23 (6.0%)

N = 384. Source: From Olsen AL, Smith VJ, Bergstrom JO, et al. Epidemiology of surgically managed pelvic organ prolapse and urinary incontinence. Obstet Gynecol 1997;89:501.

TABLE 48.2 Risk Factors for Pelvic Organ Prolapse Definite Advancing age Vaginal delivery Probable Heritable issues Race or ethnic origin Family history of pelvic organ prolapse Connective tissue disorders Obstetric factors associated with difficult birth Forceps delivery Prolonged second stage of labor Infant birth weight >4,500 g Increased abdominal pressure

Occupations entailing heavy lifting Constipation Obesity Shape or orientation of bony pelvis Previous hysterectomy Hypothesized Young age at first delivery Pregnancy in the absence of vaginal delivery Selective estrogen receptor modulators Because of the increase in pelvic organ prolapse at advancing age, it is expected that the demand for services related to pelvic floor disorders can be expected to double in the next decades, justifying the need for all obstetrician and gynecologists to be experienced in its diagnosis and management.

Risk Factors There are multiple risk factors for pelvic organ prolapse, defined as being definite, probable, or hypothesized (Table 48.2).

Figure 48.4 Age-specific incidence of surgery for pelvic organ prolapse or urinary incontinence. (UI, urinary incontinence; POP, pelvic organ prolapse.) (From Olsen AL, Smith VJ, Bergstrom JO, et al. Epidemiology of surgically managed pelvic organ prolapse and urinary incontinence. Obstet Gynecol 1997;89:501, with permission.)

Factors Associated with Definite Occurrence Age The role of advancing age in the increased occurrence of pelvic organ prolapse is obvious (Fig. 48.4). Although prolapse can occur in young women and women soon after childbirth, the number of women treated for pelvic organ prolapse increases with advancing years. Because the available information comes from counts of surgical procedures performed, there is a decrease in data for very elderly, perhaps because surgery is less likely to be performed in these women who have in increased operative risk.

Figure 48.5 Parity information for women who were operated on for pelvic organ prolapse compared with that of the national average. (Nat'l Ave., national average.) (From Timonen S, Nuoranne E, Meyer B. Genital prolapse: etiological factors. Ann Chir Gynaecol Fenn 1968;57:363, with permission.)

Vaginal Delivery Of the pelvic floor disorders, pelvic organ prolapse is the one that is most strongly associated with vaginal delivery. In studying a longitudinally followed cohort of women, the Oxford Family Planning Study reported that there was increasing relative risk for developing prolapse with increasing vaginal parity, as shown in Figure 48.5. Although the likelihood of developing stress incontinence is also related to parity, this association is weaker (relative risk 2.4) than that of prolapse and advanced parity. The strength of this relationship depends to some extent on how one defines

prolapse. This strong association is found for women who require surgery. Specific features of vaginal birth also influence whether or not a woman develops prolapse later in life. Several factors that can be grouped together as descriptors of “difficult” vaginal delivery are associated with increased occurrence of prolapse: forceps delivery, prolonged second stage of labor, and large infant birth weight have been associated with pelvic organ prolapse. Unfortunately, because of the overlapping nature of these different factors, it is difficult to determine which are causal and which are associated. Forceps delivery is often used when there has been a prolonged second stage of labor, and both of these factors are increased in infants of large size. The role of childbirth in causing damage to the levator ani muscle, which is both associated with vaginal delivery and with pelvic organ prolapse, is probably the mediating mechanism in these injuries. This will be discussed later in the chapter in somewhat more detail.

Factors Associated Probable Occurrence Heritable Issues Although there are incontrovertible data concerning the relationship between advancing age and vaginal delivery in causing pelvic organ prolapse, there are a number of factors that have supportive evidence indicating their relationship to increased risk for developing pelvic organ prolapse but for which data are less well established. For example, some data suggest that race may play a role in modulating the likelihood that a woman may develop prolapse. In the 1997 National Discharge Summary, the surgery rate for whites (19.6 in 10,000) is approximately three times greater than it is for blacks (6.4 in 10,000). Other published data have indicated that Hispanic and Asian women appear to have an increased risk of developing pelvic organ prolapse when compared with white individuals, with modest increased risks of 1.20 among Hispanics and 2.20 in Asian women and decreased risk of 0.63 for black women. Prolapse seems to also occur more often in some families than others. Women who report that their mother had pelvic organ prolapse have an odds ratio of 3.0 for having prolapse compared with those without a family history, and women with a sister who have prolapse have an odds ratio of 2.4. This is likely related to heritable changes in pelvic floor tissues. There is information that women with prolapse have a decrease in type I collagen and an increase in type 3 collagen compared with women who do not have prolapse. In addition, circumstantial evidence suggests that patients with Marfan syndrome or Ehlers-Danlos syndrome may have an increase in prolapse occurrence. However, the overall number of women with these syndromes who have prolapse is only a tiny fraction of women presenting with this prolapse. Further evidence of genetic factors is emerging from new investigations of elastin homeostasis in knock out mice.

Increased Abdominal Pressure

The structural supports of the pelvic organs are subjected to the forces created by gravity and increases in abdominal pressure. There is evidence that chronic or significant increases in abdominal pressure may be related to increased occurrence of prolapse. Women who have pelvic organ prolapse are more likely to report straining at stool as a young adult than women without prolapse, and women with stage II or greater pelvic organ prolapse are also known to have an increased risk of reporting constipation compared with women who do not have prolapse. Because difficult defecation can be a symptom of prolapse, it is somewhat difficult to prove that it is causal. In addition, women who do more physically stressful occupations have a threefold odds ratio for developing prolapse compared with professional or managerial women.

Hypothesized Factors for Occurrence Several other factors that increase the risk of prolapse have been suggested, although they are less well established. Obesity, for example, seems to have a modest increase in risk for having prolapse; however, these studies have not had substantial number of patients with clinically evident prolapse (that below the hymeneal ring). Case-control information about women with definite prolapse and definite normal support has not found a difference in body mass index (BMI). There are several authors who have called attention to differences in shape and orientation of the bony pelvis between patients with prolapse and nonprolapse controls. Ironically, these seem to have to do with the upper dimensions of the pelvis, so the biomechanical reason for this is less well known. There has long been speculation that a previous hysterectomy might alter the chance that women will develop pelvic organ prolapse. In the Oxford Family Planning cohort, women who had previously undergone hysterectomy developed prolapse at a rate of 29 in 1,000 woman-years versus 16 in 1,000 woman-years for the entire cohort. However, the gap between previous hysterectomy and prolapse is quite long, being approximately 20 years, so there must be caution in making implications about the relationship between hysterectomy and prolapse. In addition, prolapse may in some ways be part of an indication for surgery although not listed in a way that retrospective review can discern, thereby potentially confounding these analyses. A number of other factors such as young age at first delivery, pregnancy in the absence of vaginal delivery, and selective estrogen receptor modulators have also been suggested as potentially influencing prolapse, yet definitive data concerning these issues at the present time validated by independent studies has not been available.

Anatomy and Pathophysiology of the Pelvic Floor Connective Tissue Supports Anterior and Apical Anatomy The topmost layer of the pelvic floor is a combination of the pelvic viscera and their

connections to the pelvic walls and will be referred to as the viscerofascial layer. Although it is common to speak of the fasciae and ligaments as separate from the pelvic organs, unless these fibrous structures have something to attach to (e.g., the pelvic organs), they have no structural integrity of the support unit. The uterus and vagina are attached to the pelvic walls by the fibrous tissue referred to as the endopelvic fascia. It forms a sheetlike mesentery that is continuous from the uterine artery to the point at which the vagina fuses with the levator ani muscles as it passes through the urogenital hiatus. The parametria are tissues that connect the uterus, and the paracolpium are those that attach to the vagina. Although given regional names, they are one continuous entity. The parametria comprise the cardinal and uterosacral ligaments. These are two different elements of the same tissue (Fig. 48.6). The uterosacral ligaments are the visible and palpable medial margin of the cardinal–uterosacral ligament complex. As is true of the remainder of the parametria, they contain smooth muscle, nerves, and blood vessels and are not the same type of tissue seen in the fascia of the rectus abdominus muscle, which is dense regular connective tissue.

Figure 48.6 Sagittal section of the pelvis shows the support structures of the genital tract. A: The bladder, urethra, and uterine corpus (above the cervix) have been removed. B: All of the pelvic organs have been removed to show the levator ani muscles. (M., muscle.)

Opposite the external cervical os, the sheet of tissue that attaches the genital tract to the pelvic wall arbitrarily changes name from the parametrium to the paracolpium. The paracolpium has two portions (Fig. 48.7). The upper portion (i.e., level I) consists of a relatively long sheet of tissue that suspends the vagina by attaching it to the pelvic wall in

an area similar to that of the cardinal–uterosacral ligament complex. It is this portion that prevents the upper vagina from prolapsing after the uterus has been removed. In the midportion of the vagina, the paracolpium attaches the vagina laterally and more directly to the pelvic walls (i.e., level II). This stretches the vagina transversely between these two lateral attachments (Fig. 48.7B). This arrangement has functional significance. The structural layer that supports the bladder (i.e., pubocervical fascia) is composed of the anterior vaginal wall and its attachment through the endopelvic fascia to the pelvic wall. The term fascia is used commonly, but this is not a layer separate from the vagina. Fibromuscular layer of the vagina, which contains both smooth muscle and connective tissue, is the term that has been proposed for this layer. These terms are used interchangeably in the remainder of the text because the surgeon generally refers to this layer as fascia. Similarly, the posterior vaginal fibromuscular layer and its connection to the pelvic walls form the restraining layer that prevents the rectum from protruding forward. In the distal vagina (i.e., level III), the vaginal wall is attached directly to surrounding structures without any intervening paracolpium.

Figure 48.7 Support structures of the vagina after hysterectomy. The bladder has been removed to expose the vagina. A: The paracolpium. B: The different levels of support structures. C: The details of the pubocervical and rectovaginal fasciae after a wedge of vagina and urethra has been removed (inset). (From DeLancey JOL. Anatomic

aspects of vaginal eversion after hysterectomy. Am J Obstet Gynecol 1992;166:1717, with permission.)

The support that lies under the urethra has special importance for urinary incontinence. The endopelvic fascia in this region is better developed and is tougher than the tissues of the upper vagina in the area under the bladder. This provides better support for the vesical neck than for the bladder. This layer of suburethral endopelvic fascia attaches laterally to the arcus tendineus fasciae pelvis and also to the medial border of the levator ani muscles. Loss of this normal support of the urethra at the vesical neck is responsible for stress incontinence of urine.

Mechanism of Anterior/Apical Support Structural support of the upper vaginal wall and uterus is intimately related. Loss of anterior vaginal wall support and uterine descent typically are part of the same process. This can be seen in the strong correlation between the degree of anterior vaginal wall/bladder descent (cystocele) and the degree of apical descent present in women. An understanding of the structural mechanics of that interaction can be seen in Figure 48.8. From a conceptual standpoint, the bladder can be considered to rest on a trapezoidal-shaped region of the anterior vaginal wall, as seen in the diagram. The lateral margins of this trapezoid lie at the arcus tendineus fascia pelvis, with the top held in place by the apical supports and the bottom attached at the pubic bones.

Figure 48.8 Conceptual diagram showing the mechanical effect of detachment of the arcus tendineus fascia pelvis from the ischial spine. Top: The trapezoidal plane of the

pubocervical fascia. The attachments to the pubis and the ischial spines are intact (left). The connection to the spine has been lost, allowing the fascial plane to swing downward (right). Bottom: The anterior vaginal wall as would be seen with a weighted speculum in place. Normal anterior vaginal wall support (left). The effect of dorsal detachment of the arcus from the ischial spine (right). (Copyright © DeLancey.)

With loss of apical support, this supportive layer rotates downward with prolapse of the bladder. This leads to a separation between the sidewall structures at the arcus tendineus and the edge of the pubocervical fascia in what has been referred to as a paravaginal defect. At present, it is not known whether this process directly involves detachment from the ischial spine or failure of the cardinal uterosacral complex or both. Data indicating the strength of this relationship is presented in Figure 48.9A. They represent measurements taken from magnetic resonance imaging (MRI) scans made at maximal Valsalva. The most dependent point of the bladder and the location of the uterine cervix were marked in women with varying degrees of pelvic organ support, ranging from normal support to prolapse. The correlation between bladder descent and descent of the cervix is strong, with half of the variation in bladder descent being explained by descent of the apex. Increased anterior vaginal length is responsible for an additional 30% of cystocele size with other less well-understood factors responsible for the remaining contribution to anterior wall descent.

Posterior Support Anatomy The anatomical structures involved in posterior vaginal wall support are shown in Figure 48.10. The upper portion of the posterior vaginal wall is suspended by the dorsal component of the cardinal–uterosacral ligament complex. The posterior arcus tendineus fascia pelvis can be seen to extend from this upper margin to the perineal body below. It is the connective tissue at the lateral vaginal wall and is not a separate structure from the vagina itself. Distally, the vagina and arcus fuse with structures of the perineal body. The perineal body unites the perineal membrane from one side of the pelvis with the other side (Fig. 48.11). It is the connection of the two perineal membranes in the midline that provides structural continuity to this supportive apparatus. As long as the connection is intact, it can resist downward descent of the perineum. If this connection is broken (Fig. 48.11B), then this structural continuity is lost. The anal sphincter complex closes the rectum. Figure 48.12 shows a simplified version of the structural mechanics of this region. Although it does not capture all of the intricacies of this support system, it provides a useful depiction of the major elements in posterior vaginal wall support. In panel A, the borders of the posterior compartment are shown with the perineal body and anal sphincter at the bottom, the levator plate formed by the decussation of the levator muscles in the midline dorsally, and the posterior vaginal wall on the ventral side. The levator muscles are responsible for holding the posterior compartment in the normal location where the posterior vaginal wall is held against the anterior wall (panel C). In panel B, it can be seen

what happens when the levators do not adequately close the pelvic floor. In this instance, high pressures within the rectum are not counterbalanced by contact with the anterior vaginal wall, and the connective tissue supports must come into play in order to resist this downward descent.

Pathophysiology of Posterior Compartment Problems The clinical implications of the mentioned anatomical relationships can be understood by considering the different elements of posterior vaginal wall support. The posterior wall above the perineal membrane may be considered to have the form of a square ship sail that is held above and below (Fig. 48.12B). The upward forces provided by the apical supports of the posterior vaginal wall suspend it and hold it over the levator plate formed by the dorsal decussation of the levator ani muscles behind the rectum. Distally, the posterior wall is attached to the cranial margin of the perineal body. The perineal body gains its structural support laterally from attachments to the ischiopubic rami through the perineal membrane. It is the connection of the two perineal membranes by the midline tissue of the

perineal body that establishes the structural integrity of this complex. If this connection is lost, as seen in Figure 48.11, then downward descent of the rectum can occur. Failure of the levators to hold the pelvic floor closed is also a critical element of this support system.

Figure 48.9 A (left): Valsalva MRI of a patient with anterior vaginal prolapse. (U, uterus; B, bladder, arrows, at sacrococcygeal joint and inferior pubic point for sacrococcygeal inferior pubic point [SCIPP] line). Right: System marking the most dependent portion of the bladder (black dot), uterine cervix (triangle), and urethra (circle). X axis follows SCIPP line and allows the locations of points to be determined and compared. B: The relationship between the magnitude of anterior compartment descent (caudal bladder point), and descent of the cervix below normal is displayed. (Based on Summers 2006. Copyright © DeLancey 2006.)

Figure 48.10 Dissection and illustration of posterior compartment anatomy seen in midline sagittal section of a cadaver with normal pelvic organ support from a 56-yearold multipara, showing structural relationships after the rectum has been removed. Note apical connections of the upper posterior vaginal wall to the inside of the pelvic wall in a retroperitoneal position. These lie below the peritoneum and are dorsal and caudal to what is traditionally referred to as the uterosacral ligament. These structures are continuous with the posterior arcus tendineus. At the distal end of the vagina, the vaginal wall merges into the top of the perineal body. The lateral and dorsal margins of the compartment are formed by the levator ani muscles (LA) and the levator plate. The asterisk (*) denotes the region of the sacrospinous ligament overlain by the coccygeus muscle. (Copyright © DeLancey.)

Figure 48.11 Intact perineal body (*) uniting the perineal membranes (PM) (left) and perineal body disruption (right).

Loss of connection between the two sides results in the formation of a rectocele low in the vagina at the level of the perineal body. Failure of the upper supports is associated with enterocele and high rectocele. When the apical failure is most severe, vaginal vault eversion occurs.

Levator Ani Muscles For many years, damage to the levator ani muscle has been suggested as a causal factor in development of pelvic organ prolapse. Recent data in a case-control study shows that women with prolapse have major defects in their levator ani muscles much more frequently than do women who have normal support. The tonic and constantly modulated contraction of the levator ani muscles supports the pelvic organs. By closing the pelvic floor, they protect the connective tissues from excessive force that would lead to their failure. It is this load-sharing relationship between the connective tissue supports and the levator ani muscles that is disturbed in women who develop prolapse.

Figure 48.12 A: Normal borders of the posterior compartment including the posterior vaginal wall (PVW), the perineal body (PB), and the levator plate (LP). B: Under load, the posterior wall apical suspension (arrow) resists downward displacement of the posterior vaginal wall and its attachment of the perineal body. C: Action of the levator ani to keep the genital hiatus closed, in which state the posterior wall is in contact with the anterior wall (note that this is not the case in B), preventing posterior wall prolapse. (Copyright © DeLancey.)

The levator ani muscles lie below the pelvic organs (Fig. 48.6B). They span the opening within the bony pelvis, providing a “floor” to support the abdominal and pelvic organs. They have two major divisions: a medial pubovisceral and puborectal component and a lateral iliococcygeal portion.

Figure 48.13 A: Schematic view of the levator ani muscles from below after the vulvar structures and perineal membrane have been removed, showing the arcus tendineus levator ani (ATLA), external anal sphincter (EAS), puboanal muscle (PAM), perineal body (PB) uniting the two ends of the puboperineal muscle (PPM), iliococcygeal muscle (ICM), and puborectal muscle (PRM). Note that the urethra and vagina have been transected just above the hymenal ring. © DeLancey.) B: The levator ani muscle seen from above looking over the sacral promontory (SAC), showing the pubovaginal muscle (PVM). The urethra, vagina, and rectum have been transected just above the pelvic floor. The internal obturator muscles have been removed to clarify levator muscle origins. (PAM, puboanal muscle; ATLA, arcus tendineus levator ani; ICM, iliococcygeal muscle.) (Copyright © DeLancey.)

The medial portion of the levator ani muscles originates from the pubic bones and attaches to the vagina, perineal body, and rectum, with only a few insignificant fibers ending in the coccyx (Fig. 48.13). Therefore, the term pubovisceral muscle has replaced the former term pubococcygeal muscle. This strong, robust, fatigue-resistant striated muscle starts on the inner surface of the pubic bone and has fibers that attach to near the midline and passes behind the rectum, to return to the pubic bone on the other side. It attaches to the vagina (pubovaginal) and perineal body (puboperineal) and sends fibers toward the anus (puboanal). The normal resting tone of this muscle squeezes the rectum, vagina, and urethra closed by compressing them against the pubic bone. The puborectalis muscle originates lateral to the pubovisceral muscle and forms a sling behind the rectum at the anorectal angle. Arising from the lateral pelvic walls (at the tendineus arch of the levator ani muscles) is the iliococcygeal muscle that forms a horizontal shelf on which the upper pelvic organs rest.

Levator Ani Muscle Damage and Pelvic Organ Prolapse Recent studies have proven the long hypothesized link between levator ani muscle impairment and pelvic organ prolapse. The advent of modern imaging has permitted the detailed structure of the levator ani muscle to be seen in women with pelvic organ

prolapse and in normal asymptomatic controls. The degree of damage visible varies from one woman to the next and so different degrees of damage have been studied and related to the occurrence of prolapse (Fig. 48.14). Defects were classified as none, with no visible defect; minor, with less than half of the muscle damaged; and major, with more than half of the muscle damaged. In a case-control study that compared asymptomatic healthy volunteers with age- and race-matched controls, women with prolapse had major defects more often than control women (Fig. 48.15). Major defects occurred in 55.0% of women with prolapse but in only 15.6% of asymptomatic controls; an odds ratio of 7.3.

Figure 48.14 Examples of different grades of the pubovisceral portion of the levator ani muscle defects. Subjects with unilateral defects are chosen to contrast different defect severity with normal muscle showing grade 1, 2, and 3 defects contrasted with normal muscle (0) on the contralateral side.

Figure 48.15 Percentages of cases and controls with no defects, minor defects, and major defects; P _.001. (DeLancey JOL. Levator ani impairment in prolapse. Obstet Gynecol 2007.)

Muscle function can be assessed by measuring vaginal closure force. This parameter assesses the forces created by the pelvic floor muscle and connective tissue that maintain vaginal closure. It can be studied at rest, reflecting tonic muscle activity plus connective tissue elastic forces and during a maximal contraction that assesses the increased force a woman can generate by voluntary contraction. Figure 48.16 shows data from a case-control study demonstrating that women with defects had approximately 40% less force during maximal contraction compared with women who had no defect in both the prolapse and the normal support groups. The women with prolapse had a 40% lower maximum contraction force for each defect level than the normal women.

Figure 48.16 Vaginal closure force and augmentation of vaginal closure force with maximum pelvic floor muscle contraction stratified by cases and controls and by levator ani muscle defect status. Means are shown in the columns, and standard error bars are shown. Resting vaginal closure force did not differ by case and control cohorts or by levator ani defect status. (DeLancey JOL. Levator ani impairment in prolapse. Obstet Gynecol 2007.)

Levator Ani Muscle Damage during Birth Injury from Vaginal Birth Vaginal birth is a primary source of levator ani muscle impairment. Approximately 10% to 15% of women who deliver vaginally will develop a visible defect in the levator ani muscle, with 90% occurring in the pubovisceral portion of the levator ani muscle. Women who have new stress incontinence after their first birth are twice as likely to have sustained this type of injury. These injuries are visible in both MRI and ultrasound. Compared with women who did not develop a defect, women who did develop a defect were, on average, 3 years older and had second-stage lengths that were more than an hour longer. Increased odds ratios were found for forceps (14.7), anal sphincter rupture (8.1), and episiotomy (3.1). Vacuum, oxytocin, and epidural use did not differ between the groups.

Figure 48.17 Bowling-ball model. Left: Computer model of selected levator ani muscle bands before birth, with muscle fibers numbered and the muscle groups identified. Middle: Muscle band lengthening present at the end of the second stage of labor. Right: Graphic representation of the original and final muscle (top) and the stretch ratio (bottom), indicating the degree to which each muscle band must lengthen to accommodate a normal sized fetal head. Note that the pubococcygeal muscle fascicles labeled PC2 undergo the greatest degree of stretch and would be the most vulnerable to stretch-induced injury. (From Lien KC, Mooney B, DeLancey JO, et al. Levator ani muscle stretch induced by simulated vaginal birth. Obstet Gynecol 2004;103:31–40. Copyright © Biomechanics Research Laboratory 2005.) (See Color Plate)

Mechanisms of Levator Ani Muscle Injury Recent computer models have suggested that some muscle damage during the second stage of labor may come from overstretching, because those parts of the muscle that are stretched the most are those parts that are seen to be injured. Using a computer model of the levator ani muscle based on anatomy from a normal woman, the degree to which individual muscle bands are stretched could be studied (Fig. 48.17). This analysis revealed that the muscle injured most often, the pubovisceral (pubococcygeal) portion, was the portion of the muscle that underwent the greatest degree of stretch; the second area of observed injury, the iliococcygeal muscle, was the second-most stretched muscle. Furthermore, when the portion of the muscle at risk was identified in cross sections cut in the same orientation as axial MRI scans, the pattern of predicted injury matched the injury seen in MRI (Fig. 48.17). There have also been several studies based on electrodiagnostic techniques, demonstrating that birth causes changes in mean motor unit duration after vaginal birth as well as changes in pudendal terminal motor latency. Abnormal tests have been seen in women with both prolapse and stress incontinence. Although the pudendal nerve innervates the voluntary urethral and anal sphincters, it does not innervate the levator ani muscles, which receive their own nerve supply from the sacral plexus. At present, it is not clear whether the visible levator defects are from neurologic or stretch injury.

Clinical Implications of Levator Ani Muscle Injury Interaction between the Muscles and Fasciae The interaction between the pelvic floor muscles and ligaments is critical to proper function. As long as the pelvic floor musculature functions normally, the pelvic floor is closed and the ligaments and fasciae are under no tension. The levator ani closes the vagina by creating a high-pressure zone similar to the high-pressure zones created by the urethral and anal sphincter muscles. The muscles and ligaments must resist the downward force applied on the pelvic floor by the superincumbent abdominal organs as well as the forces that arise from increases in abdominal pressure during cough and sneeze or from inertial loads placed on them (e.g., when landing from a jump). Although the ligaments can sustain these loads for short periods, if the pelvic floor muscles do not close the pelvic floor, then it is more likely that the connective tissue will become damaged and eventually fail to hold the vagina in place. This normal-load sharing between the adaptive action of the muscles and the energyefficient action of static connective tissues is part of the elegant load-bearing design of the pelvic floor. When injury to one of these two components occurs, the other must carry the increased demands placed on it. When the muscle is injured, the connective tissue is subjected to increased load. If this load exceeds the strength of the pelvic tissues, they may be stretched or broken and prolapse may result. This forms a causal chain of events by which pelvic muscle injury may influence pelvic organ prolapse or urinary incontinence. In addition, there is accumulating evidence that women who are operated on for pelvic organ prolapse or urinary incontinence have higher postoperative failure rates if they have levator ani muscle impairment assessed by biopsy or muscle function testing than do women who have normal muscles.

