Ob-Gyn Platinum (1st Edition)
Ob-Gyn Platinum (1st Edition)
Ob-Gyn Platinum (1st Edition)
PLATI
F
NUM
IR S T E
FIRST D IT IO N
EDITION
2021
~
(
~)JOB-GYN
PLATINUM
-· . F I R S. lr E D I T I O N
2021
EDITOR
LILIA P. LUNA, MD
The printingofOB-GYN Platinum, First Edition is financed by Top Practice
Medical Publishing Corporation, Manila, Philippines. Proceeds from the
purchase of this book will fund the development and improvement of
future editions of this book.
Book design and layout by Manuel S. Vidal, Jr. All rights reserved. No part of this publication may
be reproduced, stored in a retrieval system, or transmitted, in any form by any means without
prior permission from Top Practice Medical Publishing Corporation.
Published by:
ISBN 978-621-95388-5-5
II
NOTICE
The information in this book has been reviewed and verified with
reliable sources, and the approaches to management have been utilized
in clinical practice. However, medicine is an ever-changing science. New
research, changes in guidelines, and human error occur. The authors,
editor, and publisher are not responsible for errors or omissions or
for any untoward outcomes from application of data in this book. The
authors, editm; publisher, and other parties who have been involved in
the preparation of this book make no warranty, expressed or implied,
with respect to the completeness, accuracy, or being up-to-date of all
the information contained in this publication. The authors, editor, and
publisher encourage the readers to confirm the information herein
with other sources, and to exercise critical thinking based on the clinical
presentation of the patient in making decisions for management.
V
PREFACE
As a young medical student, I remember wishing that our textbooks were a
lot smaller and lighter than what they were back then. Having them available
at our fingertips at any time and anywhere for a quick review before an
exam, or before going on duty or attending a conference, would have been
convenient. Having an abridged consolidation of all our reference books is
just what we needed. With the Platinum series, students will have just that.
These reference manuals do not intend to replace the textbooks prescribed
by the medical curriculum. They are meant to be a reinforcement. The
Platinum series of books aims to allow medical students to correlate what
they encounter in the clinics and in the wards real time with the handy
features the books offer. The OBGYNPlatinum Team labored to give the
students access to answers to often asked questions of the specialty, from
the long-established prerequisite basic knowledge to the latest in clinical
practice guidelines. It is our prayer that, with this book, studying Obstetrics
and Gynecology would not be any more daunting to our students than it
should be.
Ricky 0.
VI
ACKNOWLEDGEMENT
To the Lord Almighty, who makes all things possible;
To our families, for their unfailing love and support: Capt. Jaime Julian & Mrs. Ma. Rosario
Aherrera; Dr. Gil Oblepias and Mrs. Ceny Oblepias, Dr. Corito Oblepias and children, Ed, Jics,
and Kori; Mrs. Yolanda Factor, Atty. Claire Factor, Mr. john Paul Factor, Mrs. Joanna Factor,
Mstrs. Cedric and Joaquin Factor, and Mr. Raffy Taruc; Mrs. Maria Cristina Tiongson, Dr. Lalaine,
Mstr. Matthew Damian Tiongson, Atty. Virgilio, Mrs. Marilyn, Ml'. Patrick Jeanne & Ms. Patricia
Meryl Tiongson, & Mr. Dennis, Mrs. Maita, Ms. Maiden Kristine & Mr. Andrei Nikolai Tiongson;
Mr. Jose R. Soriano, Jr. and Mrs. Nelly Soriano+, Emilio Joaquin, Justino Gabriel & Lucio Nicolas
Soriano, and Samantha Dominique, Angela Katrina & Nathan Soriano Onglatco; and Mrs. Arabella
Chiong-Banzuela, Ml'.Zeus Banzuela, Ms. Angelita Chiong, Mr. Nelson Cruz, Mrs. Epifania Cruz,
Attorney Napoleon Banzuela Jr., Dr. Rocky Lim & Ms. Arabella Aurora "Bogie" Lim Banzuela;
To our patients, especially the Filipino Patients - our greatest teachers, to whom the essence and
soul of this book is rooted on. This book is for you first and foremost;
To our mentors Dr. John Aiionuevo, Dr. Felix Eduardo Punzalan, Dr. Eric Oliver Sison, Dr. Jose
Fernando Fontanilla, Dr. Maria Luz Querubin, Dr. Judy Fuentes, Dr. Rowena Rivera, Dr. Marlyn
David-Ruaro+, Dr.Ferdinand Francis Cid, Dr. Maria Concellene Laforteza, Dr. Erlyn Sana, Dr. Alvin
Mojica, Dr. Robert Arias, Dr. Rose Ann Banal, Professor jenny Zapf, Professor Bobbi Kurshan,
Mr. Jojo Fresnedi, Mrs. Rhodora Palomar-Fresnedi, Dr. Ramon Paterno, Dr. Rommel Duenas, Dr.
Pacifico Eric Calderon, Dr. Eric Calderon Jr., Dr. Mark Louie Mann for their invaluable guidance
and wisdom;
To Dr. Florante Gonzaga, Dr. Rosalinda Arceo, Dr. Lyra Ruth Clemente-Chua and DI'. Greg
Pastorfide (Reproductive Endocrinology and Infertility]; Dr. Blanca De Guia - Fuerte (Pediatric
and Adolescent Gynecology); Dr. Virgilio Oblepias, Dr. Felix Salgado, and Dr. Azucena Suplido
(Minimally Invasive Surgery, Mullerian Anomalies, and Family Planning) for having planted in us
the love and interest for Reproductive Medicine;
To our colleagues and mentors from Asian Hospital & Medical Center; FEU-NRMF Department
of Obstetrics and Gynecology, Institute for Women's Health, The Medical City, and UP-Philippine
General Hospital, especially the Department of Obstetrics and Gynecology, Division of
Reproductive Endocrinology and Infertility, Division of Family Planning;
To our colleagues, fellow teachers and bosses from San Beda University College of Medicine,
Ateneo School of Medicine and Public Health, De La Salle Medical and Health Science Institute,
Bicol University College of Medicine, and New Era University College of Medicine for enabling us
to undertake this endeavor;
To all main authors, contributing writers of the IM Platinum, Surgery Platinum, Pedia Platinum
and Philippine Medical Jurisprudence, thank you very much for all your help in making the
Platinum Series Dream come true;
To All the Teachers, Mother Geese, Mentors and Staff of Topnotch Medical Board Prep;
This book is lovingly dedicated to Atty. Virgilio Tiongson t, Mr Constantino Luis G. Factor Ill t,
and Denver's three little angels in heaven.
Ricky L., Ricky 0., Chris, Nifia, Patty, Jaime, Denver, and Broli
VII
For all the medical students,
may this OB-GYN Platinum book
help you in your rotation and exams
in Obstetrics and Gynecology.
Ricky L.
VIII
AUTHORS
THE
Jericho Thaddeus P. Luna, MD, FPOGS, FSGOP, FPSCPC
Dr. Luna is a graduate of the University of the Philippines College of Medicine (UPCM), Manila Class ofl 993 and a member
of the UPCM Phi Kappa Mu Fraternity. He has completed a 4-year residency training in Obstetrics and Gynecology
and a 3-year fellowship training in Gynecologic Oncology at the Philippine General Hospital (PGH), University of the
Philippines, Manila. Since 2001, he has been a member of the Faculty of the Department of Obstetrics and Gynecology,
UPCM where he is now a Professor 12 and the current Chief of the Division of Gynecologic Oncology. He is a Fellow of
the Philippine Obstetrical and Gynecological Society (POGS), the Society of Gynecologic Oncologists of the Philippines
(SGOP) and the Philippine Society of Cervical Pathology and Colposcopy (PSCPC). Aside from the POGS, SGOP & PSCPC,
Dr. Luna is also a member of the following Societies: Asia Oceania (research organization on) Genital Infections and
Neoplasia-Philippines [AOGIN Phils.], Philippine Society of Climacteric Medicine (PSCM), Philippine Society of Fertility
Preservation (PSFP), Philippine Society of Oncology, University of the Philippines-Manila Medical Alumni Society
(UPMAS), European Society of Gynaecological Oncology (ESGO) and International Gynecological Cancer Society (IGCS).
He has served as President in the following Societies: AOGIN-Phils. (2015-2016), UPMAS (2018), SGOP (2019) & PSCM
(2019-2020). He has been a member of the POGS Board of Trustees (BOT) where he served as Treasurer (2010-2012,
2016-2017) and Chair of both the Committees on Clinical Practice Guidelines and Scientific Works (Research) in 2015.
He has been the Editor-in-Chief of the Philippine Journal of Obstetrics and Gynecology (PJOG) since 2014. He is a
current Board Member of the PSFP and the PGH Alumni Association of the Department of Obstetrics and Gynecology
(AADOG). He has been the recipient of the following awards: Asia Oceania Federation of Obstetrics and Gynecology
(AOFOG) Young Gynaecologist Award (2002), PGH lntern's Award for Best Consultant (2002), UPCM Outstanding
Faculty in the Clinical Sciences (2005), POGS Young Researcher Award (2005), Department of Science and Technology-
National Academy of Science and Technology (DOST-NAST) Outstanding Young Scientist (2006), PSO Outstanding
Cancer Researcher Award (2010), UP Manila Gawad Chancellor Outstanding Researcher Award (2010), Metrobank
Foundation Outstanding Teacher (2011), Philippine National Health Research System (PNHRS) Best Mentor in Health
Research Award (2011), UPCM Best Teacher in the Clinical Department - LU 6 (AY 2011-2012), Philippine Medical
Association (PMA) Dr. Jose P. Rizal Memorial Award for Research (2017), POGS Honoria Acosta-Sison Award of Merit for
Research (2018) and the UP Manila Gawad Sentenaryo Professorial Chair Award in recognition of exemplary training,
service and teaching performance in Gynecologic Oncology (2019). Aside from being a known teacher, researcher and
gynecologic surgeon, Dr. Luna enjoys organizing continuing medical education (CME) activities, conducting gynecologic
surgery & cervical cancer screening workshops and missions, traveling (local and abroad), driving & going on road
trips, watching movies and gathering Starbucks collectibles.
IX
Nifi.a Katrina C. Banzuela-Cruz, MD, MHPEd, FPOGS
Dr. Banzuela-Cruz is a woman of many hats. She finished her education in Biology at The Ateneo de Manila University
and proceeded to her Doctor of Medicine Degree in the Pamantasan ng Lungsod ng Maynila. She continued further
training as a 08-GYN in the Far Eastern University-Nicanor Reyes Medical Foundation. After graduating from her
residency training, she also pursued a career in education and continues to improve herself as an educator by taking up
a Masters in Health Professions Education at the University of the Philippines-National Teachers Training Center which
aided her in inspiring students through her 08-GYN lectures in Topnotch Medical Board Prep and Physiology lectures
in San Beda College of Medicine. She believes that competence and kindness are the ideal values that all doctors should
have and these principles embody her as she continues to inspire and guide students as the head of the Mentoring
Program of Topnotch Medical Board Prep. She enjoys good food with good company. Her heft and height partnered
with her joyous laughter makes her stand out from a crowd. These traits serve as endearing qualities that makes her
well-loved by her patients, colleagues and students. Her family serves as her ultimate inspiration.
X
Enrico Paolo C. Banzuela, MD, MSEd, MHPEd, FPSP
Dr. Banzuela graduated with a 8.S. Basic Medical Sciences degree (INTARMED) from UP Manila in 2002. He obtained
his medical degree from the UP College of Medicine in ZOOS.He finished his Masters in Educational Entrepreneurship
(MSEd) at the University of Pennsylvania in 2019. He obtained his Diploma in Health Professions Education from
the UP National Teacher Training Center for the Health Professions in 2018. He also a graduate of the Management
Development Program of the Asian Institute of Management in 2018. He also has a Postgraduate Certificate in Teaching
Evidence-Based Health Care at the University of Oxford in the United Kingdom in 2020. He is currently taking a Masters
in Health Professions Education (MHPE) at the University of Maastricht in the Netherlands. Upon passing the medical
board exams in 2005, he served as a volunteer physician for the 2005 Manila Southeast Asian Games. He also worked as
a University Researcher for the UP National Institutes of Health under the Phil Health Research Study Group for 3 years.
He co•authored a book entitled "Survival Guide for Doctors (and Non·Doctors Too) with Dr. Willie Ong and D1:Liza Ong.
He is also a co-author of IM Platinum, Surgery Platinum, Pedia Platinum and now, Ob-Gyn Plaltinum. Dr.Banzuela is the
Chair of the Section of Medical Physiology (Associate Professor II) at the San Beda University College of Medicine and
has been a faculty member since 2005. he has also served previously as lecturer for Biochemisty, Neurology, Family and
Community Medicine at the same institution. He is guest lecturer for Biochemistry at the Ateneo School of Medicine
and Public Health. He currently serves as Vice-President of the Philippine Society of Physiologists. He is the President of
Topnotch Medical Board Prep where he also teaches Physiology. Dr.Banzuela has always been involved with preparing
doctors for the medical board exams since 2005, having written guides, given orientation talks, created school•specific
board exam programs and lectured subjects at various hospitals and institutions. He enjoys fishing, driving, playing
basketball, listening to vinyl records, perfecting his aquaponic setup and going on food trips with his family.
THE
EDITOR
Lilia P. Luna, MD, FPOGS
Dr. Lilia P. Luna is a cum laude graduate of FEU-NRMF Institute of Medicine and one of the 10 topnotchers in the Philippine
Medical Board Examination in 1961. She had her residency training in OBGYNat FEU Hospital, and had her fellowship in
Reproductive Infertility and Menopause (RM) at the New York University Medical Center and a postgraduate course in Family
Planning at the University of Colorado. After her fellowship, she joined the consultant staff and faculty of FEU-NRMF.She
became the chairman of the Department of OB-GYNof United Doctors Medical Center and Capitol Medical Center. She has a
degree in Master in Hospital Administration from the Institute of Public Health of the University of the Philippines. She was
appointed Chief of Clinics, and subsequently, Hospital Director of FEU-NRMF Hospital for 18 years. She was instrumental
(together with FEU-NRMF alumni) in the putting up of the Marian Medical Arts Bldg AND Marian Radiology Cente1~near
FEU-NRMF Medical Center. She established a 2-year fellowship program in Reproductive Medicine, a Consortium between
FEU-NRMF Hospital, Jose Reyes Memorial Medical Center, and Capitol Medical Center. To date, this fellowship program has
graduated 20 fellows, who have all been certified by the Phil, Board of Reproductive Medicine and some, by the Phil. Society of
Gynecologic Endoscopy. She is currently on her 55th year as faculty member of FEU-NRMF and is still very active in practice
and in training OB-GYNresidents and fellows in Reproductive Medicine.
Her expertise in OB-GYNpractice and in Reproductive Medicine is well recognized, both by her very busy OGYNpractice, as
well as her colleagues. She assumed several positions in the Philippine OB-GYNSociety, such as Treasurer, Editor in Chief,
POGS Journal, member of the Board of Trustees, Chairman of various committees, Vice-President, and President (1991 ). She
also was ve1y active in and subsequently became President of the Phil. Society of Climacteric Medicine and Phil. Society
Of Reproductive Medicine. Up to the present, she is member of the Credentialling Committee of the Philippine Society of
Gynecologic Endoscopy. She is a member of the POGS Committee on Ethics AND PSRM Credentials and Ethics committees.
She has numerous publications in scientific manuals, books, and clinical practice guidelines of POGS,and Specialty Societies.
In recognition of her expertise in obstetrics & gynecology, she received the following awards: POGSBALDOMERORoxas Award
for Academic Excellence (2000), Honoria Acosta Award for Research (2006) and the Professional Regulations Commission
of the Philippines as Outstanding in the Field of Medicine. She was cited in the Reader's Digest as one of the Philippines'
Most Trusted in the Field of Medicine (2010). Internationally, she received the Woman of the Year Award from Federation
International Obstetrics & Gynecology (FIGO) in 2009. She received various awards as Outstanding Alumni of Far Eastern
University. FEU-NRMF Medical Foundation has awarded her the following: Most Outstanding Alumni, Most Outstanding
Faculty Member; Most Outstanding Leader, Most Outstanding in Clinical Practice.
She is currently professor emeritus and senior consultant in FEU-Nicanor Reyes Medical Foundation, Medical Director
and Senior Consultant of Capitol Medical Center. She continuously participate as lecturer or attendee in various scientific
programs /webinars of POGS,PSRM,PSCMAND PSGE.
XI
CONTRIBUTING
AUTHORS
Ira Dominique T. Alatraca-Malonzo, MD, FPOGS, FPSURPS
Dr. Alatraca-Malonzo was part of the Integrated Liberal Arts and Medicine (lntarmed) Program of the
University of the Philippines College of Medicine, graduating with a bachelor's degree in Basic Medical
Science in 2004 and Doctor of Medicine in 2009. She completed her residency training in Obstetrics &
Gynecology in 2013 at the UP Philippine General Hospital and proceeded with subspecialty training
in Urogynecology and Pelvic Reconstructive Surgery in the same institution, graduating in 2015.
While in training, she won in national interesting case and research competitions, with a few published scientific papers
under her belt. She continued to present her scientific works on Urogynecology in local and international fora and won
3rd place in the Young Urogynecologists Research Competition of the Asia-Pacific Urogynecology Association in 2017.
She then joined the faculty of the UPCM,serving as a clinical associate professor, and is presently the Assistant Training
Officer of the Division of Urogynecology and Pelvic Reconstructive Surgery of UP-PGH. She is a fellow of the Philippine
Obstetrical and Gynecological Society (POGS) and was a member of its Continuing Medical Education Committee
from 2018 to 2020. She is also a fellow and is the current secretary of the Philippine Society for Urogynecology and
Reconstructive Pelvic Surgery (PSURPS). She is also a Medical Specialist II at the Dr. Jose Fabella Memorial Hospital.
In 2019, Dr. Malonzo was conferred the Constantino P. Manahan Young Researcher Award by the POGS. In the same year,
she was also one of the Shan S. Ratnam Young Gynecologist Awardees of the Asia and Oceania Federation of Obstetrics
and Gynecology. Dr. Malonzo is wife to a software architect and manager and is the proud morn of a witty 9-year old boy.
She enjoys baking, growing orchids and dancing during her free time. She is also a strong supporter of Filipino designers
and artisans, and is particularly fond of handcrahed jewelry and accessories.
XII
Agnes L. Soriano-Estrella, MD, MHPEd, FPOGS, FPSSTD
Dr. Agnes L. Soriano-Estrella obtained her medical degree from the University of the Philippines College of Medicine.
She had her residency in Obstetrics and Gynecology and fellowship training in Trophoblastic Diseases at the Philippine
General Hospital. Soon after graduation, she joined the faculty of the Department of Obstetrics and Gynecology of
the College of Medicine of the University of the Philippines, Manila where she is currently an Associate Professor and
training officer of the Division ofTrophoblastic Diseases. She obtained a Masters degree in Health Professions Education
from the National Teacher Training Center for the Health Professions of the University of the Philippines, Manila. Dr.
Soriano•Estrella is a founding member and the current President of the Philippine Society for the Study ofTrophoblastic
Diseases. She has authored several articles on general obstetrics and gynecology as well as trophoblastic diseases,
which have been published in national and international peer reviewed journals. She was the editor of the Clinical
Practice Guidelines for the Diagnosis and Management ofTrophoblastic Diseases published in 2016 and the Associate
Editor of the Handbook of Trophoblastic Diseases published in 2012. She is likewise one of the editors of the Atlas
of Trophoblastic Diseases which garnered a Book Award from the National Academy of Science and Technology. She
has also authored chapters in several books and has been a member of technical committees for some clinical practice
guidelines published by the Philippine Obstetrical and Gynecological Society. In recognition of her work in the field of
Research, she was given the Most Outstanding Young Researcher Award by the Philippine Obstetrical and Gynecological
Society in 2009
CONTRIBUTING
WRITER
FORBOARD
CORRELATES
AND
LAYOUT
EDITOR
Manuel S. Vidal, Jr., RCh, MD
Dr. Vidal graduated with a BS Biochemistry degree, magna cum laude, from the De La Salle University- Manila under the
Star Scholarship Program, with several other awards: Excellence in Chemistry, Most Outstanding Thesis, and Dr.Jose Rizal
Honors Society inductee. He ranked second in the Chemistry Licensure Examination in 2014. He finished his medical studies
at the University of the Philippines Manila - College of Medicine, and is about to embark on his PhD dissertation studies
on organ-on·chip models at the University of Texas Medical Branch, Galveston, Texas. He dreams on becoming a good
OB·GYN in the future. If not busy, he enjoys the laid-back life, collecting fragrances, sipping coffee, drinking beers, and
cooking wonderful food for his friends. He is thankful for the opportunity to work on the first edition of this book.
ILLUSTRATORS
Christian Paolo S. Vidal, RMT
Mr. Vidal is a licensed medical technologist, graduating from the University of the Philippines Manila - College of
Public Health. He is currently undertaking his Master's degree in Public Health at the same institution under the DOST·
ASTHRDP scholarship program. He is a recipient of the University of the Philippines International Publication Award in
2020. At present, he works as a teaching associate at the College of Public Health, University oFthe Philippines Manila.
He is thankful for the invitation to contribute to the Platinum book series.
XIII
TABLE
OFCONTENTS
1:ANATOMY
CHAPTER ANDPHYSIOLOGY
OFTHE
FEMALE
REPRODUCTIVE
SYSTEM
Section 1: Anatomy of the Female Reproductive Tract
Anatomy of the Female Reproductive System
External Genitalia 4
Internal Genitalia 6
Ureters 10
General Blood Supply of the Female Reproductive System 10
The Female Pelvis II
Diaphragm and Ligaments 13
Clinical Correlates 14
Section 2: The Menstrual Cycle 15
Review of the Hypothalamic-Pituitary-Ovarian (HPO) Axis 15
Overview of the Menstrual Cycle 16
Section 3: Maternal Adaptations to Pregnancy 21
Reproductive Tract 21
Breast and Skin 22
Metabolic Changes 23
Hematologic System 24
Cardiovascular System 25
Pulmonary System 26
Urinary System 28
Gastrointestinal System 29
Endocrine System 30
Neuromuscular System 31
The Placenta and the Umbilical Cord 32
Section 4: Fetal Development 33
Fetal Development 33
Amniotic Fluid 35
CHAPTER
2:APPROACH
TOTHE
PATIENT
INOBSTETRICS
Section 1: Overview 39
Definition of Terms 39
Diagnosis of Pregnancy 41
Pregnancy Tests 42
Section 2: Preconceptional Care 44
Overview of Preconceptional Care 44
Components of Preconceptional Care 44
Section 3: Prenatal Care 49
Overview of Prenatal Care 49
Initial Prenatal Evaluation SI
Prenatal Surveillance 57
Dating of Pregnancy 58
Nutritional Counseling in Pregnancy 61
Common Concerns 65
Immunization for Filipino Pregnant Women 66
Section 4: Antenatal Surveillance 68
Overview of Antepartum Fetal Surveillance 68
Non•stress Test 68
Contraction Stress Test 69
Umbilical Artery Doppler Velocimetry 69
Biophysical Profile (BPP) 70
CHAPTER
3:LABOR
ANDDELIVERY
Section 1: Mechanism of Labor 75
Section 2: Physiology of Labor 91
Preparation for Labor 91
Phases of Parturition or Labor 91
Functional Divisions (Stages) of Labor 93
Section 3: lntrapartum Assessment 100
Electronic Fetal Heart Rate Monitoring 100
Baseline Fetal Heart Activity 101
Periodic Fetal Heart Rate Changes 102
Three•tier Fetal Heart Rate Interpretation 106
Section 4: Induction of Labor 107
Section 5: Management of Labor in the Vertex Position 109
Management of the First Stage of Labor 109
Management of the Second Stage of Labor 113
Management of the Third Stage of Labor 115
Management of the Fourth Stage of Labor 118
XIV
TABLE
OFCONTENTS
CHAPTER
4:DYSTOCIA
[ABNORMAL
LABORJ
Section 1: Mechanisms ofDystocia 121
Review of Normal Labor 121
Dystocia ("Difficult Labor") 124
Diagnosis of Abnormal Labor 125
Section 2: Sepcific Causes ofDystocia 126
"Power" (Uterus) 126
"Passenger" (Fetus) 128
"Passage" (Pelvis of Mother) 133
CHAPTER
5:PROCEDURES
INOBSTETRICS
Section 1: Instruments Used in Obstetrics and Gynecology 137
Section 2: Operative Vaginal Delivery 145
Forceps Delivery 145
Vacuum Assisted Delivery 148
Section 3: Breech Delivery 150
Section 4: Cesarean Section (CS) and Vaginal Birth After CS 156
Cesarean Section 156
Vaginal Birth After Cesarean 159
Section 5: Obstetric Analgesia and Anesthesia 160
Regional Anesthesia 160
General Anesthesia 163
CHAPTER
6:PUERPERIUM
Section 1: The Puerperium 167
The Puerperium (Postpartum Period) 167
Maternal Changes During the Puerperium 167
Postpartum Care 171
Section 2: Postpartum Complications 172
Postpartum Hemorrhage 172
Puerperal Complications 174
Thromboembolic Disease 177
Uterine Complications in the Puerperium 178
Disorders of the Breast 179
Other Problems in the Puerperium 180
Section 3: Breastfeeding and Lactation 181
CHAPTER
7:BLEEDING
DURING
PREGNANCY
AND
INPOSTPARTUM
Section 1: Overview of Bleeding During Pregnancy 187
Section 2: Early Pregnancy Complications 188
Abortion 188
Ectopic Pregnancy 192
Section 3: Bleeding in the Second Half of Pregnancy 199
Placenta Previa 199
Abruptio Placenta 20 I
Morbidly Adherent Placenta (Accrete Syndromes) 205
Disseminated lntravascular Coagulation (DIC) 207
Section 4: Postpartum Hemorrhage 212
Uterine Atony 212
Retained Placenta or Placental Fragments 214
Uterine Rupture 215
Uterine Inversion 217
Genital Tract Trauma 220
CHAPTER
8:GENERAL
OBSTETRIC
ISSUES
ANDCOMPLICATIONS
Section l: Preterm Labor 227
Prelabor Rupture of Membranes 235
lntraamniotic Infection and Chorioamnionitis 237
Section 2: Fetal Demise, Postterm Pregnancy, and Prolapsed Cord 238
Section 3: Multiple Gestations 244
Section 4: Fetal Growth Disorders 248
Fetal Growth Restriction 248
Fetal Macrosomia 250
Section 5: Abnnormalities in Amniotic Fluid Volume 252
Polyhydramnios (Hydramnios) 252
Oligohydramnios 254
xv
TABLE
OFCONTENTS
CHAPTER
9:MEDICAL
ISSUES
INPREGNANCY
Section 1: Overview of the Medical Issues in Pregnancy 259
Section 2: Hypertensive Disorders in Pregnancy 261
Section 3: Hematologic and Immunologic Disorders 273
Physiologic Anemia in Pregnancy 273
Iron Deficiency Anemia in Pregnancy 274
Megaloblastic Anemia 276
Antiphospholipid Antibody Syndrome 276
Section 4: Endocrinologic Disorders in Pregnancy 280
Gestational Diabetes Mel\itus 280
Hyperthyroidism in Pregnancy 284
Hypothyroidism in Pregnancy 286
Section 5: Lung Disorders and Infection in Pregnacny 288
Bronchial Asthma in Pregnancy 288
Pneumonia in Pregnancy 289
Urinary Tract Infection (UT!) in Pregnancy 290
Sexually Transmitted Infections in Pregnancy 292
Non-sexually Transmitted Infections in Pregnancy 295
CHAPTER
10:APPROACH
TOPATIENTS
INGYNECOLOGY
Section 1; Gynecologic History and Examination 303
Approach to Patients in Gynecology 303
The Gynecologic History 305
The Gynecologic Examination 307
Section 2: Procedures in Gynecology 311
VuIvar Dermal Biopsy and Vaginal Smear 311
Pap (Papanicolaou) Smear 313
Colposcopy 318
Endometria\ Sampling 320
Other Common Procedures in Gynecology 322
CHAPTER
11:BENIGN
GYNECOLOGIC
DISEASES
Section 1: Benign Diseases of the Vulva and Vagina 327
Dermatologic Diseases 327
Benign Cysts & Tumors 329
Section 2: Benign Diseases of the Cervix, Uterus, and Fallopian Tubes 332
Diseases of the Cervix 332
Endometrial Polyp 333
Leiomyoma 333
Paratubal Cysts 336
Endometriosis 337
Adenomyosis 340
Section 3: Benign Disorders of the Ovaries 343
Functional Cysts of the Ovary 343
Benign Ovarian Tumors 344
General Approach to Adnexal Masses 345
CHAPTER
12:GENITAL
TRACT
INFECTIONS
Section 1: Overview of the Genital Tract Infections 349
Sexually Transmitted Diseases 349
Endogenous Infections 350
Iatrogenic Infections 350
Section 2: Lower Genital Tract Infections 351
Bartholin Gland Cyst and Abscess 351
VuIvar Infections 352
Genital Ulcers 353
Vaginitis 358
Cervicitis 360
Section 3: Pelvic Inflammatory Disease 362
Overview of Pelvic Inflammatory Disease 362
Management of PIO 363
CHAPTER
13:PELVIC
FLOOR
Section 1: Overview of Anatomy and Physiology of Pelvic Floor 367
Anatomy of the Pelvic Floor 367
Physiology of Voiding 368
Section 2: Pelvic Organ Prolapse 369
Pathogenesis and Manifestations of POP 369
Pelvic Organ Prolapse Quantification System 370
Management of POP 373
Section 3: Urinary Incontinence 375
Overview of Urinary Incontinence 375
Management of Urinary Incontinence 377
XVI
TABLE
OFCONTENTS
CHAPTER
14:CONGENITAL
ANOMALIES
OFTHEFEMALE
REPRODUCTIVE
TRACT
Section 1: Overview of the Congenital Anomalies 381
Section 2: Congenital Anomalies of the Uterus 384
AFS Class I: Agenesis 384
AFSClass II: Unicornuate Uterus 385
AFS Class lll: Uterine Didelphys 385
AFS Class IV: Bicornuate Uterus 386
AFS Class V: Septate Uterus 386
AFS Class VI: Arcuate Uterus 387
AFS Class Vil: Diethylstillbestrol Related Anomalies 387
Section 3: Congenital Anomalies of the Vagina and Vulva 388
Longitudinal Vaginal Septum 388
Transverse Vaginal Septum 389
Vaginal Atresia 389
lmperforate Hymen 390
Microperforate Hymen 390
Labial Hypertrophy 390
CHAPTER
15:PEDIATRIC
GYNECOLOGY
Section 1: Overview of Pediatric/Adolescent Gynecology 395
Reproductive Tract of Children & Adolescents 395
Puberty 396
Gynecologic Examination 397
Section 2: Disorders of Sexual Maturation 399
Advanced Sexual Maturation (Precocious Puberty) 399
Delayed Sexual Maturation 404
Section 3: Disorders of Sexual Development (DSD) 405
Errors in Sexual Determination 405
Section 4: Menstrual Disorders 408
Abnormal Uterine Bleeding (AUB) 408
Primary Dysmenorrhea 408
Section 5: Other Disorders in Pediatric Gynecology 409
Vulvovaginitis 409
Urethral Prolapse 409
Foreign Bodies 410
Labial Adhesions 410
Lichen Sclerosus 411
Vaginal Bleeding 411
Section 6: Gynecologic Tumors 412
Overview of Gynecologic Tumors 412
Tumors of the Vulva, Vagina, and Cervix 412
Tumors of the Ovaries 413
CHAPTER
16:REPRODUCTIVE
GYNECOLOGY
Section 1: Amenorrhea 417
Primary Amenorrhea 418
Secondary Amenorrhea 422
Section 2: Menstrual Abnormalities 425
Dysmenorrhea 425
Premenstrual Syndrome & Premenstrual Dysphoric Disorder 427
Section 3: Abnormal Uterine Bleeding 429
Review of the Normal Menstrual Pattern 429
Overview of Abnormal Uterine Bleeding 429
FlGO (PALM-COElNJ Classification System of AUB 430
Approach to Abnormal Uterine Bleeding 433
Section 4: Polycystic Ovary Syndrome 436
Section 5: Infertility 442
Evaluation and Diagnosis of Infertility 442
Approach to Female Factor Infertility 443
Approach to Male Factor Infertility 447
Intrauterine Insemination 448
Assisted Reproductive Techniques 448
Section 6: Menopause 451
Manifestations of Menopause 451
Management of Menopause 452
Section 7: Fertility Preservation 455
Gonadotoxicity of Cancer Therapy 455
Management Options 455
XVII
TABLE
OFCONTENTS
17:FAMILY
CHAPTER PLANNING
Section 1: Overview of Family Planning 463
Comparing Effectiveness of Family Planning Methods 464
Medical Eligibility 466
Section 2: Natural Family Planning Methods 467
Sexual Abstinence 467
Coitus lnterruptus 467
Fertility Awareness Methods 468
Section 3: Hormonal Contraception 470
Combined Hormonal Contraceptives 470
Progestin-Only Contraceptives 473
Section 4: Intrauterine Devices 475
Section 5: Barrier Methods 477
Section 6: Sterilization 478
Female Sterilization 478
Male Sterilization 480
Section 7: Emergency Contraception 481
CHAPTER
18:GYNECOLOGY
ONCOLOGY
Section 1: lntraepithelial Neoplasia of Lower Genital Tract 485
Etiopathogenesis 485
Prevention 487
Cervical Cytology Reporting (Bethesda System) 489
Cervical lntraepithelial Neoplasia (CIN) 493
Cervical Adenocarcinoma in Situ 494
Vulvar Atypia 495
Section 2: Cervical Carcinoma 497
Cervical Carcinoma 497
Manifestations and Staging 498
Management 500
Section 3: Neoplastic Lesions of the Uterus SOI
Endometrial Hyperplasia 501
Endometrial Cancer 504
Section 4: Ovarian Cancer 507
Etiopathogenesis 507
Manifestations and Diagnosis 509
Germ Cell Tumors 511
Sex Cord Tumors 512
Section 5: Vulvar Cancer 513
Etiopathogenesis 513
Diagnosis 513
Management 515
CHAPTER
19:GESTATIONAL
TROPHOBLASTIC
DISEASE
AND
NEOPLASIA
Section I: Overview of Gestational Trophoblastic Diseases 519
Section 2: Benign Gestational Trophoblastic Diseases 520
Complete Hydatidiform Mole 520
Partial Hydatidiform Mole 520
Section 3: Gestational Trophoblastic Neoplasia 524
Invasive Mole 524
Choriocarcinoma 524
Placental Site Trophoblastic Tumor 527
Epithelioid Trophoblastic Tumor 527
CHAPTER
20:SOARD
CORRELATES
Section I: Obstetrics 531
Section 2: Gynecology 543
XVIII
ANATOMY
AND
PHYSIOLOGY
OFTHE
FEMALE
REPRODUCTIVE
SYSTEM
SECTION
ANATOMY OF THE FEMALE REPRODUCTIVE TRACT
ONE
I
ANATOMY OF THE FEMALE REPRODUCTIVE SYSTEM
• Organs of the female reproductive tract are divided into the external and internal
genitalia (see below)
• Reproductive organs are in intimate contact with the lower urinary tract & large intestines
Uterine cavity
Cervix
Fallopian
tube
Fimbriae
Ovary
Bladder
ll':ltr-:-+s------h~'llf--+----- Cervix
\\..,_.....,.,.,..."':;,fi1'f--.W-------f'+-------+ Vagina
'\..-4---,-tl½-I------+ Urethra
1/--:::~~~~~,------ Rectum
3
II. HOMOLOGOUS STRUCTURESBETWEENMALE& FEMALEREPRODUCTIVESYSTEMS
• Sex determination involves genetic, gonadal, and phenotypic sex:
0 Genetic sex (XXor XY): established at fertilization
0 Gonadal sex: heralded by differentiation of the primordial gonad into a testis or an ova1y
Phenotypic sex: differentiation of genitalia to the male phenotype is dependent on
testicular function (in the absence of a testis, female differentiation ensues)
I MALE I FEMALE
Genital ridge • Testis • Ovary
• Epididymis, ductus deferens,
Mesonephric ducts • Gartner duct
ejaculatory duct
Paramesonephric • Prostatic utricle, appendix • Uterus, fallopian tubes, upper
ducts of testis vagina
• Glans penis
• Glans clitoris
Genital Tubercle • Corpus cavernosum and
• Vestibular bulb
spongiosum
• Cowper glands
• Bartholin glands
Urogenial sinus (bulbourethral)
• Skene glands (paraurethral)
• Prostate gland
Urogenital folds • Ventral shaft of penis • Labia minora
Labioscrotal swelling • Scrotum • Labia majora
VULVA (PUDENDA)
• Term used to describe the external organs visible in the perinea! area
• Includes all structures visible externally from the mons pubis to the perinea! body
I.MONS PUBIS
• Rounded fatty prominence anterior to the pubic symphysis, pubic tubercles, and superior
pubic rami
• Formed by a mass of fatty subcutaneous tissue covered with pubic hairs after puberty
• Surface is continuous with the anterior abdominal wall
4
II. LABIA MAJORA AND MINORA
Description
I LABIA MAJORA
• Two longitudinal folds of adipose
& fibrous tissue which extend
I LABIA MINORA
• Two small cutaneous folds
between the labia majora and the
I
from mons pubis to perinea) body introitus ( or vaginal vestibule)
Lining • Outer: KSSE
• NKSSE
epithelium • Inner: NKSSE
• Lie in close apposition
Nulliparous • Not visible behind the
• Inner surface resembles the
women non-separated labia majora
mucous membrane
Multiparous • Gape widely
• Project beyond the labia majora
women • Inner surface become skin-like
• With hair follicles • No hair follicles
Glands • With sweat glands • No sweat glands
• With sebaceous glands • With sebaceous glands
KSSE:keratinizing
stratifiedsquamousepithelium
NKSSE:non-keratinizing stratifiedsquamousepithelium
III. HYMEN
• Thin membrane (NKSSE) at the entrance of the vaginal orifice that is normally perforated
to allow egress of menstrual blood and secretions
During first coitus, laceration usually occurs at the 6 o'clock position
• Caruncle myrtiformes: remnants of hymen in adult female
IV. CLITORIS
• Erectile structure found beneath the anterior joining of the labia minora
• Very sensitive structure made up of glans, a corpus or body and two crura, which attach
to the periosteum of the ischiopubic rami
V. VESTIBULE
• Almond shaped area between the clitoris and the vaginal introitus (opening)
• Functionally mature female structure of the urogenital sinus of the embryo
• Extends from clitoris to posterior fourchette
0 Urethral opening
0 Paired Skene glands opening
0 Paired Bartholin ducts opening
s
INTERNAL GENITALIA
Intramural
Isthmus
,-----,
segment
-----~
Ampulla[ Uterine
body
,,·.-z.--.-
Infundibulum[ Uterine
FimbriaeC isthmus
*Endocervical
Lateral fornix ---~ canal
External os ------#--'
I. VAGINA
• Thin-walled, distensible, fibromuscular tube, 7-10 cm long that extends from the
vestibule of the vulva to the cervix
• Lined by rugae, which are situated in folds throughout
• Rugae in reproductive aged women has an accordion-like distensibility
I UPPER 1/3
I MIDDLE 1/3 I LOWER 1/3
• Uterine or inferior
• Ce,·vical branch of the vesical arteries • Internal
Blood
uterine artery • Internal iliac artery pudenda)
supply
• Vaginal artery • Middle rectal artery artery
(posterior vaginal wall)
• Internal, external,
Lymphatics • Internal iliac nodes • Inguinal nodes
common iliac nodes
• General
• Sympathetic via hypogastric plexus
Nerves somatic via the
• Parasympathetics via S2-S4 (low density)
pudenda) nerve
• Levator ani muscle and
transverse cervical,
Support • Urogenital diaphragm • Perinea! body
pubocervical and
sacrocervical ligaments
6
II. CERVIX
• It is the !owe, and narrow portion of the uterus
• May vary in shape from cylindric to conical
• Usually 2.5-3 cm in length and 7-8 mm at its widest point
• Cervical canal opens into the vagina at the external os of the cervix
I
• Cervical canal opens into the uterine cavity at the internal os of the cervix
A. Histology
° Consists of predominantly fibrous tissue (in contrast to the primarily muscular corpus
of the uterus)
0 The transformation zone encompasses the transition from stratified squamous
epithelium to columnar epithelium (most cervical dysplasia develops within this
transformation zone)
I ENDOCERVlX I ECTOCERVIX
Location • Supravaginal portion • Portie vaginalis
• Extends from the isthmus
• Extends from the squamo-
(internal OS) to the ectocervix
Extent columnar junction to the
and contains the endocervical
external orifice
canal
• Single layer of mucus-secreting
highly ciliated columnar • Non-keratinized stratified
Histology epithelium which is thrown into squamous epithelium
folds forming complex glands • Hormone-sensitive
and crypts
Nervous supply • Extensive amount of nerves • Few nerves only
Blood supply • Cervicovaginal branch of uterine artery located at the lateral walls
II. UTERUS
• Thick-walled, hollow, muscular organ located centrally in the female pelvis
• Nullipara: ~8 cm long, 5 cm wide, and 2.5 cm thick and weighs 40-50 g
• Multipara: each measurement is approximately 1.2 cm larger and uterine weight is 20-30 g
heavier
• The maximal weight of a normal uterus is 110 g
7
B. Histolol!V
Stratum Functionale
• Responds to fluctuating hormonal levels • Zona spongiosa
• Shed during menstruation
• Supplied by the spiral arteries
Endometrium • Zona compacta
• Superficial 2/3
Stratum Basale
• Supplied by the straight arteries
• Basal 1/3
• Inner longitudinal
Myometrium • Middle oblique
• Outer longitudinal ("hood-like" pattern)
Serosa • Visceral peritoneum
III. FALLOPIANTUBES
• The paired uterine tubes extend outward from the superolateral portion of the uterus and
open outwardly in close approximation to the ovaries
• They are between 10 & 14 cm in length and slightly <l cm in external diameter
• Each tube is divided into four anatomic sections
SEGMENT I DESCRIPTION I CLINICAL CORRELATES
• 2% of ectopic pregnancy
Intramural • 1 to 2 cm in length and is
• Ectopic pregnancy at this area
Interstitial surrounded by myometrium
result in severe maternal morbidity
• Most highly developed musculature
• Narrowest portion
• The narrow portion of the
• Preferred portion for applying
tube that adjoins the uterus,
Isthmus ligatures and clips for female
passes gradually into the
sterilization
wider, lateral portion
• Preferred portion for tubal ligation
I • 12% of ectopic pregnancy
• 4-6 cm in length & ~6 mm
in inside diameter; wider & • Site of fertilization
Ampulla
more tortuous in its course • 80% of ectopic pregnancy
than other segments
• Fimbriated extremity
Infundibulum • Tunnel shaped opening of the • 5% of ectopic pregnancy
distal end of the fallopian tube
8
.