Nerves Anatomy There are two main nerves that supply the pelvic floor relative to pelvic organ prolapse. One is the pudendal nerve that supplies the urethral and anal sphincters and perineal muscles, and the other is the nerve to the levator ani that innervates the major musculature supporting the pelvic floor. These are distinct nerves with differing origins, courses, and insertions. The nerve to the levator originates from S3 to S5 foramina, runs inside of the pelvis on the cranial surface of the levator ani muscle, and provides the innervation to all the subdivisions of the muscle (Fig. 48.13). The pudendal nerve originates from S2 to S4 foramina and runs through the Alcock canal, which is caudal to the levator ani muscles. The pudendal nerve has three branches: the clitoral, perineal, and inferior hemorrhoidal that innervate the clitoris; the perineal musculature and inner perineal skin; and the external anal sphincter, respectively.

Neural Injury and Pelvic Floor Dysfunction

A unifying neurogenic hypothesis has been well established as a contributor to pelvic floor dysfunction. Although there is a significant body of literature regarding neurogenic causes of fecal and urinary incontinence, there is comparatively little exploring the relation between nerve damage and prolapse. Prospective study of perineal descent on defecography and pudendal nerve terminal motor latency failed to show any relationship between pudendal nerve damage and increased degree of perineal descent. Two studies where prolapse patients were included did not show a difference in the pudendal nerve terminal motor latencies in patients with prolapse. However, electromyographical studies of women with pelvic floor dysfunction, including prolapse and incontinence, found changes consistent with motor unit loss or failure of central activation. This is an active field of research, and there are likely to be more insights into the important role of nerve injury in the coming years.

Diagnosis and Classification Determining the type and severity of prolapse in any given patient is a skill that should be acquired through practice and careful observation. Characterizing the degree of support loss as normal or abnormal depends on comparisons with the findings in normal multiparous women in the examiner's experience. Therefore, it is helpful to perform the same examination on a sufficient number of asymptomatic patients without prolapse to become familiar with the range of normal support. In performing an examination to determine the type and severity of prolapse, the practitioner has two important points to consider: Examination must be made with the patient straining forcefully enough that the prolapse is at its greatest. The examiner must examine each element of support independently. If a patient is not able to strain sufficiently in the lithotomy position so that the prolapse is at its largest, examination in the standing position may be necessary. This is a critical point, because it is only when the prolapse can be seen in its fullest extent that all of its various elements can be assessed. For example, a large cystocele may be seen initially when the patient strains. It may be only with continued effort by the patient that an enterocele and prolapse of the vaginal apex can be demonstrated. To make sure that all aspects of the prolapse can be evaluated, the patient should be asked how large her prolapse is at its largest, and the physician should persist in the examination until that size is achieved. Once the prolapse is visible, the elements of the vagina and pelvic organs that have prolapsed can be evaluated. Once the prolapse is maximally developed, the physician should begin by identifying how much the anterior wall, cervix, and posterior wall have prolapsed. The anterior and posterior walls should be examined separately by retracting the opposite wall with the posterior half of a vaginal speculum. A stepwise, site-specific examination is important, because a large cystocele, for example, may hold a potential rectocele in place and therefore hide it. If a rectocele is not recognized preoperatively, its repair may be overlooked and the defect can become symptomatic postoperatively. These observations

have been confirmed on dynamic colpoproctography imaging studies of the pelvic floor, with contrast placed in the bladder and rectum while the patient strains in the standing position. If the patient has a full bladder when imaging is performed, a rectocele can be obstructed and will not be evident until the patient empties her bladder. Care must also be taken to assess how much of the loss of support is from a defect of the apical (level I) support. It is not uncommon to correct the apical defects and find that much of what was considered a cystocele and rectocele has been corrected. Examination while under anesthesia is used to evaluate pelvic masses, but it is not the optimal time to identify defects caused by prolapse because of the patient's inability to perform the Valsalva maneuver and because of loss of normal levator tone.

Examination: Patterns of Pelvic Organ Support Failure Anterior Vaginal Wall Examination of the anterior vaginal wall should establish the status of urethral support as well as bladder support. The urethra is fused with the lower 3 to 4 cm of the vaginal wall, and abnormal support in this region is properly referred to as a urethrocele (Fig. 48.18). Defective support of the upper portion of the vagina is called a cystocele because the bladder lies adjacent to this portion of the vaginal wall (Fig. 48.19). The urethrovesical crease, normally visible on examination, forms the line of demarcation between these two areas of support (Fig. 48.20). When support of the entire anterior wall is defective, the term cystourethrocele is used. The anterior vaginal wall should be above the hymenal ring during straining. Descent of the lower anterior vaginal wall to the level of the hymenal ring during straining is characteristic of a urethrocele and is seen often in patients with stress urinary incontinence. This is due to loss of urethral support and corresponds to the loss of the posterior urethrovesical angle on radiographic studies of patients with stress incontinence. The lower anterior vaginal wall is mobile in all women and may move significantly in continent multiparas. Therefore, motion of this region does not establish stress incontinence but rather indicates the degree to which the support of the urethra has failed. Descent below the hymenal ring is definitely abnormal and indicates a cystourethrocele whether or not stress incontinence is present.

The anterior vaginal wall above the urethrovesical crease usually lies in a flat plane at about a 45-degree angle from the horizontal (Fig. 48.20). Descent below the level of the hymenal ring is significant. This descent can be caused by one of three entities: separation of the paravaginal attachment of the pubocervical fascia from the white line due to detachment from the ischial spine loss of the vagina's attachment to the cervix tearing in the pubocervical fascia that results in herniation of the bladder through this layer.

Uterus and Vaginal Apex The vagina and cervix are fused with one another, and prolapse of the uterine cervix is associated invariably with prolapse of the upper vagina as well. When the uterus descends below its normal level, the term uterovaginal prolapse is appropriate, although uterine prolapse commonly is used. In patients in whom the uterus has been removed, descent of the vaginal apex below its normal position in the pelvis is referred to as prolapse of the vaginal apex, and when the vagina turns entirely inside out, the term vaginal eversion is used. The location of the cervix customarily is used to gauge the severity of uterine prolapse (Fig. 48.21). Its position relative to the hymenal ring should be noted while the prolapse is at its greatest. If the cervix is not visible because of a cystocele or rectocele, then its

location may be palpated while having the patient strain. When the cervix descends to within 1 cm of the hymenal ring, there is a significant loss of support. In instances in which the uterus is not necessarily going to be removed, uterine support should be tested before it is assumed that the uterus is well supported. This can be done by grasping the cervix with a tenaculum or ring forceps and applying traction until it stops descending. Occult prolapse, in which the cervix comes below the hymenal ring, can be detected in this way.

In addition to determining how far the cervix descends, its length should be measured. Cervical elongation is frequent in individuals with prolapse, and the uterine corpus often may lie in its normal location. Awareness of cervical elongation preoperatively will allow the surgeon to proceed expeditiously with the hysterectomy rather than hoping with every pedicle that the uterine arteries will soon appear.

Posterior Vaginal Wall The posterior vaginal wall is the site of both rectoceles and enteroceles. Evaluation and correction of these two problems challenge even the most experienced gynecologic surgeon, and they are probably the most difficult to understand of all pelvic support defects. Because dyspareunia can follow repair, correction of asymptomatic posterior wall defects is not without risk. On the other hand, having a rectocele or enterocele develop after vaginal hysterectomy and anterior colporrhaphy is an undesirable outcome, and careful consideration of the

support of the posterior vaginal wall is important. Three questions should be asked by the physician when examining the posterior wall. Is it supported normally? If not, is it a true rectocele or a pseudorectocele? Is an enterocele present? A rectocele is present when the anterior rectal wall and overlying vagina protrude below the hymenal ring. An enterocele exists when the cul-de-sac becomes distended with the intestine and bulges the posterior vaginal wall outward. There are also occasions in which the posterior wall appears to bulge into the vagina, not because of poor support of the rectal wall but because of a deficiency in the perineal body. This has been referred to by Nichols and Randall as a pseudorectocele and can be differentiated easily from a true rectocele because the anterior rectal wall contour is normal on rectal examination. Another type of pseudorectocele may be suspected when there is apical descent of the upper vagina or cervix and apparent loss of posterior support. However, often when the normal apical support is restored (by temporarily supporting it with ring forceps in the office or after surgical repair of the apical descent), a suspected rectocele is not evident. This is important to determine preoperatively, because loss of tone of the levator ani muscle and anal sphincter muscle with muscle paralyzing agents during anesthesia make it harder to establish the existence of a true rectocele.

Enterocele There is always a cul-de-sac between the upper vagina and the rectum. This allows a culdocentesis to be performed and a colpotomy to be made through the posterior vaginal wall at the beginning of a vaginal hysterectomy. The peritoneal pouch normally extends 3 to 4 cm beyond the junction of the vagina and cervix. Therefore, the absence of an enterocele in normal women must be explained by factors that keep the cul-de-sac closed rather than by the absence of a peritoneal space between the upper vagina and rectum. It is the suspension of the upper vagina near the sacrum in a position where it may rest over the rectum and intact levator plate that keeps this space closed. There are two types of enterocele: pulsion enterocele and traction enterocele. A pulsion enterocele exists when the cul-de-sac is distended and appears as a bulging mass that is inflated by increases in abdominal pressure. This may occur with either the vaginal apex or uterus well suspended, in which case the cervix or vaginal apex is at a normal level and the enterocele dissects between the vagina and the rectum. When an enterocele is associated with prolapse of the uterus or vaginal apex, then the prolapse and enterocele occur together. A traction enterocele represents a situation in which prolapse of the uterus pulls the culde-sac peritoneum down with it but there is no bulging or distension of the cul-de-sac when abdominal pressure rises. This condition usually is found at the time of vaginal hysterectomy when the cervix has prolapsed. It represents a potential enterocele rather than an actual enterocele because there is no bulging mass separate from the uterus.

Unlike uterine prolapse, which is obvious because of the protrusion of the easily recognized uterine cervix, enteroceles and rectoceles rarely are evident on examination. Therefore, the key to detecting an enterocele lies in actively looking for it whenever a patient who has prolapse is examined. Detection of an enterocele is performed best in the awake, straining patient by noting a mass of small intestine between the rectum and vagina; it may not be suspected in a supine individual at rest. Anatomically, an enterocele extends from the apex of the vagina downward, whereas a rectocele typically begins in the lower portion of the vagina. An enterocele sometimes is evident as a bulge that overrides the more caudal rectocele (Fig. 48.22). Careful inspection of the posterior vaginal wall with a speculum retracting the anterior wall sometimes can suggest that an enterocele is present. The key to detecting a pulsion enterocele lies in palpating the small bowel between the vagina and rectum during rectovaginal examination, with the patient straining so that the prolapse is protruding. To do this, an index finger is placed in the rectum, and a thumb is placed in the vagina. Then, with the patient straining, the rectovaginal space may be palpated to detect the bulge of the enterocele and the presence of small bowel, omentum, or large bowel.

Rectocele The hallmark of a typical rectocele is the formation of a pocket that allows the anterior rectal wall to balloon downward through the introitus. When a rectal examination is

performed with the prolapse fully developed, a rectocele exists if there is an extension of the rectal lumen below the axis of the anus (Fig. 48.23). This not only provides the diagnosis but also illustrates the mechanism by which rectoceles create their symptoms. As long as the anterior rectal wall has a smooth contour and no sacculation, even though it may be more mobile than normal, stool will pass through the anus. However, when a pocket develops as the patient strains, stool becomes trapped in it, and difficulty with evacuation can occur.

Prolapse Subsequent to Hysterectomy Special consideration should be given to patients who have prolapse after hysterectomy to assess whether or not prolapse of the vaginal apex is present. When the uterus is in situ, the cervix calls attention to the poor support of the cervix and upper vagina. In instances of posthysterectomy vaginal prolapse, descent of the vaginal apex is more easily missed. If it is overlooked and an anteroposterior colporrhaphy is not accompanied by suspension of the vaginal apex, the colporrhaphy will fail to cure the apical prolapse and the problem is not corrected. Overlooking apical support loss also can lead to overly aggressive excision of vaginal tissues during anteroposterior colporrhaphy and a shortened vagina. Examination of patients who have previously had a hysterectomy should include a specific effort to determine the location of the vaginal apex when the prolapse is at its largest. The apex is identified by the vaginal scar at the hysterectomy site (Fig. 48.24). Vaginal prolapse is present when the hysterectomy scar lies below the level of the hymenal ring. If the apex descends to within the lower one third of the vagina with straining, a significant deficit in support of the apex is present and the vagina should be resuspended during repair.

Figure 48.23 A: Pelvic examination shows a rectocele. B: Lateral bead chain cystourethrogram with the patient supine and with contrast in the vagina and rectum shows a protruding rectocele. (Copyright © DeLancey, 1993.)

Evaluation of Pelvic Organ Prolapse Pelvic Organ Prolapse Classification Several classification systems have been used to describe the sizes and types of pelvic organ prolapse in a woman. Because many of these systems use similar words to indicate different degrees of prolapse, confusion has arisen concerning the size of prolapse. For example, grade 2 uterine prolapse in some systems indicates that the cervix descends halfway between its normal position and the introitus. In other classifications, grade 2 can mean that one half of the uterus is outside the introitus. A system that standardizes terminology has been adopted by several groups, including the International Continence Society, the American Urogynecologic Society, and the Society of Gynecologic Surgeons. This standardized terminology (pelvic organ prolapse quantification, or POP-Q) provides a system that can describe the type of prolapse as well as quantify the degree of prolapse in each area. Although this standardized system seems somewhat cumbersome when described in writing, in actual practice it is quite simple. The following section first considers the measurements that describe the type and size of prolapse and then discusses the measurements concerned with the changes in the urogenital hiatus in the levator ani muscles through which the prolapse descends.

Figure 48.24 Eversion of the vagina after hysterectomy. Note that the vaginal apex, indicated by the puckered scar where the cervix had been removed, lies below the hymenal ring. (Copyright © DeLancey, 1993.)

Measurements Describing Prolapse Type and Size To describe the nature of a woman's prolapse, it is necessary to do the following: (a) document what part or parts of the genital tract have prolapsed, and (b) indicate how far down each part of the vaginal wall or cervix has descended. Prolapse description must include a consideration of anterior vaginal wall descent, posterior wall descent, and uterine descent (or prolapse of the vaginal apex after hysterectomy). Furthermore, because different parts of the anterior wall might suffer support damage, the system provides for determining the status of each level of vaginal support. For example, the distal anterior vaginal wall adjacent to the urethra may be well supported, while the portion of the vagina under the bladder may prolapse. This system addresses the need to make individual assessments of different parts of the vaginal wall. The three levels of vaginal support (Fig. 48.7) must be assessed, corresponding to the different anatomic regions of vaginal support: Level I: support of the vaginal apex and uterus Level II: support of the bladder and rectum Level III: support of the urethra and perineal body. In levels II and III, the anterior and posterior vaginal wall are considered separately, while in level I, the cervix (or vaginal apex) and posterior fornix must be assessed. To understand the POP-Q classification system, refer to Figure 48.25. The size and type of prolapse are measured by determining the location of a series of points on the anterior and posterior vaginal walls relative to the hymenal ring. Points at each of the three levels are measured. Positive numbers reflect measurements of the vaginal points that have prolapsed below the level of the hymen, and negative numbers reflect measurements above the hymen. It should be noted that this descriptive scheme does not distinguish between rectocele and enterocele but simply provides a way to quantify the amount of vaginal wall descent in each specific area. Additional examination and written comments concerning these important differences should be made. A summary of the measurements obtained during the POP-Q examination is noted in Table 48.3. I. Vaginal points (vaginal profile): patient straining maximally A. Level I: apex and cervix, points C and D (D is omitted if patient has had a hysterectomy)

Figure 48.25 Six sites (points Aant, Bant, C, D, Bpost, and Apost), genital hiatus (gh), perineal body (pb), and total vaginal length (tvl) used for pelvic organ support quantitation.

TABLE 48.3 Stages of Pelvic Organ Prolapse based on Measurement of Specific Sites

Stage 0

No prolapse is demonstrated. Points Aant, Apost, Bant, Bpost are all at –3 cm and either point C or D is between – total vaginal length (tvl) cm and – (tvl-2) cm (i.e., the quantitation value for point C or D is ≤– [tvl-2] cm)

Stage I

The criteria for stage 0 are not met, but the most distal portion of the prolapse is >1 cm above the level of the hymen (i.e., its quatitation value is > -1 cm) The most distal portion of the prolapse is between

Stage II

1 cm above and 1 cm below the plane of the hymenal ring (i.e., its quantitation value is ≥ -1 cm but ≤ +1 cm)

Stage III

The most distal portion of the prolapse is >1 cm below the plane of the hymen but protrudes no farther than 2 cm less than the tvl in centimeters (i.e., quantitation value is > +1 cm but < + [tvl-2] cm)

Stage IV

Essentially complete eversion of the total length of the lower genital tract is demonstrated. The distal portion of the prolapse protrudes to at least (tvl-2) cm (i.e., its quantitation value is < -1 cm)

Tvl, total vaginal length. B. Level II: midvaginal points 1. Anterior wall: Ba or Bant 2. Posterior wall: Bp or Bpost C. Level III: distal vagina (perineum and urethrovesical neck) 1. Anterior wall: Aa or Aant 2. Posterior wall: Ap or Apost 3. External measurements: obtained with patient at rest and again straining A. Genital hiatus: length, gh B. Perineal body: length, pb

II. Internal digital measurements: obtained with patient at rest with vaginal apex restored to normal position A. Total vaginal length: tvl To measure the lower third of vaginal support (level III), the location of a pair of points that normally lies 3 cm above the hymenal ring is assessed. Points measured at level III are called points A. One can imagine marking these vaginal points 3 cm above the hymen with a marker and then recording the position of these points in relation to the hymen with the subject straining maximally. Anteriorly, this corresponds to the approximate location of the urethrovesical junction, and this measurement assesses urethral descent (Aa or Aant). Posteriorly, this region is normally occupied by the tissues of the perineal body (Ap or Apost).

By definition, the highest possible position of either point Aant or Apost is 3 cm above the hymen (–3), and the lowest position is 3 cm below the hymen (+3). To assess midvaginal support (level II), the most dependent part of the vaginal wall above point Aant is used. This point is called Ba, or Bant, on the anterior wall and Bp, or Bpost, on the posterior wall. Therefore, this is not a fixed point along the surface of the vagina but rather is marked at whatever location is the most caudal (distal) portion of that vaginal segment at maximal prolapse protrusion. In a normally supported vagina, this will be the same as point Aant, whereas it will be the same as point C in a woman with procidentia. The same is true for the posterior vaginal wall at point Bpost. Point C corresponds to the most distal portion of the uterine cervix or of the hysterectomy scar in the vagina in those patients who have had the uterus removed. Point D denotes the posterior fornix (that point at which the posterior vaginal wall changes direction). In addition to the positions of these points, the total length of the vagina is noted. Once these data have been gathered, a simple line diagram can be constructed by plotting these points relative to the hymen to provide a graphic representation of the prolapse (Fig. 48.26). So far, each element of the prolapse has been considered separately. It is also possible to give an overall description to the size of the prolapse by looking at the most dependent part of the protruding vagina or uterus. In this way, different stages—stage 0 through stage IV—can be defined; a description of these is shown in Table 48.3. A briefer version of the original description of the POP-Q staging system has been summarized as well. The choice of the term stage here is somewhat unfortunate, because most women with stage I and II support are anatomically normal. The implication that they have a stage of prolapse is incorrect. Hopefully, this problem with terminology will be corrected in the future.

Pelvic Floor Measurements In normal women, the levator ani muscles close the pelvic floor. In women with pelvic organ prolapse, the urogenital hiatus within the levator ani muscles is the opening through which the vagina prolapses. This hiatus is enlarged in women with pelvic organ prolapse. The size of the urogenital hiatus and thickness of the perineal body can easily be measured to describe the changes that have occurred in the pelvic floor. The anteroposterior diameter of the genital hiatus extends from the arch of the pubic bone to the front of the perineal body, while the thickness of the perineal body is measured from the anterior margin of the perineal body to the center of the anal verge. The urogenital hiatus is held closed by the constant activity of the levator ani muscles, and the diameter of this opening enlarges in many women with prolapse.

Figure 48.26 Diagram of prolapse sites. (From Viereck V, Peschers U, Singer M, et al. Metrische Quantifizierung des weiblichen Genitalprolapses: eine sinnvolle Neuerung in der Prolapsdiagnostik? Geburtshilfe Frauenheilkd 1997;57:177, with permission.)

This classification system is detailed and specific. It requires careful examination and assessment. Although at first it seems quite detailed, it is simply the quantitative documentation of the individual defects that experienced surgeons always have found necessary to assess. Some clinicians will not find it expedient to measure each of these sites, but intelligent, detailed analysis of each site of support is important to plan properly any repair for pelvic organ prolapse.

Symptoms All types of prolapse have several symptoms in common. Once the vagina prolapses below the introitus, it becomes the structural layer between the high pressures in the abdominal space and the relatively low atmospheric pressure. The downward force that this pressure differential creates puts tension on the fasciae and ligaments that support the vagina and uterus. This results in a dragging sensation where the tissues connect to the pelvic wall, usually identified by patients as occurring in the groin, and in sacral backache caused by traction on the uterosacral ligaments. This type of discomfort resolves when the patient lies down and the downward pressure is reduced. In addition, exposure of the moist vaginal walls leads to a sensation of perineal wetness that may be confused with urinary incontinence, and it also can give rise to ulceration of the vaginal wall. Most patients have an underlying sense of insecurity that is difficult for them to describe and is often expressed as a feeling that “something is just not right.” Sometimes, patients who feel the cervix or vagina protruding have fears that they have a cancer and may be relieved to find that the condition is related to prolapse. Although patients may find it difficult to put their symptoms into words, the symptoms can cause significant distress and should not be ignored.

Anterior Wall Prolapse

The symptoms of cystourethrocele are varied, and the two primary ones are paradoxical. On the one hand, loss of support of the urethra and the lower vaginal wall is associated with stress urinary incontinence, whereas loss of support of the upper anterior vaginal wall and bladder base can cause difficulty in emptying the bladder. This inability to empty the bladder completely is probably related to voiding by the Valsalva maneuver. If there is a detrusor contraction, there should be no reason for a woman with a cystocele not to empty her bladder, and many women with a significant cystocele have normal postvoid residual urine volumes. When a woman strains to void, however, the cystocele simply gets bigger, and no impulse is provided for urine to flow through the urethra. In addition to these functional symptoms, many patients with a cystourethrocele complain of urinary urgency and frequency. This probably arises from stretching of the bladder base that accompanies its prolapse through the vaginal introitus; it is often less pronounced at night when patients are supine. Patients have a varying amount of support loss under the urethra or bladder, and symptoms vary along the spectrum from incontinence to urinary retention. As is true for other forms of prolapse, it is important to correlate a patient's symptoms with the physical findings so that these problems can be addressed.

Prolapse of the Uterus, Prolapse of the Vaginal Apex, or Enterocele Few specific symptoms are related to prolapse of the uterus, prolapse of the vaginal apex, or enterocele. Patients with these conditions usually complain of the generalized symptoms of prolapse mentioned previously. Some have urgency and frequency, probably related to pressure of the prolapse on the bladder base, but this is variable. In addition, patients with large, thin enteroceles occasionally have a sense of impending rupture. Although this is an uncommon problem, it should not be overlooked.

Summary Points Annually, approximately 200,000 American women have surgery for pelvic organ prolapse. The main risk factors for pelvic organ prolapse are age, vaginal delivery, race, and family history. The combination of two mechanical factors—suspension of the genital tract by the ligaments and fasciae and closure of the pelvic floor by the levator ani—holds the vagina over the levator ani muscles and forms a flap-valve closure, preventing prolapse. The levator ani muscles and the connective tissues in the pelvic floor act together to share the load. When the muscle is injured, the connective tissue is subjected to increased load. If this load exceeds the strength of the pelvic tissues, they may be stretched or broken, and prolapse may result. The degree of anterior vaginal wall/bladder descent (cystocele)

correlates strongly with the degree of apical descent because the structural support of the two is intimately related. Approximately 10% to 15% of women who deliver vaginally develop a visible defect in the levator ani muscle. Women with prolapse have major defects in their levator ani muscles much more frequently than do women who have normal support: 55% versus 15%, respectively (odds ratio 7.3). The two main nerves that supply the pelvic floor relative to pelvic organ prolapse are the pudendal nerve (originating from S2 to S4) that supplies the urethral sphincter, anal sphincter, and perineal muscles and the nerve to the levator ani (originating from S3 to S4) that innervates the major musculature that supports the pelvic floor.