IV. OVARIES
• Lie on the posterior aspect of the broad ligament, in the ovarian Fossa
• Immediately adjacent to the ovarian fossa are the external iliac vessels, the ureter, and the
obturator vessels and nerves
• Attached to the broad ligament by the mesovarium
• Not covered by peritoneum
I
Mesovarium
Fimbria
Ovarian ligament
Mesometrium -------"~~.rr=~
-·
Ovarian ligament
ovarian ligament
• Narrow, short, fibrous band that extends from the lower pole
of the ovary to the uterus
lnfundibulopelvic • Forms the superior and lateral aspect of the broad ligament
ligament (suspensory • Contains the ovarian artery, veins, & accompanying nerves
ligament of the ovary) • Attaches the upper pole of the ovary to the lateral pelvic wall
9
URETERS
• Muscular tubes, 28-34 cm in length, extending from renal pelvis to the urinary bladder
• Retroperitoneal in location
• Found on the medial leaf of the parietal peritoneum and in close proximity to the ovarian,
uterine, obturator, and superior vesical arteries
Clinical Correlates
• Since the ureter lies underneath the uterine artery, surgical compromise of the ureter may
occur during:
• Clamping or ligating of the infundibulopelvic vessels
• Clamping or ligating of the cardinal ligaments, or
• Wide suturing in the endopelvic fascia during an anterior repair
• Two of the classic ways to differentiate a ureter from a pelvic vessel are:
• Visualization of peristalsis after stimulation by a surgical instrument
• Visualization of Auerbach plexuses, which are numerous, wavy, small vessels that
anastomose over the surface of the ureter
10
_T_H_E_F_E_M_A_L_E_P_E_L_V_IS
_________________ , __
:
I. THE PELVICBONES
• The bony pelvis consists of the two hip bones, the sacrum and the coccyx
• The hip bone is an irregularly shaped bone, also known as the pelvic girdle
• Pelvis is divided into false and true compartments
° False pelvis: lies above the linea terminalis
0 True pelvis: lies below the boundary
• Pubic symphysis: between the pubic bodies of the two hip bones
CONJUGATES
True conjugate A
Obstetricalconjugate B
Diagonalconjugate
Sacral
Sacral promontory
LIGAMENTS
Sacrospinous
Pubic symphysis spines ligament
--."J·~./-,.
i ,.; "-.J;-
-- \
'O~<T'
8 ·e5 "ej" EB
Pelvic Inlet
Antero- Transversely
Shape Round Triangular
posteriorly; oval oval
AP-Segment Equal & spacious Posterior< anterior Posterior< anterior Flat
>90° inclined >90° inclined <90° inclined >90° inclined
Sacral Angle
backwards backwards forward backwards
Sacrum Curved Curved Straight Straight
Pelvic Ca_vity
Sacrosciatic notch Wide & shallow Wider, shallower Narrow & deep Narrow & small
Straight or Straight or
Side Walls Convergent Divergent
divergent divergent
Pelvic Outlet
Lachial Spines Not prominent Not prominent Prominent Not prominent
Pubic Arch Curved Long & curved Long & straight Short & curved
Subpubic Angle Wide Slightly narrow Narrow Very wide
Bituberous
Normal Normal/short Short Wide
Diameter
Difficult delivery
Face-to-pubis with increased
Delivery No difficulty No difficulty
delivery chance of perinea!
injuries
12
_D_IA_P_H_RA_G'-'M'---A-'-N_D_L_IG--'-'--'A-"-M=E"-'N~T..;;;.S
______________ I_=.
I.DIAPHRAGM
COMPONENT I REMARKS
• Wide but thin muscular layer of tissue that forms the inferior border
of the abdominopelvic cavity
• Composed of a broad, funnel-shaped sling of fascia & muscle
• Extends from symphysis pubis to the coccyx & from one lateral
sidewall to the other
Pelvic
• Major muscles:
diaphragm
° Coccygeus
(endopelvic
0Levator ani (pubococcygeus, puborectalis, and iliococcygeus)
fascia)
• The paired levator ani muscles act as a single muscle and functionally
are important in the control of urination, in parturition, and in
maintaining fecal continence
• Supports abdominal & pelvic viscera & facilitates equal distribution of
intraabdominal pressure (e.g., during coughing, straining)
Urogenital
• Strong, muscular membrane that occupies the area between the
diaphragm
symphysis pubis and ischial tuberosities
(triangular
• Support the urethra and maintain the urethrovesical junction
ligament)
II. LIGAMENTS
• Ligaments attach the lateral border of the sacrum to various bony landmarks on the bony
pelv;s to aid stability
• Two wing-like membranous ligaments that extend from the lateral
margins of the uterus to the pelvic walls
Transverse cervical/cardinal: pass to the cervix and upper part of
0
the vagina
Broad ligament Pubocervical: from posterior surface of the pubis to the cervix;
0
end of vagina
• Divide the pelvic cavity into anterior and posterior compartments
• Provide the major support of the uterus and cervix
Cardinal • Originated from the densest portion of the broad ligament
ligament • Medially united to the supravaginal wall of the cervix
• Maintains anatomic position of the cervix & upper part of the vagina
• From posterolateral to the supravaginal portion of the cervix
Uterosacral
encircling the rectum then inserts into the fascia over S2 and S3
ligament
• Provides anatomic support to the cervix
• Extend from the lateral portion of the uterus, arising below and
anterior to origin of the oviducts, that is continuous with the broad
Round Ligament
ligament, outward and downward to the inguinal canal terminating at
upper portion of labia majora
13
CLINICAL CORRELATES
CLINICAL SCENARIO
I ANATOMICAL
INVOLVEMENT I REMARKS
• Anesthesia/hypoesthesia
• Genitofemoral nerve
or pain at the perineum
Radical hysterectomy
Iliac and obturator node • Interfere with adduction of
dissection the thigh and hip
• Obturator nerve
• Sensory function on the
medial aspect of the thigh
Improper placement of legs in • Footdrop
the stirrups or prolonged dorsal • Peroneal nerve • Sensory and motor loss
lithotomy position over the lateral lower leg
Damage due to pressure from
lateral blade of a self-retaining • Prohibits flexion of the hip,
retractor during an abdominal • Femoral nerve patient is not able to lift leg
hysterectomy/ inguinal node off the bed
dissection
Node dissection of the obturator • Severe blood loss if
• External iliac artery
fossa transected
Straddle or after giving • Injury producing a very
• Pudenda! artery
anesthetic for second stage labor large hematoma
Source:Cunningham,
FG.WilliamsObstetrics
25thEdition.2018
14
SECTION
THE MENSTRUAL CYCLE
REVIEW OF THE HYPOTHALAMIC-PITUITARY-OVARIAN
TWO
(HPO) AXIS
I
• The HPO axis is a tightly regulated system controlling female reproduction & physiology
• The axis coordinates a tightly regulated feedback loop that consists of:
0Gonadotropin-releasing hormone (GnRH) produced by the hypothalamus
Follicle-stimulating hormone (FSH) & luteinizing hormone (LH) from anterior pituitary
Sex steroids (e.g., estrogen, progesterone) from the ovaries
Positive
I feedback
I Follicular
···························►Q ANTERIOR
+--
I phase
:························•''. ~ PITUITARY I
LH
FSH
Negative
feedback
i.0·· Activin
OVARIES Luteal
···O··lnhibin phase
I
Estradiol
Progesterone
-0-1
• The hypothalamus secretes GnRH
• In response to GnRH stimulation, the anterior pituitary produces LH and FSH
• FSH and LH act primarily to activate the ovaries to produce estrogen, progesterone, &
inhibin and to regulate the menstrual and ovarian cycle.
L GONADOTROPIN-RELEASING HORMONE(GnRH)
Regulates secretion of FSH and LH
• Secreted in pulsatile manner to be effective
• Released from neurons within the anterior hypothalamus (arcuate nucleus of the median
basal hypothalamus)
15
III. OVARIAN
STEROIDS
• Biosynthesis of the ovarian steroids
• Following binding of the gonadotropins to their receptors, steroid production begins in
the ovary
• Three principal sex steroids of the ovary:
Estradiol
Progesterone
0Androgen
HORMONE I ACTIONS
• Represents a group of hormones including:
• Estrone: most common form in the post-menopausal years
• Estradiol: most potent; most common form during reproductive years
Estrogen • Estriol: least potent; most common form in pregnancy
• Secretion is regulated by FSH
• For development of secondary sex characteristics at puberty
• Thickens endometrium during the proliferative phase
• Secretion is regulated by LH
Progesterone • Maintains endometrium during secretory phase
• Prepares endometrium for implantation (during pregnancy)
• Androstenedione & testosterone are produced in the theca cells
• Regulated by LH
• At low concentrations, these are transported to the granulosa cells
for aromatization to estradiol & estrone (two-cell two-gonadotropin
Androgen
mechanism of steroidogenesis)
• At high concentrations (such as in PCOS), they are converted to 5-alpha
reduced androgens that cannot be converted to estrogens and inhibit
aromatase activity (this causes the atresia of follicles)
:::,-
0 0
3 ~
g ~-
ro ::::,
V>
0
n
<n
<
OJ
~
ro w·
::::,
m
::::,
0..
~ 0
n 3
ro ~
iii"
DO D14 D28
FOLLICULAR PHASE LUTEAL PHASE
17
OVARIAN CYCLE
I ESTROGEN I PROGESTERONE
I FSH I LH
Menstruation L L L L
Follicular phase i L i L
Ovulation i L i i
Luteal phase L i L L
Key Points to Remember:
• Dropin progesteronelevelstriggermenstruation
• Estrogenis the mainhormoneduringthe follicular
phase;itcauses selectivenegativefeedback
• Progesteroneis the mainhormoneduringthe lutealphase;itcauses non-selective negativefeedback
• EstradiolsurgeprecedesLHsurge
• LHsurgeis the triggerforovulation;
alsotriggersluteinization
of granulosacellsintoLHreceptivecells(enabling
granulosacellsto respondto LH levelsand produceprogesterone)
• FSHas the nameimpliestriggersfolliculardevelopment
I. FOLLICULAR PHASE
• First phase which involves the maturation of follicles
• Begins with the initiation of menstruation and averages 14 days in length
• The length of the follicular phase determines the cycle duration
• Can be divided into three distinct phases:
PHASE I REMARKS
Recruitment • The withdrawal of estrogen & progesterone during the luteal phase
of cohort of of the prior cycle causes a gradual increase in FSH,which stimulates
antral follicles growth of primordial ovarian follicles
• Of the primordial follicles, one becomes the dominant follicle &
develops/matures until ovulation
• It is usually the follicle that has the most vascularized theca layer and a
Selection of
higher number of gonadotropin receptors
a dominant
follicle • Follicular phase estradiol production is explained by the two-cell
two-gonadotropin mechanism (see below)
• Elevated estradiol activate the negative feedback loop, resulting to
decreased FSH that cannot sustain the growth of other follicles
Growth of • The developing dominant follicle, destined to ovulate, produces
the dominant estrogen that enhances follicular maturation & increases production of
follicle gonadotropin receptors
( ) ORCUIATION I
III. LUTEALPHASE
• This phase coincides with the secretory phase of the endometrial cycle
• Granulosa cells and theca cells hypertrophy and the follicle wall collapses; the structure
becomes the corpus luteum
• The corpus luteum secretes: progesterone, estradiol, and inhibin A
• The lifespan of the corpus luteum is 9-11 days; it may be prolonged by hCG in early
pregnancy, which serves to maintain the vital steroidogenic function of the corpus luteum
until the time that the placenta takes over
• The luteal phase is relatively constant at 14 days post-ovulation, regardless of cycle
duration
19
ENDOMETRIAL CYCLE
• Includes proliferative, secretory, and menstrual phase
• Ovarian hormones drive morphologic and functional changes of endometrium
I. PROLIFERATIVE PHASE
• Coincides with the follicular phase
• There is progressive mitotic growth of the decidua functionalis as a result of the rising
estradiol level (secondary to the growth of the dominant follicle)
• Endometrial glands become longer and tortuous
• Before ovulation, subnuclear vacuoles appear at the base of the glands
II. SECRETORYPHASE
• Coincides with the luteal phase of the ovarian cycle (where corpus luteum comes into play)
• The endometrium is optimally prepared for implantation by day 6-7 post ovulation
0 In a regular 28-day cycle, the endometrium has well-formed subnuclear glycogen-rich
vacuoles in gland lining cells and palisading cell nuclei by day 17
0 The glands become increasingly elongated, tortuous and sacculated and the spiral
arterioles are in abundance
0 There is also stromal edema
III. MENSTRUATIONPHASE
• lfno implantation takes place and there is no hCG to maintain the corpus luteum, the
withdrawal of estrogen and progesterone causes the subsequent ischemia and autolysis
of the stratum functionalis that results in menstruation
• PGF2 alpha:
Theorized to facilitate the expulsion of the sloughed endometrial tissue from uterus
° Causes arteriolar spasm, endometrial ischemia, and myometrial contractions
20
SECTION
MATERNAL ADAPTATIONS TO PREGNANCY
THREE
I
OVERVIEW
• Pregnancy is a period of adjustment to the demands and products of conception
• Profound local and systemic changes in maternal physiology are initiated by conception
and continue throughout pregnancy
• After delivery and expulsion of the placenta, these changes are rapidly reversed
Changes in pregnancy occur for the following reasons:
Maintain the pregnancy
Protect the fetus from toxic and harmful agents
Maintain the health of the fetus and mother
Protect the mother from deleterious effects of the maternal changes itself and eventual
delivery
At 20-34 weeks, the fundic height in centimeters correlates with the AOGin weeks
0
B. Uterine Contractility
Braxton-Hicks contractions: infrequent, unpredictable, sporadic, non-rhythmic
0
21
II. CERVIXAND VAGINA
• Estrogen and progesterone makes the cervix swollen and softer during pregnancy
• Towards labot; the cervix decreases in length and opens (in preparation for birth)
• Estradiol stimulates growth of columnar epithelium of cervical canal, leading to ectropion (i.e.,
extension of endocervical glands onto ectoce1vical pmtion), making it prone to contact bleeding
• Chadwick sign: greater vascularity & hyperemia in the skin and muscles of perineum,
vulva, vagina, and cervix resulting in a characteristic violet color ("violaceous" appearance)
• Goodell sign: softening of the cervix (at 6-8 weeks AOG)
• Hegar sign: softening of isthmus
~ ~
~- -=-.
'""'""~1'1
_ ......
Externalas-- -- - - ------------ --
~
· - ---- - - - - - -- --- - - -·
III. OVARIES
• Ovulation ceases during pregnancy and maturation of new follicles is suspended
• Ovarian hormones play a crucial role during pregnancy
• Corpus luteum persists up to 8 weeks (which produces progesterone) and is completely
obliterated by 20 weeks AOG (luteo-placental shift)
II. SKIN
• Hyperpigmentation in pregnancy: maybe due to estrogen and progesterone increasing
melanocyte-stimulating hormone (MSH) during pregnancy
CHANGES IN
PREGNANCY
I DESCRIPTION
Striae gravidarum or • Reddish, slightly depressed streaks seen in the abdominal skin and
stretch marks over the skin of breasts and thighs
• Rectus muscles separate in the midline
Diastasis recti • Due to muscles of the abdominal wall not able to withstand the
tension of the expanding pregnancy
Linea nigra • Pigmented skin line in the midline of the anterior abdominal wall
Chloasmaormelasma
gravidarum ("mask • Irregular brownish patches of varying size on the face and neck
of pregnancy")
• Commonly seen on the face, neck, upper chest, and arms
Angiomas or
• Minute, red skin papules with radicles branching out from a central lesion
vascular spiders
• Likely from increased estrogen
• Redness in of the thenar and hypothenar eminences of the palms
Palmar erythema
• Due to increased estrogen
Telogen effluvium • Excessive hair loss in the puerperium
22
_M_E_TA_B_O_L_I_C_C_H_A_N_G_E_S_D_U_R_l"'-N-'-G--'-P_R_E_G_N_A_N_C_Y
_________ __ =.
• In response to the demands of the rapidly growing fetus and placenta, the pregnant
woman undergoes numerous metabolic changes
I. WEIGHTGAIN
• Metabolic alterations occur in pregnancy as a result of increased demands of the growing
fetus & placenta
• Average weight gain during pregnancy is 12.5 kilograms or 27.5 pounds
II. WATERMETABOLISM
• There is greater water retention in pregnancy
• Mediated by decreased plasma osmolality of 10 mOsm/kg, relaxin and other hormones
• At term:
Volume of fetus, placenta, and amniotic fluid is ~3.5 L
Expanded maternal blood volume from uterus and breast growth (~3.0 L)
, Pitting edema of the ankles and legs due to greater venous pressure from partial vena
cava occlusion by the enlarging uterus
III. PROTEINMETABOLISM
• The placenta regulates the amino acid concentrations - it is higher in the fetal than in the
maternal compartment
• Daily requirements for dietary protein intake during pregnancy are increased.
IV.CARBOHYDRATE METABOLISM
• Normal pregnancy characterized by:
0 Mild fasting hypoglycemia
0 Postprandial hyperglycemia
0 Hyperinsulinemia
• This is secondary to pregnancy-induced peripheral insulin resistance
, This is needed to ensure sustained postprandial glucose supply to the fetus
, Factors involved: progesterone, placentally derived growth hormone, prolactin,
cortisol, tumor necrosis factor, leptin
V. FATMETABOLISM
• Increased concentrations of lipids, lipoproteins, and apolipoproteins in plasma
, Secondary to increased insulin resistance
, Positively correlated with levels of estradiol, progesterone, and hPL
• Functions ofhyperlipidemia in pregnancy:
0 Aids in fat metabolism by the fetus
, Preparatory factor in milk production
• Fat storage in pregnancy:
Functions to protect the mother and the fetus during times of prolonged starvation of
hard physical exertion
, Primarily during mid-pregnancy; in central rather than peripheral tissues
23
VI. ELECTROLYTES
AND MINERALS
II. BLOODCELLS
A. Red Blood Cells (RBC)
RBC mass begins to increase at 8-10 weeks AOGand steadily rises
0
The increase in RBC mass is smaller than the increase in plasma volume, which
0
C. Platelets
0 Platelet counts decline as pregnancy progresses, but usually remain in the normal range
0 Thrombocytopenia during pregnancy is partly due to hemodilution
--;:;160
;:,,
~
...140
C
Cardiac
output
"'
C
bO
~ 120
Q.
C.
0 Mean BP
C 100
0 ...
.,
C
80
SVR
<l.
.,
~
60
0 8 16 24 32 40
Weeks of pregnancy
I INCREASED I DECREASED
Cardiac output (CO) ✓
Arterial pressure ✓
Diastolic pressure ✓
Renin ✓
Angiotensinogen ✓
25
II.HEART
• As the diaphragm becomes progressively elevated by the uterus in the third trimester,
the heart is displaced to the left & upward and rotated on its long axis
• Apex is moved laterally, producing larger cardiac silhouette in chest radiograph seen in
the latter half of pregnancy
A. Heart Sounds
0 Exaggerated splitting of Sl and increased loudness of both Sl and S2
0 Loud S3
0 Systolic murmur in 90% of gravidas that disappears shortly after delivery
0 Diastolic murmurs are uncommon and may represent pathologic conditions
° Continuous murmurs (mammary souffle) from breast vasculature in 10% of gravidas
B. ECG Changes:
0 Slight left-axis deviation
0 Q waves in leads ll,III and aVF
0 Inverted T-waves in leads Ill, VI-V3
Thoracic circumference
increases (+6 cm)
Thoracic diameter
lengthens (+2 cm)
Key Changes
• Diaphragm rises ~4 cm
• The subcostal angle widens appreciably
• The transverse diameter of the thoracic cage lengthens ~2 cm
• The thoracic circumference increases ~6 cm
• The diaphragmatic excursion is greater in pregnant than in non-pregnant women
Source:Cunningham,
FG.WilliamsObstetrics
25thEdition.2018
26
II. LUNGVOLUMES
INCREASED I DECREASED I UNCHANGED
• Functional residual capacity*
• lnspiratory capacity (IC) • Respiratory rate
• Expiratory reserve
• Tidal volume (TV) • Totallung capacity (FRC+ IC)
volume (ERV)
• Resting minute ventilation • Lung compliance
• Residual volume (RV)
• Peak expiratory flow rates • Maximumbreathing capacity
• Total lung capacity
• Airway conductance • Forcedor timed vital capacity
• Pulmonary resistance
'Functionalresidualcapacity(FRC)= ERV+RV
IRV
vc
3200
TLC
TLC 4000
4200
ERV
550
FRC
1350
RV RV
RV 800 800
1000
ff Diaphragm elevation ff
NONPREGNANT TERMPREGNANCY
Lungvolumesare inml
• Most significant changes are reduction in FRC(along with ERV& RV)and increases in IC& TV
• FRC& RVdecreases progressively across pregnancy due to diaphragm elevation
• Enhanced respiratory drive can occur due to stimulatory action of progesterone, low ERV,
and compensated respiratory alkalosis
• 0, delivery in the maternal lungs is increased because of j TV, j hemoglobin mass,
i cardiac output
Source:Cunningham,
FG.Williams
Obstetrics25thEdition.2018
27
-
CHANGES IN THE URINARY SYSTEM
I. OVERVIEWOF THE RENALCHANGES
CHANGES CLINICAL
CORRELATES
• Increases to 1-1.5 cm
Kidney size • Resembles hydronephrosis on • Returns to normal postpartum
sonogram
Renal • GFR& renal plasma flow increase • Increased GFR results in urinary
function by ~50% due to relaxin frequency and nocturia
• Displaced laterally and compressed
at pelvic brim
• Risk for infection due to
Ureter • Ureteral dilatation (right> left) due to
compression
the dextrorotated uterus & cushioning
of the sigmoid colon on the left
• Hyperplasia of bladder muscle
• Urinary incontinence (some) by
elevate the trigone
Bladder 3rd trimester
• Reduced bladder capacity due to
• Risk for infection
uterine compression
28
;::C=H=A=N=G=E=S==IN=T=H=E==G=A=S=T=R=O=l=N=TE=S=T=l=N=A=L=S=Y=S=T=E I
I. ESOPHAGUS
• "Heart burn or pyrosis" is common in pregnancy due to reflux of acidic secretions into the
lower esophagus from:
0 Altered stomach position
Reduction in LES tone, intraesophageal pressure
Increased intragastric pressure
0 Decreased peristalsis wave speed & amplitude
II. STOMACH
• Gastric a tony (lack of tone)
• Prolonged gastric emptying time
• Stagnation of gastric contents builds up pressure causing gastro-esophageal reflux
IV.GALLBLADDER
• Progesterone potentially impairs gallbladder contraction by inhibiting cholecystokinin
(CCK)-mediated smooth muscle stimulation, which is the primary mediator of gallbladder
contraction
• Pregnancy may be associated with an increased risk for gallstones
29
CHANGES IN THE ENDOCRINE SYSTEM
I. PITUITARYGLAND
• Enlarges by approximately 135%
• Due to estrogen-stimulated hypertrophy and hyperplasia of lactotrophs
• May compress optic chiasma & reduce visual fields
PITUITARY
HORMONES I REMARKS
II. THYROIDGLAND
• Hyperplasia and increased vascularity
• Elevation of BMR (basal metabolic rate)
• Pregnancy is a mild hyperthyroid state
A. Thyroid Hormones
THYROID
HORMONES I REMARKS
30
III. PARATHYROIDGLANDS
PARATHYROID
HORMONES
Parathyroid
I REMARKS
ADRENAL
HORMONES
I DESCRIPTION
relaxin
31
THE PLACENTA AND UMBILICAL CORD
I. THE NORMAL PLACENTA
• Typical placenta at term weighs 470 g
• Round to oval with a 22 cm diameter & central thickness of 2.5 cm
• Composed of:
Placental disc
0 Extraplacental membranes
0 Three-vessel umbilical cord
• Basal plate: disc surface that lies against the uterine wall which is divided by clefts into
portions (i.e., cotyledons)
• Chorionic plate: fetal surface into which the umbilical cord inserts at the center
III. PLACENTALHORMONES
• Placenta is the main endocrine organ during pregnancy
• Supplies all materials required for fetal growth and energy production, while removing
the products of fetal catabolism (i.e., waste products)
• Secretes several hormones, such as hCG,hPL, estrogen, and progesterone
PLACENTAL
HORMONE I REMARKS
32
FETAL DEVELOPMENT
SECTION
FETAL DEVELOPMENT
FOUR
I
• The moment the ovum is fertilized, the embryonic period starts (conception)
• The first 4 months are critical: any teratogenic effects in this time may cause abortions
and congenital anomalies
I. DEFINITIONOF PERIODS
PERIOD/AGE I DESCRIPTION
• Calculated from the first day of the last normal menstrual period
Gestational or
[LNMP) and is generally used during fetal period, in ultrasound,
Menstrual Age
and in clinical practice
(Age of
Gestation)* • Time elapsed since the first day of the LNMP,a time that precedes
conception
• Time in days or weeks from ovulation
Ovulation or • Ovulation age is used when describing the embryonic period and
Conceptual Age** often, the previable fetal period
• Ovulation age is 2 weeks less than gestational age
'Becausemostwomenknowwhentheirlast periodbegan(butnotwhenovulationoccurred),the timeelapsedsince
the firstdayof the last normalmenstrualperiod(ormenstrualor gestationalage) is usedto determinethe age of
pregnancy.
"The actualembryoor fetalage (i.e.,conceptualage) is the timeelapsedfromfertilizationof the egg near the time
ofovulation.
Source:Cunningham
FG,et al. Williams
Obstetrics.25thedition;2018
IL DEFINITIONOF TERMS
TERM I DESCRIPTION
Embryonic • Time during which organogenesis takes place; begins the third week
Period after LNMP through the eight week
• Corresponds to 7 weeks after fertilization or 9 weeks after the LNMP;
Fetal Period most organ systems have developed, and the fetus enters a period of
growth and maturation
Preterm • A neonate born between 20 weeks up to 37 weeks
Term • A neonate born between 37 weeks up to 42 weeks
Post-term • A neonate born beyond 42 weeks
Infant • Between delivery to 1 year
Source:Cunningham
FG,et al. Williams
Obstetrics.25thedition;2018
33
III. FETAL DEVELOPMENT CHART
• The transition to the fetal period occurs at 7 weeks after fertilization or 9 weeks after the
last normal menstrual period
• A period of growth and maturation
DEVELOPMENTAL
STAGE EMBRYONIC
STAGE FETALSTAGE
Gestationalage
6 7 13 14 20 40
(weeks)
Conceptualage
0 0 2 3 4 5 7 8 9 10 11 12 18 38
(weeks)
••
DEVELOPING
ORGANS
Heart
■
Eyes
• The black bars in the table show the gestational age at which the specific organs or organ
systems are most susceptible to corresponding major congenital abnormalities. The dark
grey bars show the getational age at which the specific organs or organ systems are most
susceptible to functional defects and minor malformations
• The conceptus is termed an embryo at the beginning of the 3rd week after ovulation and
fertilization
• Transition from the embryonic period to the fetal period occurs at 7 weeks after
fertilization, corresponding to 9 weeks after onset of the last menses.
34
;....;A""'M"'-N"'-10"-T"""l...;;;.C....;;.F...;;;;L=U-'-'ID"--------------------I.~ .•
• Amniotic fluid is the liquid that surrounds the fetus after the first few weeks of gestation
I. FUNCTIONS
• Protection of the fetus from ' trauma to the maternal abdomen
• Cushions the umbilical cord from compression
• Antibacterial properties against infection
• Reservoir of fluid & nutrients for the fetus
• Provides necessary fluid and growth factors for fetal development of lungs,
musculoskeletal, ang gastrointestinal systems
II. REGULATION
• Derived almost entirely from the fetus
• Major inputs to the amniotic fluid are fetal urine and fetal lung secretions
• Major physiologic pathway of removal of AF is fetal swallowing and intramembranous
flow (i.e., through skin and fetal membranes)
I SOURCE I REMARKS
Early • Contains same osmolality as
• Maternal plasma as ultrafiltrate
pregnancy maternal plasma
• Transfer of water and small
• Transmembranous flow
molecules across the amnion
• Transfer of water and small
• lntramembranous flow molecules across the fetal vessels on
First half of
the placental surface
pregnancy
• Transfer of water and small
molecules across the fetal skin
• Transcutaneous flow
• Continues until keratinization occurs
at 22-25 weeks
• Produces almost 1 Lat term
• Although fetal urine production
• Fetal urination begins at 8-11 weeks ago of
gestation, it does not become a major
component until 18 weeks AOG
• Produces ·around 350 mL per day;
• Fetal lung fluid secretion half of which is immediately
Late in swallowed
pregnancy
• Resorbs 750 mL per day
• Impaired swallowing secondary
• Fetal swallowing to central nervous anomaly or a
gastrointestinal (GI) obstruction can
result in polyhydramnios
• Intramembranous flow • Resorbs 400 mL per day
• Transmembranous flow • Resorbs minimal fluid
REFERENCES
1. CunninghamFG,LeveneKJ,BloomSL,Dashe JS,HoffmanBL.CaseyBM,SpongCT(Eds.).WilliamsObstetrics.25th edition. New York:McGraw-
Hill Education,2018
2. Curran MA Fetal Development Perinatology.com.Availableonline https://perinatology.com/Reference.AccessedJuly 14, 2021
3. EngleWA;American Academyof Pediatrics Committee on Fetus and Newborn.Agetenninology during the perinatal period. Pediao-ics.2004
Nov;114(5):!362-4.
4. Ross MG,BeallMH.Physiologyof amniotic fluid volume regulation. Uptodate.AccessedJuly 14,2021
35
APPROACH
TOTHE
PATIENT
INOBSTETRICS
SECTION ONE
_Do_E:_~_:_1:_l~_:w_o_:_:_E_:H_M_:_A_P_P_R_O_A_C_H_T_O_PA_T_I_E_N_T_s_,N_O_
__
39
Gt 2010 • Preterm • NSD • Live boy, pretenn
G2 2012 • Term • cs • Live girl, term
G3 2014 • 8 weeks • Spontaneous abortion • N/A
• Twin A: live boy
G4 2016 • Preterm • CStwins • Twin B: girl died at age 3 due
to pneumonia
GS 2021 • Current pregnancy
OBScore:G5 P3 (1- 3- 1 - 3)
G - 5 pregnanciesincludingcurrentpregnancy
P - 3 pregnanciesthatreachedbeyond20 weeks(2010,2012,2016)
T - 1 termbabydeliveredin2012
P-3 preterrnbabies:1 deliveredin2010,2 deliveredin2016
A- 1 abortion/miscarriage
thatunderwentD&C
L-3 livechildrencurrently
Example 2: Determine the OB score of a patient with the following OB history, tabulated below:
40
DIAGNOSIS OF PREGNANCY
• Pregnancy is identified when a woman presents any of the following:
Presumptive or diagnostic signs and symptoms
0
Positive home pregnancy test
B-hCG result either urine or blood
Sonographic evidence of pregnancy
Source:https://www.registerednursern.com/signs-of-pregnancy-presumptive-probable-positive/
41
PREGNANCY TESTS
I. HUMAN CHORIONIC GONADOTROPHIN (p-hCG)
• Basis for endocrine assays of pregnancy
• Syncytiotrophoblast produce P-hCG in amounts that increase exponentially during the
first trimester following implantation
• Main function is to prevent involution of the corpus luteum (principal site of
progesterone formation during first 6 weeks of pregnancy)
A. Biochemistry of hCG
• Glycoprotein with high carbohydrate content
• Heterodimer composed of two subunits: alpha and beta
• Alpha-subunit: identical to LH, FSH, and TSH
• Beta-subunit: used as a basis for pregnancy detection
B. P-hCG Detection
• Detected in maternal serum or urine by 8 to 9 days after ovulation
• In normal pregnancy, the serum hCG "doubles" its level of concentration every 1.4 to
2.0 days and reaches peak levels at 60-70 days
• Not observed in cases of miscarriages, ectopic pregnancies, or molar gestations
• Concentration declines slowly until a nadir at approximately 18-20 weeks
E t d /3hCGL I . P , (Th RG t· St d )
GESTATIONAL
AGE
I MEDIAN {RANGE) I GESTATIONAL
AGE
I MEDIAN (RANGE)
A. Gestational Sac
• Small anechoic fluid collection within the endometrial cavity
• The first sonographic evidence of pregnancy
• Seen with TVS by 4 to 5 weeks gestation
• Implants eccentrically in the endometrium
42
B. Potential Indicators of Early Intrauterine Pregnancy:
0 lntradecidual sign: anechoic center surrounded by a single echogenic rim; OR
0 Double decidual sign: two concentric echogenic rings surrounding the gestational sac:
I
decidua parietalis and decidua capsularis
.
~·~, A Fetal pole
B Yolk sac
:~·,
:j,)#• C
D
E
Gestational sac
Decidua capsularis
Decidua parietalis
• Yolk sac: brightly echogenic ring with an anechoic center (confirms an intrauterine
location for the pregnancy and seen by middle of 5th week)
• Embryo: >6 weeks, linear structure adjacent to yolk sac, cardiac motion noted at this point
• Double decidual sign: (1) decidua capsularis (inner), (2) decidua parietalis (outer)
• Crown-rump length (CRL): up to 12 weeks AOG, predictive of gestational age within 4 days
I. OBJECTIVES
OF PRECONCEPTIONAL
CARE
• Improve knowledge, attitudes, & behaviors related preconceptional health
• Assure that all women of childbearing age receive preconceptional care services
(including evidence-based risk screening, health promotion, & interventions) that will
enable them to enter pregnancy in optimal health
• Reduce risks indicated by a previous adverse pregnancy outcome through
interconceptional interventions to prevent or minimize recurrent adverse outcome
• Reduce the disparities in adverse pregnancy outcomes
Source:ACOG;2017and SMFM;2014
44
II. MEDICALHISTORY
• General points include how pregnancy will affect maternal health and how a high-risk
condition might affect the fetus
Diabetes
mellitus
I REMARKS ;
Source:Cunningham,
FG.WilliamsObstetrics25thEdition;2018
American Academyof Neurology;2005
POGSPracticeBulletinNo.1,ThirdUpdate,August2021
45
III. GENETICDISEASES
• Congenital conditions that clearly benefit from patient education include neural-tube defects
(NTDs), phenylketonuria (PKU), thalassemia and other common genetic diseases
• Pedigree construction is the most thorough method for obtaining a family history as a
part of genetic screening
• Health and reproductive status of each "blood relative" reviewed for medical illnesses,
mental retardation, birth defects, infertility, and pregnancy loss
GENETIC
DISEASE
I REMARKS
IV.REPRODUCTIVEHISTORY
• Information should be sought regarding the following:
0 Infertility
0 Abnormal pregnancy outcome: miscarriage, ectopic pregnancy & recurrent pregnancy loss
0 Obstetrical complications: cesarean delivery, preeclampsia, placental abruption &
preterm delivery
0 Identification of a genetic abnormality in stillbirth
46
V.SOCIALHISTORY
A. Alcohol Intake
CONDITION I CRITERIA
Documented
Prenatal Alcohol
Exposure
• One or more required:
• ~6 drinks per week for ~2 weeks
0
0
~3 drinks per occasion for ~2 occasions
Risk identified with a validated screening questionnaire
Laboratory testing indicating alcohol intoxication or positive
alcohol-exposure biomarker
I
.
B.Smoking
• Affects the fetus in a dose dependent manner
• Increases risk of preterm labor, fetal growth restriction, and low birthweight
0Associated with increased risk for attention-deficit/hyperactivity disorder (ADHD)
and behavioral and learning problems
0Increases risk for uteroplacental insufficiency and placental abruption
C. Environmental Exposures
0 Infections: Cytomegalovirus, Respiratory Syncitial virus, Parvovirus, Rubella
• Heavy metals & organic solvents (e.g., industrial workers)
0 Pesticide & contaminated well water (e.g., women in rural areas)
D.Diet
• Craving for and consumption of ice, laundry starch, clay, dirt or
other non-food items
Pica • Should be discouraged due to its inherent replacement of healthy
food with nutritionally empty products
• Considered to be triggered by iron deficiency in some women
• Encourage intake of protein-rich food: egg, cheese, soy, legumes,
Vegetarian diets
etc.
• Associated with preeclampsia, gestational diabetes, labor
Obesity
abnormalities, cesarean delivery and operative complications
• Increase maternal risk of nutritional deficiencies, electrolyte
Anorexia and disturbances, cardiac arrhythmias and gastrointestinal pathology
bulimia • Greater risk of low-birthweight, small head circumference,
microcephaly, and small for gestational age
47
E. Recreational Drugs
DRUG I FEATURES AND EFFECTS
• Small-for-gestational age, hypertensive complications, placental
Amphetamines
abruption, preterm birth, stillbirth, behavioral abnormalities
• Maternal effects: cerebrovascular hemorrhage, myocardial damage,
and placental abruption
Cocaine • Fetal effects: cleft palate, cardiovascular abnormalities, urinary tract
anomalies, fetal-growth restriction, preterm delivery, behavioral
abnormalities and cognitive impairments
• Spina bifida, gastroschisis, cardiac abnormalities with
Opioids- periconceptional opioid exposure
Narcotics • Heroin addiction is associated with preterm birth, placental
abruption, fetal-growth restriction, and fetal death
• Cannabinoids are not considered to be major teratogens, but may
Marijuana
disrupt normal fetal brain development
Phencyclidine • Not associated with congenital anomalies
(PCP) or angel • Newborns experience withdrawal symptoms (e.g., tremors,
dust jitteriness, and irritability)
• Common solvent used in paints and glue
• Toluene embryopathy is phenotypically similar to fetal alcohol
Toluene syndrome
• Pre- & postnatal growth deficiency, microcephaly, midface hypoplasia,
short palpebral fissures, wide nasal bridge, & developmental delays
• Contains a complex mixture of nicotine, cotinine, cyanide, thiocyanate,
carbon monoxide, cadmium, lead, and various hydrocarbons
• Fetotoxic and may have vasoactive effects or reduced oxygen levels
• Associated with cardiac anomalies (dose-related), hydrocephaly,
Tobacco
microcephaly, omphalocele, gastroschisis, cleft lip and palate, and
hand abnormalities
• Electronic nicotine delivery systems have adverse effects on fetal
brain and lung development
Source:StillermanKP.et al. ReprodSci;2008
ACOG;2017
48
SECTION
PRENATAL CARE
_O_V_E_R_V_IE_W_O_F_P_R_E_N_A_I_'A_L_C_A_R_E
__ -_-_-_-_-_-_-_-_·-_-_
THREE
..._-_-_-_-_-_-_-_-_-_-_-_-•
• Prenatal care refers to healthcare provided to a woman during pregnancy
I
• It refers to early and ongoing risk assessment to prevent, recognize, and treat conditions
associated with maternal and neonatal morbidity and mortality
• Refers to a series of clinical visits and ancillary services designed to promote the health
and well-being of the mother, fetus, and family
I. GOALSOF PRENATALCARE
• It should provide opportunities for the following:
Physician and patient to be better acquainted
0 Learn something about the patient's emotional attitude toward pregnancy and labor
Instruction for the patient and her husband in optimal care for herself & the coming baby
Optimal instruction of the patient and her husband in a prepared childbirth program
COMPONENT 'FIRST~
VISIT
History
Complete history ✓
Updated history ✓ ✓ ✓
PhysicalExam -
Complete examination ✓
Blood pressure ✓ ✓ ✓ ✓
Maternal weight ✓ ✓ ✓ ✓
Fundal height ✓ ✓ ✓ ✓
49
IV.OVERVIEWOF THE COMPONENTS OF ROUTINE PRENATALLABORATORYTESTS
✓ ✓
Antibody screen ✓ A
Pap smear ✓
Urine culture 3 ✓
Rubella serology ✓
Syphilis serology ✓ C
Gonococcal screening D D
Chlamydia! screening ✓ C
Hepatitis B serology ✓ D
HIVserology B D
Tuberculosis screening•
Preeclampsia screening 5 F
A Pertormat28weeks
BTestshouldbeoffered
C High-risk
women shouldberetested
atthebeginningofthethirdtrimester
D High-risk
women shouldbescreenedatthefirstprenatal
visitagaininthethirdtrimester
E Rectovaginal
culture
should
beobtainedbetween 35to37weeks
F Pertorm
at11to13617weeks
5 Allpregnant
women should
bescreenedforearlypreecampsia
usingmaternal
riskfactors,
maternal
uterine
arteryevaluation,
and
serumbiomarkers growth
[placental factor(PIGF)
andpregnancy-associated
plasma protein
A (PAIPP-A))
Source:Cunningham.FG.WilliamsObstetrics25thEdition.2018
POGSCPGon GestationalDiabetesMellitus,2018
PhilippineCPGon the Diagnosisand Management
of UTIin Adults;2015
50
INITIAL PRENATAL EVALUATION
• Major goals include:
Define the health status of the mother and fetus
• Estimate the gestational age
• Initiate a plan for continuing obstetrical care
I. PREVIOUSAND CURRENTHEALTHSTATUS
COMPONENT I
• Name, age, status
REMARKS
I
.
51
II. OBSTETRICAND GYNECOLOGICAL
HISTORY
COMPONENT I REMARKS
• Last normal menstrual period (LNMP)
Menstrual
• Previous menstrual period (PMP)
history
• Presence of associated pain (dysmenorrhea, Mittelschmerz)
Contraceptive • Failure of current method
use • Previous methods, including complications, reasons discontinue
Cervical • Most recent Pap smear result
and vaginal • History of abnormal Pap smear: nature of diagnosis, treatment, and
cytology follow-up
• History of sexually transmitted infections
Infections • History ofvaginitis, including types, frequency, and treatment
• History of pelvic inflammatory disease
Fertility/ • Difficulty in conceiving in the past
infertility • Prior fertility evaluation and treatment
• Presence of sexual activity
• Types of relationships
Sexual history
• History of dyspareunia
• Sexual dysfunction of both patient and partner
• Describe each pregnancy and the outcome.
• Describe any maternal, fetal, or neonatal complications
Obstetrical
• 08 Score is expressed with Gravidity, Parity followed by (Ierm -
history
£reterm -Abortion - Living children)
• History of antenatal visits: place and how many visits
52
IV. GENERAL PHYSICAL EXAMINATION*
Vital signs & • Blood pressure, pulse and hea1t rate, temperature, respiratmy rate
general survey • Height and weight
HEENT
Breasts
• Conjunctiva for pallor (or signs ofanemia)
• Physiologic enlargement of the thyroid gland in pregnancy
• Chloasma or melasma ("mask of pregnancy": darkening of the face)
• Check for breast symmetry or skin retractions in the breast
• While patient is sitting up, examine the axilla & area above clavicle
I
.
for lymphadenopathy
• Ask patient to lie down and palpate the breasts
Lungs • Check for adventitious breath sounds
• Because of the enlarging abdomen, the apex beat changes in location
(lateral and upwards)
• Normal changes in heart sounds:
0 Exaggerated splitting of S1
0 No change in S2
V. ABDOMINAL EXAMINATION
A. Listening to the Fetal Heart Tone (FHT)
0 Locate where the fetal tone is heard best
0 Best place to locate the heart tone is along the fetal back
° Fetal heart rate (FHR): normally 110-160 beats per minute (bpm) with 10-15 bpm
variability from second to second
0 Inability to hear fetal heart sound should be investigated with formal ultrasound
53
Measuring the Fundal/Fundic Height
0 Measured along abdominal wall from the top of the symphysis pubis to the top of the fund us
0 Bladder must be emptied before fundal measurement
0 Between 20 and 34 weeks gestation, the height of the uterine fund us measured in
centimeters correlates closely with gestational age in weeks (e.g., at 28 weeks, the
fundic height is expected to be 28 cm)
Step 1: Palpate the fund us of the uterus prior to placement of the tape measure
~
,_-w,,>---'~
~~
~
Walk fingers up along Find the fundus Curve fingers
the side of the abdomen (hard ball under skin) into the belly
r~_o:~i:hysis
t~_'\@ of the abdomen
as long as the
'~~~~.
uterus is gently
pushed to the
~l
\W,j, ~
midline to obtain
the fundal height
54
C. Performing the Leopold Maneuvers (LM)
• Fetus can usually be palpated through the anterior abdominal and uterine walls
• Leopold maneuvers determine the fetal position
I
° Findings provide information about the presentation and position of the fetus and the
extent to which the presenting part has descended into the pelvis
~
fund us with the tips of the fund us (large, nodular mass
fingers of both hands in the fundus)
1 • Examiner palpates fundal • Breech presentation: the
area & distinguishes between head [hard and round
the irregular, nodular breech ballotable head) is in the
[buttocks) versus the round fund us
mobile and ballotable head
55
Example: Left Anterior Occiput. The occiput (posterior fontanel) is facing the left abdominal
side of the mother and near the pubis symphysis (anterior)
LMl: breech LM2: fetal back on LM3: maybe LM4: cephalic
(buttocks) occupies mother's left side engaged or not prominence on right
the fundus
~
VI. PELVICEXAMINATION
~N(~) ~
• A pelvic examination is performed with special attention to the uterine size & adnexa
• In late pregnancy, vaginal examination often provides valuable information:
° Confirmation of the presenting part and its station
° Clinical estimation of pelvic capacity and its general configuration
Amnionic fluid volume adequacy
Cervical consistency, effacement, and dilatation
External • Look for lesions and swellings
genitalia • Discoloration of skin
• Vagina:
• Assess for vaginal discharge, anomalies (e.g., septum), and masses
• Chadwick sign: violaceous discoloration due to increased blood flow
Speculum • Cervix:
examination • Bluish-red passive hyperemia of the cervix may be noted in pregnancy
• Nabothian cysts may be prominent
• Pap smear may be done and specimen obtained to check for Chlamydia and
Neisseria gonorrhea, if indicated
56
VII. PREGNANCYRISKASSESSMENT
• Purpose: identify pregnant women who are at an increased risk of maternal or fetal
morbidity and mortality
I
• Some conditions for which maternal-fetal medicine consultation may be beneficial include:
MEDICAL HISTORY I OBSTETRICAL HISTORY
• Moderate to severe cardiac disorders • COE (Rh) or other blood group .
• Uncontrolled chronic hypertension alloimmunization (excluding ABO, Lewis)
• Prior venous thromboembolism • Fetal structural or chromosomal
• Renal insufficiency abnormality
• Severe restrictive or obstructive • Desire or need for prenatal diagnosis or
pulmonary disease (e.g., severe asthma) fetal therapy
• Diabetes mellitus with end-organ damage • Periconceptional exposure to teratogens
or uncontrolled hyperglycemia • Infection with or exposure to organisms
• Family/personal history of genetic that cause congenital infection
abnormalities • Higher-order multifetal gestation
• Hemoglobinopathy • Amniotic fluid volume severe disorders
• Autoimmune disorders or other severe
systemic disease
• Poorly controlled or complicated epilepsy
• Others: HIV infection, cancer, bariatric
surgery
Source:Cunningham,
FG.WilliamsObstetrics25thEdition.2018
PRENATAL SURVEILLANCE
I. FETALSURVEILLANCE:
• Includes fetal heart rate, size (current & rate of change), amniotic fluid, presenting part
and station (late in pregnancy), and activity
II. MATERNALSURVEILLANCE:
• Vital signs: blood pressure, weight
• Check for symptoms, including headache, altered vision, abdominal pain, nausea and
vomiting, bleeding, vaginal fluid leakage, dysuria
• Abdominal exam (e.g., fundal height)
• Vaginal exam (e.g., confirm presenting part & station, pelvic capacity, and cervical
consistency, effacement and dilatation)
57
DATING OF PREGNANCY
• Pregnancy begins with the fertilization of ovum (exact time is usually unknown)
• Accurate determination of gestational length is one of the most important functions of
prenatal care
• The mean duration of pregnancy calculated from the first day of the last normal
menstrual period is very close to 280 days or 40 weeks
I. CLINICALDATING
A. Determining Age of Gestation (AOG) using the Last Normal Menstrual Period (LNMP)
Age of gestation or gestational age (AOGor GA),which is the approximate age of the
0
Example: Date Consulted: May 27 2021; EDC:June 28 2021; LNMP: September 21, 2020
09/21/20 (LNMP)
9/ 21-30/20 (from Sept 21-30) = 10 days
September = 10 days
October = 31
November = 30
December = 31
January = 31
February = 28
March = 31
April = 30
May = 27 (from May 1,2021 up to time of consult)
249 days
249 days divided by 7 days = 36 weeks and 4 days--+ AOG during consult
58
B. Determining
0
0
Expected Date of Delivery (EDD) using LNMP
Most reliable clinical indicator of gestational age is an accurate LNMP
Average duration of pregnancy is 280 days from the first day of LNMP (40 weeks)
• It is apparent that pregnancy begins on the average 2 weeks before ovulation
N-_a--'eg"-e_l_e_R_u_l_e
_____________________________ .,
I
•
• Estimation of pregnancy due date: add 7 days to the first day of LNMPand subtract 3
months then add 1 year
• Example: first day ofLNMP is September 21, 2020 ----+ due date is June 28, 2021
• When using this, we assume that ovulation and conception on the 14th day of a 28 day cycle
Expected Date of Delivery (EDD)
• To the first day of the last normal menstruation, add seven days, subtract three months
and add one year
LNMP
0
, +7 to the day
, -3 months
+l year
0
Examples:
LNMP was June 29, 2020 LNMP was July 10, 2020 LNMP was January 1, 2021
(6/29/2020) (7/10/2020) (01/01/2021)
duration of pregnancy
Used as a confirmation method rather than a primary method
0
59
D. Height of the Fundus
0 Progressive enlargement of the uterus can be followed during pregnancy
0 Height of the fundus can be used to estimate the gestational age
GESTATIONAL AGE I HEIGHT OF THE FUNDUS
12 weeks after LNMP • Above the pubic symphysis
16 weeks after LNMP • Halfway between symphysis and the umbilicus
20 weeks after LNMP • Level of the umbilicus
36 weeks after LNMP • Below the ensiform cartilage (xiphoid process)
II. ULTRASOUNDDATING
• Most reliable method for establishing fetal dating especially when the mother is unsure of
menses or the mother has irregular menses
• Ultrasound dating is most accurate in the first 12 weeks of pregnancy (1st trimester)
• The earlier sonography is performed, the more accurate the gestational age assessment
• Sonographic gestational age should be used when the LNMP-derived gestational age
differs from that obtained with sonography by the threshold value
Examples:
• Example 1: based on LNMP,AOG is 9 weeks; but based on a CRL,AOG is only 7 117 weeks:
since the difference is >5 days between the LMP and ultrasound dating, we follow the
ultrasound dating
• Example 2: based on LNMP (mother is sure of last menses & has regular menstrual cycles),
AOG is 14 weeks and based on BPD via ultrasound, AOG is 13 5/ 7 weeks: we can still use 14
weeks because the difference between the two measurements is less than 7 days
Source:ACOG;2017
60
NUTRITIONAL COUNSELING IN PREGNANCY
I. BASICTENETS FOR NUTRITIONPLAN
I
• Advise the pregnant woman to eat food types she wants in reasonable amounts and
salted to taste
• Ensure that food is amply available for socioeconomically deprived women
• Monitor weight gain, with a goal of ~25-35 lbs in women with a normal BMl
• Explore food intake by dietary recall periodically to discover the occasional nutritionally
.
errant diet
II. WEIGHTGAIN
• This table shows the body mass index (BMl) cut-off from the World Health Organization
(WHO), Institute of Medicine (!OM) and the American College of Obstetricians and
Gynecologists (ACOG)
• This table also shows the expected weight gain per week starting 2nd trimester, and the
total weight gain expected during the whole duration of pregnancy
Category
1•..(WHO)
.,,,.;,,. I {ACOG)
BMl I To<al
weight
I To<al
weight
I wo;gtrt ga;o ,.,
wee~
(kg/m 2 ) (kg/m 2 ) . (k ) . (lb ) (2nd-3rd trimester)
gain g gain s (lbs)
Ill. NUTRITIONALREQUIREMENTS
A. Calories and Protein
Formula:
Total Energy Requirement (TER) = Desirable body weight (DBW) x Activity level
61
Total Energy Intake for Gravida (kcal/kg/day)
ACTIVITY LEVEL I UNDERWEIGHT I NORMAL I OVERWEIGHT
Sedentary (mostly sitting) 35 30 25
Light (driver, nurse, MD) 40 35 30
Moderate (manual labor) 45 40 35
Very active (farming) --- 45 ---
Source:POGSCPGon MaternalNutrilion
& Supplementation,
2018
Example: Filipino, call center agent (sedentary), Normal BM/, Height =163 cm
DBW= height (cm) - 100 = 163 - 100 = 63 kg
Since patient is a Filipino: 63 kg- 6.3 (which is 10% of 63 kg)= 56.7 kg
TER = Desirable body weight (DBW) x Activity level
= 56.7 kg x 30 (activity level for a sedentary patient with normal BMI)
= 1,701 kcal
Since the patient is pregnant, add 100 to 300 kcal/day to TER
1,701 kcal (TER) + 300 kcaljd = 2,001 kcal/day
Pregnant:
TER + 300 kcal/kg/day
6-15 15-30 55-75
Lactating:
TER + 500 kcal/kg/day
Source:POGSCPGon MaternalNutrition
& Supplementation,
2018
IV. SUPPLEMENTATION
A. Minerals
MINERAL I DOSE
I REMARKS
• Calcium carbonate 500 mg • Target group: all pregnant women,
Calcium (elemental calcium) tablet, 3x a day particularly those at higher risk for
at 20 weeks AOG gestational hypertension
• 12 mg/day, but safe level for
• Deficiency: poor appetite, suboptimal
Zinc pregnant women not been clearly
growth, and impaired wound healing
established
• Use of iodized salt in preparing food
• 220 ug/day or 250 ug/day for • Sources: di/is, pusit, kuhol, lato, ta/aha,
Iodine
pregnant & lactating women tahong, alamang shrimps, crab
• Deficiency: cretinism, neurologic deficits
Source:DOHMemoNo.2016-0161Calciumsupplementation
for PregnantWomen
POGSCPGon MaternalNutrition& Supplementation,2018
RA8172:ASINLawof 1995
62
B. Iron Supplementation
, Give tablets of simple iron salts that provide at least 27 mg of elemental iron daily
, Recheck the hematocrit or hemoglobin concentration at 28 to 32 weeks' gestation to
I
detect significant anemia
INDICATION FOR DOSAGE
CATEGORY
Childbearing
I SUPPLEMENTS
I SCHEDULE I DURATION
.
• Anemia prevalence
• 3 months
age >40%
• Elemental iron: • As soon as possible
30-60 mg/day after gestation
• Universal
Pregnant • Folic acid: • Starts no later than 3rd
supplementation
400 mcg/day month and duration of
pregnancy
• Anemia prevalence
Lactating • 3 months postpartum
>40%
GROUP I RECOMMENDATION
Source:POGSCPGon MaternalNutrition
& Supplementation,
2018
63
D. Other Vitamins
~
RATIONALE FOR RECOMMENDED
VITAMIN
I NUTRIENT INTAKE (RNI)
64
COMMON CONCERNS
• In the absence of complications, most women can continue to work until
I
the onset of labor
• With physically demanding work, women had 20-60% higher rates of
Employment
preterm birth, fetal-growth restriction, or gestational hypertension
• Advise women with prior pregnancy complications that commonly recur .
to minimize physical work
• Encouraged to engage in regular, moderate-intensity physical activity for
at least 150 minutes each week
• Safe activities: walking, running swimming, stationary cycling, and low-
impact aerobics
• Contraindications to exercise during pregnancy:
Exercise
, Significant cardiovascular or pulmonary disease
, Significant risk for preterm labor: cerclage, multiple gestation,
ruptured membranes
, Obstetrical complications: preeclampsia, placenta previa, fetal growth
restriction
• Pregnant and lactating women are advised to avoid specific types of fish
Seafood
with potentially high methylmercury levels like shark, swordfish, king
consumption
mackerel, and tile fish
Lead • Significant lead exposure is associated with gestational hypertension,
screening miscarriage, low birthweight, and neurodevelopmental impairments
• Properly positioned three-point restraints against automobile crash injury:
, Lap portion of the restraining belt is placed under the abdomen and
across her upper thighs
Automobile &
, Belt should be comfortably snug
air travel
, Shoulder belt is firmly positioned between the breasts
• Pregnant women can safely travel by air up to 36 weeks AOG,in the
absence of obstetrical and medical complications
• Sexual intercourse usually is not harmful, specifically late in pregnancy.
Coitus • Whenever miscarriage, placenta previa, or preterm labor threatens,
coitus is avoided
• Examination of the teeth is included in the prenatal examination, and
Dental care good dental hygiene is encouraged
• Periodontal disease has been linked to preterm labor
• Caffeine intake during pregnancy be limited to <300 mg/day, which
Caffeine
approximates three 5-oz cups of percolated coffee
• Two types of cord blood banks:
, Public: promote allogenic donation, for use by a relative or unrelated
Cord blood
recipient, similar to blood product donation
banking
, Private: store stem cells for future autologous use and charged fees for
initial processing and annual storage.
Source:Cunningham,
FG.WilliamsObstetrics25thEdition;2018
AmericanDieteticAssociation:2008
ACOG;2016and2017
Armson;2015
65
IMMUNIZATION FOR FILIPINO PREGNANT WOMEN
I. GENERALCONSIDERATIONS FORVACCINATION
• Never administer in the buttock.
• Confirm completion of childhood (or more recent) primary vaccine series for measles,
mumps, rubella (MMR) and Tetanus-Diphtheria (Td) before initiating recommended
vaccine schedules.
• Maintain vaccine administration record in patient's chart
Simultaneous use of any vaccines is not contraindicated
• Antibiotic therapy or breastfeeding are not contraindications to vaccination
• 3 doses: 0, 1, 6 months
• Hepatitis B vaccine IM • Booster not routinely
recommended
Pregnant
• 3 doses: 0, 1, 6-12 months
0 1st dose: Td
• Tetanus-diptheria (Td)
toxoid
IM 0 2nd dose: Tdap
0 3rd dose: Td
• 3 doses: 0, 1, 6 months
• Hepatitis B vaccine IM
• Booster not routinely recommended
66
III. IMMUNIZATIONFORPREGNANTWOMEN
INDICATIONS
DURING
PREGNANCY I SCHEDULE
I REMARKS
IV.GENERALCONTRAINDICATIONS TO VACCINATION
• Severe allergy to vaccine components
• Pregnancy (or planning pregnancy within four-weeks) for live attenuated vaccines (e.g.,
measles, mumps, rubella, varicella)
• Severe immune attenuation (for live attenuated vaccines only)
• Moderate or severe acute illness
• If a live attenuated vaccine is given simultaneously with another vaccine, a four week
separation interval should be used between vaccinations.
67
SECTION FOUR
ANTENATAL SURVEILLANCE
OVERVIEW OF ANTEPARTUM FETAL SURVEILLANCE
I. INDICATIONS
• Generally, these tests are used in pregnancies with a high risk of antepartum complications
• Some conditions include the following:
MATERNAL CONDITIONS I PREGNANCY-RELATED CONDITIONS
• Antiphospholipid antibody syndrome • Pregnancy-induced hypertension
(APAS), SLE • Decreased fetal movement
• Hyperthyroidism, poorly controlled • Amniotic fluid volume abnormalities ( e.g.,
• Severe cardiac disease ( e.g., cyanotic oligo/polyhydramnios)
heart disease, hypertension) • Intrauterine growth restriction
• Post-term pregnancy
• Prior fetal demise
• Multiple gestation with significant growth
discrepancy
Source:PrebothM.ACOGguidelines.AmFam Physician;2000
II. TECHNIQUESFORANTEPARTRUMFETALSURVEILLANCE
• Electronic fetal monitoring
0 Non-stress test (NST)
° Contraction stress test (CST)
• Ultrasound modalities
0 Umbilical artery Doppler velocimetry
0 Biophysical profile (BPP)
I.PROCEDURE
• NST measures the FHR in response to fetal movements
• An external FHR monitor is positioned and the mother (or an observer) is asked to push a
button (i.e., event marker) each time she feels fetal movement
• NST involves 20 minutes of monitoring the FHR while assessing accelerations that
correlate with fetal movement
68
II. INTERPRETATIONOF THE NON-STRESS TEST
0
INTERPRETATION DESCRIPTION*
I
• ;o,2accelerations peak at ;o,15bpm, each at ;o,15secs, and all
Reactive NST
occurring within 20 minutes**
Nonreactive NST • Lacks sufficient FHR accelerations over 40 minutes .
'Presence of fetal movementsand FHRaccelerationis the most criticalfeature of the NST
.. An abnormalstress test is not alwaysominousand can occurwitha sleepingfetus. Ifa test is not reactive,FHR
shouldbe monitoredfor at least 40 minutesto accountfor the fetus sleep cycle
Source: PrebothM.ACOGgu1dehnes.AmFam Phys1c1an; 2000
I. PROCEDURE
• Fetal heart rate and uterine contractions are recorded simultaneously with an external monitor
• Contractions may be elicited using nipple stimulation or oxytocin infusion
Nipple stimulation: woman rubs her nipple through her clothing for 2 minutes or until
the contraction begins
Oxytocin: IV infusion is initiated at a rate of0.5 mU/min and doubled every 20 minutes
until a satisfactory CST result is established
• See definitions of FHR decelerations in Chapter 3
I
UMBILICAL ARTERY FLOW
FETUS
VELOCITY WAVEFORM
Normally growing fetus • High-velocity diastolic flow
Intrauterine growth restriction • Diminished diastolic flow
Extreme intrauterine growth restriction • Absent or reversed flow
69
BIOPHYSICAL PROFILE (BPP)
• It is a combination of five fetal biophysical variables:
Fetal heart rate acceleration (NST)
Fetal breathing
Fetal movements
Fetal tone
0 Amniotic fluid volume (AFV)
• Normal variables are assigned a score of 2, and abnormal variables are assigned a score of 0
II. INTERPRETATION
OF THE BPP
BPPSCORE I INTERPRETATION I RECOMMENDED MANAGEMENT
• No intervention
• Repeat test weekly except in diabetic
10 patients and postterm pregnancy
• Normal, non- (twice weekly)
NST not done (8/8)
asphyxiated fetus
• No intervention
But with normal AFV • Repeat testing per protocol
8 (8/10, AFVnormal}
But with low AFV • Suspected chronic
• Deliver
(8/10, AFV is zero) fetal asphyxia
• Deliver if:
• AFVabnormal
• Possible fetal • Normal AFV>36 weeks with
6 asphyxia favorable cervix
• Repeat test ,;6
• Repeattest >6:observe&repeat per protocol
• Probable fetal • Repeat testing on the same day
4 asphyxia • If BPP score :,6: deliver
• Almost certain
0-2 fetal asphyxia
• Deliver
: ,,
5. AmeriranCollegeofObstetridans and Gynecologists:Fetalgrowth restriction.PracticeBulletinNo.134,May2013,Reaffinned2015 ·_ •
6. AmericanCollegeofObsteOiciansand Gynecologists: Nauseaand vomitingof pregnancy.PracticeBulletinNo.153,September2015c
7. AmericanC.Ollegeof CommitteeOpinionNo700: Methodsfor Estimatingthe DueDate.ObsretGynerol2017; 129:e150.
Obstetriciansand Gynecologists.