Suggested Readings Bakas P, Liapis A, Karandreas A, et al. Pudendal nerve terminal motor latency in women with genuine stress incontinence and prolapse. Gynecol Obstet Invest 2001;51(3):187– 190. Barber MD, Visco AG, Wyman JF, et al. Continence Program for Women Research Group. Sexual function in women with urinary incontinence and pelvic organ prolapse. Obstet Gynecol 2002;99:281–289. Beevors MA, Lubowski DZ, King DW, et al. Pudendal nerve function in women with symptomatic utero-vaginal prolapse. Int J Colorectal Dis 1991;6(1):24–28. Bump RC, Mattiasson A, Bo K, et al. The standardization of terminology of female pelvic organ prolapse and pelvic floor dysfunction. Am J Obstet Gynecol 1996;175:10–17. Bump RC, Norton PA. Epidemiology and natural history of pelvic floor dysfunction. Obstet Gynecol Clin North Am 1998;25:723–746. Campbell RM. The anatomy and histology of the sacrouterine ligaments. Am J Obstet Gynecol 1950;59:1. Carley ME, Schaffer J. Urinary incontinence and pelvic organ prolapse in women with Marfan or Ehlers Danlos syndrome. Am J Obstet Gynecol 2000;182:1021–1023. Chiaffarino F, Chatenoud L, Dindelli M, et al. Reproductive factors, family history,

occupation and risk of urogenital prolapse. Eur J Obstet Gynecol Reprod Biol 1999;82:63– 67. DeLancey JOL. Anatomic aspects of vaginal eversion after hysterectomy. Am J Obstet Gynecol 1992;166:1717. DeLancey JOL. Structural anatomy of the posterior compartment as it relates to rectocele. Am J Obstet Gynecol 1999;180:815–823. DeLancey JOL. Structural aspects of the extrinsic continence mechanism. Obstet Gynecol 1988;72:296. DeLancey JOL. Structural support of the urethra as it relates to stress urinary incontinence: the hammock hypothesis. Am J Obstet Gynecol 1994;170:1713–1720. Ellerkmann RM, Cundiff GW, Melick CF, et al. Correlation of symptoms with location and severity of pelvic organ prolapse. Am J Obstet Gynecol 2001;185:1332–1337. Emge LA, Durfee RB. Pelvic organ prolapse: four thousand years of treatment. Clin Obstet Gynecol 1966;9:997. Hendrix SL, Clark A, Nygaard I, et al. Pelvic organ prolapse in the Women's Health Initiative: gravity and gravidity. Am J Obstet Gynecol 2002;186:1160–1166. Jackson SR, Avery NC, Tarlton JF, et al. Changes in metabolism of collagen in genitourinary prolapse. Lancet 1996;347:1658–1661. Jorge JM, Wexner SD, Ehrenpreis ED, et al. Does perineal descent correlate with pudendal neuropathy? Dis Colon Rectum 1993;36(5):475–483. Jorgensen S, Hein HO, Gyntelberg F. Heavy lifting at work and risk of genital prolapse and herniated lumbar disc in assistant nurses. Occup Med (Lond) 1994;44:47–49. Kammerer-Doak DN, Rogers RG, Johnson Maybach J, et al. Vasopressin as an etiologic factor for infection in gynecologic surgery: a randomized double-blind placebocontrolled trial. Am J Obstet Gynecol 2001;185:1344–1347. Kuhn RJP, Hollyock VE. Observations on the anatomy of the rectovaginal pouch and septum. Obstet Gynecol 1982;59:445. Liu X, Zhao Y, Pawlyk B, et al. Failure of elastic fiber homeostasis leads to pelvic floor

disorders. Am J Pathol 2006;168:519–528. Makinen J, Soderstrom KO, Kiilholma P, et al. Histological changes in the vaginal connective tissue of patients with and without uterine prolapse. Arch Gynecol 1986;239:17–20. Mant J, Painter R, Vessey M. Epidemiology of genital prolapse: observations from the Oxford Family Planning Association study. Br J Obstet Gynaecol 1997;104:579–585. Moalli PA, Jones Ivy S, Meyn LA, et al. Risk factors associated with pelvic floor disorders in women undergoing surgical repair. Obstet Gynecol 2003;101:869–874. Moalli PA, Shand SH, Zyczynski HM, et al. Remodeling of vaginal connective tissue in patients with prolapse. Obstet Gynecol 2005;106:953–963. Olsen AL, Smith VJ, Bergstrom JO, et al. Epidemiology of surgically managed pelvic organ prolapse and urinary incontinence. Obstet Gynecol 1997;89:501–506. Range RL, Woodburne RT. The gross and microscopic anatomy of the transverse cervical ligaments. Am J Obstet Gynecol 1964;90:460. Richardson AC, Edmonds PB, Williams NL. Treatment of stress urinary incontinence due to paravaginal fascial defect. Obstet Gynecol 1981;57:357–362. Richardson AC, Lyons JB, Williams NL. A new look at pelvic relaxation. Am J Obstet Gynecol 1976;126:568–573. Smith ARB, Hosker GL, Warrell DW. The role of pudendal nerve damage in the aetiology of genuine stress incontinence in women. Br J Obstet Gynaecol 1989;96:29. Summers A, Winkel LA, Hussain HK, et al. The relationship between anterior and apical compartment support. Am J Obstet Gynecol 2006;194(5):1438–1443. Swift SE, Tate SB, Nicholas J. Correlation of symptoms with degree of pelvic organ support in a general population of women: what is pelvic organ prolapse? Am J Obstet Gynecol 2003;189:372–377. Timonen S, Nuoranne E, Meyer B. Genital prolapse: etiological factors. Ann Chir Gynaecol Fenn 1968;57:363–370. Weidner AC, Barber MD, Visco AG, et al. Pelvic muscle electromyography of levator ani

and external anal sphincter in nulliparous women and women with pelvic floor dysfunction. Am J Obstet Gynecol 2000;183(6):1390–1399; discussion 1399–1401. Weidner AC, Bump RC. Terminology of pelvic organ prolapse. Curr Opin Obstet Gynecol 1997;9:309–312.

49 Operative Management of Pelvic Organ Prolapse Kris Strohbehn Holly E. Richter Pelvic organ prolapse (POP) is a common condition affecting women. While many women live with varying degrees of POP without treatment, it is estimated that over 200,000 surgical procedures are performed in the United States annually to treat this condition. More than 1 in 10 women will have surgical treatment of prolapse and/or urinary incontinence by the time they reach 80 years of age. The repairs are not always successful, and 1 in 3 women who undergo surgery for urinary incontinence or prolapse need to undergo a subsequent procedure. The risk factors, anatomic changes, and demographics of POP are covered in Chapter 48. Despite the fact that up to 50% of women over the age of 50 have physical findings consistent with some degree of POP, fewer than 20% seek treatment for this condition. This may be due to a number of reasons including lack of symptoms, embarrassment, or misperceptions about available treatment options for this condition. Recent estimates predict an increased demand for prolapse surgery by 45% in the next 30 years. To effectively use financial resources in the surgical management of POP, it is imperative to perform surgeries that are evidence based to improve outcomes and minimize recurrences. The authors believe that nonsurgical options, including observation or a trial of a pessary, are of low risk to patients and should be considered first, if acceptable to the patient. This chapter will review different surgical options for treating POP, including transvaginal repairs, open abdominal repairs, laparoscopic repairs, and new percutaneous needle or trocar repair kits as well as a combination of these procedures. Each of these surgical approaches to treat POP may use native ligaments and tissues for repair. Alternatively, some surgeons utilize biologic grafts for selected repairs, including xenografts, allografts, and autologous grafts. Finally, synthetic graft materials are frequently utilized via transvaginal, laparoscopic, and open abdominal repairs. A brief discussion of these options and the pros and cons of each will be included in this chapter.

Preoperative Considerations A careful preoperative evaluation of patients with POP is crucial in determining whether surgical repair is the right treatment choice for an individual and if so, which procedure is

most appropriate. The decision to operate for POP should be based on the degree of POP symptom bother that a patient is experiencing. Consideration of the patient's postrepair goals and their risks should be addressed prior to surgery. Symptom-based scoring questionnaires have been introduced and validated to assess the impact of POP on quality of life. There are a wide complex of symptoms associated with POP, including urinary incontinence, voiding dysfunction, anal incontinence, defecatory dysfunction, sexual dysfunction, and prolapse symptoms, that are also commonly reported in women without POP. However, it is more common for subjects to have symptoms when the prolapse extends to or beyond the hymen. Determination of a patient's bother prior to considering surgical approach is useful to assess whether or not surgery offers hope of alleviating her symptoms. In determining bother, it can be helpful to ask the patient if her prolapse is preventing her from doing things that she would like to do. For example, if an individual has stopped exercising because of POP, this may have great impact on her overall health. In the authors' practice, a simple but nonvalidated scoring system is used to assess bother for specific symptoms (Table 49.1). A more in-depth validated assessment of impact on quality of life has been introduced by Barber and colleagues and is validated for subscales of colorectal function, urinary incontinence, and prolapse. Whether or not a validated scoring system is used, making the effort to determine bother is useful in determining preoperative goals and postoperative outcomes.

TABLE 49.1 Bother Score to Assess Pre- and Postoperative Bother from Pelvic Organ Prolapse Setting realistic expectations and goals with the patient prior to prolapse repair is important. As part of the discussion prior to surgery, a review of possible outcomes (good and bad) should be reviewed with honesty and, if possible, with the surgeon's individual outcome data. The discussion should include potential negative impact on sexual function and visceral functions, such as bladder and bowel continence and evacuation after anatomic correction of prolapse. If a patient is bothered by prolapse but is without symptoms of urinary incontinence, she will be understandably upset with her outcome if she develops de novo urinary incontinence. By the same token, someone who has mild urinary incontinence preoperatively who develops de novo urinary retention postoperatively may have elected to live with her mild incontinence compared with the voiding dysfunction she now suffers with. A review of an individual's prior abdominal and pelvic surgeries is imperative to planning a prolapse procedure. If a patient has had several laparotomies, is morbidly obese, or there is a suspicion for severe abdominopelvic adhesions, the surgeon should consider a vaginal repair. At a minimum, preparation for possible change in the planned repair may be in order, especially if inadvertent enterotomy occurs intraoperatively. If a patient has failed prior prolapse surgeries with native tissue repairs, then consideration of a mesh-augmented or other graft repair should be entertained. Other considerations regarding the approach to repair include surgeon experience, patient age, other comorbidities, and pelvic muscle strength. Assessment of individual surgeon outcomes may help to determine which prolapse repairs are best suited for an individual's practice. A focus on outcomes in practices for procedures is being mandated with adoption of the National Surgery Quality Improvement Program (NSQIP). As part of the focus on excellent outcomes, prophylactic antibiotics should be considered prior to any POP procedure, especially in cases where the vaginal epithelium is disrupted. Within 60 minutes of the incision start, 1 g of cefazolin or a similar broad-coverage antibiotic is administered intravenously. The American College of Obstetrics and Gynecology (ACOG) practice bulletin guidelines are helpful for decisions regarding prophylaxis. Prophylaxis for deep venous thrombosis should be considered for any pelvic surgery that is anticipated to take longer than 30 minutes, and the authors employ intermittent pneumatic compression stockings in such cases. The age of the patient may help to direct which surgical approach is suitable. Many experienced surgeons advocate vaginal repairs for older patients, but using age cutoffs alone may be inappropriate. It is common knowledge that there are 80-year-old women who are more active and in better health than some 50-year-old women. As a generalization, it makes sense to consider a quicker, less invasive repair such as a

transvaginal repair or colpectomy with colpocleisis for a frail, inactive patient. This makes sense to reduce morbidity, as inactive individuals are less likely to place stress on the repair. However, the lower morbidity may be at the cost of lower success due to potential diminished strength of the native tissues that may be inherent in frail or elderly patients. The selection of repair may also depend on whether the levator ani muscles will appropriately protect the ligaments. If a patient is unable to contract her levator muscles, there is likely to be more load on her native ligaments, with possible added risks of failure over time. If it is apparent that there is no protection of the connective tissue support from the pelvic musculature, the choice of a synthetic graft to compensate for lack of muscular support seems sensible. Planning a prolapse repair requires consideration of the impact of the function of the pelvic organs in addition to anatomic support. Urodynamic evaluation has been recommended by some, even if urinary incontinence is not a symptom of the patient. Urodynamic evaluation may assist in identifying occult urinary incontinence in women with prolapse who leak with a full bladder when the prolapse is reduced. Pessary or barrier testing has also been used to try to assess risks for occult stress urinary incontinence. In the recently published CARE trial, a prophylactic Burch procedure was effective at reducing the risk of stress urinary incontinence among women without preoperative symptoms of such incontinence who underwent mesh sacral colpopexy for the treatment of prolapse. The reduction in risk of stress urinary incontinence did not result in a higher rate of voiding dysfunction or bladder storage symptoms. There are no data available regarding midurethral sling procedures as a prophylactic procedure.

Operative Repairs The aims of surgical management of POP are to: Reduce the prolapse Improve symptoms of POP, the lower urinary tract, and bowel Restore or improve sexual functioning (except after colpocleisis), and correct coexisting pelvic pathology. As mentioned previously, the surgical approach for POP includes vaginal, abdominal, and laparoscopic routes. Anatomic studies have demonstrated different levels of support, and POP may result from a single or combination of support defects (Fig. 49.1). Surgical management may therefore involve a combination of repairs including the anterior vaginal wall, vaginal apex, and posterior vaginal wall. The surgical route is typically chosen based on the type and severity of prolapse, combined with the surgeon's training and expertise as well as patient functional level and preference, rather than on primary consideration of surgical outcome. Surgical procedures for POP can be categorized into three groups: restorative procedures that use the patient's endogenous support structures to restore normal anatomy; compensatory procedures that augment defective support structures with autologous, allogenic, or synthetic graft material; and obliterative procedures that stricture the vagina. These categories are somewhat arbitrary

and not entirely exclusive. For example, graft material may be used to replace support that is deficient or to reinforce repairs. Graft use in abdominal sacral colpopexy (ASC) substitutes for the cardinal and uterosacral ligaments that would normally support the vaginal apex. When vaginal function is desired by the patient, restorative or compensatory procedures are utilized, whereas an obliterative procedure may be utilized when there is no desire to retain sexual function of the vagina.

Figure 49.1 The different levels of vaginal support structures after hysterectomy. (Reproduced with permission from DeLancey JOL. Anatomic aspects of vaginal eversion after hysterectomy. Am J Obstet Gynecol 1992;166:1717.)

Whether to repair all defects seen is controversial, especially if the patient is asymptomatic. Restorative repairs may be less successful than compensatory repairs in patients with generally “poor tissue,” and at times, one defect repair may exert more tension on the repair of another defect. Each case should be individualized based on the patient's presentation, expectations, the specific anatomical defects noted (preoperatively and, at times, intraoperatively), and on the presence or absence of lower urinary and bowel dysfunction symptoms. The following sections will describe surgical approaches of prolapse in the anterior, apical, and posterior vaginal components. Vaginal, abdominal, and laparoscopic approaches will be reviewed for each compartment.

Vaginal Approaches Anterior Compartment

Surgical management of the anterior compartment continues to be a challenge for all pelvic surgeons. In most published series, the anterior wall is the most common site of objective failure with different surgical approaches to POP.

Anterior Colporrhaphy Anatomic correction of an anterior defect or cystocele will generally relieve symptoms of protrusion and pressure and will usually improve micturition function when abnormal micturition is associated temporally with the defect and if there is no associated neuropathy. If a single, well-defined midline defect is recognized, excision of the weak vaginal wall and an imbricating closure of the defect may be performed. However, recent magnetic resonance imaging (MRI) and anatomic measurement studies indicate that at least one third of the descent of cystoceles is due to loss of apical support, so it is important to determine whether the apex needs to be suspended as well. Most central anterior defects require a more extensive dissection of the vesicovaginal space. In the case where the cuff is well suspended, the authors typically grasp the vaginal epithelium vertically with two Allis clamps cephalad to the urethrovesical junction and incise with the knife. With the use of a Metzenbaum or comparable scissors, the vaginal epithelial and subepithelial layers are separated from the fibromuscular layer out to a point lateral to the defect up to the cuff or cervix; this is followed by midline plication of this tissue with either a running or interrupted delayed absorbable suture such as polyglactin (Vicryl, Ethicon, Somerville, NJ) or no.1 polydioxanone (PDS, Ethicon, Somerville, NJ), excision of excess epithelium, and closure. The repair is similar at the time of concomitant vaginal hysterectomy or apical cuff suspension except that the dissection proceeds in a cephalad to caudad fashion. It appears of great importance to ensure that the continuum of repaired fibromuscular tissue to a well-supported vaginal apex be maintained. Recurrence rates of traditional fibromuscular connective tissue plication anterior repairs vary in the literature from 5% to 90%; however, studies define recurrence in numerous ways from minimal prolapse to stage III descent. The clinical significance of recurrent asymptomatic cystoceles (stage I and some stage II) is debatable because many of these do not progress to larger defects. The authors' interpretation of the literature is that when traditional anterior repairs are performed with patients with a pelvic organ prolapse quantitation (POP-Q) system of measurement of stage II or greater cystoceles (frequently concurrently with other procedures), a recurrence rate of stage II or greater prolapse of up to 20% to 40% is not uncommon. Many studies do not define how the subjects were evaluated postoperatively and vary in respect to patient populations, type and severity of defects, presence of concurrent defects, surgical technique, and follow-up time and length. Some studies have suggested higher recurrence rates when these repairs are performed concurrently with sacrospinous suspensions and hypothesize that this type of apical suspension may predispose the repair anterior wall to greater pressure transmission. Other possibilities of the higher failure rates in these studies are the fact that the patients having concurrent repairs may be more likely to have more complicated forms of prolapse or, possibly, more defective “pelvic floors” than other groups of patients. The addition of adjunctive graft materials has been employed in the past decade to try to

improve success rates. Two randomized trials suggest modest improvement in success after 1 year when polyglactin mesh (Vicryl, Ethicon, Somerville, NJ) was placed over the midline plication compared with standard repair. However, most surgeons have abandoned this type of mesh because of subsequent failures. Other graft materials that are discussed later in this chapter may have more promise, but long-term outcome data are lacking. Fascial autologous grafts, allografts, xenografts, and newer synthetics are presently used by many surgeons with variable short-term success and, thus far, little data on adverse effects and success after 3 years. These have been used in several ways in the anterior compartment, including placement of smaller grafts to bolster suture lines and larger grafts for complete substitution of the entire anterior support plate from the pubis to the arcus to the vaginal apex.

Vaginal Paravaginal Repair The paravaginal or “lateral defect” repair described first by White and reintroduced by Richardson and Edmonds involves reattachment of the anterior lateral vaginal sulcus to the obturator internus fascia and, at times, muscle at the level of the arcus tendineus fascia pelvis (ATFP) or “white line.” The paravaginal repair reattaches the anterolateral vaginal sulcus to the pubococcygeus and obturator internus muscles and fascia at the level of the ATFP. The original transvaginal repair used bilateral incisions along the lateral vaginal sulci to expose the arcus tendineus. Three or four sutures were then placed from the ischial spine along the ATFP to suspend the vaginal muscularis and adventitia bilaterally. Subsequently, use of a midline incision was described that facilitated the concurrent repair of central anterior defects. The typical vaginal paravaginal procedure involves the “three point closure” with incorporation of the detached edge of the pubocervical connective tissue into the ATFP and the anterior vaginal wall with a series of four to six nonabsorbable sutures (Prolene, Ethicon, Somerville, NJ) 1.5 cm apart, initiated approximately 1 cm anterior to the ischial spine. The sutures are tied sequentially, beginning with the one closest to the spine and ending periurethrally. Cystoscopy should be performed to ensure ureteral patency and inadvertent stitch placement into the bladder. This often is performed with a reinforcement of the midline pubocervical connective tissue with trimming of the vaginal epithelium (if necessary) and closure. The procedure has been described with the use of a Capio suturing device as well (Microvasive Endoscopy, Natick, MA). Observational outcome studies have reported good success (80% to 95%); however, longterm data on durability and function is lacking. Previous work has shown that most subjects with anterolateral detachments almost always have separation of the upper vaginal fornices from the arcus tendineus immediately adjacent to the ischial spine. Thus, it is important to resuspend those specific areas. It is the authors' opinion that it is difficult to achieve optimal results when vaginal paravaginal repair is used in combination with traditional central repairs because of the creation of tension on opposing suture lines. A repair that removes a weakened central vaginal wall may decrease the side-to-side dimensions of the anterior vaginal wall, making

it difficult to suspend its lateral points more laterally. When large central defects are coexistent with lateral defects, one option is an extensive central repair accompanied by a good apical support procedure. This changes the shape of the vagina to a more cylindrical structure. Another choice is placement of a graft material to span the entire anterior rhomboid-shaped plate, thus augmenting anterior paravaginal tissue strength. The graft with tension adjusted may be anchored to the arcus tendineus along with the adjacent vaginal wall from the level of the pubic rami to the ischial spine. The new synthetic graft kits utilize this principle, as described later. Although most reports indicate that repair of anterior defects with all of these procedures relieves symptoms that are directly related to prolapse, there is very little data on patient satisfaction and quality-of-life improvement over time. Such studies are much needed. There are no randomized trials that compare outcomes after anterior colporrhaphy versus vaginal paravaginal repair.

Posterior Compartment There is no consensus on what defines a rectocele or posterior vaginal wall prolapse by physical examination or the use of diagnostic imaging modalities. However, early descriptions of the traditional posterior colporrhaphy in the early 1800s addressed perineal tears sustained at vaginal delivery. The support of the rectum and posterior vagina includes the pelvic floor musculature, connective tissue, Denonvilliers (pararectal) fascia (which is the fibromuscular layer of the posterior vaginal wall), and its lateral attachments to the lateral pelvic floor (levator) musculature and its fascia. This lateral attachment site, the fascia levator ani, fuses with the ATFP at the mid to upper vaginal level and continues to the level of the ischial spine. Less dense, areolar, connective tissue surrounds the rectum and vagina and may supply some fixation of these structures as well. Richardson hypothesized, based on careful cadaveric dissections, that most rectoceles were due to discrete tears in the Denonvilliers fascia at its lateral, apical, and perineal attachments and centrally within the fascia itself. He described perineal detachment along with a defect in the perineal membrane as a perineal rectocele, which is most commonly associated with complaints of difficulty with defecation. The apical attachment defects are generally associated with enteroceles and occasionally sigmoidoceles. Once a decision is made to perform surgical repair of the posterior compartment based on symptoms, type, and location of defects, an appropriate approach should be decided on, and the patient should be made aware of what outcome she should expect and of potential adverse effects such as pain and sexual dysfunction. If the patient has defecatory dysfunction with a rectocele and has symptoms of constipation, pain with defecation, fecal or flatal incontinence, or any signs of levator spasm or analismus, appropriate evaluation and conservative management of concurrent problems should be initiated prior to repair of the rectocele. Specific types of repairs include the traditional posterior colporrhaphy, the defect-directed repair, replacement of fascia with graft materials, transanal repairs, and abdominal approaches by laparotomy or laparoscopy. An elegant review by Cundiff and Fenner has

recently summarized data on the evaluation and treatment of women with rectocele, with a focus on associated defecatory and sexual dysfunction. Surgical outcomes with available objective and subjective measures were also reported.

Traditional Posterior Colporrhaphy The first description of the posterior colporrhaphy was by Jeffcoate in 1959 and involved plication of the pubococcygeus muscles across the anterior rectum as well as perineal body reconstruction. Since that time, the technique has been modified in attempts to preserve sexual function. Typically, a midline incision is extended from the perineal body to the vaginal apex or to the cephalad border of a small or distal rectocele. The Denonvilliers fascia is mobilized from the vaginal epithelium, leaving as much of this tissue attached laterally to the levator fascia as possible. After obvious defects in the rectal muscularis are repaired, the fascia is then plicated in the midline with interrupted or continuous sutures (Fig. 49.2). The authors prefer delayed absorbable suture, no. 1–0 or no. 0 polydioxanone, for this plication. Permanent nonbraided suture material may be used as well. In our experience, braided permanent suture material is subject to a greater incidence of stitch infection and formation of granulation tissue. The vaginal epithelium is trimmed and closed with absorbable sutures.

Figure 49.2 A: To begin the posterior colporraphy, a transverse incision is made in the perineal body, and a vertical incision is extended toward the vaginal apex. B: The perirectal musculo-connective tissue is mobilized from the epithelium. C: The perirectal musculo-connective tissue is sutured, beginning above the site of the rectocele. D: The inner surface of the levator ani are approximated as necessary and redundant epithelium excised. E: the vaginal epithelium, superficial perineal muscles

and skin are closed. (Reproduced with permission from Mattingly RF, Thompson JD, eds. Te Linde's Operative Gynecology, 6th ed. Philadelphia: JB Lippincott Co, 1985:578.)