8.American Institute of Ultrasound in Medicine (AIUM):Official statements. Prudent use in pregnancy. 2012. Available at http://v ..rww.
aium.org/fficialStatements/33.
9.American Institute of Ultrasound in Medicine (AIUM):Practice guideline for the performance of fetal echocardiography. J Ultrasound
Med 32[61'\067, 2013a
10. Bertrand], Floyd LL,Weber MK;Fetal Alcohol Syndrome Prevention Team, Division of Birth Defects and Developmental Disabilities,
National Center on Birth Defects and Developmental Disabilities, Centers for Disease Control and Prevention (CDC).Guidelines for
identifying and referring persons with fetal alcohol syndrome [published correction appears in MMWRMorb Mortal Wkly Rep. 2006
May 26;55[20)568]. MMWR Recomm Rep. 2005;54(RR-11}:1-14.
11. Bilardo CM,WolfH, Stigter RH,et al: Relationship between monitoring parameters and perinatal outcome in
12. Callahan, Tamara L.(2013). Blueprints obstetrics &gynecology. Baltimore, MD :Lippincott Williams & Wilkins
13. Centers for Disease Control and Prevention: Guidelines for vaccinating pregnant women. 2016. Available at: http://www.cdc.gov/
vaccines/pubs/downloads/b_preg_guide.pdf. Accessed February 2, 2021
14. Centers for Disease Control and Prevention: Updated recommendations for use of tetanus toxoid, reduced diphtheria toxoid, and acellular
pertussis vaccine (Tdap) in pregnant women-Advisory Committee on Immunization Practices {ACIP),2012. MMWR62(7):131, 2013b
15. Clark SM, Dutta E, Hankins GD:The outpatient management and special considerations of nausea and vomiting in pregnancy. Semin
Perinatol 38(8):496, 2014
16. ClinicalPracticeGuidelineson DiabetesMellitusin PregnancyThird Edition 2018. PhilippineObstetricaland Gynecological
Societyfoundation, Inc.
17. Cunningham, F.G., Leveno, K J.,Bloom, S. L.,Spong. C. Y.,Dashe, J.S., Hoffman, B. L.,Sheffield,J.S. (2018). Williams obstetrics (25th
edition.). New York: McGraw-HillEducation.
18. Development workshop report on electronic fetal monitoring: update on definitions. interpretation, and research guidelines. Obstet
Gynecol 112:661, 2008
19. FirthHY,BoydPA.01amberlainP,etal: Severelimbabnomialitiesafter chorionvillussamplingat 56-66 days'gestation lancet 337(8744):762,1991
20. Freeman RK:The use of the oxytocin challenge test for antepartum clinical evaluation of uteroplacental respiratory function. Am J
ObstetGynecol 121:481, 1975
21. Hoyme HE, May PA,Kalberg WO,et al. A practical clinical approach to diagnosis of fetal alcohol spectrum disorders: clarification of the
1996 institute of medicine criteria. Pediatrics. 2005;115(1):39-47. doi:10.1542/peds.2004-0259
22. Hsieh FJ,Shyu MK,Sheu BC,et al: Limb defects after chorionic villus sampling. Obstet Gynecol 85( 1):84, 1995
23. Institute of Medicine and National Research Council: Weight Gain During Pregnancy: Reexamining the Guidelines. Washington, The
National Academic Press. 2009
24. Institute of Medicine: Dietary Reference Intakes: The Essential Guide to Nutrient Requirements. Washington, The National Academies
Press, 2006 [PubMed: N8K50960) [PubMed: 2388168]
25. Korevaar; T. I.,Steegers, E.A., de Rijke,Y.8., Schalekamp-Timmennans, S., Visser;W. E., Hofman, A..Jaddoe. V.W.,Tiemeier, H.,Visser;T.
J.,t..tedici,M.,& Peeters, R.P.(2015). Reference ranges and determinants of total hCGlevels during pregnancy: the Generation RStudy.
European journal of epidemiology, 30(9), 1057-1066. https://doi.org/10.1007 /s10654-015-0039-0
26. Lu, M. C.. & Lu, J.S. (2008). Prenatal Care. Encyclopedia of Infant and Early Childhood Development, 591-604. doi:10.1016/b978-
012370877-9.00127-4
27. Macones GA,Hankins GD,Spong CY,et al: The 2008 National Institute of Child Health and Human
28. Manning FA,Morrison I, Lange IR, Hannan CR,Chamberlain PF. Fetal biophysical profile scoring: selective use of the nonstress test.
Am J Obstet Gynecol. 1987;156(3),709-712. dod0.1016/0002-9378(87)90083-4
29. ManningFA.PlattW,SiposL:Anteparturnfetalevaluation:developmentofafetalbiophysicalprofile.Am J ObstetGyneml136:787,1980
30. Matthews A, Haas DM,O'Mathuna DP,et al: Interventions for nausea and vomiting in early pregnancy. Cochrane Database Syst Rev
Mar 3:CD007575, 2014
31. NijhuisJG, Prechtl HF,Martin CBJr;et al: Are there behavioural states in the human fetus? Early Hum Dev 6:177, 1982
32. OepkesD,SeawardPG,VandenbusscheFP,etal: Dopplerultrasonographyversusamniocentesisto predict fetalanemia N EnglI Med355:156,2006
33. Philippine Clinical Practice Guidelines on the Diagnosis and Management of Urinary Tract Infections in Adults 2015 Update
34. Philippine Obstetrical and GynecologicalSocietyClinicalPractice Guidelineon Diabetes Mellitus in Pregnancy November2018
35. Preboth M. ACOGguidelines on antepartum fetal surveillance. American College of Obstetricians and Gynecologists. Am Fam
Physician. 2000 Sep 01;62[5),1184, 1187-8
36. SadovskyE,EvronS,WeinsteinD:Dailyfetalmovement recording in nonnal pregnancy.RivObstetGinecolPracticaMed Perinatal59:395, 1979a
37. Severe, early intrauterine growth restriction. Ultrasound Obstet Gynecol 23:199, 2004
38. Stillennan KP,Mattison DR. Giudice LC,Woodruff TJ. Environmental exposures and adverse pregnancy outcomes: a review of the
science. Reprod Sci. 2008;15(7):631-650. doi:10.1177 /1933719108322436
39. Sumpaico,W, Ocampo-Andres, I., Blanco-Capito LR.de las Alas-Camero, S. Diamante An, Gamilla ZN. (2008). Textbook of Obstetrics
3rd edition. Chapter 15 Diagnosis of Pregnancy
40. Todros T.Sciarrone A, Piccoli E,et al: Umbilical Doppler waveforms and placental villous angiogenesis in pregnancies complicated by
fetal growth restriction. Obstet Gynecol 93:499, 1999
71
LABOR
ANDDELIVERY
SECTION ONE
MECHANISMS OF LABOR
■
I. DEFINITIONS OF TERMS
TERM I DEFINITION -
Nulligravida • Woman who has never been pregnant
Prirnigravida • Woman who is pregnant for the first time
Multigravida • Woman who has had more than one pregnancy
• Woman whose pregnancy never reached the age of viability
Nullipara (nulliparous)
(2'20 weeks)
• Woman who delivered only one fetus beyond the age of
Prirnipara (prirniparous)
viability (2'20 weeks)
Multipara (rnultiparous) • Woman who delivered ;,2 fetuses beyond age of viability
II. STATION
• Station is the extent to which the most dependent portion of the presenting part has
descended into the pelvis
• Descent of the leading edge of the presenting part to the level ofischial spines (station 0)
is defined as engagement
• Station +S means the fetal head/skull is 5 cm below the ischial spine, in which the fetal
scalp is almost separating the labia (make sure it is not the caput that is presenting)
-5
-4
-3
-2
lschial spine
+2 -·-·-·-·-·-·-·-
+3 -·-·-·-·-·-•-·-
+4 -·-·-----·---·-
+5 -·-·-·---------
Anteriorfontanelle
Posterior (bregma)
fontanelle
Biparietal
diameter Glabella
Sagittal Posterior
Nasion fontanelle
suture
Anterior Bitemporal
fontanelle diameter
(bregma)
Occipitomental
diameter
Frontalsuture
76
C. Diameters
DIAMETER
I LENGTH
AVERAGE
FOR
I DESCRIPTION
TERM FETUS
Anteroposterior (AP) Diameters*
• Presenting AP diameter during flexion,
■
when the chin is in intimate contact with
.
·Suboccipitobregmatic • 9.5 cm the thorax
• Extends from occipital bone to the
anterior fontanelle
• Presenting AP diameter in a sinciput
presentation during initial descent
Occipitofrontal • 11 cm
• Extends from external occipital
protuberance to the glabella
• Presenting AP diameter in brow
presentation
Supraoccipitomental • 13.5 cm
• Longest AP diameter of the head
• Extends from the vertex to the chin
• Presenting AP diameter in face
presentations
Submentobregmatic • 9.5 cm
• Extends from neck/lower jaw to the
anterior fontanelle
Transverse Dit:,meters
• 9.5 cm • Largest transverse diameter
Bi parietal
• Extends between parietal bones
• 8 cm • Shortest transverse diameter
Bi temporal
• Extends between temporal bones
'The APdiameterpresentingto the maternalpelvisdependson the degree of flexionor extensionof the head. It
is importantbecause these diametershave varyinglengths
77
THE PASSENGER
• Orientation of the fetus within the uterus and in relation to the pelvic canal are essential
to a successful vaginal delivery
• Determining the correct fetal lie, presentation, attitude and position would aid in the
management of labor & delivery
• Establish the station or extent to which the presenting part has descended into the pelvis
I. FETALLIE
• Relation of the long axis of the fetus to that of the mother
• It may be longitudinal, transverse, or oblique
Source:Cunningham
FG,et al. WilliamsObstetrics25thEd;2018
78
II. FETALPRESENTATION(PRESENTINGPART)
• Portion of the fetal body that is either foremost within the birth canal or closest to it (i.e.,
part that lies closest to the pelvis and will enter the birth canal first)
• Felt through the cervix during internal examination
• May be cephalic, breech, shoulder, or compound presentation
TYPESOF
CEPHALIC
I DESCRIPTION
I PRESENTING
AP
I DIAGRAM
PRESENTATION DIAMETER*
shaped)
Brow
Presentation**
• Fetal head is only
partially extended
• Usually becomes a face
presentation as labor
• Occipito-
mental
(longest)
- -~-----
-
,
-
progresses - '. _P - , -
'.
TYPESOF
BREECH
PRESENTATION
I REMARKS I DIAGRAM
Source:Cunningham
FG,et al. WilliamsObstetrics25thEd;2018
C. Other Presentations
Shoulder Presentation I Compound Presentation
• Acromion processes palpated in the cervix • Fetal hand or foot prolapses alongside
• Shoulder/acromion is usually presenting the presenting vertex or breech
into pelvic inlet in transverse lie • Combination of hand with vertex or
• Fetal back location (back down, back up) breech: tends to resolve spontaneously
helps determine type of uterine incision • Combination of foot and fetal head:
during CS complicated by cord prolapse
80
III. FETALATTITUDE (POSTURE OF THE HABITUS)
• Characteristic posture in the later months of pregnancy
• It is the relation of the fetal parts to one another
, Fetus forms an ovoid mass that corresponds roughly to the shape of the uterine cavity
IV.FETALPOSITION
• Refers to the relationship ofan arbitrary point of the presenting part to the left or right
side of the maternal birth canal
• Steps in determining fetal position:
STEP I QUESTION
I ANSWER
• For vertex (occiput) presentation: occiput or posterior
fontanelle (soft triangular depression)*
• What is the
1 arbitrary point?
• For face presentation: fetal chin (mentum)
• For breech presentation: sacrum
• For shoulder: acromion (scapula)
• What is the • Right (arbitrary point towards the right)
2 position of the • Left (arbitrary point towards the left)
arbitrary point? • Transverse (arbitrary point located in the horizontal plane)
• What is the • Anterior (arbitrary point towards the symphysis pubis)
3 direction of the • Posterior (arbitrary point towards the sacrum)
arbitrary point? • Transverse (arbitrary point located in the horizontal plane)
'2/3 of the vertex(occiput)presentationare in the leftocciputposition(e.g., the occipitalforamenor the soft triangu-
Jardepressionis on the leftside). Otherexamplesfor the vertexpresentationare:
Leftocciputanterior(leftside, towardsthe abdomen)
Rightocciputtransverse(rightside, towardsthe middle)
Rightocciputposterior(rightside, towardsthe sacrum)
81
General Cance ts in Determinin Fetal Position
posterior
__
'0 _
, ~--. ____ -Left occiput
posterior
Right occiput
transverse
RIGHT LEFT
~
Left occiput
transverse
SACRUM
OP
ROP LOP
ROT LOT
OA
PUBIC SYMPHYSIS
Possible Positions
0 LOA: left occiput anterior
0 LOT: left occiput transverse
0 LOP: left occiput posterior
0 OP: occiput posterior
0 ROP: right occiput posterior
0 ROT: right occiput transverse
0 ROA: right occiput anterior
0 OA: occiput anterior
82
SOME EXAMPLES
Example 1: LEFT OCCIPUT ANTERIOR (LOA} POSITION
Pubic symphysis
I LM 1 LM 2
R L -
mg
Occiput
Sacrum
MANEUVER I FINDINGS
• The breech occupies the fund us which gives the sensation of a large,
LM 1 nodular mass
• The fetal back is felt as a hard, resistant structure on the left side of the
abdomen of the mother. The fetal back is directed anteriorly
LMZ • The fetal parts is felt as numerous small, nodular, mobile parts on the
right side of the abdomen of the mother
• The thumb and fingers of one hand grasp the lower portion of the
LM maternal abdomen just above the symphysis pubis
LM3 • The fetal head feels hard, round and more mobile. An unengaged fetal
head is easily dislodged and mobile on palpation
• The fetal back is felt on the left side of the abdomen while the cephalic
prominence is felt on the right side of the abdomen which describes a
LM4 normal fetal attitude
• Hands diverge if the head is engaged, while the hands converge if head is
not engaged
Internal • Posterior fontanelle (or occiput) occupies the left anterior quadrant (i.e.,
examination LOA)
• FHT heard over fetal back (in this case, the maternal left, since the fetal
Others
back is on the left side of the mother) and slightly below the umbilicus
Source:Cunningham
FG,et al. Williams
Obstetrics25thEd;2018
83
Example 2: LEFT SACROANTERIOR {LSA) POSITION
Pubic symphysis
l Fetal sacrum
Maternal sacrum
MANEUVER I FINDINGS
LM 1 • Fundus is occupied by the head
• Fetal back is oriented anteriorly and occupies the left side of the
maternal abdomen.
LM2 • Fetal heart tones heard over fetal back Hence, it is best heard on the left
LM side of the maternal abdomen near the umbilicus
• If not engaged, movable breech occupying the lower pole above the
LM3 symphysis
LM4 • If engaged, breech beneath the symphysis
Internal • Fetal buttocks can be palpated (in addition, meconium staining of the
examination examining finger may occur)
• Fetal heart tones heard over fetal back (in this case, the maternal left}
Others
and slightly above the umbilicus
Source:Cunningham
FG,et al. WilliamsObstetrics25thEd;2018
84
Example 3: LEFT MENTOPOSTERIOR(LMP)
Pubic symphysis
■
.
Sacrum Mentum
MANEUVER
I FINDINGS
• Fetal back is oriented anteriorly and occupies the right side of the
maternal abdomen
LMZ • Fetal heart tones heard over fetal back. Hence, it is best heard on the
right side of the maternal abdomen near the umbilicus
• The fetal head feels hard, round and more mobile
LM3 • An unengaged fetal head is easily dislodged and mobile on palpation
LM
• Helps identify the degree of descent and fetal attitude by facing the
mother's feet and the fingertips of both hands are positioned on either
side of patient's lower abdomen moving downwards to palpate the
LM4 presenting part
• The fetal back and the cephalic prominence is felt on the right side of the
abdomen which indicates an abnormal fetal attitude or a hyperextended
fetal head which indicates a face presentation
Internal • Fetal face palpated as irregular and soft
examination
• Fetal heart tones heard over fetal back (in this case, the maternal right)
Others
and slightly below the umbilicus
85
Example 4: LEFT OCCJPUT TRANSVERSE (LOT}
Occiput
MANEUVER I FINDINGS
• The fundus is occupied by the breech (buttocks/feet are in the fund us)
LM 1 • The breech is a large nodular mass
• The plane of the fetal back is on the mother's left side
LMZ • Fetal extremities (small, nodular, mobile parts) are located on the
maternal right side
LM • If the head is engaged, presenting part is not moveable (biparietal
LM3 diameter is through the pelvic inlet already)
• If head is not engaged, fetal head is easily dislodged on deep palpation
• Hands converge if head is not engaged
LM4 • Cephalic prominence on the right
• Fetal back is on the left
Internal • The sagittal suture occupies the transverse diameter of the pelvis
examination • The posterior fontanelle (triangular shaped) is on the left of the mother
• Fetal heart tone heard on the left side of the maternal abdomen at the
Others
level of the umbilicus
Source:Cunningham
FG,et al. Williams
Obstetrics25thEd;2018
86
THE PASSAGES (THE FEMALE BONY PELVIS)
• The pelvis is divided into the false pelvis (oflittle obstetric significance) and the true
pelvis (major portion of the birth canal)
• The descent of the fetus through the pelvis occurs through three important planes:
0Pelvic Inlet: the superior strait
0Midpelvis: plane of least pelvic dimensions
0Pelvic Outlet: the inferior strait
1
rll_lu_s_t_r_a
tiio~nio;,J;t;h;e;T;riu
e_P_e_lv_i_s
1 _______________________ 7 ■
PELVIS
CONJUGATES
Sacral
True conjugate A
Obstetrical conjugate B
Diagonal conjugate C
Anteroposterior
Pubic
symphysis
The inlet of the pelvis comprises of the pelvic brim, pubic bone, and sacral promontory
• Posterior border: sacral promontory and alae of sacrum
• Lateral border: linea terminalis
• Anterior border: horizontal pubic rami and symphysis pubis
Diagonal
conjugate
• Diameters can be evaluated clinically to screen for pelvic inadequacy
• Pelvic inlet can be evaluated for its AP diameter: diagonal conjugate is measured from the
lower border of the pubis to the sacral promontory using the tip of the 2nd finger and the
point where the base of the index finger meets the pubis symphysis (see image above)
• The obstetric conjugate is estimated by subtracting 1.5-2 cm from the diagonal conjugate
• If the diagonal conjugate is c:l 1.5 cm, the AP diameter of the inlet is considered adequate
88
II. MJDPELVIS(MIDPLANE OR PLANE OF LEAST PELVICDIMENSIONS)
• Extends from the lower margin of the symphysis pubis through the level of the ischial
spines to the tip of the sacrum
• Measured at the level of the ischial spines
• A contracted midpelvis can cause transverse arrest of the fetal head
True conjugate A
Obstetrical conjugate
Diagonal conjugate
B
C
I
.
Anteroposterior diameter
of midpelvis
Sacral
Transverse of inlet E
lnterspinous diameter F
Obstetrical conjugate G
lschial spines
Pubic symphysis
Important Diameters in the Midpelvis:
• Anteroposterior (AP) diameter (2:ll.S cm): extends from the lower border of the pubis to the
sacral vertebrae (S4-SS junction)
• lnterspinous (transverse) diameter (2:10 cm): between the ischial spines
89
Ill. PELVIC OUTLET (INFERIOR STRAIT)
• Consist of two triangular planes sharing a common base formed by a line joining the two
ischial tuberosities
• The anterior triangle is formed by the pubic arch (pubic angle: 90-100 degrees)
• The posterior triangle has the tip of the sacrum as the apex and the sacrotuberous
ligaments and ischial tuberosities as the sides
Pubic symphysis
Anterior triangle A
Posterior triangle B
Bituberous diameter C
Anteroposterior diameter
Anterior sagittal diameter
Posterior sagittal diameter
90
SECTION TWO
PHYSIOLOGY OF LABOR
PREPARATION FOR LABOR
Physiologic Preparatory Events Before Actual Labor
EVENT I DESCRIPTION
• Fetal head settles into the pelvic brim, noted by the mother as a flattening
of upper abdomen & increased prominence of the lower abdomen
Lightening • Occurs ~2 or more weeks before labor in primigravids (usually at ~36
weeks AOG)
• Occurs until early labor in multigravids
• Irregular (usually painless) contractions of the uterus during the last 4-8
Braxton
weeks of pregnancy
Hicks
• Appear sporadically and are unpredictable
contractions
• Not associated with progressive cervical dilatation and effacement
• Before parturition, cervix becomes softer due to increased water content
and collagen lysis
Cervical • Effacement (or obliteration of the cervical canal) occurs as it is pulled-up
effacement and taken up into the lower uterine segment
• Onset of labor may be heralded by the passage of a small amount of
blood-tinged mucus from the vagina (i.e., "the bloody show")
• Parturition can be divided into four overlapping phases that correspond to major
physiological transitions. These four phases should not be confused with the clinical
stages of labor (i.e., first, second, and third stages), which make up phase 3 of parturition
Source:Cunningham
FG,et al. WilliamsObstetrics
25thEd;2018
91
I. PHASE 1: UTERINE QUIESCENCE& CERVICALSOFTENING (comprises 95% of pregnancy]
A. Anatomic Changes during Phase I
CHANGES 1- REMARKS
-5
-4
8 -3
E
u -2
c· "T1
~ 6 -1 "'
g_
.,"'
.!!! ~
'a
;;;
0
...
QI
o·
u +1 ::s
-~
QI
4
u +2
+3
2
+4
dilatation
+5
e
DIVISION DIVISION DIVISION
• The preparatory division covers the latent phase of the first stage of labor up to the
acceleration phase of the active phase. The dilatational division is the same period as the
phase of maximum slope where the cervix dilates rapidly. The pelvic division begins at the
deceleration phase which is at 8 cm dilatation where cardinal movements occur since the
fetal head is already navigating through the pelvis
• The first stage of labor begins at the start of true labor and ends at 10 cm dilatation.
This stage is divided into latent (relatively flat) and active (rapidly progressive) phase.
Friedman initially pegged the beginning of active phase at 4 cm. But recently, Zhang, et al
already moved the active phase at 6 cm where rapid cervical dilatation is observed. The
second stage of labor begins at 10 cm or full dilatation until the baby is delivered which
normally lasts for 1 hour
Source:CunninghamFG, et al. WilliamsObstetrics25th Ed; 2018
93
Divisions of Labor
Functional Divisibns of Labor
Preparatory • Cervix dilates little but connective tissue components change
Division • Sedation and conduction analgesia can arrest this division
Dilatational • Cervical dilation proceeds at its most rapid rate
Division • Unaffected by sedation
• Commences with deceleration phase of cervical dilatation and includes
Pelvic
the second stage of labor
Division
• Cardinal fetal movements take place in this division
Phases df Cervica{ Dilatation
• Corresponds to the preparatory division
• Ends once dilation of 3-5 cm (Friedman) or 6 cm (Zhang) is achieved
Latent Phase • Prolonged latent phase
Nullipara: >20 hours
0
Active Phase Phase of maximum slope (measure of the efficiency of the machine)
0
94
I. FIRSTSTAGE:CLINICAL ONSETOF LABOR(CERVICAL EFFACEMENT & DILATION)
• Time from onset of labor to complete cervical dilation
• Signs of labor initiation: spontaneous release ofa small amount of blood-tinged mucus
(heralded by mucus plug, "show" or "bloody show") from the vagina
Pushing or maternal intraabdominal pressure:
, Most important force in fetal expulsion
Contraction of the abdominal muscles simultaneously with forced expiratory efforts
■
with the glottis closed (as in valsalva maneuver)
Necessary to complete second-stage labor .
SEGMENT
OF UTERUS
I REMARKS
96
II. SECOND STAGE: FETAL DESCENT
• Time from complete cervical dilation to fetal expulsion/delivery
• In many nulliparas, engagement of the head is accomplished before labor begins
• Vertex enters pelvis with the sagittal suture lying in the transverse pelvic diameter in the
majority of patients
-
• Uterine contractions effect modifications in fetal attitude:
° Fetal straightening
° Closer application of the extremities to the body
CARDINAL
MOVEMENT
I PURPOSE
I REMARKS
• Allowswidest
I REMARKS
Pelvic inlet
plane
• The head position is considered to have normal synclitism when the biparietal diameter is
parallel to the pelvic plane and the sagittal suture is midway between the symphysis and
the sacral promontory. When there is lateral deflection of the sagittal suture and parietal
bone, then there is asynclitism. If the sagittal suture approaches the sacral promontory
and more of the anterior parietal bone presents itself to the examining fingers, the
condition is called anterior asynclitism, and vice versa.
FG,et al. WilliamsObstetrics
Source:Cunningham 25thEd;2018
98
Ill. THIRD STAGE:DELIVERYOF PLACENTA& MEMBRANES
• Begins immediately after fetal birth and ends with placental delivery
• After the baby has been delivered, the uterus contracts, leading to a disparity between
size of placental surface & site of placental attachment (which is the reason for separation
of the placenta)
0
Sudden gush of blood
Uterus becomes globular (round) and firmer (Calkins sign)
Lengthening of the visible portion of the umbilical cord
Rise of uterus into the abdomen
I
.
99
SECTION THREE
INTRAPARTUM ASSESSMENT
Sample Tracing
too,-+--~r ·t-FF=-==J=
r ♦-•-+ -t+--- - t=
"~-
!,(.It !- -t-t- -t- -1~:--
;-:t-rTi
--..-\.-- -:-:1* - ,-~- .! .. ( -+-+-·/,.•
'1---....-f-- "--" " -, ✓ i-- • -
4 •-,:\.--=-i=
"i:' .,+- :· ---,---• _, :::-r
,::j:::: 52 mmHg :!:EH 50 mmHg '3= 47 mm Hg ±d:± 44 mmHg =f d9mmHg ±
Speed oi tracing:1 cm/min
• Tracing A (upper figure) shows a normal or reactive FHR pattern expressed as beats per
minute (bpm). A small box corresponds to 10 fetal heart beats. In the example above, the
baseline FHR is about 120 to 130 bpm.
• Tracing B (lower figure) shows the uterine activity, which consists of the uterine
contraction pressure/intensity (0 to 100 mmHg) and contraction interval (interval
between the peak of contractions). The Montevideo Unit (MVU) can be computed using
this tracing. It is calculated by subtracting the baseline uterine pressure from the peak
contraction pressure for each contraction in a 10-minute window. In the tracing shown,
there are five contractions with contraction pressures of 52, 50, 47, 44 and 49 mmHg. The
sum of these contractions within the 10-minute period corresponds to the MVU.In this
case, the MVU is 242. Adequate uterine contraction is defined as 2200 MVU.
Source:CunninghamFG,et al. WilliamsObstetrics25th Ed;2018
100
BASELINE FETAL HEART ACTIVITY
• Refers to the modal characteristics that prevail apart from periodic accelerations or
decelerations associated with uterine contractions
• Includes rate, beat-to-beat variability, fetal arrhythmia, and distinct patterns such as
-
sinusoidal or saltatory fetal heart rates
II. BASELINEVARIABILITY
• Moment-to-moment or beat-to-beat oscillation (fluctuations) of the baseline fetal heart
rate that are irregular in amplitude and frequency
• Important index of cardiovascular function & is regulated by the autonomic nervous system
• Decreased variability is commonly caused by giving analgesic drugs during labor
• Reduced baseline heart rate variability is the single most reliable sign of fetal compromise
• Diminished variability <4.2 bpm maintained for 1 hour: diagnostic of developing
acidemia and imminent fetal death
DESCRIPTION I DIAGRAM
l_l~J~l_~l±tlil~~~--~
• Amplitude range is
Absent* undetectable (i.e.,
almost a straight line) t__
Minimal*
• Amplitude range is
,;5 bpm
lll!J•ll!~!lill
Moderate**
• Normal variability
• Amplitude range 6-25
bpm
Wrn#H#UIBI
Marked
• Amplitude range 2'25
bpm
-
'Conditionsassociated withabsent or minimalvariablityincludeextremeprematurity,preexistingneurologicinjury,
fetal sleep cycle, or medications
"Moderate baseline variability(preferred)reflectsthe oxygenationof the CNS and predictsthe absence of damag-
ing degrees of hypoxia-inducedmetabolicacidemia
Source:ArnoldKC,et al. ObstetricsEssentials;2017
101
III. SINUSOIDALOR SALTATORYHEART RATE PATTERN
• Visually apparent, smooth, sine wave-like undulating pattern in FHR baseline with a cycle
frequency of 3-5 bpm which persists for 2:20 min
• Observed with fetal intracranial hemorrhage, severe asphyxia, & severe fetal anemia
210
180
Characteristics:
~ C 150 • Stable baseline heart rate
~ .E of 110 to 160 bpm with
t
"'
a:; 120 / ' I/\ 1 I\ \I/ I\ i"\ regular oscillations
-
QJ C. I V
.c V,
• Amplitude of 5 to 15 bpm
"' "'
Q) QJ 90
I
(rarely greater)
u.. :3. • Long-term variability
60 frequency of 2 to 5 cycles
I
per minute
30 • Fixed or flat short-term
variability
-
V, 100
C ~ • Oscillation of the sinusoidal
0
.:; C waveform above or below
u ::, 75
~C 0
QJ
a baseline
0 'O
·;;; so • Absent accelerations
u
QJ
C
~
C
25
·~ 0
~
5
Overview of Terminologies
TERM I DEFINITION
102
I. ACCELERATIONS
• Abrupt FHR increases above the baseline
0 At >32 weeks AOG:acceleration has a peak of?lS bpm from baseline, lasts for ?15 secs,
but <2 mins from onset to return to baseline
At <32 weeks AOG:acceleration has a peak of?l0 bpm from baseline, lasts for ?10 secs,
0
~
'I I I
I -
60
! ' I
I
I
I ': I I I I
lO
I I I
100
II. EARLYDECELERATION
Visually apparent, usually symmetrical gradual decrease and return of the fetal heart rate
associated with a uterine contraction
Gradual FHR decrease: defined as from onset to FHR nadir of?30 seconds
0
The nadir of the deceleration occurs at the same time as the peak of the contraction
0
• It is "symmetrical": onset, nadir and recovery are coincident with the beginning, peak and end
of the contraction, respectively
~v
210 TIME
ONSET TO NADIR
~c
..
e? 'E
t'. -
• a.
.c -
180
!SO
~30:
~~
~£
110
90
I
I : :
l
100
C:vi 15
.g·E
ii.
C
·;:
~
C
0
so
,l:,
::,- "
Peak of contraction
Cause: Fetal Head Compression
• Uterine contraction causes transient fetal head compression leading to increased ICP and
reflex parasympathetic stimulation
• This causes gradual slowing of the FHR and early deceleration
• When head compression is relieved, autonomic reflexes subside and FHR returns to baseline
103
III. VARIABLEDECELERATION
• Visually apparent, abrupt decrease in FHR
0 Abrupt: from onset to FHR nadir of <30 seconds
The decrease in FHR is 2:15 bpm, lasting for 2:15 seconds but <2 mins duration
0
• Onset, depth, & duration of decelerations commonly vary with successive uterine contractions
::11111 """"
TIME
1:~T""
·················••········-············-\\0V
~----• A
Cause: Umbilical Cord Compression
Peak of contraction
• Umbilical cord compression causes initial compression of umbilical vein, leading to transient
decrease in fetal venous return. This leads to transient decrease in fetal cardiac output and BP,
causing baroreceptor stimulation and transient increase in FHR
• Umbilical artery compression causes an abrupt increase fetal peripheral resistance and BP,
causing baroreceptor stimulation and reflex parasympathetic outflow. This leads to abrupt
decrease in FHR causing variable deceleration
• When cord compression is relieved, the process occurs in reverse
IV. LATEDECELERATION
• Visually apparent, usually symmetrical gradual decrease and return of the fetal heart rate
associated with a uterine contraction
Gradual: from onset to FHR nadir of 2:30 seconds
0
• Symmetrical: onset, nadir and recovery occur after the beginning, peak and end of the
contraction, respectively
I TIME
~c I ONSETTO NADIR
~ E ISO
I \
,:: C
~ ~ .I I
.c • •' '
~1
120
'I LATE :: ~30:
T
I I
I
90 '
''
100
'
75
A
~vi' '
.g ·"§ '
'
so '
eu o" '
§i '
'
~~
·;: 0
25
'
~:,
::,- '
Peak of contraction
Cause: Uteroplacental Insufficiency
• Common causes of uteroplacental insufficiency: placental dysfunction, maternal
hypotension following epidural anesthesia or excessive uterine activity
• Decreased uteroplacental oxygen transfer to the fetus leads to chemoreceptor stimulation
and triggers an alpha adrenergic response
• This causes fetal hypertension leading to baroreceptor stimulation and parasympathetic
response causing deceleration
104
V. PROLONGED DECELERATION
• Visually apparent decrease in FHR below baseline of lasting ;,2 but <lOmin
• lfthe deceleration lasts ;elOmin, it is a baseline change
210 r,-,---,-,-.-,-,---,-.-.--,-,--,.-.--,-,-.,-.--,-,-,,-,-r,,-,-,-r,,-,-T7
"' ..
I
.