When there is a defective perineal body or perineal membrane, reconstruction is performed after accompanying posterior colporrhaphy. The superficial muscles of the perineum and bulbocavernous fascia are plicated in the midline by using delayed absorbable suture, and the skin closed as in an episiotomy repair. Detachments of the inferior portion of the Denonvilliers fibromuscular connective tissue from the perineal body are also corrected. Plication of the puborectalis muscles concurrently with these procedures is performed by some surgeons in all or selected cases, but because this has been associated with a high incidence of sexual dysfunction, the authors do not recommend that it be performed routinely. However, puborectalis plication will be performed in selected patients with severe prolapse accompanied by a large genital hiatus with palpable levator weakness or inability to contract pelvic floor muscles. Sutures are carefully placed through the puborectalis muscles at least 3 cm or greater posterior to their insertion on the pubic rami, thereby decreasing the tension of the plication. For those women who desire sexual function with findings of an enlarged hiatus and weakened puborectalis muscles, there is an attempt to plicate the muscles far enough posteriorly to easily allow two fingers through the vaginal introitus and reconstruct the distal posterior vagina and perineum so that there will not be a ledge or ridge at the site of the puborectalis plication. Outcome data on such procedures is inadequate to make conclusions regarding its efficacy; however, it is the authors' opinion that pelvic floor defects producing an enlarged genital hiatus are common reasons for failure of support procedures and that puborectalis plication may decrease the incidence of such failures. Reported anatomic cure rates for traditional posterior colporrhaphy have ranged from 76% to 90% with variable follow-up. Most studies show a benefit to ease of defecation if patients are using preoperative splinting; however, overall defecatory dysfunction (defined as constipation) is usually not relieved in the majority of the subjects. These repairs, per se, also appear to be of little to no benefit to fecal incontinence. It is not surprising that the repairs are not particularly effective for defecatory dysfunction related to disorders of constipation or for fecal incontinence since the etiology of these problems are multifactorial. De novo dyspareunia is reported to occur in up to 25% of sexually active patients who have traditional posterior colporrhaphy and is not always associated with levator plication procedures. Potential causes for dyspareunia other than vaginal strictures or introital tightness include scarring with immobility of the vaginal wall, levator spasm, and neuralgias associated with sutures and/or dissection. Dyspareunia may also occur when a Burch colposuspension procedure (or other procedures that cause anterior displacement of the vaginal canal) is combined with a posterior repair. Careful surgical technique and appropriate choice of procedure should decrease the incidence of postoperative dyspareunia.

Defect-specific Posterior Colporrhaphy Defect or site-specific posterior repairs are restorative procedures by which the posterior defects described by Richardson are corrected. These repairs begin by midline posterior vaginal incision through the epithelium and then separation of the epithelium from the fibromuscular wall (Fig. 49.3). After irrigation for better exposure, a finger is inserted in the rectum to better define defects of the rectal wall and in the fibromuscular connective tissue layer that has been dissected from the vaginal wall subepithelium. The specific defects are closed with either interrupted or running sutures (the authors prefer the delayed absorbable type). Defect closure is accomplished in such a way to minimize tension on the surrounding tissue and may involve vertical, horizontal, or oblique approximation. When there is separation of the fibromuscular tissue from the perineum, the upper anterior rectum, or a well-supported cervix or vaginal cuff, it is important to reapproximate these connections. Repairs of coexistent perineal and apical support defects are important. The goal of the surgery is to re-establish an intact plane of connective tissue that positions the rectum against the pelvic floor and obliterates any potential space between a wellsupported cervix or vaginal cuff and the cephalad edge of the tissue plane and upper rectum. The technique should minimize tension and avoid potential strictures, which may be more likely to occur with traditional posterior colporrhaphy.

Figure 49.3 A: Musculo-connective tissue defects. B: Musculo-connective tissue repair.

Just as in anterior compartment procedures, the placement of graft materials to improve the success of posterior compartment repairs has been employed. Kohli and Miklos describe the use of a dermal allograft to augment defect-directed repairs whereby the graft is sutured to the levator fascia on both sides of the defect to cover the rectovaginal plane. One concern about this technique is that in patients with relatively thin vaginal walls, removal of the fibromuscular tissue may devascularize the epithelium and make it more subject to erosion over the graft material. To improve the quality of vaginal epithelium in women with vaginal atrophy, patients in the authors' practice use vaginal for 4 to 8 weeks preoperatively. The initial surgical dissection is deep to the fibromuscular layer. Access to the lateral levator fascia is generally easily accomplished with a division of the Denonvilliers fascia at its incorporation into the posterior vaginal wall or, if the lateral attachment is not present, with combined sharp and blunt dissection to expose the paralevator fascia. This levator fascia on each side as well as any remaining lateral Denonvilliers fascia and occasionally muscle is incorporated into the edge of the graft with sutures. The posterior cephalad edge of the graft is attached to the anterior rectum at its sigmoid junction, and the anterior cephalad edge is attached to a well-suspended vaginal cuff. The caudad edge is incorporated in an appropriate repair of the perineal area. With short-term, mean follow-up of 12 to 30 months, overall results reveal good anatomic cure rates of 89% to 100% with cadaveric dermis, autologous dermis, polyglactin mesh, and polypropylene mesh. Improvement in obstipation has also been reported. Although the numbers of subjects assessed have been relatively low, de novo dyspareunia rates have been between 0% and 7%.

Transanal Rectocele Repair The aim of transanal rectocele repair, usually performed by colorectal surgeons rather than gynecologists, is to remove or plicate redundant rectal mucosa, to decrease the size of the rectal vault, and to plicate the rectal muscularis, rectovaginal adventitia, and septum. Since the vaginal epithelium is not incised or excised, this probably accounts for the procedure's reported lack of adverse affects on sexual function in contrast to the vaginal approach to posterior repair. Two randomized trials and several case series from transanal repairs with mean follow-up of 12 to 52 months report anatomic cure rates of 70% to 98%, improved constipation and fecal incontinence, and less need for vaginal digitation to expel stool. Complications included infections and rectovaginal fistulas, which were surprisingly rare in the reported series. From the gynecologic perspective, transanal posterior repair only makes sense when the procedure is performed for defecatory dysfunction and not for prolapse of the posterior vaginal wall. It is unclear whether the transanal approach with defect excision and repair improves defecatory dysfunction better than a defect-specific transperineal or transvaginal approach with imbrication of tissues to correct palpable weakness in the rectal wall and its adjacent connective tissues.

Apical Compartment

Apical vaginal prolapse encompasses the findings of uterine prolapse with or without enterocele and vaginal vault prolapse but typically with enterocele. Defects in apical support include the loss of cardinal–uterosacral support with resultant cervical–uterine or vaginal cuff descent; the detachment of the fibromuscular vagina from the anterior rectum with resultant enterocele or, at times, sigmoidocele into the rectovaginal space; and tears or attenuation of the upper fibromuscular tissue usually posthysterectomy, leading to a central apical descent that frequently presents as a ballooning defect. Often, these defects occur concurrently. The general principles of the repair should include management of the specific apical defects: (a) if present, the attenuated part of the upper vaginal wall (fibromuscular defect) should either be repaired or covered by graft material; (b) the vaginal cuff, or in some instances the cervix, should be suspended without excessive tension; and (c) any defect in the attachment of the upper vagina to the rectum at or below its sigmoid junction should be corrected. Enterocele repairs may include (a) removal of the peritoneal sac with closure of the peritoneal defect and then closure of the fascial and/or fibromuscular defect below it, (b) dissection and then reduction of the peritoneal sac and closure of the defect, or (c) obliteration of the peritoneal sac from within with transabdominal Halban- or Moschowitz-type procedures or transvaginal McCall or Halban procedures. Historically, the “standard” for the treatment for symptomatic uterine prolapse has been hysterectomy, which is performed vaginally or abdominally in combination with an apical suspension procedure and repair of coexisting defects. Apical support procedures that have been described for use when the uterus or cervix is to be kept in place include the Manchester-Fothergill procedure, described later, and the Gilliam procedure, which suspended the uterus with the round ligaments. The latter has been abandoned due to high rates of failure. In addition, fixation of the cervix to the sacrospinous ligament, uterosacral ligament plication, and fixation of mesh from the cervix to the sacrum (mesh sacral hysteropexy) have been described. Adequate outcome data on such uterine-sparing procedures are not yet available. One randomized trial in Europe compared Gortex sacral hysteropexy to vaginal hysterectomy with uterosacral ligament suspension without mesh. The authors found higher failure rate and reoperation rate among the group who had uterine conservation with mesh sacral hysteropexy. When the cervix is absent, it is the authors' opinion that in addition to repair of fibromuscular defects, both fibromuscular planes anterior and posterior to the vaginal cuff should be attached to whatever suspension is employed.

Enterocele Repair Enterocele repair usually is performed in the setting of concomitant procedures for prolapse, more often as related to posterior compartment repair and apical repair. Whether by vaginal, abdominal, or laparoscopic access, the enterocele repair is traditionally performed by sharply dissecting the peritoneal sac from the rectum and bladder. A purse-string suture can be used to close the peritoneum as high (cephalad) as possible; whether excision of the peritoneum itself is necessary has not been determined. Care must be taken to identify and avoid the ureters during peritoneal closure. More important than closing the enterocele sac is approximating the anterior to the posterior

fibromuscular connective tissue of the vagina. Suspension of the vaginal apex is almost always necessary except in those rare cases when the enterocele occurs in the presence of adequate apical support.

Sacrospinous Ligament Suspension The fixation of the vaginal apex to the sacrospinous ligament, the tendineus component of the coccygeus muscle, was first described in mid 20th century. Traditionally, access is extraperitoneal via the rectovaginal space with penetration of the pararectal (Denonvilliers fascia) at the level of the ischial spine to expose the muscle and ligament. The rectum and surrounding connective tissue typically are swept medially with blunt dissection, and visualization of the ligament prior to suture placement can be facilitated with the use of Breisky Navratil retractors. The authors typically use a delayed absorbable suture material such as polydioxanone placed with a Miya hook or free needle such that a long suture can be brought through the ligament, grasped, and cut, resulting in two sutures to incorporate into the vaginal apex (Fig. 49.4). Bilateral sacrospinous ligament suspensions have also been advocated; however, they may create a greater degree of tension on the sutures and at times create a band of apical vagina across the rectum at the level of the suspension. The advantages of the sacrospinous fixation procedure include (a) its transvaginal extraperitoneal approach, (b) resultant posterior vaginal deflection, and (c) the fact that it is a relatively durable repair if performed correctly. Reported success for apical support has been good at approximately 97%, with follow-up times ranging from 1 month to 11 years. There have been subsequent reports of high rates of anterior vaginal prolapse. It is debatable as to whether this observation is due to the procedure and its exaggerated posterior vaginal deflection or due to other inherent factors for anterior prolapse in those subjects having the procedures. Other disadvantages cited by critics include relative difficulty in adequately exposing the ligament; an unnatural lateral vaginal deflection toward the fixation site; an inability to perform without excessive tension when the vaginal length is compromised, as may be the case in repeat procedures; potential risk for sciatic nerve or pudendal nerve or vessel injury; and occasional need to shorten or narrow the upper vagina when a fibromuscular defect involves much of the apical area. Additionally, some patients experience buttock pain that has been ascribed to entrapment of the nerve to the levator ani. Some of these problems are not unique to this procedure.

Figure 49.4 Penetration of the sacrospinous ligament. The right pararectal space has been entered, and the ischial spine palpated and identified. The use of 2 Breisky retractors can be helpful to hold the rectum medially and the cardinal ligament anteriorally. The coccygeus muscle-sacrospinous ligament complex running posteriomedially from the ischial spine to the sacrococcygeal area is exposed and grasped with a long-handled Allis or Babcock clamp as shown or delineated with the use of a notched half speculum. The tip of the ligature carrier is pushed under and upward through the ligament-muscle complex approximately 2 cm medial to the ischial spine. The suture is grasped with a nerve hook and held as the ligature carrier is removed.

Iliococcygeal Vaginal Suspension The iliococcygeal vaginal suspension involves bilateral attachment of the vaginal apex to the iliococcygeus muscle and fascia. Extraperitoneal access is achieved via the posterior vagina. Briefly, the dissection of the area to the ischial spine is approached from a midline posterior vaginal wall incision by using the ischial spine as a landmark for identifying the sacrospinous ligament and the anterior iliococcygeal fascia and caudad to it. A no. 1 polydioxanone suture is placed through the fascia and attached to the vaginal apex as a pulley stitch. This procedure is more easily performed bilaterally than the sacrospinous suspension and should be considered particularly in the setting of a shortened vagina. Risk of major vessel, nerve, or ureteral injury should be relatively low compared with injury

found in other transvaginal suspensions.

Uterosacral Ligament Vaginal Vault Suspension Surgical variations of the uterosacral ligament suspension originally described by McCall have been used prophylactically at hysterectomy or therapeutically for vaginal apical suspension. The original McCall culdoplasty begins with the placement of several rows (on average, three rows, with each row superior to the previous) of nonabsorbable suture (“internal” McCall sutures) starting at the left uterosacral ligament approximately 2 cm above its cut edge and reefing across the redundant cul-de-sac to the right uterosacral ligament. Prior to tying, three “external” absorbable sutures are placed incorporating the posterior vaginal epithelium, uterosacral ligaments, and the contralateral vaginal epithelium in a mirror image to the first pass through the vagina. Multiple rows are placed each superior to the last to move the cuff to the highest point on the uterosacral ligament. In 2000, Shull and colleagues described a therapeutic procedure in which the vaginal t apex is suspended to the uterosacral ligaments above the level of the ischial spines and reported excellent success rates in a large observational study. Once access to the posterior cul-desac has been attained, the uterosacral ligament remnant can usually be found adjacent to the pelvic side wall peritoneum just cephalad to the palpable ischial spine. Shull described placement of up to three sutures in each ligament and incorporated into the anterior and posterior fibromuscular layer of the vagina. Other surgeons suspend the right and left vaginal apex to the ipsilateral uterosacral ligament, leaving the cul-de-sac open to avoid impinging on the rectum and adversely affecting bowel function. The most common serious complication has been ureteral obstruction secondary to ureteral kinking or incorporation of a ureter in a suspension stitch. This has been shown to occur in up to 11% of cases. Therefore, intraoperative cystoscopy with documentation of ureteral patency after administration of indigo carmine dye is recommended. Aronson and associates emphasize placement of the sutures deep toward the sacrum, along the posterior segment of the ligament, rather than cephalad. In the lithotomy position, this caution may reduce risks of ureteral injury. Their series had a low rate of injury.

Figure 49.5 Diagrams illustrating open vaginal apex with a modification of the high uterosacral vaginal suspension described by Shull, whereby single monofilament permanent sutures are placed through the residual uterosacral remnants cephalad to

and at the same posterior level of the iscial spines. (A) exposure of site to suture placement on lateral pelvic sidewall. (B) Suture placement through ligament and then through the posterior and anterior paravaginal tissue where they may be locked to enable pulley action to the ligaments when tied. (Reproduced with permission from Berek JS. Berek and Novak's Gynecology, 14th ed. Philadelphia: Lippincott Williams & Wilkins, 2007.)

The authors have employed a modification of Shull's technique to minimize complications of ureteral kinking and injury and the number of sutures and knots present at the vaginal apex. It is thought that, at times, multiple sutures may increase the incidence of tissue devascularization and necrosis—thus, failure of the suspension. Exposure is accomplished through the vaginal cuff after hysterectomy, a transverse incision at the vaginal cuff in cases of vaginal vault prolapse or descent, and rarely through a posterior colpotomy when uterine or cervical conservation is desired. Attenuated areas of the apical vaginal wall are excised. The pelvic side wall, lateral to the sigmoid colon, is exposed by using Breisky Navratil retractors and a pack to hold the small bowel cephalad and to place the sigmoid colon and side wall peritoneum on stretch (Fig. 49.5A). After palpation of the ischial spine, single permanent sutures of no. 0 or no. 1 polypropylene are placed through the peritoneum and adjacent uterosacral ligament approximately 1 cm cephalad to and at the same posterior level as the ischial spines. Traction on the sutures and palpation of the site should reveal good purchase of the ligamentous structures. The sutures are tagged for use after repair of defects of the anterior compartment. The peritoneum is dissected off the vaginal fibromuscular wall posterior to the vaginal cuff. The suspension sutures are then secured with large bites into the posterior vaginal fibromuscular tissue and anterior fibromuscular tissue and then locked in place in order to well approximate anterior to posterior connective tissue and to fix the suture to the vaginal apex so that it may be pulleyed up to the ligament (Fig. 49.5B). If a rectovaginal enterocele is present, it is dissected and reduced, and the defect is closed approximating the prerectal fascia or anterior rectal wall to the posterior fibromuscular vaginal tissue just caudad to the suspension sutures. Absorbable cuff closure sutures are placed at each cuff angle (usually no. 0 polyglactin), and one to two bites are taken to approximate anterior-to-posterior vaginal cuff over the suspension suture sites. When indicated, plication of the central cuff anterior to the posterior fibromuscular tissue with a box stitch is also performed. These sutures are secured after the suspension (pulley) sutures are tied, then cuff closure is completed from each side with the absorbable sutures in a running fashion. Cystoscopy is performed to document ureteral patency. Ureteral compromise has been noted in only 2 of 150 cases performed. The authors have also found adequate support of POP-Q point C and D in all 88 subjects evaluated 24 months postoperatively by an unbiased observer.

Manchester-Fothergill Procedure There are several options to preserve the uterus with prolapse repairs at the apex,

including shortening the uterosacral ligaments as a vaginal, open, or laparoscopic approach and mesh or other biomaterial suspension of the cervix to the sacrum. The ManchesterFothergill procedure, first performed in 1888, is primarily of historic interest but continues to be done in some parts of the world. For this procedure, the vaginal wall is dissected off of the cervix around its circumference. The elongated cervix is amputated and then the cardinal ligaments are ligated and sutured over the anterior cervical stump. The procedure is summarized by Skiadas and associates and, for the interested reader, includes photographs of the procedural steps.

Abdominal Approaches Anterior Compartment Anterior Abdominal Colporrhaphy A high central defect may also be corrected via a transabdominal approach by dissecting between the base of the bladder and the upper one third of the anterior vaginal wall. The defective tissue may then be wedged out and the defect closed with running or interrupted sutures. This may be of use when performing a transabdominal procedure for apical suspension.

Paravaginal Repair The paravaginal or “lateral defect” repair described first by White and reintroduced by Richardson and Edmonds involves reattachment of the anterior lateral vaginal sulcus to the obturator internus fascia and, at times, muscle at the level of the ATFP. It usually is performed as a bilateral procedure. The procedure, in a sense, restores normal anatomy; however, since it is not practical to rebuild the defective endopelvic–fascial bridge to the pelvic sidewall, it attaches the vaginal wall itself. Previous work has shown that most subjects with anterolateral detachments almost always have separation of the upper vaginal fornices from the arcus tendineus immediately adjacent to the ischial spine. Thus, it is important to resuspend those specific areas.

Figure 49.6 Open paravaginal defect repair. The paravaginal musculo-connective tissue was separated from the arcus tendineus fascia pelvis from the inferior pubic ramus to the ischial spine. (A) With a finger elevating the vagina, a full thickness bite of pubocervical connective tissue and partial vaginal wall are incorporated into the arcus (B) Completed procedure.

After entry into the retropubic space, careful blunt dissection is performed to mobilize the bladder, urethra, and paravaginal tissue. A Foley catheter helps to delineate the urethrovesical junction. The ATFP is identified along the obturator internus muscle from the inferior pubic ramus to the ischial spine as the bladder is reflected medially with a sponge stick. The nondominant hand is placed in the vagina to elevate the lateral superior vaginal sulcus, and a permanent suture is used to reattach the vaginal sulcus with its overlying fibromuscular connective tissue to the ATFP. The first stitch is usually placed 1.0 cm caudal to the ischial spine, with subsequent sutures placed 1.0 to 1.5 cm apart. The procedure is performed bilaterally as needed (Fig. 49.6). After all of the sutures are placed, they are tied and cystoscopy is performed.

Posterior Compartment Mesh Abdominal Sacral Colpoperineopexy When ASC is planned for apical vaginal prolapse and a concomitant rectocele is present, some have advocated extending the posterior graft arm down the posterior vaginal wall to correct the defect. Cundiff and coworkers described the technique of sacral colpoperineopexy to replace the normal vaginal suspensory ligaments and to augment or replace the posterior fibromuscular plane with graft material that runs from the sacrum to the perineal body. Its purpose is to both correct the posterior compartment defects and to suspend the perineal body, thus preventing descent and opening of the genital hiatus. It has been performed transabdominally or as a combined abdominal

and vaginal procedure with both Mersilene mesh and dermal allografts. Mesh erosion occurred frequently when the vagina was open (40% with transvaginal placement of mesh and 16% with transvaginal placement of sutures).

Apical Compartment Uterosacral Ligament Suspension Abdominal uterosacral colposuspension has been used prophylactically after hysterectomy and therapeutically for apical prolapse with cardinal–uterosacral defects. It can be performed through laparotomy incision or by laparoscopic techniques. For the therapeutic procedure, a no. 1 polypropylene or delayed absorbable suture is placed cephalad and at the same level posterior as the ischial spines, which may be palpated transabdominally or with a vaginal finger to push a vaginal fornix to the spine. The authors' technique has been to place one or two permanent sutures through one ligament, then, after reefing across the cul-de-sac peritoneum at the sigmoid border, through the contralateral ligament, then through the fibromuscular tissue just anterior to the vaginal cuff from each end of the suture, creating a box-type configuration. Tying the suture suspends the vaginal cuff and obliterates any enterocele defect. Another technique employs separate sutures placed at the same level into each uterosacral ligament and anchored to the ipsilateral side of the anterior and posterior vaginal cuff—similar to transvaginal procedures performed. If a uterus is in place, it can be tracked superiorly to more clearly delineate the ligamentous structure; if a cuff is present, an end-to-end anastomosis (EEA) sizer can likewise be utilized. Cystoscopy is performed after the procedure to document ureteral patency. The authors are unaware of outcome data on large series of subjects who have undergone such procedures.

Abdominal Sacral Colpopexy ASC uses graft material attached to the anterior and posterior vaginal apex and suspended to the anterior longitudinal ligament of the sacrum. Different graft configurations and materials have been utilized, and numerous other modifications exist, including the extent to which the anterior and posterior vagina are attached to the graft, different graft and suture materials, peritoneal closure over the graft, and obliteration of the cul-de-sac for treatment or prevention of enterocele. Cure rates range from 78% to 100% for apical prolapse; when cure is defined as no postoperative prolapse, the range widens from 56% to 100%. The peritoneum overlying the vaginal apex is removed and macroporous polypropylene mesh, fashioned in a Y configuration (or two separate layers), is affixed to the posterior vaginal apex at the rectovaginal junction and to the anterior vaginal apex at the bladder reflection. Two permanent sutures are then used to affix the mesh to the anterior longitudinal sacral ligament (Fig. 49.7). No overt tension is placed on the vagina while attaching the mesh to the anterior sacral ligament. The authors reperitonealize over the mesh. In the setting of a deep cul-de-sac, Halban culdoplasty sutures with no. 1 polydioxanone are placed. Cystoscopy is performed at the end of the procedure.

The most common complications associated with performing a sacral colpopexy include bleeding and graft erosion. Intraoperative hemorrhage that occurs when lacerated sacral veins retract into the sacrum can be difficult to control; the use of hemostatic sutures, pressure, and bone wax has been found to help manage this potential complication. Other options for management of bleeding of presacral veins include applying sterile thumbtacks into the bone to tamponade the veins. It is helpful to apply bone wax under the rim of the tack. More recently, a technique has been described by several authors where a small 1-cm piece of rectus abdominus muscle is harvested and placed over the bleeding veins and then electrocautery is applied. The authors have used this technique with excellent success and find it preferable to other options, as it reduces risks of creating new bleeding sites. Synthetic graft material holds the highest risk of infection or erosion, although these complications have been reported with all types of graft material. As with small bowel obstruction, mesh erosion or infection has been reported years after the index surgery. While mesh erosion usually can be treated successfully with a relatively minor transvaginal excision of the exposed mesh, the entire graft occasionally must be removed with high levels of potential surgical morbidity. The risk of erosion ranges from approximately 3.5% to 9.0%. Other complications associated with the procedure are those associated with laparotomy, including postoperative ileus, small bowel obstruction, and the development of intra-abdominal adhesions.

Laparoscopic Approaches Laparoscopic approaches to treat POP were first introduced in 1992. The decision to use a laparoscopic approach must be partly directed by the surgeon's skill, but the authors' goal with laparoscopic repairs is to try to perform the same procedure that would be performed via an open approach. It is common for pioneers in laparoscopic procedures to change the overall technique for established open laparotomy procedures. Any change in technique, however, such as introducing anchoring screws or changing suturing locations or mesh applications may change the outcome. Outcomes may not be comparable and should ideally be tested with randomized trials. To date, there are no such trials available, and thus the high success rates reported with an open sacral colpopexy may not be recognized with a laparoscopic approach. There is one randomized trial comparing laparoscopic rectopexy with open rectopexy with favorable outcomes and earlier hospital discharges in the laparoscopic cohort. For positioning in laparoscopic repairs, the table height should be adjusted as low as possible during laparoscopic suturing. This allows for the surgeons' shoulders to be in a more normal resting position. The patient is positioned in low lithotomy with adjustable boot-type stirrups (Fig. 49.8). Lithotomy positioning is important to allow access to the urethra, vagina, and rectum.

Figure 49.7 Sacrocolpopexy. (A) Illustration of (i) graft attachment to the posterior area of prolapsed vagina to or below the recto-sigmoid junction after the overlying

peritoneum has been dissected and flapped laterally (ii) exposure of the presacral space with permanent suture placement through the anterior sacral ligament. A second graft is placed anteriorly. (B) Attachment of both grafts to the sacrum without tension. Closure of the cul-de-sac peritoneum and graft reperitonealization is performed per surgeon preference. EEA, end-to-end anastomosis sizer. (Reproduced with permission from Berek JS. Berek and Novak's Gynecology, 14th ed. Philadelphia: Lippincott Williams & Wilkins, 2007.)

The location of trocar placement for complex laparoscopic surgery is important to optimize suturing. The authors use three 5-mm ports and one 10-mm port (Fig. 49.9). One 5-mm port is placed at the umbilicus. The 10-mm port is placed on the primary surgeon's side and is the port of entry for the needles and suture. If both surgeons are introducing and tying needles, two lateral 10-mm ports can be used. An alternative to using a 10-mm port is to use a 5-mm port. By back-loading the suture, a 5-mm port can be utilized rather than a 10mm port, but the authors find this approach too time-consuming because this requires removal and reinsertion of the port with each suture. Two accessory 5-mm ports are placed, including one lateral port on the assistant's side and the other either on the operating surgeon's side or in the midline. This port allows the operating surgeon to retrieve sutures and grasp tissues.

Anterior Compartment Laparoscopic Paravaginal Defect Repair A paravaginal repair can be performed as an open procedure, a transvaginal approach, or via the laparoscope. Purported advantages of an abdominal approach include lack of disruption of the neurovascular supply at the anterior vagina, but this concern remains theoretical. The authors find that the laparoscopic paravaginal repair is technically more challenging than other laparoscopic repairs, including laparoscopic sacral colpopexy. The difficulties with laparoscopic paravaginal repairs stem partly from the limitations of the bony pelvis angles coupled with long laparoscopic suturing instruments. These confines make suturing more challenging than open paravaginal repairs or laparoscopic mesh sacral colpopexy. The authors perform paravaginal repairs with an intraperitoneal laparoscopic approach. Once the ports are placed, the peritoneum above the dome of the bladder is incised in the midline. A transverse incision is carried bilaterally to the obliterated umbilical artery. Filling the bladder retrograde can be helpful in determining the proper plane. The threedimensional shape of the bladder dome can be difficult to appreciate with two-dimensional imaging. The tendency for the dissection to drift in a posterior direction should be avoided to avoid bladder dome injury. Once the proper plane is identified, the dissection is carried through the loose adventia easily. As the peritoneal incision is established, the insufflating gas often distends this space well and helps to delineate the structures. Dissection can

proceed bluntly or sharply. Care is taken to avoid anterolateral dissection in the region of the obturator canal. Once the space of Retzius is exposed (from the anterior pubovesical attachments adjacent to the pubic symphysis to the posterolateral ischial spine), the extent of the defect is assessed. Using a vaginal finger to elevate the vaginal at the defect, interrupted sutures are place from the lateral ATFP to the fibromuscular layer of the vagina medially. Sometimes, there is not much supportive ATFP left overlying the obturator internus muscle and fascia. In this case, there usually is strong connective tissue adjacent to the ischial spine. Alternatively, sutures can be placed in the obturator internus fascia. Approximately four to five interrupted no. 2–0 braided polyester (Ethibond, Ethicon, Somerville, NJ) or other permanent suture are placed on each side. The authors tie the sutures with an extracorporeal knot. The medial bite is more anterior, and the lateral bite is posterior and cephalad to help provide both lateral and apical support. Once the sutures are placed and tied, irrigation is performed. After assuring hemostasis, a Burch retropubic urethropexy can also be placed laparoscopically. The data suggest that the stress incontinence outcomes may not be as good with a laparoscopic Burch approach when compared with that achieved by an open approach.

Figure 49.8 Laparoscopic positioning for pelvic support defects. The arms at both padded and then tucked at the sides. The legs are wrapped with knee-high intermittent pneumatic compression stockings and positioned in adjustable hydraulic boot stirrups. The table height is adjusted to its lowest position and the legs are positioned low so that the thighs will not inhibit the laparoscopic instruments.

Once the space of Retzius is irrigated, the authors close the space with peritoneal closure. Some centers leave this space open, but this closure is preferred to prevent herniation of bowel. A purse-string closure of the peritoneum is run by using a monofilament delayed absorbable suture.

Posterior Compartment Laparoscopic Mesh Sacral Colpoperineopexy As described previously for open ASC, some centers have advocated laparoscopic attachment of the perineal body to laparoscopically placed sacral colpopexy mesh. There has been a higher rate of mesh erosion reported when comparing historical controls, although true comparison studies are lacking. The technique described includes opening the posterior vagina, affixing mesh to the perineal body, and then retrieving the mesh via laparoscopy to attach to the sacrum.

Apical Compartment Laparoscopic resuspension of the vaginal apex can be performed by shortening the uterosacral ligaments or with sacral colpopexy. The choice of suture and technique can be very similar to that described for open or vaginal repairs.

Laparoscopic Mesh Sacral Colpopexy Mesh sacral colpopexy via the laparoscope requires a skilled laparoscopist who is facile at laparoscopic suturing. The overall technique is similar to that of an open procedure. Positioning is as described previously, but left lateral tilt is often helpful to rotate the rectosigmoid away from the sacral promontory. Dissection begins at the sacral promontory after first assuring that there are no pelvic or abdominal abnormalities that need to be addressed on laparoscopic survey. The avascular spaces are utilized to sharply or bluntly expose the anterior longitudinal ligament of the sacral promontory. The authors choose to start at the promontory, as this is the region that is at most risk for bleeding. At this step, if uncontrollable bleeding ensues due to iliac, middle sacral, or presacral bleeding, conversion to laparotomy should rapidly be considered. Weislander and colleagues recently reviewed the presacral vascular anatomy. The vascular structures of most concern include (a) the left iliac vein, which is not protected by the artery as it is on the right side; (b) the middle sacral vessels; and (c) the presacral venous plexus. By isolating the deeper dissection to the sacral promontory rather than attempting to expose the anterior longitudinal ligament at lower levels, injury to the presacral veins is unlikely. The right ureter, iliac vessels, and colon should be identified prior to incision. The peritoneum over the sacral promontory is elevated and incised with scissors. Alternatively, electrodissection (or a harmonic scalpel) can be utilized, but the authors prefer to reduce risks of thermal damage by using sharp dissection. The peritoneal incision is carried into the pelvis, lateral to the rectum but medial to

the right ureter. Once the peritoneal incision is completed, it can be valuable to run a suture along the medial side of the peritoneum and sometimes through epiploica. The suture can then retract the rectum medially out of the field by exiting it through a separate small stab incision. The suture ends are retrieved through the stab incision in the skin by using a fascial closure device. The suture can then be against the anterior abdominal wall (which is protected by a moistened sponge) on mild tension using a hemostat.

Figure 49.9 Laparoscopic port placement options for pelvic support defects. A: The position of the lateral ports should be at or above the level of the anterior superior

iliac spines to avoid injury to the ilioinguinal and iliohypogastric nerves. (Reproduced with permission from Whiteside JL, Barber M, Walters M, et al. Anatomy of ilioinguinal and iliohypogastric nerves in relation to trocar placement and low transverse incisions. Am J Obstet Gynecol 2003;189(6):1574–1578.) B: The inferior epigastric vessels should be identified bilaterally as they initiate just cephalad and lateral to the junction of the round ligament and the obliterated umbilical artery; identification at this location facilitates location of the more cephalad vessels by tracing them upward. The superior epigastric vessels can often be identified by transillumination in thin patients. (Reproduced with permission from Hurd WW, Bude RO, DeLancey JO, et al. The location of abdominal wall blood vessels in relationship to abdominal landmarks apparent at laparoscopy. Am J Obstet Gynecol 1994;171(3):642–646.)

Next, dissection of the rectovaginal is initiated. With a probe in the vagina and another in the rectum, the proper plane can be established. The authors utilize EEA sizers, with a small sizer placed in the rectum and a large placed in the vagina. This space is dissected prior to the anterior vesicovaginal space to avoid obstructing the view if there is bleeding at the anterior site. Sharp dissection is utilized, and the dissection can often proceed down to the lower half of the posterior vagina via the rectovaginal space. Care should be taken to avoid straying laterally with the dissection to avoid bleeding. The vesicovaginal space is then dissected in a similar fashion and with careful attention to be sure that the bladder is dissected away anteriorly. If the plane of dissection is difficult to develop, then retrograde filling of the bladder can be helpful. The authors utilize two leaves of polypropylene macropore mesh fashioned from a 10 ×15 cm piece (Gynemesh, Ethicon, Somerville, NJ). Occasionally, a larger-length piece is desired to be able to reach from low on the posterior vagina to the sacral promontory. The first leaf of mesh is attached to the posterior vagina. By manipulating the vaginal probe so that the tip of the probe is directed toward the rectum, the most distal suture can be placed far down the rectovaginal septum. The mesh is then threaded over the suture and guided into the pelvis and tied in place. At least six permanent monofilament no. 2–0 polypropylene (Prolene, Ethicon, Somerville, NJ) or Gortex (W. L. Gore & Associates, Flagstaff, AZ) sutures are then placed through the mesh and into the vaginal wall to secure it. (Fig. 49.10). A second leaf of mesh is then attached to the anterior vagina in a similar fashion. If a concomitant hysterectomy has been performed, then the sutures attaching the mesh should not be placed near the cuff closure to avoid future mesh erosion. At this point, both leaves of the mesh are brought back to the sacral promontory, and a determination of the appropriate tension is made. Ideally, there should be little tension on the mesh so that it follows the curve of the sacrum to some extent. The authors adjust the tension by finding a location on the mesh that will allow the mesh to be slack with pressure on the EEA vaginal probe but with tension taken up slightly with the probe removed. Two permanent no. 2–0 sutures are passed through the mesh and then through the anterior longitudinal ligament at the sacral promontory.

The authors prefer extracorporeal knot tying, as it has been found that this approach is faster than intracorporeal knot tying. There are disadvantages to extracorporeal knot tying, however, in that there is more leakage of the insufflation gas. Therefore, a properly functioning and self-sealing trocar is imperative.

Laparoscopic Uterosacral Ligament Suspension While uterosacral ligament suspension is commonly performed via a vaginal approach, purported advantages of the laparoscopic approach to uterosacral ligament suspension include direct visualization of the ureters and bowel. Additionally, lysis of adhesions can be performed with improved visualization. Disadvantages include greater risks for bowel injury with port placement, greater discomfort, and the potential for more adhesions. Trocar placement is similar to that described previously for laparoscopic mesh sacral colpopexy. After survey of the abdomen and pelvis, identification of both ureters is imperative. The uterosacral ligaments normally attach from the upper vagina and cervix back to the lateral sacrum at the S2–3 level. The uterosacral suspension sutures are placed in the proximal third of the ligament, where it is broader. Care must be taken to identify the ipsilateral ureter and rectum prior to and during placement of the sutures. The first suture of no. 2–0 polypropylene or braided polyester is placed through the middle segment of the ligament and then into the ipsilateral vaginal cuff. A second suture is placed in the more proximal (sacral) portion of the ligament and into the medial ipsilateral cuff (Fig. 49.11). Injury to the rectum is avoided by placing a small EEA sizer and mapping out the location of the rectum prior to placing the sutures. The contralateral sutures are placed in a similar fashion. At times, it is helpful to incise the peritoneum medial to the ureter but lateral to the rectum to be sure that these structures are not at risk. Once the sutures are tied, cystourethroscopy should be performed to assure normal bladder integrity and ureteral patency, as described elsewhere.

Obliterative Procedures In selected patients, an obliterative procedure may be offered rather than a reconstructive procedure. The success

of obliterative procedures has been reported to be in the 90% to 95% range, with variable follow-up. However, obliterative procedures usually are reserved for patients with significant comorbidities who are not interested in retaining a vagina for sexual relations. There is an approximate 10% risk of regret following colpocleisis procedures, thus counseling of options and discussing potential future life changes, including loss of a current partner, and/or gaining a new partner, is important. An excellent review of colpocleisis was recently written by Fitzgerald and associates in 2006.

Figure 49.10 Laparoscopic mesh sacral colpopexy. A: Sagittal view with two leaves of macropore polypropylene mesh attached from the anterior and posterior vaginal apex to the anterior longitudinal ligament of sacral promontory with several permanent sutures. B: View from laparoscope with mesh attachments to sacral promontory.

Figure 49.11 Laparoscopic high uterosacral ligament suspension. Two uterosacral ligament permanent sutures are placed through the deep portion of the ligament and to the ipsilateral vaginal cuff. A: Placement of right uterosacral ligament suspension suture to lateral vagina. Care is taken to avoid the ureter laterally and the rectum medially. B: Four uterosacral ligament sutures have been tied, resuspending the vagina over the rectum.

Total Colpectomy with Colpocleisis Total colpectomy (vaginectomy) is an option among patients who have posthysterectomy vaginal vault prolapse or in selected patients in which vaginal hysterectomy is combined with total colpectomy. Total colpectomy combined with vaginal hysterectomy is associated with higher morbidity, including transfusion risks, infection risks, and ureteral injury risks, than that found with colpectomy alone.

Figure 49.12 Total colpocleisis after colpectomy. A: The vaginal epithelium is removed in four quadrants with care to leave the distal 2 cm of vagina above the hymenal remnants. B, C: A pursestring closure is started at the apex, with sequential purstring closure progressing distally. (Reproduced with permission from DeLancey JOL, Morley GW. Total colpocleisis for vaginal eversion. Am J Obstet Gynecol 1997;176(6):1228–1235.)

Colpectomy is initiated by mapping out the region of vaginal epithelium that is to be denuded. The authors feel that it is important to leave a 1- to 2-cm margin of distal vagina to assure that the axis outlet of the bladder is not adversely altered. The vagina is marked

into quadrants to facilitate dissection (Fig. 49.12A). The subepithelium may be infiltrated with a vasoconstrictive agent such as dilute vasopressin (the authors utilize 20 U diluted in 100 cc of normal saline) or epinephrine. Alternatively, colpectomy under local anesthetic has been described by Miklos and Kohli. Prior to injecting a vasoconstrictive agent, communication with the anesthesiologist is important to assure that the patient's comorbidities do not preclude its use. The authors begin the dissection in one of the two posterior quadrants first to take advantage of better exposure by avoiding blood obscuring the operative field if the anterior quadrants are started first. The dissection begins at the apex of the vagina if the prolapse is extensive and then proceeds to the distal vagina. After initially scoring the epithelium with a scalpel, the epithelium is undermined with Metzenbaum scissors. It often is helpful to use countertraction with a finger from the nondominant hand behind the vagina. The proper plane can then be dissected with pressure applied from this finger against the vagina (Fig. 49.12B). Countertraction can be applied by an assistant with a smooth or Russian forceps. As dissection continues out to the distal vagina, the epithelium is completely removed. Similar excision is performed in all four quadrants. Once all four quadrants are denuded, a purse-string closure of the fibromuscular layer of the vagina is initiated at the apex (Fig. 49.12C). Care must be taken to avoid taking bites that are too deep during the purse-string closure, as the bladder and bowel are at risk of injury. The authors generally use no. 2–0 polyglactin or polydioxanone delayed absorbable suture. Sequential purse-string closure is performed with each subsequent suture placed approximately 1 cm distal to the last. As the closure reaches the distal cut edge of the vaginal epithelium, the vagina is closed from front to back with interrupted no. 2–0 polyglactin suture. The authors leave the medial 1 to 2 cm open to leave room to perform an aggressive posterior colpoperineorrhaphy, as described previously. To provide extra support at the distal vagina and perineum, the puborectalis muscle across the space between the distal vagina and the rectum is plicated. The concerns for dyspareunia described previously with puborectalis muscle plication sutures are not an issue after colpocleisis. The authors place a midurethral synthetic sling (retropubic or transobturator) in selected individuals who demonstrate stress urinary incontinence on cough stress testing. It is important to leave the distal vagina intact to be able to preserve the landmarks of the bladder neck and midurethra.

Partial Colpectomy with LeFort Colpocleisis Partial colpectomy and colpocleisis was first performed by Neugebauer in 1867 but first published by LeFort in 1877. This procedure antedates hysterectomy and was a procedure to treat advanced prolapse without the added morbidity that accompanies hysterectomy. There have been many modifications to the initial descriptions of the procedure, and several have been named after surgeons who have described the modifications. Most of the modifications have changed the shape or amount of vaginal epithelium removed.

Figure 49.13 Partial colpectomy with colpocleisis. Trapezoids of anterior and posterior vagina are excised. The apex is closed with interrupted delayed absorbable suture, leaving channels laterally for drainage of the cervix and uterus. (Reproduced with permission from Reiffenstuhl G, Platzer W, Knapstein PG, eds. Vaginal operations: Surgical Anatomy and Technique, 2nd ed. Baltimore: Williams & Wilkins 1996:167.)

Anterior and posterior trapezoids of vaginal epithelium are excised (Fig. 49.13). As with other vaginal surgeries, the authors prefer to start with the posterior dissection first to prevent blood running down into the posterior operative field. A dilute vasopressin solution or local anesthetic with epinephrine may be helpful for hemostasis and to establish dissection planes. The vaginal epithelium is left intact from the cervix and along two lateral tracts to allow drainage from the uterus and cervix. The vaginal excision is also usually left intact for 1 to 2 cm above the hymenal remnants to prevent change in the urethral axis. Once the trapezoids are excised, closure begins at the cervicovaginal junction. The anterior vagina is reapproximated to the posterior vagina with interrupted no. 2–0 polyglactin or polydioxanone suture. This effectively reduces the cervix by imbricating it above the vaginal closure line. Similar rows of suture are continued, closing anterior to posterior fibromuscular layers of the vagina. At the lateral edges, the sutures bring the anterior and posterior vagina together at the epithelium to make lateral channels

contiguous with the cervix (Fig. 49.13). Similar to the total colpectomy with colpocleisis, the authors recommend leaving room distally to perform an aggressive posterior colpoperineorrhaphy. As described previously, plication of the puborectalis muscle across the midline is performed because dyspareunia is not a concern. Room is left at the distal anterior vagina as well, to prevent axis change at the bladder neck that can occur if the distal anterior vagina is sewed to the posterior vagina. If urethral hypermobility is a concern, sometimes a Kelly plication of the urethra can be considered. If stress urinary incontinence is documented, a midurethral sling may be considered.

Other Technology Percutaneous Kits New technologies have recently and rapidly been marketed to treat POP (Table 49.2). Most of these technologies have been derived from the success of the midurethral mesh slings, originally described with the tensionfree vaginal tape (TVT) procedure (Gynecare, Somerville, NJ). Despite very different placement and mechanisms of action than the original TVT, these surgical devices have been approved under the Food and Drug Administration (FDA) 510(k) mechanism. They are categorized as class II devices, and for this reason, clinical outcome, safety, and efficacy studies are not required before device implementation. Until there is safety and efficacy data available, these devices should be used with caution and with appropriate patient counseling. The kits utilize polypropylene macropore mesh coupled to percutaneous needles. The mesh is inserted via vaginal incisions and retrieved through percutaneous needles placed through perineal skin sites. A vaginal incision is made in the compartment to be augmented with mesh. Percutaneous lateral needles are then placed via different sites and directed to the vaginal incision. The needles are used to retrieve small extension arms of mesh that are pulled back through the percutaneous sites.

TABLE 49.2 Permanent Synthetic Percutaneous Mesh Kits (U.S. Market) Vaginal Support Defect

Procedures

Anterior vagina

Perigee (American Medical Systems, Minnetonka, MN) Avaulta (anterior) (C. R. Bard, Cranston, RI)

Prolift (anterior) (Gynecare, Somerville, NJ) Posterior vagina

Apogee Avaulta (posterior) Prolift (posterior)

Apical prolapse

Apogee Avaulta (posterior) Prolift (posterior)

Prolapse all segments

Perigee combined with Apogee Avaulta (anterior and posterior) Prolift (complete)

Anterior prolapse kits primarily access the anterior wall through percutaneous lateral sites that pierce the medial anterior and posterior margins of the obturator foramen. Placement is designed to have the mesh arms pierce the ATFP. Posterior prolapse kits tend to access the vaginal incisions through the ischiorectal fossa. The posterior kits often use posterior needle placement through or near the sacrospinous ligament to provide apical support. Ostensible advantages of macropore mesh (with pore size of at least 75 µm) are that the loose weave promotes fibroblast integration into the mesh and that the macrophages can permeate the mesh to reduce infection. The concept with the kits is to provide tensionfree mesh supports at the anterior vagina, apex, and posterior compartments. To date, there is limited safety data and limited follow-up. Mesh erosion is reported in the 0% to 18% of patients. There are no comparison trials with traditional repairs. Altman and colleagues recently published a registry of all subjects undergoing transvaginal mesh repairs in Sweden over a 6-month study period. They found a serious perioperative complication rate of 4.4%, dominated by visceral injury. There are not follow-up data regarding erosion risks, dyspareunia, or pain.

Biologic Grafts Xenografts Xenografts are biologic materials harvested from other species. Xenografts have been used in other surgical subspecialties for decades. The market for biomaterials is rapidly changing, and thus a list of available product has not been included. Tissues utilized commonly include porcine small intestinal submucosa and bovine pericardium. One concern regarding xenografts is the potential for latency of animal zoonoses. The FDA does have strict guidelines regarding knowledge of the animal herd, screening for bovine spongiform encephalopathy, feed source, and vaccination status. Evidence-based data regarding different products are limited. One randomized multicenter trial by Meschia and

associates compared porcine dermal graft to augment anterior colporrhaphy. They found lower recurrence rates with the graft-augmented repair. Studies to date on posterior colporrhaphy have not shown benefit with augmented repair, and in one randomized trial (Paraiso and coworkers), there was a higher recurrence rate when xenograft augmentation was utilized. Xenograft extrusion has been reported in some series.

Allografts Human allografts are tissues harvested from cadavers. Fascia lata is commonly marketed for POP and has been used in the orthopedic field for years. Human dermal products and human-derived dura mater are also available commercially for POP. Allograft material is screened for infection, including HIV, hepatitis B and C, and T-cell lymphocyte virus type 1. FDA guidelines require irradiation and freeze-drying. While under FDA control, there was a recall in 2005 of cadaveric human tissue from Biomedical Tissues Services, Ltd, that may not have been procured with appropriate screening. Even with adequate testing, there may be a small risk of HIV or prion transmission. Allografts used for pubovaginal sling procedures have had variable results. Autolysis and evidence for graft versus host reaction has been identified histologically on some products. Several authors have suggested that the preparation of the tissue may be a factor in its long-term integrity after implantation. Tissue preparation, including freezing, irradiating, and the storage medium, may affect durability and integrity. There are limited data on allograft tissues for prolapse. Flynn and colleagues describe favorable results using cadaveric fascia lata allograft for ASC with follow-up of 6 to 12 months. Another series by Gregory and associates found unfavorable results compared with those found with mesh, but they used fascia that was freeze-dried and irradiated.

Autologous Grafts Autologous fascia lata and rectus abdominus fascia have also been utilized to augment prolapse repairs at the anterior, posterior, and apical compartments. The disadvantages of autologous grafts include perioperative morbidity associated with harvesting tissue, infection or pain at harvest site, incisional hernia, and unsatisfactory cosmesis. There is little comparison data available on outcomes in the literature.

Conclusion Surgical treatment of POP is common. Surgical approaches to treat POP are varied, both with respect to the approach (vaginal, abdominal, and laparoscopic) as well as the materials used (native ligaments and other biomaterials). Selection of a procedure for an individual should be strategized based on her risks, comorbidities, and prior surgical history. Obliterative procedures may be best for selected individuals when penetrative vaginal intercourse is still desired. In the three randomized studies included in a 2005 Cochrane review, abdominal mesh sacral colpopexy has lower rates of failure, dyspareunia, and reoperation compared with rates associated with vaginal suspension. Nonetheless, there may be higher rates of adhesions and serious morbidity with abdominal approaches.

Recurrent prolapse and complications associated with traditional repairs have led investigators and biomedical companies to seek alternatives that are less invasive, quicker, and perhaps more durable. Their primary focus has been on the marketability. The surgical treatment of POP is rapidly changing due to rapid introduction of synthetics and biomaterials and new ways to introduce them. Unfortunately, most of these materials and techniques have come to market without safety and efficacy data, and their use in patients should be used cautiously until more data is available.

Summary Points POP is a prevalent condition that may manifest with a variety of symptoms and not necessarily reflective of the specific prolapse defect. The goal of surgical management of POP is to restore normal vaginal anatomy; improve symptoms of POP, the lower urinary tract, and bowel; restore or improve sexual functioning; and correct coexisting pelvic pathology. The goal of surgical intervention needs to be individualized to the patient and is dependent on patient physical activity level, desire for sexual function, and medical status. A variety of surgical approaches exist, including open abdominal and transvaginal, and outcomes from these different approaches may vary widely depending on the surgeon, operative materials, and technique utilized as well as patient factors. New operative approaches utilizing synthetic graft material need to be studied in a prospective robust fashion in order to get the information with which to more fully counsel patients about shortand long-term complications and outcomes.

Suggested Readings Altman D, Falconer C. Perioperative morbidity using transvaginal mesh in pelvic organ prolapse repair. Obstet Gynecol 2007;109(2 Pt 1):303–308. Altman D, Lopez A, Gustafsson C, et al. Anatomical outcome and quality of life following posterior vaginal wall prolapse repair using collagen xenograft. Int Urogynecol J Pelvic Floor Dysfunct 2005;16(4):298–303. Altman D, Zetterstrom J, Mellgren A, et al. A three-year prospective assessment of rectocele repair using porcine xenograft. Obstet Gynecol 2006;107(1):59–65. American College of Obstetricians and Gynecologists. Pelvic organ prolapse. ACOG Practice Bulletin No. 79. Obstet Gynecol 2007;109(2 Pt 1):461–473.