1 -+--+i-,,,-¥4c-.-+-"+-+~-
120 H-+-+-+-t-t-+-+--"'--+"'=..;...ch,JM...q>'--1~f'1'\.H- 1
Hv-+-l-+-H-+-+--+---l
90 >-+-t--+-+-+-<-t--+-+-+-<-+-t-+-+-<r-+-+--+-+-,r-+-+--+-+->-+-+--t-+-t--t-t--+-+-t
60 H-+-+-+-t-t-+-+-+-t-1-t-+-+-t-ir+-++-+-cr+-+-l--t-t-t-+-t-+-t-t-+-+--+---l
75
25
105
THREE-TIER FETAL HEART RATE INTERPRETATION SYSTEM
• Fetal heart rate (FHR) monitoring during labor is essential to determine if a fetus is well
oxygenated
• A three-tiered system for categorization of intrapartum FHR pattern is used
• This categorization evaluates the fetus only at that point in time
• The FHR tracing may move back and forth between these categories at any time during
labor, depending on the clinical situation
CATEGORY I FEATURES
• Strongly predictive of normal fetal acid-base status
• Can be followed-up in a routine manner without specific action
Bradycardia
0
•Management
of CategoryI is routinemonitoring
.. Management of Categories II andIll aimto improvefetaloxygenationanduteroplacental bloodflow,stepsto
diminishuterineactivity,andreliefof umbilicalcordcompression. Potentialinterventions
arelateraldecubitus
positioning,
administering maternaloxygen,discontinue oxytocin,or amnioinfusion
for variabledecerations
Source:ArnoldKC,et al. Obstetrics
Essentials;
2017
106
SECTION FOUR
INDUCTION AND AUGMENTATION OF LABOR
OVERVIEW OF INDUCTION AND AUGMENTATION OF LABOR
• Goal of induction & augmentation is to effect uterine activity sufficient to produce cervical
change and fetal descent, while avoiding development of a non-reassuring fetal status
• Indicated when benefits to mother/fetus outweigh those of pregnancy continuation
• Intervention designed to:
0
Artificially initiate regular uterine contractions
Progressively dilate and efface the cervix
I
'
I INDUCTIONVERSUSAUGMENTATION
OF LABOR
• Process whereby labor is initiated by artificial means
Induction of
• Stimulation of contractions before the spontaneous onset of labor, with
labor
or without ruptured membranes
• Effecting regular uterine contractions by artificial means in cases of
Augmentation spontaneous labor with irregular & inadequate uterine contractions
of labor • Stimulation of spontaneous contractions considered inadequate
because of failure of the cervical dilatation or descent of the fetus
II. BISHOPSCORE
• Quantifiable method used to predict labor induction outcomes
Bishop score of 9: high likelihood for a successful induction
• Bishop score of 4 or less: unfavorable cervix which may require cervical ripening
SCORE I DILATATIONI EFFACEMENT I STATION ICONSISTENCYI POSITION
0 Closed 0-30% -3 Firm Posterior
1 1-2 cm 40-50% -2 Medium Midposition
2 3-4cm 60-70% -1 Soft Anterior
3 ;,S cm ;,80% +1, +2 --- ---
Dilatation:averagediameterof cervicalopening
Effacement: degreeofdecreasein the cervicallength
Station:levelof presentingpartin relationto the ischialspine(station0)
Positionof the cervix:relationship
ofthe cervicalos to the fetalhead
• Posterior(lessfavorable):cervixpointedposteriorly
• Midposition (favorable):
cervixin midline
• Anterior(morefavorable):cervixpointedanteriorly
Source:Cunningham, FG.Williams Obstetrics25thEd1t1on,
2018and Bishop,1964
III. INDICATIONSAND CONTRAINDICATIONS
FORINDUCTIONOF LABOR
INDICATIONS I CONTRAINDICATIONS
• Perform abdominal examination to obtain the fundic height and perform the Leopold
maneuver to determine fetal presentation & fetal heart tones
• Unless contraindicated, do a vaginal exam under aseptic technique to determine cervical
dilation and effacement, presentation, station and asses the pelvis
• Monitor and document progress of cervical dilation and descent every hour once in the active
phase to diagnose abnormal labor (plot in a partograph)
• Monitor the vital signs at least every hour once in the active phase
• Monitor FHR & uterine activity regularly either by:
0 Auscultation after a contraction at least every 30 mins (low-risk) or 15 mins (high-risk)
0 EFM with tracing evaluated at least every 30 mins (low-risk) or 15 mins (high-risk)
• Anesthesia consultation should take place prior to admission
• Oral intake of modest amounts of clear liquids (e.g. water, pulp-free juices) may be allowed
I. DIAGNOSISOF LABOR
A. Criteria for the Diagnosis of Labor
• Uterine contractions* (1 in 10 mins; 4 in 20 mins) by direct observation or by electronic
fetal monitor (at least 200 Montevideo units or MVU)
• Documented progressive changes in cervical dilatation & effacement
• Cervical effacement of>70-80%
• Cervical dilatation >3 cm
•uterinecontractionswithoutcervicalchangesDOESNOTmeetthe definition
of labor.
110
VI. WORLD HEALTH ORGANIZATION (WHO) PARTOGRAPH
• Used to record all observations made on a woman in labor in low-resource settings
• It aids the primary health care giver in a primary health facility (health center) to
determine whether there is a need to transfer the patient to a tertiary center
■
• Expected rate of cervical dilation is 1 cm/hour, regardless of gravidity
.
• Normal cervical dilatation should fall within the ''ALERT"line
• If cervical dilation crosses the ALERTline, then there is a need to transfer to a tertiary facility
Some Examples
Cervical dilation not crossing Alert Line
Name Gravida Para Hospital Number
Date of Admission Time of Admission Ruptured membranes Hours
10
9 V
v ,,,.,,,,,,,I
1,,,./ I ,,,,v
I/
/
8
i,,,:...,_~
./ ./ ,o'1' ,,,.v
7
k"'~ /./ .,.c-v
./
6 - p
IJ v/ / /
1:
Descent of ,,i,.
ro,
V
V / /
HT~::1
12
111111111111111
1 2 3 4 5 6 7
IIIIIIIII
8
PM PM PM PM PM PM PM PM PM
10 !// //
9 I 1,,,,V ,, I I v"'
8
,_'<.¢-/~ .... ,o'1' ,/
V
7 ,,,I" i,.◊ V
/
6
,~i,..-°// I//
1; .,,v v"'
Descent of 3
Fetal head (Plot 0) ,.
~ ..........
-
1
I 0
~~
~
H~::1111111111111111
12 1 2 3 4 S 6 7
IIIIIIIII
8
PM PM PM PM PM PM PM PM PM
111
Cervical dilation crossing Alert Line but not crossing Action Line
Name Gravida Para Hospital Number
Date of Admission Time of Admission Ruptured membranes Hours
10 1,,..V IY ,,/
t-t-t-t-t-t-
I i,,,v l.,r'I r ,,/
,.-..----1r--t-t-t-+-+---1
8 <. ,/ 1 .,,...... I /
1>-'-::,
/ ,,.... c-'o~,.,/+--+--+--+-+-+-+--+--+--+
7 / i.,I"" I>',,/
6- -
// ~......... //
,,C+-+-+--+--+--+-+-+-+--+--+--+
1 5 ,,,,... ,v
41'11""1/4----,c......1-1-1-1-+-+"/+-+-+--+--+--+-+--+---+--+--+--,--+-I-!--,
'
Descent of '"fflc::t--t----+-+-+--+--1-r-r-t-+-+-+-+-+-+-t--t----t---t----t--t-+-I
HT~::1
12
I I I I I I I 11111111111111111
1 2 3 4 6 7 8
PM PM PM PM PM PM PM PM PM
10 // ,_,/
9 I 1,,,,,, ,,v
8
,.,¢-// V
7 1>-"
Cervix (cm) ,,,..✓ i...,, ~ / /
(PlotX) 5--
c-'o;,,,
// I,,, ~ I>'/
....
1:
Descent of 3 '
_/.,:;. ,../
1
~ ........
I 0
r- r-,..
--
H~::1I I I I I I I I I 111111111111111
12 1 2 3 4 5 6 7 8
PM PM PM PM PM PM PM PM PM
112
MANAGEMENT OF THE SECOND STAGE OF LABOR
• Second stage of labor starts when cervix is fully dilated up to the delivery of the fetus
• At the time of full dilatation, the parturient (woman in labor) feels the urge to bear down
• Average duration of this stage is 50 mins for nulliparas and 20 mins for multiparas
■
placed on the stirrups. Bed is elevated to >45 degrees or Fowler position
.
• Asepsis and antisepsis is done
• Sterile drapes are placed
• Bladder drained with straight catheter
• Fetal heart tones are noted after every contraction every 15 minutes
• Patient is encouraged to bear down during a uterine contraction. She can bear down as
long as she is able and exhale slowly. Rest between contractions.
• Once fetal head reaches the perineum and the scalp is seen with a diameter of 2-3 cm,
episiotomy is done after administering adequate anesthesia
• The perineum is supported with one hand using a hand towel (Ritgen maneuver) and the
other hand tries to keep the head flexed to control delivery of the baby
• Once head is delivered determine for presence of nuchal cord and either slip it over the
shoulders or cut between 2 clamps. Clear baby's nose and mouth.
• Await external rotation or assist by bringing shoulders into anterior posterior position
• Deliver anterior shoulder by gentle downward traction followed by upward traction to
deliver posterior shoulder
• Gently deliver rest of the baby
• Apply the Essential intrapartum Neonatal Protocol (EINC): immediate drying of the baby,
skin-to-skin contact, timely cord clamping, and non-separation for early breastfeeding
I. PREPARATIONFOR DELIVERY
A. Delivery of the Head
0 With each uterine contraction, perinea] opening becomes ovoid to circular with
progressive dilatation
0 Perineum is stretched to paper-thin and rectal opening may also stretch
° Crowning is when the fetal head is seen encircled by the vulvar ring
° Failure to perform an episiotomy at this point invites perinea! lacerations
0 See cardinal movements of labor discussed in Section 2
113
II. EPISIOTOMY
• An incision into the perineum to enlarge the space at the outlet, thus facilitating the birth
of the child
• Restricted use is preferable to routine use
• Median episiotomy is the first choice for episiotomy (but mediolateral episiotomy may be
preferable in selected cases, such as big babies, short perinea! body, and forceps delivery)
A. Indications to do an Episiotomy
' Expedite delivery in the 2nd stage of labor
' When spontaneous laceration is likely
' Maternal or fetal distress
' Breech position
0Assisted forceps
0Large baby
, Maternal exhaustion
I MEDIAN (MIDLINE)
EPISIOTOMY
I MEDIOLATERAL
EPISIOTOMY
~ ~
Diagram
~£
• Begins at the fourchette
continuing to the perinea!
• Begins at the midline of the
fourchette and is directed
Description body at the midline and ends
to the right at an angle 60
before the external anal
degrees off the midline
sphincter is reached
• Done if perinea] body is long
• Done if perinea! body is short
Characteristics enough
• Likely to cut blood vessels
• Less chance to cut blood vessels
Surgical repair • Easy • More difficult
Healing • Good healing • Prone to faulty healing
Postoperative
pain • Minimal • Common
114
MANAGEMENT OF THE THIRD STAGE OF LABOR
• Starts from the delivery of the baby up to the delivery of the placenta
• Goals include the following:
0 Delivery of intact placenta
0 Avoidance of postpartum hemorrhage & uterine inversion
• Separation of the placenta usually occurs within 5 mins of delivery
__________ _, ■
~B_a_s,_·c_P_r_in_c,.:..·p_le_s_,_·n_t_h_e_M_a_n...;ag:::.....em_e_n_t_o::..f_th_e_T_h_ir_d_S_t_a-=g-e_o.:..f_L_a_b_o_r
• Await for signs of placental separation
• Do controlled cord traction. Place hand below fundus facing the mother's head. Push
fund us upward while placing gentle traction on the cord with opposite hand. As the
placenta reaches the perineum, slightly lift the cord
• Deliver placenta, slowly rotating as you pull
• Inspect placenta for completeness
• Massage fund us until contraction is felt. Start on oxytocin drip or give ergot derivatives, if
not contraindicated
• Inspect for lacerations. Do repair of episiotomy or lacerations
• Check for hematoma formation and integrity of the anal sphincters
I. UTEROTONICDRUGS
UTEROTONIC DRUGS I REMARKS
• Effective first line prophylactic uterotonic
• Safe to use on all patients
Oxytocin
• Lesser unpleasant side effects (e.g., nausea, vomiting &
hypertension)
Oxytocin analogues
• Synthetic analogue of oxytocin with a longer duration of action
(e.g., Carbetocin) -
115
B. Techniques in Manual Extraction of the Placenta
• Perform by carefully
Feel if the proceeding slowly all
placenta has
around the placental
7 been peeled or
bed until the whole
detached from
the uterine wall placenta has been
detached
Palpate uterine
cavity to ensure
8 complete
removal of • One complications is
placental tissue
incomplete placental
delivery
• Cotyledons must be
Examine the complete
9 placenta and
membranes
Consideradministeringoxytocin,whichfavorsuterinecontraction
andstopsbleeding
Thingsto remember:
• Donotexerttractiononthecordandtheplacentaseparately
• Donotmassage theabdomen
• Donotinfuseoxytocintoomuch(it cancauseretraction of theplacenta)
Source:SOGC.ALARMCourseSyllabus.Postpartum Hemorrhage; 2010
Source:Cunningham
FG,et al. WilliamsObstetrics
25thEdition;2018
116
III. INSPECTION OF THE VAGINA & PERINEUM FOR LACERATIONS
A. Types of Lacerations
FIRST SECOND THIRD FOURTH
INVOLVEMENT
Fourchette
I DEGREE
✓
I DEGREE
✓
I DEGREE
✓
I DEGREE
✓
Perineal skin ✓ ✓ ✓ ✓
■
Vaginal mucosa ✓ ✓ ✓ ✓ .
Fascia --- ✓ ✓ ✓
Firstdegree:tearonlypenetrates
vaginallining
Seconddegree(mostcommon): tearpenetrates thevaginallining& underlying
vaginaltissues
Thirddegree:tearextendsthroughvaginallining/tissues
andpartof theanalsphincter
Fourthdegree:tearextendsthroughvaginallining/tissues,
analsphincter,andrectallining
B. Performing the Episiotomy Repair
MEDIAN EPISIOTOMY REPAIR I MEDIOLATERAL EPISIOTOMY REPAIR
;M C
D~/
REFERENCES
!.American Academyof Pediatricsand the AmericanCollegeof Obstetriciansand Gynecologists: Guidelinesfor PerinatalCare,
8th ed. Elk Grove Village, MP, 2017
2.AmericanCollegeof Obstetriciansand Gynecologists. Fetalheart rate patterns:monitoring.interpretation,and management
ACOGtechnical bulletin 207, 1995
3.Arnold, K. C., & Flint, C. j. (2017). lntrapartum fetal heart rate monitoring: Nomenclature, interpretation, and general
managementprinciples.In ObstetricsEssentials(pp. 101-107). Springer;Cham.
4.Cunningham,F.G.,Leveno,K.]., Bloom,S. L.,Spong.C.Y..Dashe,J.S.,Hoffman,8. L.,Sheffield,J.S. (2018). Williams obstetrics
(25th edition.).New York:McGraw-HillEducation.
5.Eberle RL,Norris MC, EberleAM, et al: The effectof maternal positionon fetal heart rate during epidural or intrathecallabor
analgesia. Am J Obstet Gynecol 179:150, 1998
6.FreemanRK,Garite TH, NageotteMP: FetalHeart RateMonitoring,3rd ed. Philadelphia,LippincottWilliams & Wilkins, 2003
?.GilstrapLC111, Hauth JC.HankinsGD,et al: Secondstagefetal heart rate abnormalitiesand type of neonatalacidemia.Obstet
Gynecol 70:191, 1987
8.Hobel CJ, Zakowski M. Normal labor,delivery,and postpartum care. Obstetricsand Gynecology.Availableonline: https://
clinicalgate.com/normal-labor-delivery-and-postpartum•care/
9.https://www.perinatology.com/Fetal%20Monitoring/lntrapartum%20Monitoring.htm
10. littps:/ /www.youtube.com/watch?v=un3HxiD3BUQ
11. KentonK, Mueller M: Episiotomyand obstetricanal sphincterlacerations.In YeomansER. Hoffman BL,GilstrapLCIII, et al
(eds): Cunninghamand Gilstrap'sOperativeObstetrics,3rd ed. New York,McGraw-HillEducation,2017
12. Murata Y,Martin CB,lkenoueT, et al: Fetalheart rate accelerationsand late decelerationsduring the courseof intrauterine
death in chronicallycatheterizedrhesusmonkeys.Am I ObstetGynecol144:218, 1982
13. National Institute of Child Health and Human Development ResearchPlanning Workshop: Electronic fetal heart rate
monitoring:researchguidelinesfor integration.Am JObstetGynecol177:1385, 1997
14. Paul RH, Snidon AK, Yeh SY:Clinical fetal monitoring. 7. The evaluationand significanceof intrapartum baseline FHR
variability. Am I Obstet Gynecol 123:206, 1975
15. Smith JH,Anand KJ,CotesPM, et al: Antenatal fetal heart rate variation in relation to the respiratoryand metabolicstatus
of the compromised human fetus. BJOG95:980, 1988
16. SOGC.(2010) Advances in Labour and Risk Management Textbook (ALARM)Course Syllabus. Postpartum Hemorrhage.
SOGC.Ottawa, Ontario
17. Yang M, Stout MJ, Lopez JD, et al: Association of fetal heart rate baseline change and neonatal outcomes. Am J Perinatal
34(9):879, 20 I 7
18. Young BK,Weinstein HM: Moderate fetal bradycardia. Am J Obstet Gynecol 126:271, 1976
118
DYSTOCIA
(ABNORMAL
LABOR)
SECTION ONE
MECHANISMS OF DYSTOCIA
--~-o-rw_a-rd_p_r_es_s_u_r_e_e_x_e_r-te_d_b_y-th_e_le_a_d_i_n~g-fe_ta_l_p_a-rt---~-------------,
..I. THE DIVISION AND PHASES OF LABOR (Friedman Curve)
■.·
-5
-4
8 -3
E
u -2
c'
.g
J3
6
-1 ..
....
g_
.!l! a
'5 ~
"iii
.!:!
er
+1 ::,
..
C:
u
4
+2
+3
2
+4
+5
e
DIVISION DIVISION DIVISION
• First stage: time from onset of labor (contractions ;,200 MVU,every 3-5 mins) up to full
cervical dilatation (10 cm)
0 Latent phase: characterized by gradual cervical change, which begins with perception of
contractions from closed cervix up to 4 cm (Friedman) or 6 cm (Zhang)
0 Active phase: characterized by rapid & predictable cervical change from 4 cm
(Friedman) or 6 cm (Zhang), up to full cervical dilatation (10 cm)
• Second stage: time from complete cervical dilation to fetal expulsion
• Third stage (not shown above): time from fetal expulsion to placental expulsion
I NULLIPARA
I MULTIPARA
121
II. NORMALLABOR USING DIFFERENTPARTOGRAMS
I FRIEDMAN CURVE
I ZHANG CURVE
I WHO PARTOGRAPH
• Improve labor
management in
developing countries
• Define normal labor • Prevent premature • Intended for GPs
Purpose
progress cs and paramedical
personnel to know
when to refer to OB-
Gyn specialists
• Sigmoid curve • Exponential staircase
Shape of
• Slow cervical dilation line
labor curve • Diagonal straight
until ~4 cm, followed • Increase in cervical
(cervical lines
dilatation) by an abrupt dilation is more
acceleration gradual
• Active phase starts
• Active phase starts • Active phase starts at4cm
at 4 cm at6 cm • After line starts at 4
Progression , 1.2 cm/hr for • Progression is slow cm, action line is 4
pattern nulliparas before 6 cm hours from alert line
, 1.5 cm/hr for • Duration is <4 hours • Cervical dilatation
multi paras after 6 cm during the active
labor is 1 cm/hr
I. MECHANISMSOF DYSTOCIA
• Abnormal progress of labor (spontaneous, induced, or augmented) related to the 3 P's:
Uterine factors (power)
, Fetal factors (passenger)
Bony pelvis (passage)
FACTOR
I REMARKS
I SOME CAUSES
122
II. GENERALMECHANISMS
• Most common etiology of dystocia is cephalopelvic disproportion (CPD)
Cephalopelvic disproportion: fetal head that is large on a small pelvis or abnormal fetal
head position on a normal or small sized pelvis
Fetopelvic disproportion: disparity of the size of the fetus for a small pelvis
• Hypocontractile uterine activity is the most common risk factor for protraction and/or
arrest disorders in the first stage of labor
MECHANISM I REMARKS I FEATURES
• Relationship between the power and the • Protracted labor: slow
I
passenger progress
• Uterine dysfunction can result from • Arrested labor: no
Uterine
overdistention, obstructed labor, or both progress
dysfunction
• Fetopelvic disproportion can also cause • Inadequate expulsive
uterine dysfunction effort: ineffective
• Can be managed medically pushing
• Relationship between passenger &
• Excessive fetal size
passage (i.e., disparity between fetal head
Cephalopelvic • Inadequate pelvic
and maternal pelvis)
(fetopelvic) capacity
• More apparent once 2nd stage is reached
disproportion • Malpresentation or
(CPD) • Ineffective labor is generally accepted as a
position of the fetus
possible cause of fetopelvic disproportion
• Abnormal fetal anatomy
• Managed by cesarean section (CS)
Source:Cunningham,FG.WilliamsObstetrics25thEdition;2018
B. Perinatal Complications
Fetal sepsis rises with longer labors
° Caput succedaneum and molding develop
0 Mechanical trauma such as nerve injury, fractures, and cephalhematoma
123
DIAGNOSIS OF ABNORMAL LABOR
I. ABNORMALLABORCRITERIAFOR DIAGNOSIS
~
p repa,:a ory D IVISlf?l!g
ABNORMAL LABOR CRITERIA FOR DIAGNOSIS
Dilatti'tional Dlvisio~ .,
True active • Active phase arrest is defined as cervix of .e6 cm with ruptured bag
phase: of waters with no cervical dilatation for:
6-7cm phase of • ;,4 hours with adequate uterine contractions (.e200 MVU), OR
maximum • .e6 hours with inadequate uterine contractions despite oxytocin
slope • Arrest disorder as indication for CS will only apply at this phase
Pelvic Division JI
Prolonged deceleration phase:
• Nullipara: ;,3 hours
• Multipara: .el hour
Secondary to••:
10cm Second
• Failure of descent due to contracted pelvic inlet: fetal head only at
(fully) Stage
station "O" or above (-1 to -5) for >l hour. Delivery by CS
• Arrest of descent due to contracted pelvic mid plane: fetal head at
station + 1 to +5 for> 1 hour. Delivery by CS
• If fetal scalp is already seen separating the labia (station +5) & fetal
head is in occiput anterior, outlet forceps delivery can be attempted
'Must meetcriteriaof prolonged
decelerationphase beforeaddingseconda,ydiagnosisofeither'failure"or "arrest ofdescent'
"Must meet criteriaof prolonged2nd stage beforeaddingthe seconda,y diagnosisof either'failure"or "arrestof descent'
Source: PhilippineObstetrical& GynecologicalSociety;2021
124
Guide to use the table from the previous page:
• Perform internal exam to determine cervical dilatation, station, and Bishop Score
• Check the indication for induction of labor
• Patient meets the criteria ofadequate labor (contractions with ;,200 MVUat least every 2-3 minutes)
• Check the phase of labor the patient is in
• Check if the patient's labor pattern fits the criteria for abnormal labor
Some Sample Cases
1. Failed induction of labor: GlPO 39 weeks AOG with GDM for induction of labor.
Internal examination (IE) was 2 cm, 50%, station -3, (+)bag of waters (BOW); with
no perceived uterine contractions. Induction with oxytocin drip started which made
uterine contractions regular with ;,ZOO MVU intensity. Amniotomy was done to further
1.·
augment labor. Twelve (12) hours from complete induction (oxytocin drip, ruptured
BOW, and regular contractions of ;,ZOOMVU), the cervix remained in the latent phase.
2. Active phase arrest or arrest of cervical dilatation: GlPO 39 weeks AOG with
ruptured bag of waters on admission. IE revealed: 6 cm, 70% station -1, (-) BOW with
clear fluid. Augmentation of labor with oxytocin was done. After 4 hours with regular
strong uterine contraction, IE remains unchanged at 6cm, 70%, station -1.
3. Prolonged deceleration phase secondary to failure of descent secondary to
contracted pelvic inlet: GlPO 39 weeks AOG came in due to watery vaginal discharge.
Augmentation of labor with oxytocin was started with normal progress of labor until
IE was 8 cm, 80%, station -1, (-) BOW. For 4 hours, it remained the same. This is
prolonged deceleration phase secondary to failure of descent since the fetal head did
not descend below station 0.
4. Prolonged second stage secondary to arrest of descent secondary to contracted
pelvic midplane: GlPO 39 weeks AOG came in due to watery vaginal discharge.
Augmentation of labor with oxytocin was started with normal progress of labor until
IE was 8 cm, 80%, station +1, (-)BOW.For 3 hours, it remained the same. This is
prolonged 2nd stage secondary to arrest of descent since the fetal head remained in
that same station for> 1 hour.
Sources:WilliamsObstetrics,25th Edition,2018;PhilippineObstetrical& Gynecological
Society
PracticeBulletinNumber2, April5, 2021;Cohen,et al. UniversityPark Press; 1983
II. ABNORMALLABORPATTERNS,DIAGNOSTICCRITERIA,AND TREATMENT
CRITERIA
LABOR PATTERN TREATMENT
Prolongation Disor.der
I NuIiiparas I Multiparas I
• Bed rest*
Prolonged latent phase >20 hours >14 hours • Oxytocin or CS for
urgent problems
Protracition Disorders
Protracted active-phase dilation <1.2 cm/hr <1.5 cm/hr • Expectant & support*
Protracted descent <l cm/hr <2 cm/hr • CSfor CPD
Arrest Disord·ers
-
Prolonged deceleration phase >3 hours >1 hour
Secondary arrest of dilation
>2 hours >2 hours • CSif with CPD*
(arrest of cervical dilatation)
• Oxytocin if no CPD*
Arrest of descent >l hour >l hour • Rest if exhausted
No descent in deceleration phase
Failure of descent
or second stage
>3 hours:(+) RA >2 hours:(+) RA • Forceps or vacuum*
Prolonged second stage • cs
>2 hours:(-) RA >l hour:(-) RA
•Preferredtreatment
125
"POWER"
• Cervical dilation & propulsion and expulsion of the fetus are brought about by
contractions of the uterus
• During second-stage labo,; uterine contractions are also reinforced by "pushing" of the
mother (voluntary or involuntary muscular action of the abdominal wall)
• Either of these factors may lack intensity & result in delayed or interrupted labor:
0 Uterine Contractility
0 Expulsive Powers
I. PHYSIOLOGYOF UTERINECONTRACTION
• A uterus with a good power should have a fundal dominance: uterine fundus contracts
effectively pushing the fetus towards the birth canal & retracting the cervix to fully dilate
• Power is defined as uterine contractility multiplied by the frequency of contractions
I
-1-tH+-
i . I I I 1J
+t
11
I 11
\--- --t+
126
II. UTERINE DYSFUNCTION
• As labor normally progresses, there is an increase in intensity, duration, & frequency of
uterine contraction (i.e., uterine contraction increases from latent phase to the active phase)
• Failure of the cervix to dilate or the presenting part to descend is cause for concern
PARAMETERS
I HYPOTONIC UTERINE
DYSFUNCTION
I HYPERTONIC UTERINE
DYSFUNCTION
Low uterine activity (hypotonic) I High uterine activity (hypertonic)
Ettopathogenesis
- -··
General
features
• Absence of basal hypertonus
• Normal gradient pattern with
fundal dominance
• Elevated basal tone (basal
hypertonus) due to absence of
fundal dominance, and/or
• Complete asynchronism of the
I
impulses originating in each cornu
• Gradient pattern is distorted
(e.g., incoordinate uterine
dysfunction)
• The slight rise in pressure during
• Uterine pain that appears out
Pathology contraction is insufficient to
of proportion to the intensity
dilate the cervix
of the contractions and their
effectiveness in effacing and
dilating the cervix
Prevalence • More common • Less common
• Uterine overdistention (e.g.,
• Contraction of the midsegment
macrosomia, polyhydramnios)
of the uterus
Etiology • Grand multiparity
• Asynchronism of the impulses
• Sedation
originating from each cornu
• Regional anesthesia
Manifestations and Diggnosis ;
'
Clinical
• Painless • Painful
symptoms
Fetal distress • Late • Early
,,,~
Management i ' ~
127
III. OTHER POWER ABNORMALITIES FROM LABOR DISORDERS
A. Maternal Pushing Efforts
° Combined force created by contractions of the uterus and abdominal musculature
propels the fetus downward.
° Factors that affect maternal pushing:
• Heavy sedation or regional anesthesia reduce the reflex urge to push
• Intense pain created by bearing down overrides urge to push
0 Approaches to improve pushing with epidural anesthesia:
• Pushing forcefully with contractions after complete dilation, regardless of the urge
to push
• Analgesia infusion is stopped and pushing begins only after the woman regains the
sensory urge to bear down
I NORMAL
I ABNORMALITIES
• Malposition
Position • Occiput anterior (OA) Persistent occiput transverse (OT) position
0
• Malpresentation
• Vertex cephalic Brow /face presentation
0
Presentation
presentation Breech presentation
0
Transverse presentation
0
I. BROW PRESENTATION
• Cephalic presentation wherein the head is "partially extended" (usually converts to a face
or occiput presentation)
• Rare presentation when the portion of the fetal head between the orbital ridge and
anterior fontanel presents at the pelvic inlet
• Fetal head occupies a position midway between full flexion (occiput) and extension (face)
128
B. Management
0 A larger diameter must pass through the pelvis
0 Iffetus is extremely small (e.g.,preterm) or pelvis is particularly large, the brow presentation
may convert to vertex or face presentation (mentum anterior) to deliver vaginally
Cesarean section
0 Spontaneous conversion into an occiput or face (mentum
anterior] presentation
• Done in cases of persistent brow presentation
I
II. FACEPRESENTATION
• In this presentation, the fetal head is fully extended (hyperextended)
• The occiput is in contact with the fetal back and the chin (mentum) is presenting
• Fetal face may present with mentum anterior or posterior
A. Etiopathogenesis
0Preterm fetus (a smaller head can engage before conversion to vertex position]
0Marked enlargement of the neck or coils of cord around the neck may cause extension.
° Fetal malformations and hydramnios are risk factors for face or brow presentations
0Anencephalic fetuses naturally present by the face
° Contracted pelvis or a large fetus
0High parity (a pendulous abdomen permits the back of the fetus to sag forward or
laterally, often in the same direction in which the occiput points which promotes
extension of the cervical and thoracic spine)
B. Diagnosis
C. Management
0 Mentum anterior: the only face presentation that will allow for a vaginal delivery,
since symphysis pubis serves as a fulcrum allowing for flexion of the hyperextended head
0 Mentum posterior or transverse: CS is necessary because fetal brow (bregma) is
pressed against the maternal symphysis pubis (not amenable to vaginal delivery)
0 Mentum posterior:
• Spontaneous rotation to mentum anterior may occur in some multiparous patients
with an adequate pelvis & smaller fetus compared to previous babies. Trial of labor can
be attempted with a low threshold for CS
• In multiparous patients with previous babies smaller than current one or in
nulliparous patients, CS may be done early in the course of labor
129
III. BREECHPRESENTATION
• Occurs when the breech (fetal buttocks) or lower extremities present into the maternal pelvis
• Types of breech (e.g., frank complete, incomplete) discussed in previous chapter
A. Etiopathogenesis
RISK FACTORS FOR
BREECH PRESENTATION
I COMPLICATIONS OF
BREECH PRESENTATION
• Prematurity (20-30%)
• Perinatal morbidity /mortality (e.g.,
• Uterine relaxation (multiparity)
preterm delivery, birth trauma, congenital
• Multiple pregnancy
anomalies)
• Hydramnios, oligohydramnios
• Low birth weight (prematurity, lUGR)
• Hydrocephalus
• Prolapsed cord
• Anencephaly
• Placenta previa
• Uterine anomalies/tumor
• Uterine anomalies/tumors
• Placenta previa
I FRANK BREECH
PRESENTATION
I COMPLETE
BREECH
PRESENTATION
I FOOTLING
BREECH
PRESENTATION
Illustration
(-j-,
~...
.'->\
.
/ ,;
_.,,
(~-,
'\ 1
"\.~ \~·,
/
'?'~
/_./
~
(?/
>~_,,.---'-....
~:::--_c~) '<·/-,<:_,,.. )
130
2. Leopold Maneuvers
LM 1 I LM 2 I LM 3 I LM 4
. . .
. - =-- t -
) • ) ) >
C. Management of Breech
0 Planned vaginal versus planned CS for term, singleton delivery
0 External version may be attempted (repositioning the breech baby)
131
IV.TRANSVERSEPRESENTATION
• This position occurs when the long axis of the fetus is perpendicular to that of the mother
• There is no mechanism of labor for transverse lie
• Always delivered by cesarean section
A. Etiology
0Abdominal wall relaxation
0Preterm fetus
0Placenta previa
0Abnormal uterine anatomy (e.g., multiple myoma, especially if occupying the lower
uterine segment)
, Polyhydramnios
'Contracted pelvis
B. Diagnosis
1. Abdominal and Vaginal Examination
2. Leopold Maneuver
V. EXCESSIVEFETALBODYAND HEADSIZE
• Fetal size alone is seldom suitable explanation for failed labor
• There is no current method of measurement satisfactorily predicts fetopelvic
disproportion based on head size
ABNORMALITY REMARKS
• Definition: birth weight ~4,000 grams irrespective of AOGor
>90th percentile for gestational age after correcting for neonatal sex
Fetal
& ethnicity
Macrosomia
• Total length of labor is not prolonged - but the second stage of labor is
prolonged
• Excessive accumulation of cerebrospinal fluid (CSF)with consequent
cranial enlargement
Hydrocephalus
• Gross cephalopelvic disproportion is the rule, with dystocia as the
usual consequence
132
"PASSAGE" (PELVIS OF MOTHER)
• Fetopelvic disproportion arises from diminished pelvic capacity, excessive fetal size, or both
• Any contraction of the pelvic diameter that diminishes the pelvic capacity can create
dystocia during labor
• Pelvic contraction is discussed below
The Inlet
t--P_e_lv_i_c_b_r_im_(_fo_r_e_p_e_lv_i_s_)-+-_•_R_o_u_n_d
Diagonal conjugate
____________________
• e,11.5 cm
----t I
The Midpelvis
Symphysis pubis • Parallel to the sacrum and with average thickness
Sacrum • Hollow with average inclination
Side walls • Non-convergent
lschial spines • Blunt
Interspinous diameter • e,10 cm
Sacrosciatic notch • Sacrospinous ligament is 2.5-3 fingerbreadths
The Outlet
Suprapubic angle • Admits 2 fingerbreadths
Coccyx • Mobile
Anteroposterior
• e,11 cm (from tip of sacrum to inferior edge of symphysis)
diameter
Clinicalpelvimetryfindingsof a contracted
pelvis:
• Diagonal conjugate<11.5cm • Prominentischialspines
• Pelvicsidewallsareconvergent • Subpubic
archangle<90degrees
• Sacrumis flat • Nodescentof vertexwithValsalvaor fundalpressure
(Muller-Hiilis
maneuver)
Overview of Pelvic Contraction
LJJUUJ:Si
rtr
PELVIC INLET MIDPLANE PELVIC OUTLET
'
CONTRACTION CONTRACTION CONTRACTION
• Causes transverse • Defined as an
arrest of fetal head interischiat tuberous
General • Shortest AP diameter is
• Spines are sharp & diameter of <8 cm,
description <10 cm
prominent sidewalls roughly measured
or clinical long or if its greatest
are convergent using the length of a
pelvimetry transverse diameter
• Narrow sacrosciatic closed fist against the
findings <12 cm
notch perineum
• Flat sacrum • Narrow pubic arch
• Obstetrical conjugate
• Often associated
(AP diameter) <10 cm • Interspinous
Measurement with a contracted
• Transverse diameter diameter <8 cm
midplane
<12 cm
• Frequently causes
• More frequent face and transverse arrest of • May play an
shoulder presentations the fetal head, which important part
Effects
• More frequent cord can lead to difficult in production of
prolapse midforceps operation perinea! tears
or cesarean delivery
Sources:WilliamsObstetrics,
25thEdition,2018;DrennanK, 2021.
133
REFERENCES
I.CohenW, FriedmanEA:Managementof Labor.Baltimore,UniversityPark Press,1983
2.CohenWR. Friedman EA Perilsof the new labor managementguidelines.Am J ObstetGynecol2015; 212:420.
3.Cunningham, F.G., Leveno, K. J., Bloom, S. L.,Spong, C. Y.,Dashe, ). S., Hoffman, B. L.,Sheffield,). S. (2018). Williams Obstetrics
(25th edition.).New York:McGraw-HillEducation.
4.Drennan K. Abnormal labor: diagnosis and management I GLOWM [Internet]. [cited 2021 Oct 7). Available from: http://
www.glowm.com/section-view /heading/abnormal-labor-diagnosis-and-rnanagement/item/13 2
5.Ehsanipoor RM, Satin AJ.Normal and abnormal labor progression. Uptodate. Available online: https://www.uptodate.com/
contents/normal-and-abnonnal-labor-progression?. Accessed on Sept 21, 2021
6.EI-Movafi DM. Obstetrics simplified: Contracted pelvis. Available onlinehttps://www.gfmer.ch/ Obstetrics_simplified/.
Availableonline Sept 21, 2021
?.FriedmanE.The graphicanalysisof labor.Am J ObstetGynecol1954; 68:1568.
8.Friedman EA.Labor:ClinicalEvaluationand Management.2nd ed, Appleton-Century-Crofts, New York 1978.
9.Myles TD, SantolayaJ.Maternal and neonatal outcomesin patients with a prolongedsecondstageof labor.ObstetGynecol
2003; 102:52.
10. PhilippineObstetrical& Gynecological SocietyPracticeBulletin Number 2, April 5, 2021
11. Zhang I, Duan T.The physiologic pattern of normal labour progression. BJOG2018; 125:955.
12. Zhang I, Troendle J, Mikolajczyk R, eta!. The nan,ral histo,y of the normal firststageoflabor. ObstetGynecol 2010; 115:705.
134
PROCEDURES
INOBSTETRICS
SECTION ONE
INSTRUMEN:rS USED IN OBSTETRICS AND GYNECOLOGY
I. SURGICALSUTURES
• Used to ligate bleeding vessels or approximate tissue
• PolyglycolicAcid
• Polyglactin 910
I
• Lactomer 9-1, and
Glycomer 631
• Nylon
• Plain • Polyglyconate and • Surgical silk or
• Polyester
• Chromic Catgut Polydioxanone cotton
• Polypropylene
• Poliglecaprone 25
• Polyglactin 910
(Rapide)
• Polyglytone 6211
II. SURGICALNEEDLES
• Characteristics of needles include their attachment to the suture, shape of the tip, suture
lever in tissue, and the curve of the needle
• Necessary to carry suture material through tissue
•Needlepoint (or sharp apex): sharpness
and geometry are critically important
characteristics
Needle point\ • Body: portion of the needle which is
Needle eye
grasped by the needle holder
l'-''lr-•Needle diameter • Needle length: the circumferential length
of the needle
• Needle cord length: linear distance between
the pointed tip & the end of the needle
• Eye: opening where to manually insert
non-atraumatic sutures (Note: atraumatic
sutures have eyeless needles with the
Needle length suture already permanently attached into
a hollow end which is less traumatic to the
tissues, hence the name)
137
III. NEEDLEHOLDERS
• Required when curved needles are used
• With broad tips having a variety of inner surfaces to prevent needle from slipping/rotating
WAGENSTEEN (STRAIGHT) I HEANEY (ANGLED)
• Can place sutures deep inside the pelvis • Useful for vaginal surgeries since angled
head allows easy placement of curved
needles & sutures at any angle
-+ ¥ :-4
IV.SCALPEL
• Best instrument for dividing tissue with minimal trauma to surrounding tissue
• Scalpel blades come in various sizes and shapes depending on the cutting task at hand
Function follows form when it comes to surgical blades
0 In general: larger blades are used for coarser tissues or larger incisions
A. Scalpels
SIZE 10 I SIZE 11 I SIZE 15 I SIZE 20 I SIZE 22
~
/,,
/
/
Source:Yeomans
ER.et al. Cunningham
andGilstrap'sOperative
Obstetrics
(3rdEd);2017
138
B. Two Methods for Gripping
• Scalpel is held as one would a pencil, and • Scalpel is held between the thumb and
movement is directed by the thumb and third finger
index finger • The end of the blade is forced up against
• Motion comes predominantly from the the thenar muscles of the hand
thumb & index finger, allowing for precise • Primarily used for making long skin
cutting of tissue incisions, using arm motion, rather than
finger motion
I
Source:YeomansER,et al. Cunningham
andGilstrap'sOperativeObstetrics(3rdEd);2017
V. SCISSORS
• For cutting and for blunt dissection
• May be:
Straight: designed for cutting body tissues near the surface of a wound
° Curved: cut tissue in a smooth curve & horizontal fashion, cutting deep into a wound
• Used when • For retro peritoneal • For delicate • With a blunt and
dividing tough dissection or for dissection a hooked tip for
tissue (e.g., fascia, developing tissue suture removal
parametrial tissue planes in adhered (not used on
of vaginal cuff) or distorted tissue tissue)
139
VI. TISSUE/THUMB FORCEPS
• Consists of two strips of metal joined at one end
• Used to grasp and hold tissue during dissection, suturing, or cutting
RING- BONNEY
SMOOTH DEBAKEY TOOTHED ADSON
TIPPED TISSUE
FORCEPS
I FORCEPS
I FORCEPS
I FORCEPS
I FORCEPS
I FORCEPS
• For • Have long • Bites into • Have fine • Increase • Heavy-
handling fine smooth tissue, teeth the toothed
friable or tips that providing and are grasping forcepswith
delicate provide a firm commonly force serrations
tissue precise grip with used to without along the
control of minimal approximate using teeth shaft for
small or pressure skin for when a maximum
delicate staple or secure gripping
tissue (e.g., suture hold is powerused
vascular placement needed whensewing
i
.
surgery)
I :
fascia
-
VII. CLAMPS/GRASPINGFORCEPS
To grasp and apply pressure or traction to tissues
• With finger rings and locking mechanism
140
HEANEY I HEANEY- BALLENTINE I MASTERSON
• Heavy hysterectomy clamps with ridged shaft for clamping the parametrial and
paracervical tissue during hysterectomy
I
.
VIII. RETRACTORS
• Instrument to separate edges of a surgical incision/wound, or to hold back underlying
organs/tissues so that body parts within the incision may be accessed (to improve
exposure)
A. Self-Retaining Retractors: to hold incision apart
BOOKWALTER I BALFOUR
• Consists of a circular metal ring to which a wide • Two lateral blade with one additional
variety of retractors can be attached at any point retractor blade
O'CONNER-0-SULLIVAN
141
B. Manual Retractors
HEANEY I DEAVER I RICHARDSON
BRIESKY-NAVRATIL
VAGINAL SPECULUM
I ARMY-NAVY I PARKER
• Special curved jaws help • For retraction of shallow • Two concave blades with
visualize the genital tract or superficial incisions double ended design and
• For opening the vagina central handle
and visualization of • For strong tractions to
cervix, vaginal walls and widen surgical field or
uterine cavity pull back soft tissues
• For pap smear and other
gyne procedures
142
DILATORS AND CURETTES FOR DILATION & CURETTAGE
• Dilation and curettage (D&C) is a procedure in which the physician explores a cavity
beyond his/her view
• "Dilation" refers to the opening of the cervix
• "Curettage" refers to the removal of tissue within the uterus with an instrument called a curette
I. DILATORS
• Metal or plastic cylindrical rods of increasing diameter used to dilate the cervical os to
sufficient size to admit other surgical instruments into the uterine cavity
• Dilation of the internal os should be done slowly, allowing the fibers of the internal os to
stretch gradually
HANK I PRATT I HE GAR
■
• Tapered tips that reach • Long tapered tips that • Rounded tip (short)
deep into the cervix enables easier dilation • For small or atrophic
• Cause cervical relaxation • Less traumatic but may uterus
and uterine dilation perforate smaller uterus • Usually a set of dilators of
• Smooth edges allow increasing caliber
comfortable insertion with
minimal damage and less
chance of piercing
,=,o
I J
:
I I I
Source:Yeomans
ER,et al. Cunningham
andGilstraps Operative
Obstetncs(3rdEd),2017
Hulka,J, Glob.libr.women'smed;2008
143
SECTION TWO
OPERATIVE VAGINAL DELIVERY
I. INDICATIONS:
• Termination of 2nd stage of labor indicated in conditions where threat to mother/fetus is
relieved by delivery. The following must be observed:
Must be non-elective
0 Should fulfill the criteria for an outlet forceps delivery
STATION I ROTATION
144
III. PREREQUISITES FOR OPERATIVE VAGINALDELIVERY
Mnemonic: "FORCEPS":
• Fully dilated cervix, no fetal coagulopathy or fetal demineralization disorder
• Occiput/vertex presentation
• Ruptured membranes
• Cephalopelvic disproportion is not suspected, Consent completed
• Engaged head (at least +4 station), experienced operator, emptied maternal bladder
• Position of fetal head is known, painless (adequate anesthesia)
• Size (fetal weight) estimated
■
• Fetal demineralizing disease (e.g., osteogenesis imperfecta)
• Fetal bleeding diathesis (e.g., fetal hemophilia)
• Unengaged head (i.e., head is engaged when biparietal diameter has reached pelvic inlet) ..
• Fetal position: unknown or in brow /face position
• Suspected fetal-pelvic disproportion
Source:AGOG.ObstelGynecol;2020
FORCEPS DELIVERY
• Elective forceps delivery should be done only when criteria for outlet forceps have been met
• Forceps is usually called the "Iron Hand" (designed for extraction of the fetus)
TBr T
• Thin smooth blades Handle Lock
~~
Piper
• Shanks are long
• It has a reverse pelvic curve
Cephalic curve
IV. FORCEPSPROCEDURE
Ask for
• Authorization (consent), Anesthesia, Assistance
Assistance
Bladder • Empty bladder
Cervix • Fully dilated; membranes ruptured
Determine • Station, position, adequate pelvis, shoulder dystocia
Equipment • Quality, functionality
• Phantom application; correct pair
• Left blade, left hand, maternal left side
• Pencil grip, vertical insertion, left thumb directing
• Right blade, Right hand, maternal right side
Forceps
• Pencil grip, vertical insertion, right thumb directing
• Lock & support
• Posterior fontanelle 1 cm above plane of shank
• Sagittal suture perpendicular to plane of shank
Gentle
• Traction with contraction or pushing
traction
STEPS I ILLUSTRATION
147
VI. FAILEDFORCEPS
• If satisfactory application of forceps cannot be achieved, abandon procedure and deliver
either by vacuum extraction or CS
• If after 3 gentle downward pulls do not result in descent, abandon the procedure and
deliver by CS
• Factors for failed forceps-assisted delivery:
0 Persistent occiput posterior
0 Absence of regional or general anesthesia
0 Birthweight >4 kg
Source:AGOG,2012
I. INSTRUMENT:VACUUMEXTRACTOR
• Contains a cup (metal or plastic), shaft, handle and vacuum generator
Shaft
I
Vacuum
Handle generator
I
Vacuum
Handle generator
Source:Cunningham
FG,et al. Williams
Obstetrics;2018
148
II. TECHNIQUE(Remember A·B·C·D·E·F·G-H-1-J)
• Adequate pain relief
Anesthesia
• Analgesia is not essential but is recommended, if available
A s· tan e Neonatal support
Au horiz tion • Informed consent
• Bladder should be empty
Bladder
• May do straight catheterization
Cervix • Cervix must be fully dilated, and membranes ruptured
Determine
Equipment
• Position, station and pelvic adequacy
• Think possible shoulder dystocia
• Make certain that the vacuum cup, pump and tubing are
I
'. ·
functioning properly 7 ;
--------1-----------------------------1
posterior fontanelle
• Position the cup over the
• The cup is applied by compressing it in an anteroposterior diameter
Fontanelle and then introducing it into the posterior fourchette while protecting
maternal tissues and making space with the opposite hand
• Sweep finger around cup to clear maternal tissue
• 100 mm Hg initially and between contractions
• Pull with contractions only
• As contraction begins:
Gentle traction 0 Increase pressure to 600 mmHg
0 Prompt the woman for good expulsive effort
0 Traction in axis of birth canal
• No progress with 3 traction-aided contractions
Halt • Vacuum pops off3 times
• No significant progress after 20 minutes of operative vaginal delivery
Incision • Consider episiotomy iflaceration imminent
Jaw • Remove vacuum when fetal jaw is visible, or delivery assured
of Canada;2012-2013
andGynecelogists
Source:ALARM.Societyof Obstetricians
149
SECTION THREE
BREECH DELIVERY
III. VERSION
• Fetal presentation is altered by physical manipulation, either by substituting one pole of
a longitudinal presentation for the other, or converting an oblique or transverse lie into a
longitudinal presentation.
• It is simply changing an unfavorable presentation to a favorable one
Procedure
■
Done Before ECV:
• Sonographic examination to check the following:
° Confirm nonvertex presentation
0Amniotic fluid adequacy
0Exclude fetal anomalies
0Placental location
• Fetal heart rate monitor
• Anti-D lg given to Rh-D (-) women
• Administer betamimetics (e.g. terbutaline 250 mcg SC,salbutamol)
• Forward roll of the fetus is attempted first, each hand grasps one fetal pole, and the fetal
buttocks are elevated from the maternal pelvis and displaced laterally
• Buttocks gently guided toward the fund us, while the head is directed toward the pelvis
• Backflip is attempted if forward roll is unsuccessful
• Discontinue when there is excessive discomfort, persistently abnormal fetal heart rate,
or multiple failed attempt
Contraindications to ECV:
ABSOLUTE CONTRAINDICATIONS I RELATIVE CONTRAINDICATIONS
151
VAGINAL BREECH DELIVERY
• Decision regarding the mode of delivery should depend on the experience of the health
care provider
• Planned vaginal delivery of a term singleton breech fetus may be reasonable under
hospital-specific protocol guidelines
I. CARDINALMOVEMENTSIN BREECH
1 · EN;;s~EE~~NT & I 2. INTERNAL ROTATION I J. LATERAL FLEXION
152
II. PLANNED VAGINAL BREECH CRITERIA:
Skilled OB,anesthesiologist, and delivery room staff
No contraindication to attempted vaginal birth
Facilities for possible CS available
Patient is informed of risks
EFW: 2500-4000 g
Frank or complete breech
Flexed fetal head
Absence of fetal anomalies (e.g., hydrocephalus)
Continuous fetal heart monitoring
Induction is not recommended
• Oxytocin augmentation if with hypotonic uterine dysfunction
• Passive 2nd stage without active pushing for 90 min allowing breech to descend into pelvis
• Once active pushing commences & delivery not imminent after 60 min, CSis recommended
Spontaneous
than support of the baby as it is born
Breech Delivery
• Occurs infrequently and may happen in multi paras
• Delivered by natural forces as far as the umbilicus
• Rest of the body is delivered by the obstetrician
Partial Breech • Delivery ofaftercoming head using (discussed below):
Extraction 0 Mauriceau-Smellie-Veit maneuver
0 Piper Forceps
0 Modified Prague Maneuver
Frank Breech
Extraction
153
IV. BREECHDELIVERYSTEPS
A. General Steps of Breech Delivery
Anesthesia • Request for anesthesia
Episiotomy • Do episiotomy
Spontaneous • Partial breech extraction
delivery • Wait! Don't pull! Hold baby until umbilicus is delivered
Legs • Pinard: lateral rotation of thighs, flex knees
• Delivery when wing of scapula is seen
Arms • Rotate arm to anterior
• Loveset maneuver
Nape • Fetal body rests on arm and apply suprapubic pressure
• Mauriceau-Smellie-Veit maneuver
Aftercoming
• Modified Prague Maneuver
head
• Piper Forceps
Inspect • Check for fetal fractures/injuries or perineal lacerations
Source.ALARM.TheSocietyof 0bstetnc1ansand Gynecologists ofCanada,2012-2013
154
C. Maneuvers in the Management of Head Entrapment
MANEUVER I PROCEDURE I FIGURE
I
• Under local anesthesia, the
symphyseal cartilage is
Symphysiotomy
divided surgically to widen the
symphysis pubis up to 2.5 cm
Source:Cunningham
FG,et al. WilliamsObstetrics;
2018
15S
SECTION FOUR
CESAREAN SECTION
CESAREAN SECTION (CS)
• Fetus is delivered through an incision on the anterior uterine wall accessed through
an incision on the maternal abdominal wall
• Causes for 85% of CS: prior CS, dystocia, fetal jeopardy, abnormal fetal presentation
I. DEFINITIONOF TERMS
TERMS I DEFINITION
Laparotomy • Abdominal wall incision to gain access into the intrabdominal cavity
Hysterotomy* • Uterine wall incision to gain access into the intrauterine cavity
Cesarean section • Uterine wall incision specifically done to deliver a fetus of viable AOG
'The termis alsousedto referto a uterineincisionperformed
to delivera nonviable
fetusformaternalindications
II. INDICATIONSFORCS
• Prior cesarean delivery (depending on type, number, and indication)
• Abnormal placentation
• Prior classical hysterotomy
• Unknown uterine scar type
• Uterine incision dehiscence
• Prior full-thickness myomectomy
• Genital tract obstructive mass
• Invasive cervical cancer
• Prior trachelectomy
Maternal
• Permanent cerclage
• Prior pelvic reconstructive surgery
• Pelvic deformity
• HSVor HIVinfection
• Cardiac or pulmonary disease
• Cerebral aneurysm or arteriovenous malformation
• Concurrent pathology requiring intraabdominal surgery
• Perimortem cesarean delivery
• Maternal request*
• Cephalopelvic disproportion
Maternal-Fetal • Failed operative vaginal delivery
• Placenta previa or placental abruption
• Non-reassuring fetal status
• Malpresentation
• Macrosomia
Fetal • Congenital anomaly
• Abnormal umbilical cord Doppler study
• Thrombocytopenia
• Prior neonatal birth trauma
'If a patientrequestsforCesareansectionwithouta clearindication,
reasonforrequestshouldbe examined,
discussed
anddocumented.Thediscussionshouldincludethe overallbenefitsand risksofcesareandeliverycomparedwith
vaginalbirth.
Source:Cunningham
FG,et al.Williams
Obstetrics;
2018
POGS.CPGon Cesareansection.2012
156
III. TECHNICAL ASPECTS OF CS
A. Types of Uterine Cesarean Incisions (Hysterotomy)
0 The type of CS is determined by the incision on the uterus, and not the abdomen
0 May be classified as:
• Lower segment incision (transverse or vertical)
• Classical cesarean incision
CLASSICAL CS ~
• Upper segment is incised
longitudinally from
above the lower segment
upwards to about 10 cm
_____
1--(_m_o_r_e_o_r_I_e_ss_)
• Preferred over classical incision because it has low
tendency to rupture in the next pregnancy (subsequent
VBAC possible)
• Kerr Incision is preferred since there is only moderate
__________
t-_d_i_ss_e_c_ti_o_n_o_f_t_he_b_Ia_d_d_e_r_,..... ~;
I
· ·
;
Advatanges
• Less blood loss
• Any fetus can be
• Placenta is rarely incised
delivered, regardless of
• Fetal head is easier to extract if fetus is in vertex position
orientation in uterus or
• Uterine muscles easier to approximate
gestational age
• Less incidence of uterine rupture
Disadvantages
• Greater blood loss
• Higher risk of post-
operative adhesions • Risk of bladder injury
• Contraindicated to VBAC • Lower uterine segment must be formed
• Increased risk of uterine
rupture
157
• A straight incision
• Also called the that is 3 cm below
• Also called the median transverse supra pubic the line joining both
infraumbilical longitudinal incision incision or "bikini" anterior superior
• Incision begins 2-3 cm above the incision iliac spines.
superior margin of the symphysis • Preferred for aesthetic • Advantages over
and 12-15 cm in length reasons Pfannenstiel include:
• Quickest to make • Low curvilinear 0Shorter duration of
• Allows faster abdominal entry, incision made at the surgery
causes less bleeding and superficial level of the pubic 0Less blood loss,
nerve injury, and can be easily hairline, 3 cm above fever, and pain
extended cephalad if more space is the superior border of ° Fewer analgesic
required for access symphysis pubis requirements
• 12-15 cm in length 0Shorter
hospitalization
158
VAGINAL BIRTH AFTER CESAREAN (VBAC)
• Describes a vaginal delivery in a woman who has given birth via CS in the past
• May be considered in patients with:
Baby on vertex presentation
,;2 previous low transverse uterine scar (2 previous transverse CS should be offered
and counseled regarding VBAC)
No contraindication to vaginal birth
Operative records which may include opinion of the obstetrician of previous delivery
Source:
AGOG.Practice
BulletinNo.205.2019
If the patient has had one previous CS, would she still be able to deliver vaginally?
• It depends on the type and on the reason why the CSwas done in the first place
• If the CS was a low transverse incision, a VBACmay be considered
• If the reason is a non-permanent indication, a VBACmay be considered (i.e., placenta
previa, non-reassuring fetal status, malpresentation)
• If the reason is a permanent indication, VBACis contraindicated (i.e., contracted pelvis,
pelvic deformity)
I .
B F Aff VBACO
INCREASES LIKELIHOOD OF
SUCCESSFULVBAC
I DECREASES LIKELIHOOD OF
SUCCESSFULVBAC
REGIONAL ANESTHESIA
• Most commonly used technique in obstetric procedures
• Includes subarachnoid block, epidural block, peripheral nerve block
160
III. LANDMARKS
A. Iliac Crest
0 Transverse line connecting highest points of iliac crest (Tuffier line)
0 At L4-LS intervertebral space where lumbar puncture is usually done, and spinal
anesthesia is introduced
• Saddle and epidural block can also be given in this area
B. Lumbar Puncture
° Common vertebral level: L4-LS interspace
0 Avoids injury to the spinal cord
I
• Skin infections at puncture site*
• Clotting defect
• Hypovolemia / dehydration / shock
• Sepsis
• Increased intracranial pressure (risk of herniation)
• Neurologic diseases (including psychiatric diseases)
• Deformities of spine or vertebral column
• Prolapsed vertebral disk
•Absolutecontraindications
to regionalanesthesia
161
VI. FREQUENTLYUSED DRUGS IN REGIONALANESTHESIA:
DRUGS
I ONSET I DURATION
I CLINICAL USE
• Epidural for cesarean & labor
• 3 hours
• 4-10 analgesia
Bupivacaine • Extended to 4 hours if
minutes • Spinal for CS
with epinephrine wash
• Saddle block for vaginal delivery
• 2-2.5 hours
• 2-10 • Low spinal block
Tetracaine • Extended to 3 hours if
minutes • Spinal for CS
with epinephrine wash
• Limited to 1.5 hours
• 1-3 • Pudenda! block
Lidocaine • Extended to 2.5 hours if
minutes • Epidural for CS
with epinephrine wash
162
GENERAL ANESTHESIA
• Includes inhalation and intravenous types
• Usually avoided because of greater risk for mother and baby during procedure
• Complications
• Mendelson syndrome (aspiration pneumonitis): a complication from vomiting and
aspiration of gastric contents
• Possibility of anesthetics crossing the placental barrie1; thereby causing
fetal depression
I. TYPES OF GENERALANESTHETICS
ANESTHETIC I REMARKS
Inhalational Anesthetics
Enflurane
Halothane
• Can be used for labor analgesia during vaginal delivery
• No adequate studies in pregnant women
• High risk for uterine atony
I
. '
163
REFERENCES
l.ACOG Practice Bulletin No. 205: Vaginal birth after cesarean delivery. (2019). Obstetrics & Gynecology, 133(2), el 10-e127.
https://doi.org/10.1097 / AOG.0000000000003078
2.ACOG
CommitteeOpinionNumber761. Cesareandeliveryon maternalrequest.January2019
3.Advancesin Labour and Risk Management (ALARM) Course Manual, 19th Edition, The Society of Obstetriciansand
Gynecologists of Canada. 2012-2013
4.Barash, P.G. (2017). Clinical Anesthesia 8th edition. Philadelphia: Wolters Kluwer.
S.Chestnut,D.H. (2014). Chestnut'sObstetricAnesthesia:Principlesand Practice5th edition.Philadelphia:ElsevierSaunders.
6.Cunningham, E G., Levene, K J.. Bloom, S. L.. Spong. C. Y.,Dashe, J.S., Hoffman, B. L.,Sheffield,). S. (2018). Williams obstetrics
(25th edition.). New York: McGraw-Hill Education.
7.Handa,Victoria L; Van Le, Linda (2019) Te LindesOperativeGynecology12th edition Lippincott Williams & Wilkins
8.Hofmeyr GJ,Shweni PM: Symphysiotomyfor feta-pelvicdisproportion.CochraneDatabaseSystRev 10:CD005299, 2012
9.Hulka,). Glob. libr. women's med.,(ISSN: 1756-2228) 2008; DOI 10.3843/GLOWM.10037
10. LandonMB, HauthJC,LeveneKJ,SpongCY,LeindeckerS,Varner MW, et al. Maternal and perinataloutcomesassociatedwith
a trial oflabor after prior cesarean delivery. N Engl J Med 2004;351(25):2581-9.
11. LandonMB, SpongCY,Thom E, et al: Riskof uterine rupture with a trial of labor in women with multiple and singleprior
cesareandelivery.ObstetGynecol108:12, 2006
12. National Institutes of Health ConsensusDevelopment Conference Panel: National Institutes of Health Consensus
Development conference statement: Vaginal birth after cesarean: new insights. March 8-10, 2010. Obstet Gynecol
115:1279, 2010
13. Operative Vaginal Birth: ACOGPractice Bulletin, Number 219. Obstet Gynecol 2020; 135:el49.
14. Postgraduate Manual of Obstetrics & Gynecology for Practical Examination by By Neerja Goel, Shalini Rajaram, Sandhya
Jain,SumitaMehta
15. Sandberg EC: Shoulder dystocia: associatedwith versus caused by the Zavanelli maneuver. Am J Obstet Gynecol
197(1):115, 2007
16. SOGC.(2010) Advances in Labour and Risk Management Textbook (ALARM)Course Syllabus. Operative Vaginal Delivery.
SOGC.Ottawa, Ontario
17. SOGC.(2010} Advances in Labour and Risk Management Textbook (ALARM) Course Syllabus. Vaginal Breech Delivery.
SOGC.Ottawa, Ontario
18. The Societyof Obstetriciansand Gynaecologists of Canada.Advancesin Labourand RiskManagement.19th Edition.2012-
2013
19. Yeomans ER. Hoffman BL, Gilstrap LC, Cunningham FG. Cunningham and Gilstrap's Operative Obstetrics (3rd Ed).
McGraw-Hill Education. 2017
164
PUERPERIUM
AND
POSTPARTUM
COMPLICATIONS
SECTION ONE
THE PUERPERIUM
THE PUERPERIUM (POSTPARTUM PERIOD)
• From Latin "puer" (child)+ "parus" (bringing forth)
• The time after delivery when maternal physiologic changes related to pregnancy return
to the non-pregnant state usually by 6 weeks post-delivery
• Begins as soon as placenta is expelled and lasts for ~6 weeks when uterus regresses to
almost the non-pregnant size
DIVISION
I BIRTH CANAL
I CERVIX
I UTERUS
I
PLACENTAL
SITE
I
• Becomes firm &
• Soft and relaxed retracted with
• Contracts
immediately alternate hardening
rapidly
after birth & softening
• Vagina is • Raised surface
Immediate • Begins to • Fundus lies
greatly • Measures~ 7.5
(within 24 contract slowly just below the
distended with cm (palm-size)
hours) • Cervical as umbilicus
smooth walls • Consists of
(dilated at 10 • Lower segment
thrombosed
cm) closes becomes thin, and
vessels
gradually collapsed
• Weighs ~1000 g
• Fundus descends
halfway between
• Remains • Decreases in
symphysis pubis
edematous and size: ~3-4 cm
and umbilicus
thin for several by the end of
• Within 2-3 days,
days the 2nd week
• Thickening of the decidua
• Possible to • Initially
Early vaginal mucosa differentiates into
introduce 2 consists of
(up to 7 with return two layers:
fingers into thrombosed
days) of ovarian • Superficial layer
cervical os vessels,
function is sloughed in
for first 4-6 ultimately
the lochia
postpartum days undergoes
• Basal layer is the
(i.e., admits 2 organization
11 source of new
fingers)
endometrium
• Weighs ~500 g
• Vaginal rugae • Complete
• Returns to its
reappear at involution
normal state • Remains
3rd week • Lower segment
at 4 weeks elevated
• lnvolutes over reverts back to
postpartum • Decreases in
Remote 4-8 weeks normal shape &
• External os does size: ~1.5 cm
(up to 6 • Regains tone, size of the isthmus
not completely • Complete
weeks) but never to the • Endometrium at
resume its extrusion of
virginal state the placental site is
pregravid placental site
• Proliferation restored
appearance
of the vaginal • Weighs ~SOg
epithelium
Source:Cunningham
FG,et al. WilliamsObstetrics
25thEdition;2018
167
I. BIRTH CANAL:VAGINA& VAGINALOUTLET
• Early in puerperium, the vagina & its outlet form a spacious, smooth-walled passage that
gradually diminishes in size but rarely return to nulliparous dimensions
• By the 4-6th week postpartum, vaginal epithelium begins to proliferate, coincidental with
resumed ovarian estrogen production
• Lacerations or stretching of the perineum during delivery may result in relaxation of the
vaginal outlet
II. CERVIX
• External os is usually lacerated laterally
• By the end of 1st week:
° Cervical opening narrows, the cervix thickens, and endocervical canal reforms
0External os remains wider and bilateral depressions at the site of lacerations become
permanent (changes characteristic ofa parous cervix)
• Cervical epithelium undergoes considerable remodeling
III. UTERUS
A. Uterine Involution
Delivery day
2 days postpartum
4 days postpartum
6 days postpartum
8 days postpartum
• After placental expulsion, fund us of the contracted uterus lies slightly below umbilicus
• Fundus descends about 1-2 cm every 24 hours
• By 6th postpartum day, fund us is located halfway between symphysis pubis & umbilicus
• It takes up to 8 weeks for the uterine cavity to regress to its nonpregnant state.
B. Lochia
Vaginal discharge from sloughed off decidual tissue which consists of erythrocytes,
0
TYPE I DESCRIPTION
• Blood from first few days after delivery
Lochia rubra
• Flow in amounts like a heavy menstrual period
(red)
• Persistence ofred lochia means subinvolution
• From 4 to 12 days (~2 weeks postpartum)
Lochia serosa • Color becomes paler
• Flow is light to moderate in amount
• At about 10th day to 3 weeks postpartum
Lochia alba
• Because of admixture of leukocytes & reduced fluid content, it
(pale white)
assumes a white or yellowish-white color
168
C. Clinical Correlations
I
CORRELATION REMARKS I MANAGEMENT
• Secondary to uterine involution
• Similar to but milder than labor
contractions
• More pronounced as parity increases
and worsens when the infant suckles
0 Primipara: uterus tends to remain
Afterpains tonically contracted after delivery • Analgesics as needed
0 Multi para: contracts vigorously at
intervals similar to (but milder) the
pain of labor contractions
• Occur during the first 2-3 days of
puerperium (intensity decreases after
1st postpartum day)
■
• Arrest or retardation of involution • Methylergonovine (if not
• Suspected when there is prolongation contraindicated)
of lochial discharge and irregular or • Prostaglandin-E analogue
excessive uterine bleeding (e.g., Carboprost,
Subinvolution • Uterus is larger & softer than would be Misoprostol*)
expected • Antibiotics if due to
• Retention of placental fragments, metritis
anemia, and pelvic infection may also • Hematinics if with
cause subinvolution anemia
• Oxytocin
• Methylergonovine (if not
contraindicated)
• Prostaglandin-E analogue
(e.g., Carboprost,
• Bleeding 24 hours to 12 weeks after
Misoprostol*): if
delivery
sonography reveals an
Secondary • Usually due to abnormal involution of
empty cavity
Postpartum the placental site
• Gentle suction curettage if
Hemorrhage • Occasionally due to retention of a
with large clots in cavity
placental fragment or a uterine artery
• Antibiotics for infection
pseudoaneurysm
• Curettage not routinely
performed (it may
worsen bleeding)
• Hematinics if with
anemia
• Misoprostol
is notFDAapprovedforuse in the localsetting
169
IV.LACTATION
• In breastfeeding mothers, lactation is the most dominant physiologic event of the puerperium
• After delivery, estrogen and prolactin levels decrease - however with suckling, amount of
prolactin produced by the pituitary is elevated (let-down reflex)
• Colostrum ( deep lemon-colored liquid) is secreted by the breasts and can be expressed
from the nipple by the second postpartum day and may persists for 5 days to 2 weeks
• Gradual conversion of "transitional milk" to mature milk may take place in 4-6 weeks
I LACTATING
(BREASTFEEDING) MOTHERS*
I NON-LACTATING MOTHERS
170
POSTPARTUM CARE
I. HOSPITALCARE(FACILITY-BASED)
ASPECT I REMARKS
• BP and pulse every 15 minutes for the first 2 hours after delivery
• Temperature every 4 hours for the first 8 hours after delivery
• Amount of vaginal bleeding
• Uterus is closely monitored at least 1 hour after delivery
Monitoring
° Fund us palpated to ensure that it is well contracted
0 If there is relaxation, it should be massaged through abdomen until it is
contracted
• Take note if regional anesthesia or general anesthesia was used
• Should be done as soon as possible
0 Vaginal delivery: ambulate within 12 to 24 hours
° Cesarean delivery: ambulate after 24 hours
■
Early • _Advantages of early ambulation:
ambulation ° Fewer bladder complications
0 Less frequent constipation
0 Reduced puerperal venous thrombosis
0 Reduced pulmonary embolism
• Cleanse vulva from anterior to posterior, toward the anus
• Ice bag applied to the perineum may reduce edema & discomfort from a
laceration or episiotomy
• Local anesthetic spray may also provide periodic relief; analgesics if needed
Perinea[ • Severe perinea!, vaginal, or rectal pain always warrants careful inspection
care and palpation, and may indicate:
0 Hematoma (if within 24 hours postpartum)
0 Infection after 3rd or 4th day
• Episiotomy incision normally is firmly healed and nearly asymptomatic by
the 3rd week
• If abdomen is unusually flabby or pendulous, an ordinary girdle is often
Abdominal s.atisfactory
wall • Exercise to restore abdominal wall tone may be started any time after
relaxation vaginal delivery and as soon as abdominal soreness diminishes after
cesarean delivery
• Uncomplicated vaginal delivery: may be given food after 2 hours with no
dietary restrictions
Nutrition
• Increased caloric and protein requirements because of lactation.