Aronson MP, Aronson PK, Howard AE, et al. Low risk of ureteral obstruction with “deep” (dorsal/posterior) uterosacral ligament suture placement for transvaginal apical suspension. Am J Obstet Gynecol 2005;192(5):1530–1536. Baessler K, Hewson AD, Tunn R, et al. Severe mesh complications following intravaginal slingplasty. Obstet Gynecol 2005;106(4):713–716.

Barber MD, Walters MD, Cundiff GW. Responsiveness of the Pelvic Floor Distress Inventory (PFDI) and Pelvic Floor Impact Questionnaire (PFIQ) in women undergoing vaginal surgery and pessary treatment for pelvic organ prolapse. Am J Obstet Gynecol 2006;194(5):1492–1498. Benson JT, Lucente V, McClellan E. Vaginal versus abdominal reconstructive surgery for the treatment of pelvic support defects: a prospective randomized study with long-term outcome evaluation. Am J Obstet Gynecol 1996;175(6):1418–1421; discussion 1421–1422. Boyles SH, Weber AM, Meyn L. Procedures for pelvic organ prolapse in the United States, 1979–1997. Am J Obstet Gynecol 2003;188(1):108–115. Brown JS, Waetjen LE, Subak LL, et al. Pelvic organ prolapse surgery in the United States, 1997. Am J Obstet Gynecol 2002;186(4):712–716. Brubaker L. Controversies and uncertainties: abdominal versus vaginal surgery for pelvic organ prolapse. Am J Obstet Gynecol 2005;192(3):690–693. Brubaker L, Cundiff GW, Fine P, et al. Abdominal sacrocolpopexy with Burch colposuspension to reduce urinary stress incontinence. N Engl J Med 2006;354(15):1557– 1566. Collinet P, Belot F, Debodinance P, et al. Transvaginal mesh technique for pelvic organ prolapse repair: mesh exposure management and risk factors. Int Urogynecol J Pelvic Floor Dysfunct 2006;17(4):315–320. Culligan PJ, Blackwell L, Goldsmith LJ, et al. A randomized controlled trial comparing fascia lata and synthetic mesh for sacral colpopexy. Obstet Gynecol 2005;106(1):29–37. Cundiff GW, Fenner D. Evaluation and treatment of women with rectocele: focus on associated defecatory and sexual dysfunction. Obstet Gynecol 2004;104:1403–1421. Daneshgari F, Paraiso MF, Kaouk J, et al. Robotic and laparoscopic female pelvic floor

reconstruction. BJU Int 2006;98(Suppl 1):62–68; discussion 69. Deprest J, Zheng F, Konstantinovic M, et al. The biology behind fascial defects and the use of implants in pelvic organ prolapse repair. Int Urogynecol J Pelvic Floor Dysfunct 2006;17(Suppl 1):S16–S25. De Tayrac R, Gervaise A, Chauveaud A, et al. Tension-free polypropylene mesh for vaginal repair of anterior vaginal wall prolapse. J Reprod Med 2005;50(2):75–80. De Tayrac R, Picone O, Chauveaud-Lambling A, et al. A 2-year anatomical and functional assessment of transvaginal rectocele repair using a polypropylene mesh. Int Urogynecol J Pelvic Floor Dysfunct 2006;17(2):100–105. Elkadry EA, Kenton KS, FitzGerald MP, et al. Patient-selected goals: a new perspective on surgical outcome. Am J Obstet Gynecol 2003;189(6):1551–1557; discussion 1557–1558. FitzGerald MP, Edwards SR, Fenner D. Medium-term follow-up on use of freeze-dried, irradiated donor fascia for sacrocolpopexy and sling procedures. Int Urogynecol J Pelvic Floor Dysfunct 2004;15(4):238–242. FitzGerald MP, Richter HE, Siddique S, et al. Colpocleisis: a review. Int Urogynecol J Pelvic Floor Dysfunct 2006;17(3):261–271. Flynn MK, Webster GD, Amundsen CL. Abdominal sacral colpopexy with allograft fascia lata: one-year outcomes. Am J Obstet Gynecol 2005;192(5):1496–1500. Gandhi S, Goldberg RP, Kwon C, et al. A prospective randomized trial using solvent dehydrated fascia lata for the prevention of recurrent anterior vaginal wall prolapse. Am J Obstet Gynecol 2005;192(5):1649–1654. Govier FE, Kobashi KC, Kozlowski PM, et al. High complication rate identified in sacrocolpopexy patients attributed to silicone mesh. Urology 2005;65(6):1099–1103. Gustilo-Ashby AM, Jelovsek JE, Barber MD, et al. The incidence of ureteral obstruction and the value of intraoperative cystoscopy during vaginal surgery for pelvic organ prolapse. Am J Obstet Gynecol 2006;194(5):1478–1485. Handa VL, Garrett E, Hendrix S, et al. Progression and remission of pelvic organ prolapse: a longitudinal study of menopausal women. Am J Obstet Gynecol 2004;190(1):27–32.

Higgs PJ, Chua HL, Smith AR. Long term review of laparoscopic sacrocolpopexy. BJOG 2005;112(8):1134–1138. Huebner M, Hsu Y, Fenner DE. The use of graft materials in vaginal pelvic floor surgery. Int J Gynaecol Obstet 2006;92(3):279–288. Hullfish KL, Bovbjerg VE, Gibson J, et al. Patient-centered goals for pelvic floor dysfunction surgery: what is success, and is it achieved? Am J Obstet Gynecol 2002;187(1):88–92. Hullfish KL, Bovbjerg VE, Steers WD. Patient-centered goals for pelvic floor dysfunction surgery: long-term follow-up. Am J Obstet Gynecol 2004;191(1):201–205. Jelovsek JE, Barber MD. Women seeking treatment for advanced pelvic organ prolapse have decreased body image and quality of life. Am J Obstet Gynecol 2006;194(5):1455– 1461. Jelovsek JE, Sokol AI, Barber MD, et al. Anatomic relationships of infracoccygeal sacropexy (posterior intravaginal slingplasty) trocar insertion. Am J Obstet Gynecol 2005;193(6):2099–2104. Kearney R, DeLancey JO. Selecting suspension points and excising the vagina during Michigan four-wall sacrospinous suspension. Obstet Gynecol 2003;101(2):325–330. Maher C, Baessler K, Glazener CM, et al. Surgical management of pelvic organ prolapse in women. Cochrane Database Syst Rev 2004; issue 4:CD004014. Maher CF, Qatawneh AM, Dwyer PL, et al. Abdominal sacral colpopexy or vaginal sacrospinous colpopexy for vaginal vault prolapse: a prospective randomized study. Am J Obstet Gynecol 2004;190(1):20–26. Mattox TF, Moore S, Stanford EJ, et al. Posterior vaginal sling experience in elderly patients yields poor results. Am J Obstet Gynecol 2006;194(5):1462–1466. Meschia M, Pifarotti P, Bernasconi F, et al. Porcine skin collagen implants to prevent anterior vaginal wall prolapse recurrence: a multicenter, randomized study. J Urol 2007;177(1):192–195. Milani R, Salvatore S, Soligo M, et al. Functional and anatomical outcome of anterior and posterior vaginal prolapse repair with prolene mesh. BJOG 2005;112(1):107–111.

Molsted-Pedersen L, Rudnicki M, Lose G. Transvaginal repair of enterocele and vaginal vault prolapse using autologous fascia lata graft. Acta Obstet Gynecol Scand 2006;85(7):874–878. Nieminen K, Hiltunen KM, Laitinen J, et al. Transanal or vaginal approach to rectocele repair: a prospective, randomized pilot study. Dis Colon Rectum 2004;47(10):1636–1642. Nygaard IE, McCreery R, Brubaker L, et al. Abdominal sacrocolpopexy: a comprehensive review. Obstet Gynecol 2004;104(4):805–823. Paraiso MF, Barber MD, Muir TW, et al. Rectocele repair: a randomized trial of three surgical techniques including graft augmentation. Am J Obstet Gynecol 2006;195(6):1762– 1771. Rooney K, Kenton K, Mueller ER, et al. Advanced anterior vaginal wall prolapse is highly correlated with apical prolapse. Am J Obstet Gynecol 2006;195(6):1837–1840. Roovers JP, van der Vaart CH, van der Bom JG, et al. A randomised controlled trial comparing abdominal and vaginal prolapse surgery: effects on urogenital function. BJOG 2004;111(1):50–56. Silva WA, Karram MM. Scientific basis for use of grafts during vaginal reconstructive procedures. Curr Opin Obstet Gynecol 2005;17(5):519–529. Skiadas CC, Goldstein DP, Laufer MR. The Manchester-Fothergill procedure as a fertility sparing alternative for pelvic organ prolapse in young women. J Pediatr Adolesc Gynecol 2006;19(2):89–93. Solomon MJ, Young CJ, Eyers AA, et al. Randomized clinical trial of laparoscopic versus open abdominal rectopexy for rectal prolapse. Br J Surg 2002;89(1):35–39. Toglia MR, Nolan TE. Morbidity and mortality rates of elective gynecologic surgery in the elderly woman. Am J Obstet Gynecol 2003;189(6):1584–1587; discussion 1587–1589. Weber AM. New approaches to surgery for urinary incontinence and pelvic organ prolapse from the laparoscopic perspective. Clin Obstet Gynecol 2003;46(1):44–60. Weber AM, Richter HE. Pelvic organ prolapse. Obstet Gynecol 2005;106(3):615–634. Weber AM, Walters MD, Piedmonte MR, et al. Anterior colporrhaphy: a randomized trial of three surgical techniques. Am J Obstet Gynecol 2001;185(6):1299–1304; discussion

1304–1306.

Wheeler TL 2nd, Richter HE, Burgio KL, et al. Regret, satisfaction, and symptom improvement: analysis of the impact of partial colpocleisis for the management of severe pelvic organ prolapse. Am J Obstet Gynecol 2005;193(6):2067–2070. Wheeler TL 2nd, Richter HE, Duke AG, et al. Outcomes with porcine graft placement in the anterior vaginal compartment in patients who undergo high vaginal uterosacral suspension and cystocele repair. Am J Obstet Gynecol 2006;194(5):1486–1491. Whiteside JL, Weber AM, Meyn LA, et al. Risk factors for prolapse recurrence after vaginal repair. Am J Obstet Gynecol 2004;191(5):1533–1538. Winters JC, Fitzgerald MP, Barber MD. The use of synthetic mesh in female pelvic reconstructive surgery. BJU Int 2006;98(Suppl 1):70–76; discussion 77.

50 Nonsurgical Treatment of Pelvic Organ Prolapse Ingrid E. Nygaard While surgery is considered the primary treatment for pelvic organ prolapse (POP), pessaries have been used to reduce prolapse for centuries and continue to fill an important niche in treating this disorder. Additionally, there is some, albeit scant, evidence that pelvic muscle exercises may hinder prolapse regression. In 2001, 86% of American gynecologists queried prescribed pessaries, though most received minimal training in this area in their residencies. Further, 77% of American Urogynecologic Society members responding to a questionnaire about pessary use reported using them as first-line therapy for prolapse; 12% used pessaries only when surgery was contraindicated. Some patients choose to wear a pessary as primary therapy for POP, while others use one temporarily when awaiting surgery. For some women, the option of a pessary allows flexibility in scheduling surgery. Others may wear a pessary only when doing an activity that exacerbates symptoms such as exercise. A pessary may useful diagnostically. Patients generally have a variety of symptoms that may or may not be related to POP. By reducing the bulge for several days with a pessary, the patient and clinician get clues about whether reducing the prolapse surgically is likely to resolve symptoms that the patient may have, such as pelvic and back pain, urinary urgency and frequency, or voiding dysfunction. This may improve the chance that the patient has reasonable expectations of what surgery can and cannot “fix.” Limited data from a small study by Handa suggest that wearing a pessary may have a therapeutic effect in women with POP: 19 of 56 women fitted with a pessary continued its use for at least 1 year. Four women had an improvement in stage of prolapse, and no women had worsening.

Choosing a Pessary Today's pessaries are made from medical-grade silicone, which is not allergenic or toxic, does not absorb odors, can be sterilized, and lasts for several years. Some pessaries are easier for a woman to manage herself than are others. Pessaries can be loosely grouped into supportive pessaries, in which levator muscle tone is needed to keep the pessary in place (Fig. 50.1), or space occupying pessaries (Fig. 50.2), which, as their

name implies, keep prolapse reduced by filling the vagina. Space-occupying pessaries are particularly useful for women with advanced POP who have minimal levator muscle tone and wide genital hiatuses. Wu found that 70% of women with POP were successfully fitted with a size 3, 4, or 5 ring pessary. Pott-Grinstein also reported that the ring and donut pessaries were the most common pessaries used. In contrast, Sulak fitted 96 of 107 women with symptomatic POP with a Gellhorn pessary and gave the following reasons why they chose this pessary: the design makes it easy to insert and remove, the base of the pessary is large enough to support the proximal prolapse without exerting excessive pressure in any particular area, the concave base provides suction, and this pessary can be removed by the patient “with minimal discomfort.”

Figure 50.1 Support pessaries used to treat POP. Top: Ring with support (Milex Inc, Chicago, IL) (left), Shaatz (Mentor Corporation, Santa Barbara, CA) (right). Middle: Oval with support (Mentor Corporation, Santa Barbara, CA). Bottom: Gehrung (Milex Inc, Chicago, IL) (left), Hodge (Milex Inc, Chicago, IL) (right).

Most women can be fit successfully. In a prospective cohort study by Clemons and associates, 94 of 100 women with POP were fitted successfully in the office, while two women had pain and four expelled all pessaries tried. Clinicians tried an average of 2.2 pessaries per patient to achieve the best fit. The strategy of the clinic was to try a ring pessary with support first, followed by a Gellhorn if the ring was expelled. One week later, 54% of women were satisfied with the pessary, but it was expelled in 29% and caused pain or discomfort in 17%. Of the dissatisfied women, 29 were refit, 76% successfully. Overall, 73% of women had a successful 2-week pessary fitting trial. Women with a vaginal length of ≤6 cm and those with a wide introitus (four fingerbreadths wide or greater) had a lower chance of being successfully fitted. Ring pessaries with support were used in 100% of women with stage II prolapse and 71% of women with stage III prolapse. Gellhorn pessaries were used in 64% of women with stage IV prolapse.

Figure 50.2 Space-occupying pessaries used to treat POP. Top: Gellhorn (Mentor Corporation, Santa Barbara, CA) (left), Inflataball (Milex Inc, Chicago, IL) (middle), cube with drainage holes (Mentor Corporation, Santa Barbara, CA) (right). Bottom: Mar-Land (left), doughnut (middle), cube (right) (all three by Milex Inc, Chicago, IL).

Cundiff and colleagues conducted a randomized crossover design in which women with stages II or greater POP were initially randomly assigned to be fitted with a ring or a Gellhorn pessary and then 3 months later crossed over to the other type. In the first randomization, 71 and 63 women were assigned to the ring and Gellhorn pessary groups, respectively. In the ring group, 65 (92%) were fitted successfully, 51 at the initial visit and 14 after refitting. In the Gellhorn group, 57 (90%) were fitted successfully, 36 at the initial visit and 21 after refitting. Thus, randomized trial evidence suggests that clinicians can successfully fit most women with either a ring or Gellhorn pessary. In our clinical experience, women find it easier to manage a ring pessary on their own than the Gellhorn.

Pessary Care Before a pessary fitting session, the author treats women who demonstrate vaginal atrophy for 6 weeks with estrogen cream. The women are then instructed to come to the fitting session with a moderately full bladder so that it can be seen that the pessary induces stress incontinence and to ensure that the woman can void with it in place. The author recommends that women remove the pessary at least weekly, leave it out overnight, and then reinsert in the morning. When removed, the pessary is simply washed with warm water. As seen by experience, women rarely develop excessive or foul-smelling vaginal discharge if they remove the pessary at this interval and thus have little use for creams other than occasionally estrogen. If women are unwilling or unable to remove the pessary, an attempt is made to estimate the best interval for office or visiting nurse visits for pessary removals. Women are examined 2 weeks after initial pessary insertion. If discharge is minimal and no erosions are present, the patient is examined at 4 weeks.

Similarly, if the examination is reassuring, the patient is examined again after 6 weeks and so on. The appropriate pessary interval is either a maximum of 3 months or the interval at which foul-smelling discharge or early erosion is seen. Visiting nurses are a valuable resource for women who are unable to care for the pessary on their own. They are often able to visit the woman at home, remove the pessary in the evening, and return in the morning to replace it. The nurse can arrange follow-up if she sees excessive foul-smelling discharge or bleeding. After an initial 2-week and 3-month check, the author examines women who manage their own pessary without difficulty on a yearly basis. (In premenopausal women, women are generally seen only once after fitting and then yearly.) In those unable to remove the pessary themselves, the vagina is inspected visually at least twice yearly. It is important to examine the anterior and posterior vaginal walls during the examination (by turning the speculum 90 degrees) as well as the obvious lateral walls that are visible when the speculum is placed in the usual fashion. Several women have been seen with large rectovaginal or vesicovaginal fistulas caused by pessaries; in all cases, they were undergoing regular examinations by a physician. It is possible that unseen erosions under the speculum blades may have heralded the beginnings of such pressure ulcers.

Effectiveness of Pessaries in Treating Prolapse Effectiveness of pessaries is usually described as either continued use or by reduced symptoms. In two separate studies by Wu and Sulak, each with about 100 women, 41% and 49% were still using the pessary a year or more later. Wu identified no clear factors that correlated with unsuccessful pessary use. Others reported that previous hysterectomy and previous prolapse surgery decreased the chance of success. However, a large enough number of women with prior surgeries were able to use a pessary successfully for several years to warrant trying this modality in women with this history. Almost all women wearing a pessary for symptomatic POP report that the sensation of a bulge resolves; symptoms of pressure, discharge, splinting, urge incontinence, and voiding difficulty improve; and prolapse-specific quality of life improves.

Adverse Events In Wu's series, in which pessaries were generally kept in situ for 3 months at a time, 8 of the 110 women developed vaginal erosions. Five were using a cube, and 3 others were using a ring pessary. Overall, 5 of 6 women using cube pessaries developed vaginal erosions, compared with 3 of 101 using ring pessaries. Ten women had pelvic pain with the pessary in place; 3 were using cube pessaries and 7 were using ring pessaries. Only 2 women discontinued pessary use because of discharge, while 1 did so because of difficulty evacuating the rectum. This study highlights the need for extra caution when using a cube pessary. The suction cups on each side of the cube allow this pessary to stay in when other pessaries fall out, but the same suction cups can cause significant ulceration in the vagina. The author has seen several postmenopausal women who developed large, weeping ulcers

after wearing the cube pessary for only 2 or 3 days. Anecdotally, some colleagues have not had similar experiences; however, based on the author's observation, the use of this type of pessary is now reserved for women with healthy vaginal tissue who are able to remove it nightly. Patients and clinicians must take care to release the suction by sweeping a finger between the pessary and the upper vaginal wall before attempting removal. In the Clemons study, 6 of 73 women (8%) using a pessary discontinued it before 2 months because of severe stress incontinence (4 women), de novo voiding difficulty (1 woman), and de novo defecation difficulty (1 woman). Two women developed vaginal erosions that subsequently resolved with daily vaginal estrogen cream and continued pessary use.

Pelvic Muscle Exercises In a 2006 Cochrane review by Hagen and associates, the authors found three trials that assessed the role of pelvic muscle exercises in treating prolapse. However, the trials were either very small or had substantial limitations that preclude the ability to draw any conclusions. Future research is needed to understand what role, if any, pelvic muscle exercises play in preventing or treating primary or recurrent POP.

Conclusion Pessaries are an important part of the treatment armamentarium for POP. However, they are not without risk, and women using pessaries must be followed carefully. Whether pelvic muscle strengthening can prevent or retard prolapse progression must be studied in carefully designed trials.

Summary Points Most women with POP can be successfully fitted with a ring or Gellhorn pessary. One year after fitting, about half of women continue to use a pessary. While rare, pessaries can cause serious harm, and women using them must be followed closely. Data are insufficient to understand what role pelvic muscle strengthening may play in preventing or treating POP.

Suggested Readings Clemons JL, Aguilar VC, Tillinghast TA, et al. Patient satisfaction and changes in prolapse and urinary symptoms in women who were fitted successfully with a pessary for pelvic organ prolapse. Am J Obstet Gynecol 2004;190:1025–1029. Clemons JL, Aguilar VC, Tillinghast TA, et al. Risk factors associated with an unsuccessful pessary fitting trial in women with pelvic organ prolapse. Am J Obstet

Gynecol 2004;190:345–350.

Cundiff GW, Amundsen CL, Bent AE, et al. The PESSRI study: symptom relief outcomes of a randomized crossover trial of the ring and Gellhorn pessaries. Am J Obstet Gynecol 2007;196:405.e1–405.e8. Cundiff GW, Weidner AC, Visco AG, et al. A survey of pessary use by members of the American Urogynecologic Society. Obstet Gynecol 2000;95;931–935. Fernando RJ, Thakar R, Sultan AH, et al. Effect of vaginal pessaries on symptoms associated with pelvic organ prolapse. Obstet Gynecol 2006;108:93–99. Hagen S, Stark D, Maher C, et al. Conservative management of pelvic organ prolapse in women. Cochrane Database Syst Rev 2006;18(4):CD003882. Handa VL, Jones M. Do pessaries prevent the progression of pelvic organ prolapse? Int Urogynecol J 2002;13:349–352. Maito JM, Quam ZA, Craig E, et al. Predictors of successful pessary fitting and continued use in a nurse-midwifery pessary clinic. J Midwifery Womens Health 2006;51:78–84. Mutone MF, Terry C, Hale DS, et al. Factors which influence the short-term success of pessary management of pelvic organ prolapse. Am J Obstet Gynecol 2005;193:89–94. Pott-Grinstein E, Newcomer JR. Gynecologists' patterns of prescribing pessaries. J Reprod Med 2001;46:205–208. Sulak PJ, Kuehl TJ, Shull BL. Vaginal pessaries and their use in pelvic relaxation. J Reprod Med 1993;38:919–923. Wu V, Farrell SA, Baskett TF, et al. A simplified protocol for pessary management. Obstet Gynecol 1997;90:990.

51 Female Urinary Incontinence: Epidemiology and Evaluation Peggy A. Norton

Epidemiology of Urinary Incontinence Urinary incontinence (UI) is a common problem in women that affects quality of life and results in over $16 billion in direct medical costs annually in the United States (1995 figures). UI can be surveyed by using standardized questionnaires, which have been used to estimate the prevalence of UI in the general population and in affected women seeking treatment. Unfortunately, severity of UI is not always correlated with level of bother: one woman may leak several times a day and not be bothered at all, while another would report an occasional leak as having severe impact on her quality of life. Thus, some measure of bother is considered when reporting UI.

Definitions Rates vary in populations because of differences in definition, but good standardization with regular updates has been provided by the International Continence Society (ICS) for more than 20 years. The ICS has the following definitions for UI: Urinary incontinence: the complaint of any involuntary urine leakage. The main types in women are stress, urge, and mixed. Stress urinary incontinence (SUI): the complaint of involuntary leakage associated with effort or exertion or on coughing or sneezing. If the incontinence is diagnosed on urodynamic testing, this is termed urodynamic stress incontinence (USI). Urge urinary incontinence (UUI): the complaint of involuntary loss of urine accompanied by or immediately proceeded by urgency. If the incontinence is diagnosed on urodynamic testing with increased detrusor pressures reproducing symptoms during filling, the diagnosis is detrusor overactivity with incontinence (DOI.) Because some women are bothered by frequency, nocturia, and urgency but do not actually leak urine with urge, a broader term, overactive bladder, may incorporate all of these symptoms. Mixed incontinence: the presence of both stress and urge incontinence in the same patient.

Prevalence The prevalence of any UI in community-dwelling women ranges from 10% to 40%; while this seems surprisingly high, women with UI often underreport or delay seeking treatment for UI for several years after the condition has become bothersome. Approximately one in four women with UI is considered to have “severe” UI: in studies that differentiate “any” UI from “severe” UI, the prevalence is 29% (11% to 72%) versus 7% (3% to 17%), respectively. In institutional-dwelling adults, the prevalence of UI is 50% or higher. Overall, half of women with UI complain of pure SUI, 30% to 40% complain of mixed urinary incontinence (MUI), and 10% to 20% complain of pure UUI. However, these proportions vary with age: middle-age women complain of SUI, while MUI predominates in older women.

Incidence and Regression It was thought previously that UI was a progressive condition, but some recent reports have highlighted the fact that a certain number of women develop UI and a certain number resolve UI at any given time. It is less known whether the resolution of UI is a direct result of effective medical and surgical intervention or due to the waxing and waning of UI in any single woman. Why would UI resolve in the absence of treatment? It may be that some modifying factor has improved, such as weight loss or change in job, or that the natural history of UI is variable in its severity.