• Continue iron supplementation for at least 3 months after delivery
Bladder
• Urinary retention & bladder overdistention: common in early puerperium
function
Source:Cunningham
FG,et al. WilliamsObstetrics25thEdition;2018
II. HOMECARE
• May resume after 2 weeks based on desire and comfort
Coitus
• Hypoestrogenic state may cause dryness, requiring vaginal lubricants
Common • Fatigue, breast problems, anemia, backache, hemorrhoids, headache,
morbidity "blues", constipation, suture breakdown, and vaginal discharge
• Uncomplicated vaginal delivery: can resume most activities like bathing,
Follow-up driving, household chores
care • Postpartum visit: maybe done 1 week after to identify early problems,
then 4-6 weeks after to initiate contraceptive practices
Source:Cunningham
FG,et al. WilliamsObstetrics25thEdition;2018
171
POSTPARTUM HEMORRHAGE
Discussed in detail in Chapter 7
I. DEFINITIONS
Postpartum • ;,1000 mL blood loss after completion of the third stage of labor with
Hemorrhage signs and symptoms of hypovolemia
• Bleeding after 24 hours to 12 weeks after delivery
• May be due to abnormal involution of placental site or retention of
Late placental tissue (e.g., placental polyp)
postpartum • Initial treatment: medical control of bleeding (e.g., oxytocin, ergonovine,
hemorrhage prostaglandins)
• Curettage is carried out only if appreciable bleeding persists or recurs
after medical management
I DESCRIPTION
I MANAGEMENT
• Uterotonic agents
• Bimanual uterine compression
• Most frequent cause of • Tamponade (e.g.. Bakri balloon)
obstetrical hemorrhage • Surgical procedures
Uterine atony • Inability of the uterus to 0 Uterine compression sutures (e.g.,
contract sufficiently after 8-Lynch sutures)
delivery 0 Pelvic vessel ligation (internal iliac)
0 Angiographic embolization
0 Total or subtotal hysterectomy
• May be cause by • Gentle suction cur!;!ttage (if with
Placental site retention of a placental sonographic evidence retained
subinvolution fragment or uterine artery placental fragments/blood clots)
pseudoaneurysm • Uterotonic agents
• Primary: rupture of a
previously unscarred uterus
Uterine • Uterine repair
• Secondary: rupture due to a
rupture • Total or subtotal hysterectomy
preexisting incision, injury
or myometrial abnormalities
Uterine • Uterine fundus turns partially • Manual repositioning of uterine fund us
inversion or completely inside out • Surgery
• Suturing of lacerations
• Includes vulvovaginal and
Genital tract • Large, expanding hematomas
lacerations & puerperal
trauma repaired surgically by evacuating
hematomas
clots and ligating bleeding vessels
• Intravascular activation of
Consumptive
clotting • Prompt identification and removal of
Coagulopathy
• Most common cause: the cause of the coagulopathy
or DIC
placental abruption
Source:Cunningham
FG,et al.WilliamsObstetrics
25thEdition;2018
172
III. UTEROTONIC
AGENTS
• Uterotonics are pharmacologic agents that induces uterine contractions are given for the
prevention and treatment of postpartum hemorrhage
MECHANISM OF
AGENT
I ACTION
I DOSE
I REMARKS
.,
First Line
• Binds to oxytocin
• Prevention: 10 lU IM • Overdose or
receptors in the
or 5-10 !U IV bolus prolonged use
myometrium
• Treatment: 20-40 lU can cause water
stimulating
Oxytocin + lL normal saline: intoxication
contractions
infuse 500 mL over • Possible hypotension
by increasing
10 mins, then infuse with IV use following
permeability of
at 250 mL/hr cesarean delivery
uterine myofibrils
■
I>
Second{.ine r:I .~ .,.,
Methyl- • Ergot alkaloids • Used as second line to
• Treatment: 0.2
ergonovine & increase uterine treat uterine atony
mg IM, every 2
Ergonovine muscular tone by • Do not give IV since it
to 4 hours if with
(Ergot causing sustained may cause dangerous
Alkaloids) bleeding
uterine contractions hypertension
• Maybe given during
• Prevention: delivery of the
125 ug IM anterior shoulder
• Treatment: • Should not be used
• Prostaglandin F2 250 ug IM & may for women with
Carboprost
alpha analogues be repeated at asthma, preeclampsia
15-90-minute or those suspected
intervals up to a for amniotic fluid
maximum of8 doses embolism.
• May cause diarrhea
• Prevention: 600mcg
orally • Caution in those with
• Prostagladin El • Treatment: 800 to cardiovascular disease
Misoprostol*
analogue 1000 mcg rectally • Side effects include
or 600 to 800 mcg shivering and fever
sublingually
• Long acting
analogue of oxytocin
with agonist
properties
• Binds to oxytocin
receptors in uterine • Can cause
smooth muscle hypotension and
• 100 mcg IV over 1
Carbetocin resulting in: tachycardia
minute
0 Rhythmic • Can cause water
contractions retention
0 Increased
frequency of
contractions
0 Increased uterine
tone
• Misoprostolis not FDAapprovedforuse in the localsetting
Source:CunninghamFG,et al. WilliamsObstetrics25th Edition:2018;EvensenA, et al. AmFam Physician;2017
WHO;2018
173
PUERPERAL INFECTIONS
• General term used to describe any bacterial infection of the genital tract after delivery
• Part of the lethal triad of maternal death (puerperal infections, preeclampsia, and
obstetrical hemorrhage)
I. PUERPERAL FEVER
• Oral temperature ;c38°C on any 2 of the first 10 days postpartum, exclusive of the first 24
hours, taken at least four times daily
• Most persistent fever after childbirth are caused by genital tract infection
DIFFERENTIALS
I REMARKS
Genital tract infection • Infections involving the perineum, vagina, cervix, and uterus
• The basalis layer of the uterus is iatrogenically disrupted where infection can
Cesarean traverse the layers of the uterus
section • Presence of foreign body (e.g., sutures), myometrial injury, hematomas and
necrosis at the suture line further enhance the potential for infection
3. Microbiology
• Most pelvic infections are caused by bacteria indigenous to the female genital tract
• Bacteria commonly responsible:
• Streptococci,Enterococcus,Gram(-) Bacteria(£ coli,Klebsiella,Proteus),
Aerobes
Staphylococcusaureus,Staphylococcusepidermidis, Gardnerellavaginalis
• Bacteroidesfragilis,Peptococcusspp, Peptostreptococcusspp, Prevotellaspp,
Anaerobes
Clostridiumspp, Fusobacteriumspp, Mobiluncusspp
Others • Mycoplasmaspp, Chalmyd.iatrachomatis.Neisseriagonorrhea
174
B. Manifestations
° Fever: most important criterion for the diagnosis of postpartum metritis (temperature
commonly exceeds 38°C)
0Abdominal pain, bothersome afterpains, malaise
0Parametrial tenderness
° Foul smelling discharge or lochia
0Uterine or parametrial tenderness on bimanual exam
C. Management
SEVERITY
I MANAGEMENT*
• Oral or intramuscular antimicrobials:
Non-severe
, Ampicillin + Gentamicin, OR
metritis 0 Amoxicillin-clavulanicacid orally q12 x 7 days
Moderate to severe • IV broad-spectrum antibiotics:
metritis (including ° Clindamycin+ Gentamicin (gold standard), PLUS
■
those following CS) 0 Ampicillin(if with sepsis syndrome or suspected enterococcalinfection)
'Improvement
followsin48-72hrs (persistenceof fevermandatessearchforcauses of refractorypelvicinfection)
D. Prevention of Infection
Perioperative antimicrobial • Single-dose Ampicillin 2g or first-generation cephalosporin
prophylaxis (e.g.,cefazolin 2 g IVANST)
• Allow placenta to separate spontaneously
Operative technique
• Avoidexteriorizing the uterus to close the hysterotomy
Source:Cunningham
FG,et al. Williams
Obstetrics25thEdition;2018
B. Manifestations
, Local pain and dysuria, with or without urinary retention
Most common findings: pain, purulent discharge, fever
0
Vaginal lacerations may become infected directly or by extension from the perineum
0
° Cervical lacerations are common, and the cervix normally harbors potentially
pathogenic organisms
17S
IV.UTERINE& PELVICINFECTIONS
ETIOPATHOGENESIS
I MANIFESTATIONS
I MANAGEMENT
Peritonitis
,, • Peritonitis may be severe
• Most often caused by uterine • Adynamic ileus may be the • Antibiotics with or
incisional necrosis and dehiscence; first symptom without surgical
others: ruptured adnexal abscess or • Severe pain intervention
inadvertent bowel injury at CS • Abdominal tenderness
Parametrial Phlegmon
• Parametrial cellulitis that forms an • Fever persists > 72 hours • Antibiotics
area of induration (phlegmon) within despite IV antibiotics • Surgery
the leaves of the broad ligament, • CTscan (hysterectomy &
seen in those who develop metritis debridement) for
following Cesarean delivery uterine incisional
• Most common form of extension is necrosis because of
laterally along the broad ligament. ileus & peritonitis
with a tendency to extend to the • CT-directed needle
pelvic sidewall aspiration
Septic Pelvic Thrombophlebitis
• Arises as an extension along venous • Presence of metritis with • Antibiotics
routes and may cause thrombosis. fever despite ;eS days of
• Puerperal septic thrombophlebitis is appropriate antibiotics
likely to involve one or both ovarian • Abdominal pain & chills
venous plexuses because they drain • Diagnosis confirmed by
the upper uterus and therefore the either pelvic CT or MRI
placental implantation site
Toxic.ShockSyndrdlne .
• Acute febrile illness with severe • Fever. headache, confusion, • Supportive (principal
multisystem derangement diffuse macular erythematous therapy]
• Most common etiologic agent: rash, subcutaneous edema, • Antibiotics
Staphylococcus aureus, exotoxin nausea, watery diarrhea, and • If with pelvic
(TSST-1) marked hemoconcentration infections: requires
• Others: group A B-hemolytic • Complications: renal failure wound debridement
streptococcus serotypes M1 and M3, followed by hepatic failure, and possibly
Clostridium sordellii DIC and circulatory collapse hysterectomy
Source: CunninghamFG, el al. WilliamsObstetrics25th Edition;2018
176
THROMBOEMBOLIC DISEASE
I. ETIOPATHOGENESIS
A. Incidence
° Five times more common in pregnancy and puerperium
0 Early ambulation after delivery decreases the risk ofthromboembolic disease
B. Predisposing Factor:
0 Stasis
0 Oral contraceptive use before conception
0 Jobs where pregnant women sits for long period of time (sedentary lifestyle)
0 Deficiency of proteins involved in coagulation inhibition or in fibrinolytic system (e.g.,
Antithrombin-111, Protein-C, Protein-S, Plasminogen)
II. MANIFESTATIONS,
DIAGNOSIS,MANAGEMENT
MANIFESTATIONS I DIAGNOSIS I MANAGEMENT
■
Superficial Venous, Thrombo$is ·
• Thrombosis limited to the • Clinical • Analgesia
superficial veins of the saphenous • Elastic support
system
'!''i'1-
Deep Venq,us Thrombosis (DVT)
• Phlegmasia alba do lens or milk leg: • Compression • Anticoagulation
reflex arterial spasm causes a pale, ultrasonography throughout
cool extremity with diminished • D-dimer (if with low pregnancy and
pulsations probability of disease) postpartum
• Most are confined to the deep veins
of the lower extremity, leading to
pain, edema of the leg & thigh
Pulmonar,y Embolism-(PE)
• Causes 10% of maternal deaths • High index of suspicion • Anticoagulation
• May present with dyspnea, chest • Chest X-ray • Placement of
pain, syncope, hemoptysis • Ventilation/perfusion vena caval filters
• Massive PE: embolism causing scintigraphy considered
pulmonary instability with sudden • Computed tomographic • Thrombolysis
onset pulmonary hypertension and pulmonary angiography • Embolectomy
circulatory collapse
Source:Cunningham
FG,et al. WilliamsObstetrics25thEdition;2018
Iii. ANTICOAGULATION
THERAPY
THERAPY I REMARKS
• Anticoagulation is initiated using either unfractionated heparin
(UFH) or Low molecular weight heparin (LMWH)
Heparin • UFH: initial treatment of thromboembolism and during delivery,
surgery or thrombolysis
• LMWH:preferred for acute venous thrombosis
• Vitamin K antagonist: contraindicated during pregnancy but can be
Warfarin
given orally during postpartum along with heparin
Newer oral • Dabigatran: thrombin inhibitor
anticoagulants • Rivaroxaban and apixaban: factor-Xa inhibitor
177
UTERINE COMPLICATIONS IN THE PUERPERIUM
178
DISORDERS OF THE BREAST
• Breast fever: not unusual for breasts to become distended with transient elevation of
temperature for the first 24 hours after commencement of lactation
• Puerperal fever from breast engorgement is common
• Fever seldom persists for> 16 hours
I. ABNORMALITIESOF SECRETION
• Marked individual variations in the amount of milk secreted
• It is not dependent on general health/ appearance of woman but on development of
glandular portion of breast:
0 Agalactia: no milk secretion
0 Polygalactia: excessive milk secretion
• Pituitary microadenoma: most common cause of galactorrhea, amenorrhea, estrogen
deficiency
II.OTHERS
I MANIFESTATIONS I MANAGEMENT
■
ETlOPATHOGENESIS
__ ____ =---------.------------'-~~-=....c..,~----~------"--------------1
1-B_r:~e~a"'s""C_'E_n"'g_o_11_y_e_m
e~n-t
• Due to exaggeration of normal • Pain • Support with brassiere
venous and lymphatic channels of • Transient increase • Cold compress
breast of temperature • Analgesic, antipyretic
• Breast pump/manual
expression of milk
Mastitis
• Infected breasts: parenchymatous • Chills or actual rigor, • Culture & sensitivity
infection of the mammary glands followed by fever & of milk
• Occurs on 3rd-4th week postpartum tachycardia • Antibiotics (penicillin /
(symptoms seldom occur in the first • Breast engorgement cephalosporin)
week postpartum) • Inflammation • Stop breastfeeding
• Infection is unilateral & marked temporarily
engorgement precedes inflammation • Drainage of abscess
• Staphylococcusaureus (most common)
179
OTHER PROBLEMS IN THE PUERPERIUM
ETIOPATHOGENESIS I MANIFESTATIONS I MANAGEMENT
Maternityl'_Postpartum Blues
"
• Emotional letdown that • Emotionally labile • Self-limited: 2-3 days
follows the excitement and • Insomnia up to 10 days
fears experienced during • Weepiness • Effective treatment
pregnancy & delivery • Depression includes anticipation,
• Common within the first week • Anxiety recognition, and
postpartum • Poor concentration reassurance
• Usually secondary to: • Irritability • May be improved
0 Discomforts of early • Affective !ability with counselling and
puerperium & delivery psychotherapies
° Fatigue from loss of sleep
0 Anxiety over capability to
care for the baby
,ii . •,;: .. ·- "
Neuromuscular &Join_tProblems ~
.,
• Obstetrical neuropathies: • Intense neuralgia and • Anti-inflammatory
labor can cause pressure cramp like pains • Physical therapy
on the branches of the • If nerve is injured, pain,
lumbosacral nerve plexus sensory loss, & muscle
• Musculoskeletal injuries: paralysis may ensue
stretching/tearing injuries • Median duration of
during normal or difficult symptoms- 2months (2
delivery weeks to 18 months)
Urinary Retentio~f& Blaffder Qverdisteniion
• Antidiuretic effects of • Enlarged bladder on • Examine for perinea!
oxytocin palpation and genital-tract
• Local or conduction analgesia • Inability to void within 4 hematomas
may cause inability of bladder hours after delivery • Insert indwelling foley
to empty spontaneously catheter for 24 hours,
• Trauma to the bladder until factors causing
(episiotomy, lacerations or retention have abated
operative vaginal delivery) • Intermittent self
catheterization
Source:Cunningham
FG,et al. WilliamsObstetrics25thEdition;2018
180
J. LEGALFRAMEWORKSRELATEDTO BREASTFEEDING
LEGAL
FRAMEWORK I REMARKS
Republic Act 7600: • An act providing incentives to all government and private health
Rooming-in and
institutions with rooming-in and breastfeeding practices for other
Breastfeeding Act
of1992 purposes
■
Promotion Act of
2009
Standards for
Rooming-in & • Rooming-inwithin 30 mins to 1 hour after delivery
Administrative
Order 2009-0025: Breastfeeding • Infants without complications shall be given to
Essential Newborn for Vaginal their mothers to hold and caress (skin-to-skin
Care Protocol deliveries contact) immediately after birth after the first
with awake 30 seconds of thorough drying
mothers
181
LEGAL
FRAMEWORK
I REMARKS
World Health • To improve, through optimal feeding, the nutritional status, growth
Assembly and & development, health, and survival of infants & young children
UNICEF:Global • Supports exclusive breastfeeding for 6 months, followed by timely,
Strategy on Infant adequate, safe and appropriate complementary feeding, while
and Young Child continuing breastfeeding for two years and beyond.
Feeding in 2002 • Supports maternal nutrition, and social and community support
II. HUMANBREASTMILKCOMPOSITION
COMPONENT I AMOUNT
Fats
-
Total • 4.2 g/l00mL
Fatty acids • Trace
Polyunsaturated • 0.6 g/l00mL
fatty acids (PUFA)
Cholesterol • 0.016 g/1 00mL
Proteins
-
Total • 1.1 g/l00mL
182
III. MILKPRODUCTIONSUPPLEMENT
• Malunggay capsule supplements can increase the breast milk quantity without affecting
its quality
Estrellaet al.,2000
■
effectively or get the milk easily
V. BABY'SSUCKLING
GOOD SUCKLING I POOR SUCKLING
• The baby takes slow, deep sucks, • Rapid, shallow sucks and smacking or
sometimes pausing for a short time clicking sounds
• You can see or hear the baby swallowing • Has cheeks drawn in
• Baby's cheeks are full and not drawn • Feeds very frequently
inward during a feed • Feeds for a very long time - for more than an
• Baby finishes the feed & releases the hour at every feed
breast by him/herself & looks contented • Does not release breast & seems unsatisfied
• Mother feels no pain • Mother feels pain
VI. BREASTCARE
• Clean breasts with water only. Soaps, lotions, oils, and vaseline all interfere with the
natural lubrication of the skin
• Washing the breasts once a day as part of general body hygiene is sufficient
• It is not necessary to wash the breasts directly before feeds (this removes protective oils
and alters the scent that the baby can identify as his or her mother's breasts)
• Brassieres are not necessary, but can be used if desired
Source:WHO/UNICEF; 2009
CunninghamFG,et al. Williams
Obstetrics25thEdition;2018
183
REFERENCES
!.American Academy of Pediatrics, American College of Obstetricians and Gynecologists: Guidelines for Perinatal Care, 8th ed.
Elk GroveVillage, MP. 2017
2.American College of Obstetricians and Gynecologists: Inherited thrombophilias in pregnancy. Practice Bulletin No. 138,
September 2013, Reaffirmed 2017c
3.American College of Obstetricians and Gynecologists: Postpartum hemorrhage. Practice Bulletin No. 183, October 2006,
Reaffirmed 2017
4.American College of Obstetricians and Gynecologists: Thromboembolism in pregnancy. Practice Bulletin No. 123, September
2011, Reaffirmed 2017
S.American College of Obstetricians and Gynecologists: Use of prophylactic antibiotics in labor and delivery. Practice Bulletin
No. 120, June 2011, Reaffirmed 2016
6.Atkinson MW. Owen J.Wren A, et al: The effect of manual removal of the placenta on post-cesarean endometritis. Obstet
Gynecol 87:99, 1996
7.Bamigboye AA, Hofmeyr GJ: Closure versus non-closure of the peritoneum at caesarean section. Cochrane Database Syst
Rev 8:CD000!63, 2014
8.Bates SM, Greer IA, Middledorp S, et al: VTE, thrombophilia, antithrombotic therapy, and pregnancy. Chest 141:e691S, 2012
9.Breastfeeding promotion and support in a baby-friendly hospital. Baby-friendly Hospital Initiative. WHO/UNICEF. 2009
10. Buhimschi CS, Buhimschi IA, Malinow AM, et al: Myometrial thickness during human labor and immediately postpartum.
Am) Obstet Gynecol 188:553, 2003
11. Chelmow D, Rodriguez EJ,Sabatini MM: Suture closure of subcutaneous fat and wound disruption after cesarean delivery:
a meta-analysis. Obstet Gynecol 103:974, 2004
12. Cunningham FG, Nelson DB: Disseminated intravascular coagulation syndromes in obstetrics. Obstet Gynecol 126(5):999,
2015
13. Cunningham, F.G.,Levene, K.)., Bloom, S. L.,Spong, C.Y.,Dashe, ). S., Hoffman, B. L.,Sheffield, ). S. (2018). Williams obstetrics
(25th edition.). New York: McGraw-Hill Education.
14. Dagdeviren H, Cengiz H, Heydarova U, et al: Intramuscular versus intravenous prophylactic oxytocin for postpartum
hemorrhage after vaginal delivery: a randomized controlled study. Arch Gynecol Obstet 294(5):911, 2016
15. Estrella, M.C.P.& Mantaring. Jacinto & David, G.Z.. (2000). A double-blind, randomized controlled trial on the use of
malunggay (Moringa oleifera) for augmentation of the volume of breastmilk among non-nursing mothers of preterm
infants. Philipp) Pediatr. 49. 3-6.
16. Evensen A. Anderson J.Chapter JM, Fontaine P. Postpartum Hemorrhage: Prevention and Treatment. Am Fam Physician.
2017; 95 (7):442-449
17. Goldhaber SZ, Visani L, De Rosa M: Acute pulmonary embolism: clinical outcomes in the International Cooperative
Pulmonary Embolism Registry (!COPER). Lancet353:1386, 1999
18. Hauth JC, Owen J, Davis RO: Transverse uterine incision closure: one versus two layers. Am J Obstet Gynecol 167:1108,
1992
19. Jackson, Emily MD,MPH; Glasie1;Anna MD Return of Ovulation and Menses in Postpartum Nonlactating Women, Obstetrics
& Gynecology: March 2011-Volume 117 - Issue 3 - p 657-662 doi: 10.1097 /AOG.Ob0!3e31820ce18c
20. facobs-fokhan D, Hofrneyr G: Extra-abdominal versus intra-abdominal repair of the uterine incision at caesarean section.
Cochrane Database Syst Rev 4:CD000085, 2004
21. Lee CY, Madrazo 8, Drukker BH: Ultrasonic evaluation of the postpartum uterus in the management of postpartum
bleeding. Obstet Gynecol 58:227, 1981
22. Lobo RA,Gershenson DM, Lentz GM, Valea FA.Comprehensive Gynecology. 17th Ed. Philadelphia: Elsevier; 2017.
23. Mackeen AD, Berghella V, Larsen ML: Techniques and materials for skin closure in caesarean section. Cochrane Database
Syst Rev I l:CD003577, 2012
24. Meaney-Delman D, Bartlett LA, Gravett MG, et al: Oral and intramuscular treatment options for early postpartum
endometritis in low-resource settings: a systematic review. Obstet Gynecol 125(4):789, 2015
25. Mulder FE, Hakvoort RA. de Bruin JP,et al: Comparison of clean intermittent and transurethral indwelling catheterization
for the treatment of overt urinary retention after vaginal delivery: a multicentre randomized controlled clinical trial. Int
Urogynecol J August 30,2017
26. Quinlan DJ, McQuillan A, Eikelboom JW: Low-molecular-weight heparin compared with intravenous unfractionated
heparin for treatment of pulmonary embolism: a meta-analysis of randomized, controlled trials. Ann Intern Med 140:143,
2004
27. Schauberger CW, Rooney BL, Brimer LM: Factors that influence weight loss in the puerperium. Obstet Gynecol 79:424,
1992
28. Schimmer BP, Parker KL Contraception and pharmacotherapy of obstetrical and gynecological disorders. In Brunton LL,
Chabner BA, Knollmann BC (eds): Goodman and Gilman's The Pharmacological Basis of Therapeutics, 12th ed. New York.
McGraw-Hill, 2011
29. Stern JM, Kenner M, Herman TN, Reichlin S. Nursing behaviour, prolactin and postpartum amenorrhoea during prolonged
lactation in American and !Kung mothers. Clin Endocrine! (Oxf). I 986;25(3):247
30. Tapson VF: Acute pulmonary embolism. N Engl) Med 358:1037, 2008
31. Tuuli MG, Rampersad RM, Carbone JF, et al: Staples compared with subcuticular suture for skin closure after cesarean
delivery: a systematic review and meta-analysis. Obstet Gynecol 117(3):682, 2011
32. Tyson JE, Ito P, Guyda H, et al. Studies of prolactin secretion in human pregnancy. Am) Obstet Gynecol 1972; 113:14
33. WHO recommendations: uterotonics for the prevention of postpartum hemorrhage. Geneva: World Health Organization;
2018. License: CC BY-NY-SA
3.0 IGO
184
BLEEDING
DURING
PREGNANCY
AND
INPOSTPARTUM
SECTION ONE
OVERVIEW OF BLEEDING DURING PREGNANCY
CAUSES OF BLEEDING DURING PREGNANCY
• Bleeding per vagina is common at ail stages of pregnancy
• Source of bleeding is almost always maternal, rather than fetal
DURING EARLY I DURING THE SECOND I POSTPARTUM
PREGNANCY HALF OF PREGNANCY HEMORRHAGE
• Abortion • Placenta previa • Uterine atony
• Ectopic pregnancy • Abruptio placenta • Retained placenta
• Cervical, vaginal, or • Morbidly adherent • Uterine rupture
uterine pathology (e.g., placenta (placenta accrete • Uterine inversion
infection, polyps) syndromes) • Genital tract trauma
I. EARLYPREGNANCYBLEEDING
• History of 2:2 early pregnancy losses or a condition associated with
History
Abdominal
early pregnancy loss (e.g., APAS)may suggest impending pregnancy loss
• Heavy bleeding, pelvic pain/cramping, passing of tissue may suggest
ectopic pregnancy or early pregnancy loss
• Midline pain: may suggest pregnancy loss
I
examination • Lateral pain: may suggest ectopic pregnancy
• To check for fetal heartbeat if pregnancy >10-12 weeks AOG
Doppler
• Doppler confirmation of fetal cardiac activity is reassuring, indicating
ultrasound
that bleeding is not related to fetal demise or ectopic pregnancy
External • Visual inspection and palpation to check for abnormalities (e.g.,
genitalia laceration, neoplasm, warts, polyps)
• Direct visualization of gestational sac in a dilated internal cervical os
Cervical os signifies that early pregnancy loss is inevitable
• A closed internal cervical os suggests a threatened early pregnancy loss
• There is no role for monitoring hCG concentrations once the presence of
an intrauterine pregnancy has been established sonographically
• Serial measurements are useful in the first 6 weeks of pregnancy if
~-hCG ultrasonography is non-diagnostic (i.e., location & viability of the
concentration pregnancy are not revealed)
• Failed pregnancy (i.e., nonviable intrauterine pregnancy): ~-hCG
levels plateau or fail
• Ectopic pregnancy: slowly rising hCG levels ( <35% over 48 hours)
Ultrasound • Cornerstone in the evaluation of bleeding in early pregnancy
Ill. POSTPARTUMHEMORRHAGE(PPH)
• PPH is an obstetric emergency
• Hemostasis normally occurs upon placental separation because uterine bleeding is
controlled by a combination of two mechanisms:
Contraction of the myometrium (which compresses the vessels)
• Local decidual hemostatic factors which cause clotting
187
SECTION TWO
El,4\RLYPREGNANCY eOMPLICATIONS
OVERVIEW
• Vaginal bleeding is common in the first trimester
• The five major sources of nontraumatic bleeding in early pregnancy are:
Ectopic pregnancy
Early pregnancy loss
0
Abortion
° Cervical, vaginal, or uterine pathology (e.g., polyps, inflammation, infection)
ABORTION
I. NOMENCLATURE
TERM I DEFINITION
• Pregnancy termination or loss before 20 weeks of
Abortion
gestation or with a fetus delivered weighing <500 g
• May be threatened, inevitable, incomplete, complete or
Spontaneous abortion
missed abortion
Septic abortion • Abortion that is complicated by infection
• 2:3 early consecutive spontaneous abortions OR
Recurrent pregnancy loss
• 2:2 late consecutive spontaneous abortions
• Positive for ~-hCG testing but without a confirmed
Pregnancy of unknown sonographic location (gestational sac not yet sonological!y
location (PUL) visible transvaginally)
• ~-hCG<1500 mIU/mL
Source:POGSCPGonAbortion.2ndEdition.November
2015
II. PATHOGENESIS
• More than 80% of spontaneous abortions occur within the first 12 weeks of gestation
• Incidence increases significantly with advancing maternal age
• Most commonly presents with vaginal bleeding & suprapubic pain
• Hemorrhage into the decidua basalis & necrotic changes cause detachment of the embryo,
stimulating uterine contractions and expulsion
III. ETIOLOGY
FIRST TRIMESTER ABORTION I MIDTRIMESTER ABORTION
• Chromosomal anomaly (most common) • Cervical insufficiency
• Infections • Infections
• Medical disorders (e.g., thyroid disease, • Maternal uterine or cervical anatomic
DM,SLE,APAS) defects*
• Exposure to chemotherapy /radiation • Medical disorders
• Maternal uterine/cervical anatomic defects* • Exposure to fetotoxic agents
• Social and behavioral factors** • Trauma
• Paternal factors: increasing paternal age,
chromosomal abnormalities in spermatozoa
*Includesleiomyomata,
uterinesynechiae,cervicalincompetence
••HIV,uncomplicatedsurgicalprocedures,
dietarydeficiency
of anyonenutrientarenotassociated
withexcessive
abortionrisk.Traumaseldomcausesfirst-trimester
abortion.
"Heavy"caffeineconsumption
{morethan3 cupsper
day)coupledwithsmokingis associatedwithhigherriskof abortion.
188
A. Chromosomal Abnormalities
0 Responsible for most cases of early abortion (i.e., fetal factors)
0 Abnormalities in zygote development are the most common findings in early
spontaneous abortions
1. Management
TIMING I MANAGEMENT
If fetus previable • Expectant management
(<24 weeks) • Emergency cerclage
If with viable
pregnancies
•
•
•
•
Expectant management with strict bed rest
Steroid therapy*
Tocolysis during steroid therapy
Emergency cerclage
I
'Dependson cervicaldilatationand state of amnionicsac
2. Cercla2e
• Suture placed vaginally around the cervix either at the level of
the cervical-vaginal junction (McDonald) or at the internal os
(Shirodkar)
Emergency
• Goal is to close the cervix
cerclage
• Maintained until 36 - 38 weeks if possible
• Possible complications: rupture of membranes, preterm labor
(PTL), and infection
• Offered if with suspected cervical insufficiency in a previous
Elective cerclage at
pregnancy
12-14weeks
• Maintained until 36 - 38 weeks if possible
189
III. CLINICAL CLASSIFICATION OF SPONTANEOUS ABORTION
TYPE
I DESCRIPTION I CERVIX I UTERUS• 1~·1 RiT< I PLAN
• Any bleeding
<20 weeks AOG,
without dilatation
of cervix or • Bed rest
Threatened
abortion
expulsion of Closed Compatible + + • Tocolysis
any products of
conception (i.e., a
normal pregnancy
with bleeding)
• Dead products
of conception • Cervical
Missed
abortion
that have been
retained for days
Closed Compatible + - ripening±
curettage'
or weeks
• Complete • Observe
expulsion of Incompatible • Measure
Complete
abortion
all products of
conception (POC)
Closed (small for
AOG)
- - hCG
• Trasvaginal
<20 weeks AOG ultrasound
• Partial expulsion
• Manage
(i.e., passage of
expectantly
meaty material) of Incompatible
Incomplete • Curettage•
abortion
some, but not all
POC <20 weeks
Open (small for
AOG)
- - • Prostaglandin
analog (e.g.,
• Part of placenta is
misoprostol•)
retained in uterus
• No expulsion
but with vaginal
bleeding & dilation
of the cervix such
• Expectant
that maintaining a
Inevitable • Oxytocin
abortion
viable pregnancy
is unlikely
Open Compatible - +/- • Curettage'
• There is rupture
of the membranes
in the presence of
cervical dilatation
• Uterus: compatible or incompatiblein relation to the age of gestation
'BOW: bag of water(+ would mean an intact BOW,i.e., not yet ruptured BOW)
'FHT: Fetal heart tone
'Await passage of fetus priorto curettage in late abortions (;?:12weeksAOG)
• Misoprostolis not approved for use in the local setting
190
IV.OTHERTYPES OF ABORTION
TYPE I DESCRIPTION
• ;?3 early consecutive spontaneous abortions or
Recurrent
;?2 late consecutive spontaneous abortions
pregnancy loss
(RPL) • Work-up for anatomic, metabolic immunologic, genetic, and infectious
causes
• Abortion with infection of the products of conception (POC), uterus,
and adnexa
• Usually polymicrobial
• Diagnosis of septic abortion:
0 Temperature ;?38°Cof at least 24-hrs duration & unattributable to
Septic abortion
any other cause
0 History of mechanical instrumentation for the purpose of inducing
an abortion
0 Presence of septic discharge from the cervix
Tenderness of the uterus, parametrium or adnexa
I
0
V. DIAGNOSIS
DIAGNOSTICS I REMARKS
• Urine or serum 8-hCG
Basic tests • CBC,blood typing
• Transvaginal ultrasound
• Sonographic findings in early pregnancy loss:
° Crown-rump length (CRL) ;?7 mm and no heartbeat
0 Mean gestational sac diameter (MSD) ;?25 mm and no embryo
0 An initial ultrasound shows gestational sac with yolk sac, and
Ultrasound
after "11 days
no embryo with heartbeat is seen
0 An initial ultrasound shows a GSwithout yolk sac, and after <:2weeks
no embryo with a heartbeat is seen
191
ECTOPIC PREGNANCY
• Implantation of the fertilized ovum outside the endometrial lining of the uterine cavity
• May implant in the fallopian tube, ovary, cervix, abdomen (normal: should be intrauterine)
• All women with early pregnancy bleeding and pain are assumed to have ectopic
pregnancy until excluded by laboratory and sonography
I. ETIOPATHOGENESIS
A. Risk Factors
0 Prior ectopic pregnancy (strongest risk factor)
0 Previous tubal surgery
0 Smoking >20 cigarettes per day
0 PID confirmed by laparoscopy or positive test for Chlamydia trachomatis
0 ;;,3 prior miscarriages
0 Age e,40 years old
0 Prior abortion (medical or surgical
0 Infertility >l year
0 Lifelong sexual partners > 5
0 Prior IUD use
lsthmic (12%)
Tubal
(95-96%)
Ampullary (70%)
Fimbrial (11%)
Ovarian(3%)
Cervical (<1%)
-----------------------< Non-tubal
(4-5%)
L------==----------------A-b-do_•~_
0
_i~_:_~~_l:_y~-)
________ ..J ■
Source:Cunningham
FG,et al. WilliamsObstetrics25thEd;2018
II. MANIFESTATIONS
• Classic triad of symptoms:
Amenorrhea
0
Symptoms
Abdominal pain (95%)
0
Vaginal bleeding/spotting
0 (60-80%)
• Uterus may be slightly enlarged and pushed to one side
• Vital signs: normal (unruptured) or hypotension (ruptured)
• Adnexal mass that is often tender
Signs
• Small corpus compared to AOG
• Cervical motion tenderness
• Bulging of posterior vaginal fornix (accumulation of blood in cul-de-sac)
Presents with severe hemorrhage due to close proximity to uterine & ovarian arteries
0
Management
0
193
III. DIAGNOSIS
DIAGNOSTICS I REMARKS
• Findings in ectopic pregnancy: P-hCG Levels are lower than those in
normal intrauterine pregnancies
• Normal rate of increase in P-hCG Levels or "doubling time" does not
fl-hCG: urine or occur in ectopic pregnancy
serum • Intrauterine pregnancy not seen on transvaginal ultrasound after
attaining discriminatory serum P-hCGlevel ofeel,500 mlU/mL
• Fetal heartbeat, whether intrauterine or ectopic should be seen on
transvaginal ultrasound at P-hCGlevels ee5,000 mlU/mL
• Should be 10-25 ng/mL
Serum
• Levels are lower compared to normal gestation
progesterone
• There is no viable pregnancy if serum progesterone is <0.5 ng/mL
• Presence of
° Complex adnexal mass separate from the ovary and fluid in cul-de-sac
0Pseudogestational sac/pseudosac: fluid collection that is seen in the
midline within the endometrial cavity
• In contrast, gestational sac of normal pregnancy (seen between
4-5 weeks AOG)implants eccentrically within the endometrial cavity
Ultrasound
and has the double decidual sac sign
• Absence of an intrauterine gestational sac on transvaginal ultrasound
(TVS) when the ~-hCGlevel is eel,500 mlU/mL
• Presence of an intrauterine gestational sac rules out an ectopic
pregnancy, except in a heterotopic pregnancy (an ectopic pregnancy
occurs at the same time as a normal intrauterine pregnancy)
I
• Aspiration of non-clotting blood from cul-de-sac through the posterior
vaginal fornix is indicative ofhemoperitoneum
• Hemoperitoneum is extravasated blood that has clotted & lysed
Culdocentesis • False negative interpretations may be due to:
Blood aspirated from pelvic vessels (clotting blood}, or
0 •
IV.MANAGEMENT
A. Expectant Management
0 Observing the ectopic pregnancy to resolve naturally without intervention
0 Recommended ~-hCG monitoring is every 48 hours (three consecutive decreasing
measurements is reassuring)
2. Dose ofMethotrexate
Dosing
I SINGLE DOSE
• One dose
I MULTIDOSE
C. Surgical Management*
• Used to remove unruptured pregnancy that is <2 cm in size
• 10- to 15-mm linear incision is made at the antimesenteric border;
Saipingostomy products of conception is flushed out
• Incision is not sutured and left to heal via secondary intention
• Hemostatic control is done by bipolar cauterization
• Same as salpingostomy, except that the incision is closed with
delayed-absorbable suture
Salpingotomy
• No longer done because of more tubal scarring and adhesion
formation observed
Salpingectomy • Complete excision of the fallopian tube
'Laparoscopicsurgeryis preferredunlesspatientis hemodynamically
unstable(versuslaparotomy)
195
ABORTION VERSUS ECTOPIC PREGNANCY
..~11~-
_.,
,.