Risk Factors Most of the studies of risk factors have involved cross-sectional studies, with the beststudied factors being parity, age, and obesity. Specific risk factors for UI type are more developed for SUI (all of those mentioned), but risks for urge incontinence may include childbirth and obesity. Pregnancy and childbirth are the most significant risk factors: half of all women experience UI increases during pregnancy, and leakage both before and during pregnancy seems to be associated with parity, age, and body mass index (BMI). Multiple studies demonstrate that episiotomy is not protective. Current epidemiologic studies suggest that cesarean delivery is somewhat but not completely protective. Although some UI resolves during the postpartum period, women who still experience UI at 3 months postpartum are likely to be incontinent 5 years later. Increasing parity and birth weight may be additive, but there is conflicting data in the literature. Most epidemiologic studies demonstrate that increasing age is associated with increasing UI, but surprisingly, the highest prevalence of UI peaks first at age 50 years (Fig. 51.1). SUI predominates in middle-age women, but urge incontinence increases with age. This is not to say that UI is a normal part of aging; rather, factors that contribute to UI are increased with age as well. Obesity defined as >20% over ideal weight or BMI >30 is a risk factor for both urge and stress incontinence, the mechanism in stress being increases in intraabdominal pressure. UUI is also increased in women with obesity.

Several recent studies in differing populations indicate that family history of UI in firstdegree relatives increases the risk of UI four to six times for individual women. Sexual abuse has been identified recently as an important contributor to overactive bladder symptoms.

Figure 51.1 Prevalence of any UI by age from the Norwegian EPINCONT study. (From Hannestad YS, Rortveit G, Sandvik H, et al. A community-based epidemiological survey of female urinary incontinence: the Norwegian EPINCONT study. J Clin Epidemiol 2000;53:1150–1157, with permission.)

It is less clear whether UI is affected by the menopause and hysterectomy, and there is conflicting evidence as to the role of estrogen replacement. Other risk factors include functional and cognitive impairment, constipation, smoking, and pelvic organ prolapse.

Prevention Some of the mentioned risk factors are potentially modifiable. Weight loss has been shown to reduce the severity of UI in women with BMI >30. With increasing request for cesarean delivery, more information is needed as to whether cesarean performed solely to prevent pelvic floor damage is really effective in defined patient populations. Few studies of primary prevention of UI have been undertaken, but women with a family history of UI may be an ideal group to study with regard to childbirth interventions such as elective cesarean. Smoking cessation and resolution of constipation have general benefits in addition to possibly preventing UI.

Evaluation of Urinary Incontinence UI is so common that evaluation and treatment cannot be limited to specialists and subspecialists. UI continues to be embarrassing for some women to report, and this leads to delay and underreporting of symptoms to health care providers. Most of the basic evaluation of UI is within the scope of primary care providers, and many first-line treatments are readily available without specialized instructions or training. The main role of the primary care provider in basic evaluation of UI is to arrive at a presumptive

diagnosis and to exclude complicating factors that would necessitate referral for a more complex evaluation. Thus, a woman complaining of UI may undergo basic triage by any interested clinician, who may be able to arrive at some initial treatment options or who may decide that more complex evaluation is needed.

Basic Evaluation Most UI is diagnosed on history alone, with lesser contributions from the exam or testing. It has been argued that a simple questionnaire to evaluate UI subtypes and a review of potentially complicating factors is all that is required of the primary care provider. Several such questionnaires are included in Table 51.1.

History The history is the most important basic evaluation of UI in women and focuses on the type and desire for treatment. Important questions include the frequency of UI episodes; the degree of bother; stress versus urge symptoms; and relationships to medications, voiding habits, or fluid intake. Reversible causes of UI should be explored, including medications, comorbidities, stool impaction, or acute urinary tract infection (UTI). Pharmacologic agents that contribute to incontinence are listed in Table 51.2. Conditions such as poorly controlled diabetes mellitus or diabetes insipidus may result in excess urine output, thus overwhelming the normal continence mechanism. Gastroesophageal reflux disease (GERD) can lead to a chronic cough. Stool impaction distends the distal sigmoid and rectum and inhibits sacral parasympathetics, resulting in inadequate detrusor contractility and compromised bladder emptying.

TABLE 51.1 Questionnaires for the Evaluation of Urinary Incontinence Sandvik Incontinence Severity Index: Sandvik et al 1995 1. Do you lose urine during sudden physical exertion, lifting, coughing or sneezing? 2. Do you experience such a strong and sudden urge to void that you leak before reaching the toilet? (1) SUI: 0.66 sensitive, 0.88 specific for SUI. (2) UUI: sensitive, 0.96 specific for UUI. (1) and (2) MUI: 0.84 sensitive, 0.66 specific for MUI.

31Q: Brown et al 2000 1. During the past month, have you leaked urine (even a small amount?) 2. id you (a) leak urine when you were performing some physical activity such as coughing, sneezing, lifting, or exercise? (b) when you had the urge or feeling that you needed to empty your bladder but you could not get to the toilet fast enough? (c) without physical activity and without a sense of urgency? 3. Did you leak urine most often with a, b, c, or equally a and b? (a) SUI, 0.86 sensitive, 0.60 specific for SUI; (b) UUI, 0.75 sensitive, 0.77 specific for UUI; (c) unclear incontinence; (a) and (b) MUI.

TABLE 51.2 Medications Affecting Bladder Function, Type of Urinary Incontinence Associated with the Drug, and Presumed Mechanism ACE-inhibitors

SUI: produce chronic cough in 15% of women

Alpha-blockers

SUI: decrease urethral tone

Anticholinergics

Voiding problems: reduce bladder contraclility

Diuretics

UUI: rapid bladder filling and fluid overload to bladder

Lithium

UI: causes excess fluid

Sedatives

Voiding problems: produces overflow incontinence

UI urinary incontinence; SUI stress urinary incontinence; UUI urge urinary incontinence

Acute UTI usually presents with typical symptoms of dysuria, frequency, and urgency but sometimes with urge incontinence. Asymptomatic bacteriuria detected in a woman undergoing evaluation for UI is a management dilemma: if the urge incontinence is a symptom of UTI, then the primary care physician should treat the infection and evaluate for improvement in UI. But asymptomatic bacteriuria otherwise is not treated in women unless they are pregnant, and in truth, few individuals see dramatic resolution of their UI with a course of antibiotics. A relatively full bladder increases the likelihood of urine loss and decreases bladder control. However, many women drink excessive amounts of fluid in an effort to treat constipation, incontinence, or bladder infections or for weight loss. The Food and Drug Administration (FDA) recommends that in the absence of other factors, normal fluid intake for adults should be the equivalent of six to eight 8-oz glasses of fluid per day, much of which can be in the form of solid food. Urine output in excess of the normal 1,300 to 1,500 mL may lead to frequency, urgency, or UI. The primary care physician should screen for the presence of these exacerbating or reversible factors, and in fact, most women presenting with a complaint of UI will have few or none of these issues. When such factors are present and are beyond the scope of the primary care physician, these patients should be referred for a complex evaluation with a specialist or subspecialist.

Exam The physical exam is somewhat less helpful in the evaluation of UI compared with the history, but essential elements include visualization of urine loss per urethrum, confirmation of history, and exclusion of UTI or hematuria. Pelvic organ prolapse and vaginal atrophy are modifiable physical findings that when treated may affect continence. Evidence of vaginal atrophy may be seen in loss of rugae or urethral caruncle. The strength of the pelvic floor muscles (pubococcygeus muscles) should be assessed during the bimanual examination. The patient should be able to voluntarily contract the muscles around the examining fingers and sustain the contraction for several seconds. Patients can be categorized those with good pelvic floor strength who would benefit from skill training, those with poor pelvic floor muscular strength who would benefit from strength training, or those with absent (possibly denervated) pelvic floor musculature who need further assessment. SUI should be demonstrated as leakage per urethrum, asking the patient to cough vigorously while the clinician watches for leakage of urine. This can be done in the standing position over a disposable absorbent pad, and/or in the supine position with the cautious examiner directly observing the urethra. Women who demonstrate urine leakage in the supine position with an empty bladder relatively are thought to be at increased risk of having a severe degree of stress incontinence. The bimanual examination should evaluate for pelvic mass and should include a rectal examination to check anal sphincter tone and, for fecal impaction, the presence of occult blood or rectal masses.

Tests Some tests to consider in a basic UI evaluation include a frequency/volume diary, urinalysis, possible postvoid residual (PVR), and possibly simple cystometry. The frequency/volume chart or bladder diary is the simplest and most important initial evaluation tool. These charts may recorded over 2 to 3 days, may record intake and output, and may allow the clinician to distinguish women who void 2 to 3 oz from the women who void 20 oz at time. Both groups of women may complain of urgency and urge incontinence, but the recommended treatments will be different. Both groups should have normal voided volumes of 7 to 10 oz without incontinence, but the former need bladder retraining and anticholinergic medications while the latter need to reducing voided volumes, possibly by normalizing fluid intake and urine output (“normal” is 50 to 70 oz intake and 40 to 50 oz output). Other simple tests include evaluation for UTI, assessment of PVR by catheterization or ultrasound, and simple cystometry. For clinical purposes, a PVR 200 mL is considered abnormal. In older women, residuals 54 - Fecal Incontinence and Defecation Disorders

54 Fecal Incontinence and Defecation Disorders Dee E. Fenner Catherine Ann Matthews Bowel control problems cover a broad range of symptoms and pathophysiology that encompass disorders of bowel evacuation and storage, bowel motility, anorectal pain syndromes, and anatomic abnormalities such as hemorrhoids, anal fissures, and tumors. Patients may present to the obstetrician–gynecologist with symptoms that range from excessive straining, having to support the perineum or posterior vaginal wall to defecate, or suffering from frank fecal incontinence. Bowel and anorectal disorders are divided into two major categories: those arising from a defined structural or neuropathic defect versus a functional disorder in which no such pathology can be detected. For example, obstructed defecation may be caused by an anatomic defect of the posterior vaginal wall (rectocele or perineocele) or may result from the functional inability to voluntarily relax the muscles of the pelvic floor (pelvic floor dyssynergia). The Rome III criteria are a set of consensus agreed-on criteria that standardized definitions about functional disorders of the bowel, rectum, and anus. The broad category of functional bowel disorders includes irritable bowel syndrome (IBS), functional abdominal bloating, functional constipation, and functional diarrhea. Included in the category of functional anorectal disorders is functional fecal incontinence and functional anorectal pain syndromes including levator ani syndrome, proctalgia fugax, and pelvic floor dyssynergia. The specific diagnostic criteria for each of these functional disorders are listed in Table 54.1. The prevalence of bowel disorders is higher in women than in men. Highly variable rates of defecatory dysfunction and fecal incontinence have been reported, which most likely reflects the heterogeneity of the populations studied, the use of nonstandardized questionnaires, a variety of definitions in terms of frequency of defecation or fecal loss, and patient reluctance to disclose these potentially embarrassing problems. Constipation, defined as less than three stools per week, affects 2% to 28% of those surveyed. Obstructed defecation occurs in approximately 7% of the adult population affected by constipation, and while many of these women demonstrate posterior vaginal wall defects radiologically, it is unclear whether this is a cause or a consequence of chronic straining. Fecal incontinence is defined as the inability to defer the elimination of liquid or solid

stool until there is a socially acceptable time and place to do so. Anal incontinence includes the inability to defer the elimination of gas, which may be equally socially embarrassing. The community-based prevalence of fecal incontinence has been reported as 1.4% to 2.2%. Aging has been consistently identified as a major risk factor for the development of fecal incontinence, and the prevalence has been reported to approach 50% in nursing home residents. A recent study of more than 3,000 community-dwelling women found a population-adjusted prevalence of 7.7% when fecal incontinence was defined as loss of liquid or solid stool at least monthly. The prevalence of fecal incontinence increased linearly with age (Fig. 54.1). Significant independent risk factors included age, depression, vaginal parity, and a history of operative vaginal delivery. A recent study of the prevalence of anal incontinence in women seeking general gynecologic care suggested that the prevalence of symptoms when asked in this population is higher. In a group of 457 women seeking general gynecologic care, the overall rate of bothersome anal incontinence was 28.4%. The mean age of this cohort was 39.9 years and after logistic regression analysis, IBS (odds ratio [OR] 3.2; 95% confidence interval [CI] 1.75 to 5.93), constipation (OR 2.11; CI 1.22 to 3.63), age (OR 1.05; CI 1.03 to 1.07), and higher body mass index (OR 1.04; CI 1.01 to 1.08) remained significant risk factors. It is unclear if it was the type of questionnaire or comfort of the patients in disclosing this information to their gynecologist that resulted in such a dramatically higher affirmative response. This study certainly raises the question of anal incontinence being a silent affliction for many women.

TABLE 54.1 ROME III Criteria for Functional Disorders

IBS

At least 12 weeks or more, which need not be consecutive, in the preceding 12 months of abdominal discomfort or pain that has two of three features: 1. Relief with defecation, 2. Onset associated with a change in the frequency of stool, and/or 3. Onset associated with a change in form (appearance of stool).

Functional abdominal bloating

At least 12 weeks, which need not be consecutive, in the preceding 12 months of: 1. Feeling of abdominal fullness, bloating, or visible distension; and 2. Insufficient criterion for the diagnosis of dyspepsia, IBS, or other functional disorder.

At least 12 weeks, which need not be consecutive, in the preceding 12 months of two or more of the following: 1. Straining >1/4 of defecations, 2. Lumpy or hard stools >1/4 of defecations, Functional 3. Sensation of incomplete evacuation >1/4 of constipation defecations, 4. Sensation of anorectal obstruction/blockage >1/4 of defecations, 5. Manual maneuvers to facilitate >1/4 of defecations, and/or 6. 3/4 of the time, and 3. No abdominal pain.

Recurrent uncontrolled passage of fecal material for >1 month, in an individual with a developmental age of at least 4 years, Functional associated with: fecal incontinence 1. Fecal impaction, 2. Diarrhea, or 3. Nonstructural anal sphincter dysfunction.

Levator ani syndrome

Pelvic floor

At least 12 weeks, which need not be consecutive, in the preceding 12 months of: 1. Chronic or recurrent rectal pain or aching, 2. Episodes last 20 minutes or longer, and 3. Other causes of rectal pain such as inflammatory bowel disease, cryptitis, fissure, hemorrhoids, and the like, have been excluded. 1. Patient must satisfy diagnostic criteria for functional constipation; 2. There must be manometric, EMG, or radiologic evidence for inappropriate contraction or failure to relax the pelvic floor muscles during repeated attempts to

dyssynergia

defecate; 3. There must be evidence of adequate propulsive forces during attempts to defecate; and 4. There must be evidence of incomplete evacuation.

IBS, irritable bowel syndrome; EMG, electromyography. Fecal incontinence is also significantly more common in women with other pelvic floor disorders; 7% to 30% of women with urinary incontinence and/or pelvic organ prolapse also have fecal incontinence. The presence of both urinary and fecal incontinence is known as dual or double incontinence. In a recent case-controlled study of women with and without pelvic floor disorders, those with pelvic organ prolapse and/or urinary incontinence were five times more likely to report bothersome anal incontinence than a group of healthy control women. The presence of this “double” incontinence has been associated with a significantly higher adverse effect on quality of life. It is clear that while screening for bowel problems in the general gynecologic population is important, it is imperative that any woman with pelvic floor dysfunction is comprehensively evaluated for concomitant fecal incontinence. Many patients are reluctant to seek medical attention for bowel disorders because of embarrassment and social stigma. Primary care providers, including obstetricians and gynecologists, are therefore integral to the successful disclosure of such problems by routinely inquiring about bowel function during periodic health care visits. Ideally, a few written questions such as “Do you have difficulty emptying your bowels” and “Do you leak gas, liquid, or solid stool” should be part of the standard office intake questionnaire. Several reports have shown that twice the number of patients complain of fecal or flatal incontinence when given written questionnaires than when answering verbal questions. If an affirmative response if obtained, then further quantification of the problem is obviously required. The Wexner fecal incontinence scale is a quick and simple questionnaire that has been validated to track changes in symptoms and is a useful tool to assess and track patient progress (Table 54.2).

Figure 54.1 Prevalence of fecal incontinence by decade of age. (FI, fecal incontinence.) (From Melville JL, Fan MY, Newton K, et al. Fecal incontinence in US women: a population-based study. Am J Obstet Gynecol 2005;193(6):2071–2076.)

Because approximately 10% of women will experience some alteration in bowel habits after one vaginal delivery, it is especially critical to incorporate open-ended questions concerning flatal or fecal incontinence and fecal urgency at the 6-week postpartum visit. Other high-risk groups that should be targeted for additional questions regarding bowel storage and evacuation are women with other pelvic floor disorders and those over age 65. A critical component of screening for anorectal disorders includes colon cancer screening. The recommended screening guidelines from the American Cancer Society are presented in Table 54.3. In general, screening guidelines are for “asymptomatic” patients and those not at an increased risk for colon cancer. First-degree relatives of patients with colon cancer or patients with acute changes in bowel habits, including gross or occult blood, should be referred to a gastroenterologist or surgeon for colonoscopy and other evaluation.

TABLE 54.2 Wexner Scale for Anal Incontinence, a Validate Instrument to Quantify the Type and Severity of Incontinen How often…

Sometimes Usually Rarely Al Never (1

Are you incontinent of: Solid stool

Liquid stool

Gas/flatus

Do you wear a pad due to stool incontinence

Do you alter your lifestyle due to stool incontinence

Adapted from Jorge JM, Wexner SD. Etiology and management of f incontinence. Dis Colon Rectum 1993;36:77–97.

Anatomy The anorectum comprises the distal-most portion of the gastrointestinal tract. The rectum is a hollow muscular tube, 12 to 15 cm long, composed of a continuous layer of longitudinal smooth muscle that interlaces with the underlying circular smooth muscle. It is separated from the anus by the dentate, or pectineal line that demarcates a transition in the type of epithelium and innervation. The rectum is lined by columnar epithelium and is under autonomic control. In contrast, stratified squamous epithelium, innervated by the somatic nervous system, is found in the anal canal. The anal sphincter complex is made up of the internal anal sphincter (IAS) and external anal sphincter (EAS), which provide both resting and increased voluntary tone to the anal canal. The IAS is a thickened expansion of the circular smooth muscle of the bowel wall, a predominantly slow-twitch, fatigue-resistant muscle that contributes approximately 70% to 75% of the resting sphincter pressure but only 40% after sudden rectal distension and 65% during constant rectal distension. The anus is therefore normally closed by the tonic activity of the IAS that is primarily responsible for maintaining anal continence at rest. This barrier is reinforced during voluntary squeeze by the EAS. The anal mucosal folds, together with the expansive anal vascular cushions, provide a tight seal. These barriers are further augmented by the puborectalis muscle, which when tonically contracted forms a flaplike valve that creates a forward pull and reinforces the anorectal angle. Figure 54.2 demonstrates a simplified drawing of the sphincter complex. Through voluntary contraction, the EAS can contribute an additional 25% of anal squeeze pressure. Because the

EAS is made up of fast-twitch, fatigable fibers, this increased tone cannot be maintained over a prolonged period. The EAS is integral to maintaining voluntary control over the evacuation of gas and liquid stool. The pudendal nerve, which arises from the second, third, and fourth sacral nerves, innervates the EAS. A pudendal nerve block creates a loss of sensation in the perianal and genital skin and weakness of the anal sphincter muscle but does not affect rectal sensation that is most likely transmitted along the S2, S3, and S4 parasympathetic nerves. These nerve fibers traverse along the pelvic splanchnic nerves and are independent of the pudendal nerves.

TABLE 54.3 Colon and Rectal Cancer Screening Recommendations Beginning at age 50, both men and women should follow one of these five testing schedules: yearly FOBTa or FIT flexible sigmoidoscopy every 5 years yearly FOBTa or FIT, plus flexible sigmoidoscopy every 5 yearsb double-contrast barium enema every 5 years colonoscopy every 10 years. All positive tests should be followed up with colonoscopy. People should talk to their doctor about starting colorectal cancer screening earlier and/or undergoing screening more often if they have any of the following colorectal cancer risk factors: a personal history of colorectal cancer or adenomatous polyps a strong family history of colorectal cancer or polyps (cancer or polyps in a first-degree relative [parent, sibling, or child] younger than age 60 or in two first-degree relatives of any age) a personal history of chronic inflammatory bowel disease a family history of an hereditary colorectal cancer syndrome (familial adenomatous polyposis or hereditary nonpolyposis colon cancer). FOBT, fecal occult blood test; FIT, fecal immunochemical test. aFor FOBT, the take-home multiple sample method should be

used. bThe combination of yearly FOBT or FIT flexible sigmoidoscopy every 5 years is preferred over either of these options alone.

Anorectal Physiology The successful storage and evacuation of fecal material relies on normal stool consistency and bowel motility, rectal compliance, an intact anal sphincter complex, and the ability to voluntarily relax the puborectalis muscle and sphincters to facilitate defecation. The physiology of voluntary bowel evacuation relies on the rectoanal inhibitory reflex (RAIR). When a bolus of fecal material is delivered to the rectum, increased rectal pressure and distension causes transient relaxation of the IAS, allowing a small sample of the rectal contents to come in contact with the sensory afferent somatic nerves innervating the anoderm. The amplitude and duration of this relaxation increases with the volume of rectal distension and is mediated by the myenteric plexus. The RAIR facilitates the discrimination of gas, liquid, or solid fecal material that is present in the rectum and permits voluntary evacuation in a socially acceptable manner. Once the conscious decision has been made to permit evacuation, the puborectalis muscle relaxes, increasing the anorectal angle and allowing passage of solid fecal material. Patients who experience paradoxical contraction of the puborectalis muscle and sphincter complex with straining suffer from severe obstructed defecation and require biofeedback and physical therapy to reverse this pathology.

Figure 54.2 Anatomy of the external anal sphincter. (EAS-m, main body of the external anal sphincter; SQ-EAS, subcutaneous external anal sphincter; EAS-w, lateral wing portion of the external anal sphincter.)

Fecal Incontinence Etiology and Pathophysiology

The etiologies of fecal incontinence are many and are listed in Table 54.4. It is helpful to divide the etiologies between those that start outside or above the pelvis versus those within the pelvis. In many cases, patients will have several abnormalities that lead to fecal incontinence, such as diarrhea-predominant IBS and a chronic third-degree laceration. The etiologies outside the pelvis include all the pathologies that cause diarrhea or increased intestinal motility. Neurologic conditions such as multiple sclerosis, diabetic neuropathy, trauma, or neoplasms in the spinal cord or cauda equina initially begin as pathologies outside the pelvis, and the pelvic floor is presumed normal. As these neuropathies progress, the pelvic floor muscular function or rectal sensation may become impaired, resulting in fecal incontinence.

TABLE 54.4 Etiologies of Fecal Incontinence Pathology outside the pelvis Diarrheal states Infectious diarrhea IBS Inflammatory bowel disease Short-gut syndrome Bacterial overgrowth (common in cases of diabetic gastroparesis) Laxative abuse Radiation enteritis Carcinoid tumor Malabsorption Neurologic diseases Congenital anomalies (e.g., myelomeningocele) Multiple sclerosis Diabetic neuropathy Neoplasms or injury of the brain, spinal cord, or cauda equina Scleroderma (reduced rectal compliance) Pathology within the pelvis Obstetric injury Disruption of IAS Disruption of EAS Pelvic floor/anal sphincter denervation Trauma Pelvic fracture Anorectal surgery Anal intercourse

Rectovaginal fistula Rectal neoplasia Rectal prolapse Rectocele/perineocele Hemorrhoids Overflow Impaction Encopresis Fecal incontinence that arises from pathology within the pelvis is largely attributed to two broad categories: direct anatomical disruption of the sphincter complex, with or without neuropathy, usually occurring with the first delivery that results in an earlier presentation of fecal incontinence and neurogenic dysfunction of the pelvic floor and sphincter complex that appears to be cumulative and leads to a presentation of fecal incontinence in later life. Historically, incontinence secondary to pelvic floor/anal sphincter denervation has been designated as “idiopathic” and represents as many as 80% of patients with fecal incontinence. Denervation may be secondary to pregnancy, vaginal delivery, chronic straining with constipation, rectal prolapse, or descending perineal syndrome. Histologic studies of the EAS and puborectalis in women with idiopathic fecal incontinence show fibrosis, scarring, and fiber-type grouping consistent with nerve damage and reinnervation. Electromyographic studies (EMGs) have demonstrated reinnervation of the pelvic floor with increased fiber density and prolongation of nerve conduction.

Obstetric Anal Sphincter Injury In younger women, a common cause of fecal incontinence is anatomic damage to the anal sphincter that is sustained at the time of vaginal delivery, with or without neuronal injury. Damage to the anal sphincter can occur by mechanical disruption or separation of the IAS or EAS or by damage to the muscle innervation by stretching or crushing the pudendal and pelvic nerve. In a landmark study from England in 1993, 13% of primiparous women and 23% of multiparous women developed fecal incontinence or fecal urgency at 6 weeks postpartum. All but one of the symptomatic women had evidence of anatomic anal sphincter disruption on endoanal ultrasound. While pudendal nerve studies initially showed prolongation, the vast majority demonstrated full neuronal recovery by 6 months postpartum. This study suggested that the contribution of an anatomic sphincter injury was a greater determinant of developing symptoms than denervation injury, highlighting the need to identify obstetric risk factors that are associated with anal sphincter tears. The prevalence of clinically recognized anal sphincter lacerations varies widely and has been reported to occur in 0.6% to 20.0% of vaginal deliveries, with higher rates documented after operative vaginal delivery. Results obtained from endoanal ultrasound studies of the anal sphincter complex after one vaginal delivery demonstrate an incidence of “occult” anal sphincter disruption in 11% to 35%. Occult sphincter lacerations are not recognized at

delivery, and in fact, the perineal skin may be intact with an underlying muscle tear not visible. Risk factors for both occult and clinically recognized anal sphincter disruption include midline episiotomy, operative vaginal delivery (both forceps and vacuum), persistent occiput posterior head position, prolonged second stage of labor (>2 hours), and delivery of macrosomic infants. Persistent symptoms of anorectal dysfunction are reported by 20% to 50% of women who sustain an anal sphincter injury and have a primary repair. Overall, the prevalence of anal incontinence and fecal incontinence following visible sphincter lacerations has been reported at approximately 40% and 13%, respectively. Current evidence suggests that if a primiparous woman presents with symptoms of fecal incontinence, there is a 76.8% chance of an anal sphincter defect being identifiable on endoanal ultrasonography. Several studies that investigated women up to 5 years postpartum following a third-degree tear and a primary repair have shown that as many as 85% will have persistent structural defects with approximately 58% subsequently running the risk of developing fecal incontinence.

Anal Incontinence and Symptoms Distant from Delivery Differences in rates of incontinence reported by women with and without lacerations may fade with advancing age, depending on the time since delivery. Several retrospective studies have looked at the impact of sphincter laceration on anal incontinence symptoms and report different long-term risks. A retrospective cohort study on 125 matched pairs of women with and without a history of sphincter laceration, with a median follow-up of 14 years after index delivery, found a threefold higher risk of anal incontinence in the tear group. In contrast, a 30-year retrospective cohort study reported equal rates of anal incontinence among women who delivered vaginally with an overt sphincter rupture, in those with episiotomy without sphincter rupture, and in those who only delivered by cesarean section. Another study of 4,569 women 18 years after delivery found that only 6% of the reports of fecal incontinence were attributable to a prior sphincter tear. One prospective cohort study of 242 women 5 years after vaginal delivery identified age (OR 1.1; 95% CI 1.0 to 1.2) and prior overt sphincter laceration (OR 2.3; 95% CI 1.1 to 5.0) as well as subsequent vaginal delivery (OR 2.4; 95% CI 1.1 to 5.6) as predictive of anal incontinence symptoms.

Effect of Subsequent Vaginal Delivery Severity of anal incontinence symptoms may be affected by subsequent vaginal delivery. A study following 117 women with a history of third- or fourth-degree lacerations 1 to 10 years after primary repair found that the 43 women who underwent another vaginal delivery had an increased risk (relative risk [RR] 1.6; 95% CI 1.1 to 2.5) of anal incontinence when compared with the risk found in the 74 women without more deliveries. The chance of developing permanent anal incontinence after a subsequent delivery may also be affected by the severity of the tear in the index pregnancy. In a series of 177 women, severe anal incontinence was reported more commonly after a second delivery in those who had sustained a fourth-degree laceration in their first delivery when compared with

women who had only third-degree lacerations (P = 0.043). The presence of transient incontinence after sphincter laceration and repair is also predictive of the likelihood of developing permanent incontinence with a subsequent delivery. In a study of 56 women with complete EAS tears, 23 (41%) had transient incontinence and 4 (7%) had permanent incontinence following their first delivery. Among the 23 with transient incontinence, 9 (39%) had recurrent symptoms with a subsequent delivery, and in 4 (17%), these symptoms became permanent. Not all studies, however, conclude that subsequent delivery negatively affects anal continence. A comparison of 125 women with third- and fourth-degree lacerations to 125 controls 14 years after their first delivery identified sphincter laceration as an independent risk factor for fecal incontinence (RR 2.54; 95% CI 1.45 to 4.45), but there was no observed increased risk with subsequent vaginal deliveries. In another retrospective analysis, 234 women who had sustained a complete third-degree laceration were contacted for phone interviews regarding continence. In this cohort, no differences were found between women with zero, one, or two subsequent deliveries, nor were there any differences between women who sustained additional third-degree laceration and those without any subsequent deliveries. These studies question whether increases in anal incontinence are due to subsequent vaginal delivery or to other influences, including age.

Anal Incontinence and Cesarean Delivery The role of pregnancy and the protective effect of cesarean delivery on anal incontinence are unclear. A prospective cohort study of 184 primiparous women 6 weeks following delivery found that none of the sixteen women who delivered by cesarean had altered fecal incontinence, whereas 42 of 169 (25%) women undergoing vaginal delivery had impairment of fecal continence. In contrast, a European study that evaluated 46 women 3 months following delivery reported that 2 of the 6 patients having elective cesarean delivery complained of anal incontinence even though the results of endoanal ultrasounds and anal manometry were normal. An observational questionnaire study of 1,004 women also found no significant difference in fecal incontinence when comparing women who delivered via cesarean only to women who had at least one vaginal delivery. The study reported an overall prevalence of bothersome fecal incontinence of 13% and found a significant increase in prevalence when comparing multiparous with nulliparous women (OR 2.26; 95% CI 1.22 to 4.19). Similarly, another study from Australia suggested that pregnancy itself, not route of delivery, impacted the risk of fecal incontinence. Two prospective randomized studies, in secondary analyses, have evaluated the impact of vaginal delivery versus cesarean on the development of anal incontinence. The first was a randomized trial of 949 women on the effect of perineal massage on vaginal delivery. Three months postpartum, 29 women (3.1%) reported fecal incontinence, and 242 (25.5%) had involuntary escape of flatus. Multivariate analysis of predictors of postpartum anal incontinence showed a significant independent association with forceps versus spontaneous vaginal delivery but not with vacuum extraction, episiotomy, or cesarean. When episiotomy and type of delivery were replaced by degree of perineal injury in the analysis, incontinence of flatus or stool was predicted by anal sphincter laceration but not by lesser

degrees of perineal trauma. The second study was a secondary analysis of a multicenter, international trial of 2,088 women with a singleton breech fetus who were randomized to cesarean versus vaginal delivery. Mothers completed a structured questionnaire at 2 years postpartum to determine relationships of the index delivery to various health problems, including anal incontinence. Overall, the prevalence of fecal and anal incontinence was 2.3% and 12.1%, respectively. No differences were found between delivery groups in the incidence of fecal or flatal incontinence in an intent-to-treat analysis. Conflicting results from these studies make it challenging to recommend the optimal mode of delivery to maximally reduce the chance of developing anorectal dysfunction, even in women with a prior history of an anal sphincter tear. What is known is that anal incontinence following vaginal delivery is strongly associated with both overt and occult sphincter lacerations. The use of forceps has been consistently identified as an independent risk factor for fecal incontinence, and they should be used cautiously in women with increased risk factors for sustaining an anal sphincter tear. It is important to note that cesarean deliveries, especially those performed late in labor, may not confer all the benefit to the pelvic floor than was previously expected.

Evaluation History Because of the complex nature of the stool continence mechanism and the myriad disorders that can affect the normal functioning of the posterior compartment, a detailed and precise history regarding the problem is imperative. The practitioner needs to understand the duration of the symptoms, what exactly was happening when the symptoms first started, the precise quality and consistency of stool that is successfully stored versus that which is leaked, the patient's bowel habit history, and normal dietary habits. Specific questions concerning diarrhea, loose or mushy stools, the presence or absence of fecal urgency (especially after eating), passage of mucus, average number and quality of stools per day, presence of pain or bloating, difficulty wiping clean, feelings of incomplete evacuation and straining to empty, splinting the vagina or perineum to empty, bowel control during sexual intercourse, practicing anal intercourse, and frequency/severity of incontinent episodes should all be determined. It is important to identify if the patient can sense when she needs to have a bowel movement and how that relates to any possible leakage versus just finding stool in her underclothes. A sensory impairment is suggested when stool leakage occurs without warning, whereas a motor impairment is likely if the patient is merely unable to get to a toilet on time. A prospective diary of food intake, bowel habits, and incontinence episodes can be useful. Several standardized questionnaires and fecal incontinence severity scoring systems are available, including the Wexner scale in Table 54.2. A complete review of systems should be obtained, including abdominal pain or cramping, lower back or pelvic pain, any changes in pelvic or lower extremity sensation, and any urinary retention or leakage. Any acute change in neurologic function should direct the practitioner to rule out central nervous system disorders such as multiple sclerosis or a

neoplasm of the brain or spinal cord. A comprehensive obstetric history including mode of delivery, length of second stage, use of forceps/vacuum, birth weights, episiotomies or lacerations, and any wound complications should be obtained. As always, a full understanding of the patient's other medical conditions that may be impacting the continence mechanism should be sought. A review of all laxatives and other medications, both prescription and over the counter, can yield important information. Many medications including nonsteroidal anti-inflammatory drugs (NSAIDs), iron, anticholinergics, antidepressants, narcotics, and pseudoephedrine can cause chronic constipation that may contribute to overflow incontinence or pelvic floor neuropathy secondary to straining. Finally, patients should be queried about all prior investigations including flexible sigmoidoscopy, colonoscopy, and barium enemas. Any previous operative reports relating to the posterior compartment should be reviewed.

Physical Examination Examination begins with careful inspection of the perineum and anal region. It is important to note the presence or absence of fecal material and whether or not there is discoloration and irritation of perianal skin, which is commonly seen in patients with significant incontinence. The perianal skin creases or folds should completely encircle the anus. In cases of complete anal sphincter disruption, a “dovetail” sign is usually present in which only a semicircular presence of creases or folds is present. Attention to the presence of any protruding tissue around or from the anus should be made, as in the case of external hemorrhoids or rectal mucosal prolapse (Fig. 54.3). Careful inspection for a rectovaginal fistula should be performed, and any dimpling should be probed with a silver wire or lacrimal probe. The size of the genital hiatus and perineal body should be measured, and the vagina should be examined for evidence of genital prolapse, which may be an indicator of pelvic floor neuromuscular function. Any prior episiotomies, lacerations, or surgical scars should be noted. Whether or not the anal mucosal skin is completely coapted is important to note as well. Eliciting the clitoral-anal or bulbocavernosus reflex can grossly test the innervation of the EAS. If this is intact, the reflex implies that the pudendal nerve afferents and the rectal or external hemorrhoidal branch of the pudendal efferent nerves are functional. Sensation in the S2–4 dermatomes should be screened by dull and pinprick discrimination when touching the perineum. Abnormalities in either the perianal reflexes or sensation should prompt further neurologic testing.

Figure 54.3 Dovetail sign and rectovaginal fistula. A silver wire probe is placed through the rectovaginal fistula. A gloved index finger palpates for rectal tone at rest and with a pelvic floor contraction. Note loss of the perianal fold from 9 o'clock to 3 o'clock.

Next, the patient should be asked to squeeze “as if trying not to pass gas.” Inspection of the perianal folds should be evaluated for a concentric contraction and some upward movement of the perineal body. Substitution with contraction of the buttocks, upper thighs, or abdomen should be noted. The patient should then be asked to bear down “as if trying to have a bowel movement.” She should be reassured that it is expected that she may pass flatus or even some fecal material during this part of the examination. The practitioner should note the degree of perineal descent and any prolapse of the vagina, pelvic viscera, or rectum. If there does appear to be any pelvic organ prolapse, the examination can then be repeated in the standing position or after straining on the commode to maximize the prolapse. A rectal examination is then used to assess both the resting and squeeze tone of the anal canal. The resting tone of the anal canal is an indicator of IAS function. When the patient is asked to squeeze, a circumferential contraction and tightening should be felt in addition to some upward movement of the rectum and posterior compartment. On vaginal examination, the levator ani should be palpated for strength and symmetry. Any scarring or retraction of the posterior vaginal wall should be noted. In addition to assessing rectal tone, the anal canal and rectum should be palpated for masses, a dilated rectum, or the

presence of stool in the rectal vault. A chronically distended rectum with stool, a tumor, or with intussusception of the bowel will disrupt the normal RAIR. If this reflex is suppressed, the anal canal remains dilated, the EAS becomes fatigued, and incontinence will occur.

Testing The clinical diagnosis based on physical examination and history alone will be accurate in a majority of patients. However, further evaluation, including radiologic and physiologic tests listed in Table 54.5, have been shown in a prospective study at a tertiary colorectal referral center to alter the final diagnosis of the cause of fecal incontinence in approximately one out of five cases. The specific historical and physical examination findings that are helpful in determining the sequence of tests that are ordered are any abnormalities in stool consistency and frequency and the degree of rectal tone on digital rectal examination. The algorithm presented provides a flow diagram based on these findings. The presence of normal resting and squeeze tone of the anal canal directs the clinician away from an abnormality of the sphincter complex and instead focuses on etiologies outside the pelvis. Poor resting tone or the inability to voluntarily squeeze the anal sphincter, in contrast, then focuses attention on the neuromuscular evaluation of the sphincter complex itself (Fig. 54.4).

Treatment The treatment of fecal incontinence includes medications, biofeedback, electrical stimulation, and surgery. In every patient, regardless of the integrity of the sphincter complex, maintaining normal stool consistency and frequency is the first step in management. The goal for every patient is to have a predictable bowel movement every morning that is the size of a six-inch log and of moderately firm consistency. Soft, mushy stools can be very difficult for patients to control and evacuate completely, a problem that leads to constant seepage and the inability to ever wipe clean. If patients are having several bowel movements throughout the day, this implies rapid colonic motility or an enhanced gastrocolic reflex, both of which can create symptoms of fecal urgency and incontinence.

Dietary and Behavioral Treatments The successful evacuation of a formed, bulked stool every morning can be achieved by taking a fiber supplement at night such as methylcellulose or psyllium. High-fiber cereals and a hot beverage for breakfast the next morning will usually prompt the gastrocolic reflex, and before leaving the comfortable home environment, patients will typically experience a defecatory urge. For some patients, especially those with retained stool within a rectocele pocket (not that common if the stool is sufficiently bulked), the use of a daily cleansing enema eliminates the seepage of residual fecal material. If patients report several further bowel movements throughout the rest of the day following the complete morning evacuation, then the use of an agent to slow the intestinal transit time is indicated. Commonly used medications that

can be used to slow the gastrointestinal tract are listed in Table 54.6. Titration of the selected medication over the course of a month is frequently necessary to achieve the desired result of a single bowel movement in the morning. Patients with diarrhea dependent IBS also should be conscious of the specific foods that exacerbate their symptoms. Additional doses of antimotility drugs are frequently required before eating in restaurants.

TABLE 54.5 Commonly Used Tests to Evaluate Bowel Function Colonoscopy: A colonoscopy is indicated for any patient with chronic diarrhea or a history of nonhealing perineal lacerations to rule out inflammatory bowel disease or malignancy. Sphincter Ultrasound (Transanal or Transperineal): Transanal endosonography that utilizes a rotating rectal probe provides excellent visualization of all layers of the anal canal and sphincter complex. The IAS, comprised of smooth muscle, appears as a dark, hypoechoic ring. The striated EAS, which lies external to the IAS, has a brighter, hyperechoic appearance. Breaks in the EAS appear as “gaps” or dark spaces within the hyperechoic ring (Fig. 54.6). Transperineal ultrasound with a high-frequency probe can be used to visualize the sphincter complex. Anal Manometry: Anal manometry, once a mainstay of evaluation, is rarely indicated as most experienced clinicians can estimate the pressure in the anal canal with a simple rectal examination. It is helpful for patients who have had surgery to the anorectal canal or radiation therapy to determine rectal sensation and rectal capacity. Electromyography: EMG evaluates the bioelectrical action potentials that are generated by depolarization of skeletal striated muscle. EMG is rarely indicated outside of the research laboratory. Pudendal Nerve Terminal Motor Latencies: Nerve conduction studies measure the time from stimulation of a nerve to a response in the muscle that it innervates. The pudendal nerve is stimulated at the ischial spine, and the latency is determined by the amount of time it takes for the external sphincter to contract, which is normally about 2 msec. Prolonged PNTMLs have been found in patients with idiopathic fecal incontinence and in patients with rectal prolapse; however, there is often poor correlation between

nerve conduction studies, patient symptoms, and surgical outcomes such that the test is rarely done. Defecography: Defecating proctograms are very helpful in some patients with fecal incontinence because all components of the pelvic floor can be visualized during attempted storage and evacuation. Sigmoidoceles, rectal intussusception, rectal prolapse, retention of stool within a rectocele pocket, and perineal descent can be visualized. Defecography is also useful when evaluating chronic constipation and obstructed defecation. Patients should be warned that while this test is potentially embarrassing, it can yield important information. Magnetic Resonance Imaging: Specialized dynamic MRI may replace defecography in the future, as it has the ability to also evaluate the anatomy of the anal sphincter complex and levator muscles, along with pelvic organ prolapse and perineal descent. At present, this test is not readily available and remains considerably more expensive than standard radiologic tests. Colon Transit or Sitz Marker Study: A transit study is used to evaluate colonic motility and is used in the evaluation of constipation and obstructed defecation. It may be indicated with suspected overflow incontinence. There are numerous variations of the study. Patients ingest a capsule containing 25 to 30 radiopaque rings. Five days later, an abdominal flat plate is obtained, and normally, 80% of the markers should have passed. Global colon dysfunction is indicated if the rings are dispersed throughout the colon, whereas segmental dysfunction is suggested if rings are clustered together in one area. IAS, internal anal sphincter; EAS external anal sphincter; EMG, electromyography; PTNMLs, pudendal nerve terminal motor latencies, MRI, magnetic resonance imaging.

Biofeedback Biofeedback for fecal incontinence, like urinary incontinence, requires a motivated patient, a feedback device, and a planned exercise program. This typically is conducted by a trained pelvic floor physical therapist. In order for biofeedback to be successful, a patient must have an intact neurologic system, and through biofeedback, she will learn to perceive normal sensation and the ability to contract the pelvic floor muscles voluntarily.

Several studies have found biofeedback in correctly selected patients to be very successful in that 60% to 70% of patients with fecal incontinence secondary to abnormalities of the pelvic floor will have a 90% reduction in their incontinence. A measuring device, either an electrode or pressure transducer, is used transvaginally or transanally to record and give feedback to the patient. She then uses this feedback to increase or lengthen pelvic floor contraction. If the patient has incontinence secondary to a sensory deficit in the rectum, rectal balloons can be used to “retrain” the patient to perceive rectal distention and respond by squeezing the EAS. It is important to remember that while biofeedback and physical therapy are initially labor intensive, they have no side effects or morbidity and frequently are used in conjunction with other treatment modalities, including surgery. In addition, for patients with double incontinence, single therapy with biofeedback may well improve both conditions. As long as the patient can follow instructions, there does not appear to be an age limit on the use of biofeedback and pelvic floor training. In fact, in a randomized trial of electrical stimulation therapy, biofeedback, and nursing intervention, older women were more likely to respond to treatment, including education, fiber, and diet management for fecal incontinence when compared with response in younger women.

Figure 54.4 Fecal incontinence evaluation. Any diarrhea or functional bowel component should be managed prior to anal ultrasound and possible surgical therapy. (AI, anal incontinence.)

TABLE 54.6 Antidiarrheal Medications Drug

Dosage

Mechanism of Action

Loperamide

2 mg three times/d or 4 mg followed by 2 mg after loose bowel movement

Inhibits circular and longitudinal muscle contraction

Diphenoxylate with atropine

10 mg up to four times/d

Direct action of circular smooth muscle to decrease peristalsis

Hyoscyamine sulfate

0.375 mg two times/d

Anticholinergic

4-g pack one to four times/d

Binds bile acids after cholecystectomy (helpful for patients who develop diarrhea after cholecystectomy)

Cholestyramine

Electrical Stimulation Therapy Functional electrical stimulation therapy has been shown to reduce fecal incontinence in patients with a weakened pelvic floor who are unable to contract their EAS or puborectalis muscle on command. Because of the expense, electrical stimulation generally is reserved for patients who are unable to respond to traditional biofeedback protocols. Both transvaginal and transrectal probes are available. Most protocols recommend highfrequency stimulation at maximum tolerable stimulation of 50 MHz for 15 to 20 minutes twice a day. Response to therapy usually is seen by 6 weeks, with maximum improvement by 12 weeks.

Surgery Surgical management of fecal incontinence includes the repair of rectal prolapse, anal sphincteroplasty, and the implantation of artificial anal sphincters. Postanal repair or posterior levatorplasty has not been shown to be effective in the treatment of fecal

incontinence in most patients and thus will not be discussed. In women with anal sphincter defects and anal incontinence remote, the mainstay of surgical intervention is overlapping anal sphincteroplasty. Unfortunately, the reports of long-term results for a mean follow-up of 3 to 10 years are less than promising, with cure rates ranging from 0% to 28% after overlapping repair. A comparison of outcomes from five different studies is presented in the Table 54.7. A recent study of 86 women who underwent anal sphincteroplasty with a mean follow-up of 5.1 years reported that only 11% were completely continent. A remarkable 75% were incontinent of liquid and/or solid stool, and this correlated with an adverse effect on quality of life. As a retrospective study, the authors were not able to determine improvement of symptoms, and most patients subjectively said that they were better. In addition, the number of bowel movements per day and the amount of liquid stool were not determined. Therefore, it is possible that the outcomes may be better for women with well-formed stools and no undertreated motility disorders. However, women should be counseled appropriately of the low probability of complete continence with sphincteroplasty. In addition to poor long-term outcomes, short-term complications are common, with a high rate of wound infection and superficial wound breakdown.

TABLE 54.7 Long-term Outcomes of Anal Sphincteroplasty Remote from Delivery Author/Year

Malouf 2000 (UK)

Karoui 2000 (France)

Patient with Follow-up(%)

38/55 (69)

74/86 (86)

Mean Follow-up (years)

Outcomes

6.4

0% continent 10% incontinent of flatus only 63% passive soiling

3.3

28% continent 23% incontinent to flatus only 49% incontinent of stool

Halverson 2002 (USA)

BravoGuitierrez 2004 (USA)

Trowbridge 2006 (USA)

49/71 (69)

130/191 (71)

59/86 (70)

5.8

14% continent 32% incontinent to flatus only 54% incontinent of stool

10.3

6% continent 18% incontinent to flatus only 60% incontinent of solid stool

5.6

10% continent 15% incontinent to flatus only 75% incontinent of solid stool

Modified from Rogers RG, Abed H, Fenner DE. Current diagnosis and treatment algorithms for anal incontinence. BJU Int 2006;98(Suppl 1):101.

Neosphincters There are two types of neosphincters: one using the patient's own skeletal muscle, usually the gracilis, and the other using an artificial Silastic cuff connected to a fluid reservoir to occlude the anal canal. The gracilis muscle wrap has shown inconsistent results, but improvement may be seen with the use of preoperative low-frequency electrical stimulation to produce fatigue-resistant muscle fibers. Artificial sphincters are indicated in patients with anal incontinence caused by neuromuscular disease or trauma. Complications include infection and mechanical breakdown. Success rates of 75% and complication rates of 33%, similar to muscle transposition, have been reported.

Defecation Disorders

Etiology and Pathophysiology Normal defecation requires normal colonic motility, anorectal sensation, and a coordinated expulsive force with relaxation of the pelvic floor and anal sphincters. Constipation has many definitions and descriptions. For some women, constipation means not having a daily bowel movement, while for others having to push or having a hard stool is constipation. The Rome III criteria, as listed in Table 54.1, divides constipation into functional or slow colonic transit constipation including IBS and obstructed defecation. In reality, many women appear to have difficulty having regular bowel movements because of both slow colon transit and some component of obstructed defecation.

Functional Constipation The pathophysiology of slow-transit constipation has been difficult to delineate in large measure because of the influence of a multitude of changing factors such as sleep, diet, physical activity, and emotional stressors. Patients with this disorder demonstrate a significant impairment in phasic colonic motor activity and also have a blunted gastrocolic reflex. In addition, a loss of ganglion cells in the myenteric plexus suggests an underlying neuropathy.

Diagnostic Studies The acute onset of constipation should prompt the clinician to rule out an underlying metabolic (e.g., hypothyroidism) or pathologic disorder (e.g., colon cancer). Women with a long-standing history of constipation generally do not warrant an extensive laboratory workup beyond what is recommended for standard colon cancer screening. A colonic transit study can provide valuable objective information about motility throughout the colon (Table 54.5).

Management While general measures such as increasing hydration, performing physical exercise, and dedicating time for passing bowel movements are frequently recommended, little evidence actually exists to support their efficacy. Colonic motor activity is greatest after awakening and following a meal, and efforts to make use of this fact are encouraged.

TABLE 54.8 Medication to Facilitate Defecation Type of Laxative

Examples

Description

Bulking agents

Psyllium Citrucel

Absorbs liquid in intestines and swells to form a soft, bulky stool

Stool softeners

Docusate

Helps liquids mix into stools (eases straining rather than causing a bowel movement)

Osmotic laxatives

PEG Saline laxatives: Magnesium hydroxide Magnesium citrate Poorly absorbed sugars: Lactulose Mannitol Sorbitol Glycerin suppositories

PEG and lactulose have been shown to increase stool frequency and improve consistency

Stimulant laxatives

Diphenylmethane derivatives: Bisacodyl Sodium picosulfate Castor oil Mineral oil Anthraquinones: Senna Cascara sagrada Aloe

Insufficient data to make a recommendation regarding use (no placebo-controlled trials)

5-HT4 agonists

Tegaserod

Improves stool frequency, consistency, and straining

PEG, polyethylene glycol. Before initiating a treatment for constipation, a caref

Title: Danforth&#39;s Obstetrics and Gynecology, 10th Edition - PDFCOFFEE.COM (2024)

Title: Danforth's Obstetrics and Gynecology, 10th Edition - PDFCOFFEE.COM (2024)