. ~
.
• ( +) mass/tenderness
~
,,
~ ".ii''-'
Serum
• <5 ng/mL • <25 ng/ml
progesterone
• Insufficient to maintain the • Does not reach the normal pregnant
(normal is
225ng/ml) pregnancy levels
196
SECTION THREE
'
■
-:-<
Non-obstetric causes
Cervical • Severe cervicitis, polyps, cervical dysplasia/cancer
Vaginal/vulvar . • Lacerations, varices, cancer
Other • Hemorrhoids, bleeding disorder, trauma, hematuria
Source:HackerN, et al. Essentialsof ObstetricsandGynecology.
Philadelphia, PA:WBSaunders;1992:155.
II. PLACENTAPREVIAVERSUSABRUPTIOPLACENTA
I PLACENTA PREVlA I ABRUPTIO PLACENTA
• Placenta abnormally implanted • Premature separation of a
in the lower uterine segment normally implanted placenta prior
or lower uterine segment (LUS) to delivery
Definition
(passive segment)
• Internal os covered partially or
completely by the placenta
Illustration
197
I PLACENTA PREVIA I ABRUPTIO PLACENTA
Clinical 11.ist_ory
Hemorrhages • Profuse bleeding • Single episode
Abdominal Pain* • Absent • Common
Physical Examinat1o_n . -
198
PLACENTA PREVIA
• Normally, the placenta is implanted near or at the fund us of the uterus (which is part of
the active segment)
• Placenta previa means placenta goes first before fetus in the birth canal ("Previa" means
"going before")
• Condition wherein the placenta is abnormally implanted in the lower uterine segment
(passive segment), either over or near the internal cervical os
I. ETIOPATHOGENESIS
A. Classification of Placenta Previa
C. Risk Factors
• Maternal age (>35 years old) • Low socioeconomic status
• Multiparity • Short interpregnancy interval
• Prior uterine surgery (e.g., CS) • Cocaine use
• Recurrent abortions • Abnormally elevated maternal serum
• Smoking alpha-fetoprotein (MSAFP)levels
• Uterine leiomyoma • Infertility treatment/assisted
• Multiple gestation reproductive technology (ART)
• Erythroblastosis • Others (e.g., digital exam, abruptio
• Non-white ethnicity placenta, trauma)
199
II. MANIFESTATIONS
• Suspected in any woman >20 weeks AOGwith painless vaginal
bleeding (classic presentation) usually near the end of the second
trimester
Symptoms
• Repeated "warning" hemorrhages ("sentinel bleed")
• Absent abdominal pain ("painless vaginal bleeding")
• Not associated with toxemia (in contrast to abruptio placenta)
• Normal uterine ton~ & non-tender
• Patient rarely in labor
• Presenting part is unengaged (in 35% of cases: non-cephalic presentation)
Signs
• Fetal parts are usually palpable abdominally
• Fetal heart tones usually present on abdominal auscultation
• Internal examination is contraindicated
III. DIAGNOSIS
DIAGNOSTIC I REMARKS
• Speculum examination may be done gently
• Internal examination is contraindicated in cases of placenta previa
Vaginal • If unknown placental location in patients clinically suspected with
examination placenta previa, internal examination can be done in a double set-up
(i.e., performed in the operating room prepared for an emergency CS
delivery)
• Can already make a diagnosis (even the type of placenta previa)
Ultrasound
• Placenta is seen in the LUS
Basic • CBC,blood typing, PT/PTT
laboratory • Fibrinogen, D-dimer if suspecting disseminated intravascular
work-up coagulation (DIC)
IV.MANAGEMENT
Initial • Secure IV access and blood products
stabilization • Continuous fetal monitoring
• Steroid therapy for fetal lung maturity.
Prepare for
• Magnesium sulfate (between 24-32 weeks) for neuroprotection if
preterm
delivery is occurring within 24 hours
delivery
• Cautious use of tocolytics as long as mother and fetus are stable
• Depends of final placental localization (usually determined between
32-36 weeks)
• Vaginal delivery:
0If placental edge >2 cm away from os: trial of labor
0If placental edge within 0-20 mm from os: vaginal delivery is still
Route of possible, but proceed with caution
delivery • Cesarean section (delivery of choice):
° For all women with placenta previa
° For near term and with no bleeding, schedule elective CS at term
[usually 38 weeks)
0Midline vertical laporotomy incision: recommended for rapid entry in
case of bleeding or in case hysterectomy is needed
Indications
• Active labor
for immediate
• Fetal distress
CS regardless
ofAOG • Life-threatening hemorrhage
200
ABRUPTIO PLACENTA
• Premature separation of normally implanted placenta before birth of a viable fetus
I. ETIOPATHOGENESIS
• Premature separation of a normally implanted placenta
• Diagnosis is typically reserved for pregnancies over 20 weeks of gestation
0nset of Manifestations
Acute abruptio • Sudden onset of signs and symptoms
• Shows non-expanding or shrinking retroplacental hematoma
formation on serial ultrasound
• Chronic abruption-oligohydramnios sequence (CAOS):
Chronic abruptio ° Chronic abruption severe enough to result to oligohydramnios
0 Mean AOG at delivery: 28 weeks
° Continuous fetal heart rate monitoring does not universally
Severity
Mild abruptio
guarantee good fetal outcomes
• Partial abruption
- - I
• Mother and fetus are undisturbed
• Maternal tachycardia with orthostatic hypotension
Moderate abruptio
• Fetal distress
• Maternal shock
Severe abruptio
• Fetal demise
Partial
separation
201
C. Types Based on Mode of Bleeding
TYPE I REMARKS I ILLUSTRATION
D. Pathophysiology
• Likely begins with rupture of a decidual spiral arteries resulting in an expanding
retroplacental hematoma
• Extravasation into the decidua basalis causing the decidua to split, leaving a thin layer
adhered to the myometrium
• This leads to decidual hematoma and expands to cause separation and compression of
the adjacent placenta
•Maybe due to acute process from one of the following:
• Uncontrolled hypertension
• Shearing forces resulting from trauma
• Sudden uterine decompression from membrane rupture associated with hydramnios
• Cocaine usage leading to acute vasoconstriction with resultant placental separation
E. Risk Factors
• Increased age and parity • Single umbilical artery
• Race • Multifetal gestation
• Pregnancy-induced hypertension • Low fetal weight
(most common associated condition) • Uterine leiomyoma (especially if located
• Prior abruption near the mucosa! surface behind the
• Hydramnios placental implantation site)
• Preterm ruptured membranes • Cigarette smoking
• Chorioamnionitis • Cocaine use
202
II. MANIFESTATIONS
A. Clinical Manifestations
• Most common presentation: sudden-onset abdominal pain, vaginal
Symptoms bleeding, and uterine tenderness
• Abdominal pain, uterine tenderness or back pain
• Vaginal bleeding >20 weeks AOG
• Hypertonic/tetanic "woody" uterus
• Frequently associated with hypertension
• Patient usually in labor
Signs
• Presenting part often engaged
• Fetal parts may be difficult to palpate
• Fetal heart tones may be difficult to detect (due to tetanic uterus) or
absent (i.e., dead fetus)
I MILD
I MODERATE
I SEVERE
• Stable
I
• Elevated pulse rate
• Minimal
Mother • Hypotension • Shock/unstable
manifestations
• Reduced CVP
• Normal CVP
• Normal (reassuring) • Alive but+/- signs • Fetal distress
Fetus
FHT of fetal distress • Fetal death
• None • None
• Renal failure
Complications • Good urine output • Marginal urine
• Coagulopathy
• No clotting problems output
• Irritable • Severe pain &
• Irritable
Uterus • More pain tenderness
• Pain tenderness
• Severe tenderness • Tetanic contractions
• <500 mL
Bleeding • 500-1000 mL • >1000 mL
• No active bleeding
Placental
• < 1/6 • 1/6 to 2/3 • >2/3
Separation
C. Differentials
0Placenta previa
0Appendicitis
0Preterm labor
° Fibroid degeneration
0Ovarian pathology
0Muscular pain
'UT!
D. Complications
0Perinatal mortality
0Acute renal failure
0Hypovolemia/hemorrhagic shock
0Uterine atony
° Couvelaire uterus (uteroplacental apoplexy)
0DIC (abruptio placenta is most common etiology)
203
III. DIAGNOSIS
Vaginal • Done under double set-up if unsure of placental location
examination • Findings: no placenta within S cm of internal os
• Placenta seen in the upper uterine segment (UUS)with retroplacental
Ultrasound
clot/hematoma
• Recurrent late or variable decelerations
• Reduced variability, bradycardia or a sinusoidal pattern
EFMtesting
• Often associated with observed increased baseline uterine tone on
tocomonitoring
• Put sample of blood in a test tube
Clot
• Coagulation defect is positive if:
observation
test ° Clot does not form within 6 mins, or
° Forms and lyses within 30 mins
IV:MANAGEMENT
A. Overview of Management
• Stabilize the patient
• Prepare for the possibility of hemorrhage to worsen
Initial
• Prepare for delivery (if preterm, give steroids, magnesium sulfate as
management
indicated)
• Deliver if bleeding is life-threatening or fetal testing is non-reassuring
• Amniotomy (both diagnos!ic and therapeutic)
° Confirms diagnosis with observed bloody amniotic fluid
0 Prevents further placental separation with the baby having a
tamponade effect on the retroplacental hematoma
0 Prevents further release of thromboplastins into the circulation
• Vaginal delivery:
0 Both maternal and fetal status are stable, consider induction with
Term/
close monitoring
near term
° Cervix almost fully dilated
° Fetus is dead but mother is stable
• Cesarean Section (CS):
0 There is fetal compromise
• Severe uterine hypertonus
0 Life-threatening vaginal bleeding or DIC,or
0 Vaginal delivery is not imminent
204
MORBIDLY ADHERENT PLACENTA (ACCRETE SYNDROMES)
I. ETIOPATHOGENESIS
• Abnormally adherent villi to the myometrium:
• Partial or total absence of the decidua basalis or
• Imperfect development of the fibrinoid or Nitabuch layer
• Microscopically, placental villi are anchored to muscle fibers rather than to decidual cells
• Normally, cytotrophoblasts should control decidual invasion through factors such as
angiogenesis and growth expression
TYPE I DESCRIPTION
• Villiare attached to
Accreta*
the myometrium
• Villi penetrate
through the
Percreta
myometrium to or
through the serosa
'Typesof placenta
accreta
• Totalaccreta:abnormal adherence mayinvolveall lobules
• Focalaccreta:all or partof a lobuleis abnormally
attached
B. Risk Factors
• Prior cesarean delivery (especially if done as emergency CS)
• Risk factors associated with placenta previa (see previous section on Placenta Previa)
• Maternal serum: MSAFPlevels >2.5 Multiples of the Median or MoM (Bx) or
B-hCGlevels >2.5 MoM (4x)
• Prior myomectomy or reconstructive surgery
• Asherman syndrome
• Submucous leiomyomata
• Multiparity (>G6)
II. MANIFESTATIONS
AND DIAGNOSIS
• In some with no associated previa, accreta may not be identified until the 3rd stage labor
• Diagnosed via ultrasound with Doppler studies:
Loss of hypoechoic retroplacental zone, which correspond to the decidua basalis,
myometrium, and dilated venous channels
Progressive thinning of the retroplacental hypoechoic zone to <2 mm on serial exams
Placental vascular lacunae or "lakes" which represent dilated vessels extending from
the placenta through the myometrium having a "Swiss cheese" appearance (placenta
increta/placenta percreta)
Thinning/focal disruption of uterine serosa-bladder wall complex (placenta percreta)
Focal mass-like elevation with the same echogenicity as the placenta beyond the
uterine serosa (placenta percreta)
205
III. MANAGEMENT
A. Criteria for Consideration of Delivery in an Accrete Center of Excellence
• Suspicion for morbidly adherent placenta on ultrasound
• Placenta previa with abnormal ultrasound appearance
• Placenta previa with >3 prior cesarean deliveries
• Prior CS delivery and anterior placentation
• Prior endometrial ablation or pelvic irradiation
• Inability to adequately evaluate or exclude placenta accrete
• Suspicion of morbidly adherent placenta
Source:Silver,et al. 2015
CunninghamFG,et al. WilliamsObstetrics25thEd;2018
206
DISSEMINATED INTRAVASCULAR COAGULATION (DIC)
I. ETIOPATHOGENESIS
• DICis a syndrome characterized by:
Widespread systemic activation of coagulation
Thrombotic obstruction of small and midsize vessels, eventually causing tissue
0
A. Pathogenesis
DICis a systemic thrombohemorrhagic disorder seen in association with well-defined
clinical situations and laboratory evidence of:
• Procoagulant activation
• Fibrinolytic activation
• Inhibitor consumption
• Biochemical evidence of end-organ damage or failure
• Associated with septic abortion and chorioamnionitis
Intrinsic • Damage of the vessel wall and subsequent exposure of collagen
pathway
activates factors XII initiating the coagulation cascade
(Endothelial
damage) • Slow process, since circulating coagulation factors which are inactive
are subsequently activated
■
Extrinsic • Associated with abruptio placenta, amniotic fluid embolism, retained
pathway dead fetus, saline-induced abortion
(Massive • Rapid process, wherein procoagulant materials from tissue injury are
tissue injury) not usually present in the blood stream
Preeclampsia/eclampsia
0
Hemorrhage
0
II. MANIFESTATIONS
• Bleeding at sites of modest trauma
• Bleeding from venipuncture site, nicks from shaved area of perineum or abdomen,
trauma from insertion of a catheter
• Bleeding from the gums or nose
• Petechiae and purpuric rash
III. DIAGNOSIS
• Excessive bleeding
Bioassay • Purpura and petechiae at pressure sites
• Surgical procedure with intractable bleeding
• Fibrinogen (300-600 mg/dL)
• Elevated fibrin and degradation product levels
Laboratory
• Decreased platelet count (thrombocytopenia)
tests
• Prolonged prothrombin time (PT) & partial thromboplastin time (PTT)
• Elevated D-dimer levels
IV.MANAGEMENT
• Cornerstone of the therapy: eliminate or treat the triggering process (i.e., prompt
identification and removal of inciting source of the coagulopathy)
• Replacement of pro coagulants for planned or anticipated extensive surgeries (e.g.,
transfusion of blood components)
• Vigorous restoration and maintenance of circulation to treat hypovolemia
207
SECTION FOUR
POSTPARTUM HEMORRHAGE
OVERVIEW OF POSTPARTUM HEMORRHAGE (PPH)
• An obstetric emergency
• Normally, hemostasis occurs upon placental separation because uterine bleeding is
controlled by a combination of two mechanisms:
° Contraction of the myometrium, which compresses the uterine sinuses and vessels
0Local decidual hemostatic factors which cause clotting
I. DEFINITIONOF TERMS
• The following are suggested definitions of postpartum hemorrhage but there is a lack of
agreement on what constitutes excessive blood loss:
• Blood loss 2'500 mL for vaginal delivery and > 1,000 mL for CS
POGSCPG • Blood loss ;;,500 mL in the first 24 hours following delivery
0
10% decrease in hemoglobin or hematocrit level
0
Need for transfusion
• 2'1000 mL blood loss regardless ofroute of delivery accompanied
Williams, 25th ed.
by signs and symptoms ofhypovolemia
Source:POGSCPGon ThirdTrimesterBleeding
and PostpartumHemorrhage.
November 2012
Williams'
Obstetrics.25thed. 2018
I VOLUME
BLOOD HEART
I SYSTOLIC BP I SIGNS AND
BLOOD LOSS
I RATE SYMPTOMS
500-1000 mL 10-15% <100 bpm Normal • None
208
C Class1"fication base d on 0 nset of Hemorrhal!e
Third Stage
• Postpartum hemorrhage before placental delivery
Hemorrhage
Early Postpartum
• Blood loss of> 500 mL during the first 24 hours after delivery
Hemorrhage
Late Postpartum
• If bleeding occurs after 24 hours to 12 weeks after delivery
Hemorrhage
ObstetGynecol;2017
Source:Committeeon PracticeBulletins-Obstetncs.
• Multiple gestation
Overdistended uterus • Polyhydramnios
■
• Macrosomia
Tone • Prolonged labor
(Abnormal Uterine muscle fatigue • Augmented labor
uterine • Prior postpartum hemorrhage
contractility)
Chorioamnionitis • Prolonged rupture of membranes (ROM)
SYSTEM
I
BLOOD
LOSS
I
HEART
RATE I BP I c~LL YI
uo
[mL/hr)
I MENTAL
STATUS
Normal or
Compensated <l,000 mL <100 bpm Normal Normal >30
agitated
1,000 to Orthostatic Maybe
Mild >100 bpm 20-30 Agitated
1,500 mL change delayed
1,500 to Marked Usually
Moderate >120 bpm 5-20 Confused
2,000 mL fall delayed
Profound Always Lethargic,
Severe >2,000 mL >140 bpm Anuria
fall delayed obtunded
Source:MartelMJ.J ObstetGynaecolCan;2018
IV.GENERALMANAGEMENTOF POSTPARTUMHEMORRHAGE(PPH)
• Simultaneous, coordinated, multi-disciplinary management (OB-GYN,anesthesiologist,
hematologists, radiologists, nurses, laboratory and blood bank technicians) to concur
timely management in the presence of obstetric hemorrhage
• Preoperative preparedness is important especially for patients identified as high risk
• Details in the management (depending on etiology) are discussed in the succeeding section
A. Initial Management
I
INITIAL
REMARKS
APPROACH
• Constant awareness of the hemodynamic status as well as evaluation
Assessment
to determine the cause of bleeding.
Breathing • Administration of oxygen
• Obtaining intravenous (IV) access and adequate circulating blood volume
through infusion of crystalloid and blood products
Circulation
• Second large-bore IV catheter is needed
• Notify the blood bank
210
B. Review of the Management of the Third Stage of Labor
APPROACH I COMPONENTS
• Recommended by guidelines
• Consists of (discussed in detail below):
Active 0 Routine administration of a prophylactic uterotonic just before
management of
labor or immediately after the birth of the baby
0 Delayed cord clamping
° Controlled cord traction to deliver the placenta
1. Uterotonics
I
■
UTEROTONIC REMARKS
• Preferred uterotonic in the active management of the third stage of
labor because of fewer side effects, but similar efficacy with others
• Can also be used in CSdeliveries
Oxytocin
• Preferred route for oxytocin is intravenous
• There is still insufficient evidence to issue a recommendation as to the
timing of giving oxytocin (before or after placental delivery)
• May be used in cases where PPH is refractory to oxytocin
• Should only be given in the presence of trained personnel
Carboprost
• Should not be given among patients with increased intraocular
(IM)
pressure, hypertension/hypotension, cardiovascular /pulmonary/
renal disease, anemia, epilepsy and jaundice
• Ergometrine
Other agents • Syntometrine
• Carbetocin
V. IMPORTANTCAUSESOF POSTPARTUMHEMORHAGE
• Uterine atony
• Retained placenta
• Uterine rupture
• Uterine inversion
• Genital tract trauma
211
UTERINE ATONY
• Most frequent cause of obstetrical hemorrhage
• Women with risk factors for uterine atony should be delivered in a hospital with adequate
facilities to manage PPH
I. ETJOPATHOGENESIS
A. Pathogenesis
° Caused by the failure of the uterus to contract sufficiently after delivery and to arrest
bleeding from sinuses at the placental implantation site
B. Risk Factors
0 Primiparity or multiparity
0 Overdistended uterus (e.g., women with large fetus, multiple fetus, or hydramnios)
0 Labor abnormalities
III. MANAGEMENT
A. Overview
• Active management of the 3rd stage of labor with use of uterotonics
(most important component)
• Drugs:
0 Oxytocin: given IM or via IV infusion after placental delivery
Pharma co logic
0 Methylergonovine (Methergine): second-line treatment;
contraindicated in hypertensive patients
0 Prostaglandin analogues: carboprost, misoprostol
0 Oxytocin analog: carbetocin
• Vigorous fundal massage
• Bimanual uterine compression, balloon tamponade
• If ineffective: B-Lynch procedure, internal iliac artery ligation,
Non-
hysterectomy
pharmacologic
• Uterine artery embolization
• Manual placental removal: indicated when heavy bleeding persists
after delivery & while placenta remains partially or totally attached
Source:CPG on ObstetricHemorrhage.POGS;2014
212
C. Some Maneuvers/Procedures
213
RETAINED PLACENTA OR PLACENTAL FRAGMENTS
I. RETAINEDPLACENTA
• Retention of the placenta in utero for >30 minutes
• More common cause of late postpartum bleeding (after the first 24 hours)
• The bleeding may be visible or may manifest only by the increasing size of the uterus
In the absence of any evidence of placental detachment, consider the diagnosis of
complete placenta accreta or a variant.
II. RETAINEDPLACENTAL
FRAGMENTS
• May interfere with the complete uterine involution preventing adequate compression of
the uterine sinuses and vessels at the exposed placental implantation site
• Manifests as late postpartum hemorrhage, presenting as prolonged postpartum bleeding
• May be avoided by awaiting signs of placental separation before delivering placenta and
inspecting the placenta for completeness upon delivery
214
UTERINE RUPTURE
I. ETIOPATHOGENESIS
• Rare & catastrophic complication with a high incidence of fetal and maternal morbidity
• Usually involves a thinned out lower uterine segment or a weakened uterine scar
A. Etiology
ETIOLOGY I REMARKS
• Surgery involving the myometrium: CS,previously repaired
uterine rupture, myomectomy, cornual resection of the interstitial
Preexisting
fallopian tube
uterine injury or
anomaly • Coincidental uterine trauma: abortion with instrumentation, trauma
• Congenital: connective tissue disorder, pregnancy in undeveloped
uterine horn
• Before delivery: labor stimulation, uterine overdistension, external
Uterine injury version
I
or abnormality
• During delivery: internal version of 2nd twin, difficult forceps
incurred
delivery, difficult manual removal of placenta
in current
pregnancy • Acquired: placenta accrete, adenomyosis, gestational trophoblastic
neoplasia ; :
Source:CPGon ThirdTrimesterBleedingandPostpartum
Hemorrhage.
POGS,Inc;2009
II. MANIFESTATIONS
• Initial manifestations are nonspecific, which makes the diagnosis difficult and sometimes
delays definitive therapy:
Fetal distress (evidenced by pattern of abnormalities in FHR)
0 Recession of the presenting fetal part into the maternal pelvis
Diminished baseline uterine pressure or loss of uterine contractility
Abnormal labor pattern or failure oflabor to progress, abdominal pain
, Hemorrhage and shock
• Fetal morbidity occurs as a result of catastrophic hemorrhage, fetal anoxia, or both.
215
III. UTERINERUPTUREVERSUSDEHISCENCE
• Uterine rupture: separation of old uterine scar throughout most of its length with rupture
of fetal membranes (uterine cavity and peritoneal cavity communicate)
• Uterine dehiscence: occult and incomplete disruption that does not lead to any serious
maternal or neonatal consequences
UTERINE
DEHISCENCE
IV.MANAGEMENT
• Definitive therapy for the fetus is immediate abdominal delivery.
• Conservative surgical management involves revision of the edges of the prior incision
following primary closure and should be reserved for women who have the following
findings:
0 Type of uterine rupture: low transverse uterine rupture
0 Extent of rupture: no extension of the tear to the broad ligament, cervix, or paracolpos.
0 Degree of hemorrhage: easily controllable uterine hemorrhage
0 General condition of the mother: hemodynamically stable
0 Desire for future childbearing
0 No clinical or laboratory evidence of an evolving coagulopathy
• Hysterectomy is the treatment of choice when intractable uterine bleeding occurs or when
the uterine rupture sites are multiple, longitudinal, or low lying.
Source:CPG on ObstetricHemorrhage2nd Edition.POGS, Inc:2014,2019
216
UTERINE INVERSION
• Inside-out displacement of the fund us of the uterus during the third stage of labor
• Prevents myometrium from contracting and retracting, and it is associated with life-
threatening blood losses as well as profound hypotension from vagal activation
I. ETIOPATHOGENESIS
• Rare condition, occurring in 0.05% of deliveries
• Almost always due to vigorous traction of the umbilical cord prior to detachment of a
fundally implanted placenta
A. Etiology:
, Overly aggressive management of the third stage of labor
, Excessive umbilical cord traction while the uterus is relaxed
, Extrinsic factors: use of magnesium sulfate or oxytocin (some studies)
, Intrinsic factors:
• Primiparity
• Uterine hypotonia secondary to twin pregnancy and use of P-mimetics
• Placenta accrete (involving the uterine fundus)
• Fundal myoma
• Short umbilical cord
■
• Rapid emptying of the uterus after prolonged distention
• Congenital weakness or anomalies of the uterus
B. Risk Factors
'Fundally implanted placenta
, Uterine atony
'Cord traction applied before signs of placental detachment, which are:
• A sudden gush of blood
• Lengthening of the visible portion of the umbilical cord
• Uterus becomes globular and firm
• Uterus rises to the abdomen
, Abnormally adherent placentation
II. MANIFESTATIONS
• Clinical signs and symptoms: hemorrhage, shock and severe pelvic pain
• Bimanual exam will confirm the diagnosis and reveal the degree of inversion.
Uterus not palpable abdominally in complete uterine inversion
, Internal examination shows a palpable mass
IV.MANAGEMENT
• Application of active management of the third stage of labor including controlled cord
traction decreases incidence of acute uterine inversion following vaginal delivery
AO verv1ew o fM anagement
• Tocolysis may be initiated, if necessary to relax the uterus
• If uterus has not contracted & has retracted completely and placenta
has separated, uterus is replaced by pushing up on the inverted fund us
with the palm and fingers* in the direction of the long axis of the vagina
Manual • If placenta is still attached, attempts are made to reposition with the
replacement placenta in situ. After uterus is replaced, placenta is manually removed
ofuterus and delivered
• If uterine repositioning fails with placenta attached, it is peeled off and
steady pressure with fist, palm, or fingers* is applied to the inverted
fundus in an attempt to push it up into and through the dilated cervix
• Once uterus is repositioned, tocolysis is stopped and oxytocin is infused
• Done when manual replacement fails (possible cause: tight myometrial
Surgery constriction ring)
• Exploratory laparotomy, Huntington procedure, Haultain incision
'Cautionis observedwheneverusingthe fingersin repositioningthe uterusto preventperforation
218
D. Replacement of the Uterus
METHOD I ABORTION
Initial Replacement
• Patient is placed in lithotomy position and two bottles of 1 liter
warm (40°C) irrigation fluid (0.9% NSS) are attached to a cystoscopy
irrigation set
Hydrostatic • Nozzles of the rubber tubes should be directed to the posterior fornix
reduction of the vagina
(O'Sullivan
hydrostatic • Run the warmed fluid by gravity or pressure and prevent the water
maneuver) from leaking out of the vagina (up to 4 liters may be required)
• As the vaginal wall distend, the fundus and the uterus will begin to rise
• Reduction can be achieved in about 5-10 minutes
• After complete replacement, start oxytocin drip & give ergometrine IV
• Grasp the inverted uterus with the placenta with one hand
• The fundus is allowed to rest on the palmar surface of the operator's
hand with fingertips exerting equal pressure around the collar of the
uterus within the cervical opening
■
• The fundus is then replaced with upward pressure
Johnson
• After repositioning the uterus, the placenta is manually removed
maneuver
followed by uterine exploration
• Operator's hand is kept inside the uterus, slowly removed as it begins
to contract around the hand
• A tight uterovaginal pack may be inserted before the hand is removed
from the uterine cavity (pack can be removed after 24 hours)
Surgical Replacement
• Grasping the round ligaments to locate the depression of the uterine
fundus formed by the inversion
Huntington
• Clamps are placed on the inverted fund us below and within the
procedure
cervical ring, and gentle upward traction is applied
• Repeated clamping & traction continues until inversion is corrected
• Incision is made on the uterine wall at the posterior rim of the cervical
ring
• Length of the incision should be sufficient to permit passage of the
Hultain uterine fundus
procedure • Fundus is restored by combined traction on the uterine wall from
above by the surgeon and pressure from the vagina by an assistant
• When the uterus is completely restored, the incision is closed with
interrupted sutures
Source:CPGon ObstetricHemorrhage2nd Edition.POGS,Inc;2014,2019
219
GENITAL TRACT TRAUMA
• Genital tract traumas are the second most common causes of PPH (20%)
• Includes lacerations to the perineum/vagina/cervix, large episiotomy (including
extensions)
• Types of genital tract trauma:
Genital tract lacerations (1st, 2nd, 3rd, and 4th degree)
0 Genital tract hematoma
I. GENITALTRACTLACERATION
• Occurs at the vaginal vault as the fetal head passes through
• It can involve the perineum, vagina and the cervix
• Genital tract laceration should be suspected if bleeding will persist despite a well-
contracted uterus
A. Types of Lacerations
1. Perinea! Lacerations
• Trauma may occur spontaneously or arise from episiotomy during vaginal delivery
• May reach to involve the anal sphincter (causing incontinence & rectovaginal fistula if
untreated)
CLASSIFICATION I REMARKS
Classificatio'l, by Location_ Pi'
Anterior perinea I • Injury involving the labia, anterior vagina, urethra or clitoris
trauma
Posterior perinea! • Injury to the posterior vaginal wall, perinea! muscles or anal
trauma sphincters and may extend through the rectum
- --
Classificatiortlbase_don Depth or Degr,ee
• Fourchette, perinea! skin, and vaginal mucous membrane
1st degree
• Does not reach the underlying fascia and muscle
• Aside from skin and mucous membrane, the fascia and
2nd degree
muscles of the perinea! body are involved
• Lacerations extend through skin, mucous membrane, perinea!
body and anal sphincter
• Royal College of Obstetricians & Gynecologists (RCOG)
3rd degree subclassification:
0 3a: <50% of external anal sphincter thickness torn
0 3b: >SO% of external anal sphincter thickness torn
0 3c: internal anal sphincter torn
• Extension of laceration through the rectal mucosa to expose
4th degree
lumen of the rectum
2. Vaginal Lacerations
• Associated with forcep/vacuum deliveries or in precipitous deliveries
• May extend to the underlying tissues and cause significant hemorrhage
• Considered if there is vaginal bleeding while the uterus is firmly contracted
3. Cervical Lacerations
• lntrapartum cervical lacerations are more common and most are asymptomatic
• Suspected in cases of profuse bleeding if uterus is well contracted
• Cervix should be routinely inspected after the 3rd stage of labor in all difficult
deliveries, even if there is no bleeding
• Any cervical tear, which is actively bleeding and/or >2 cm in length should be sutured
• May be incurred during forceps deliveries when performed through an incompletely
dilated cervix with the blades applied over the cervix
220
B. Prevention of Genital Tract Lacerations
0 Optimize episiotomy to reduce occurrence of severe perinea! trauma
0 Minimizing operative vaginal delivery can decrease incidence of trauma (vacuum
extraction is less associated with severe perinea! trauma compared with forceps)
0 Antenatal perinea! massage reduces perinea! trauma
■
• Polyglycolic acid and
Perineum • Loose, continuous, non-locking
Polyglactin 910
to appose the vaginal tissue,
perinea! muscle and skin
221
II. GENITALTRACT HEMATOMA
• Pregnant uterus, vagina and vulva have rich vascular supplies that are at risk of trauma
during the birth process, and trauma may result in formation of a hematoma
• Hema to mas are rarely a potentially life-threatening complication of childbirth.
• Good surgical technique, with attention to hemostasis in the repair of lacerations, should
limit the occurrence of puerperal hematoma
B. Manifestations
0 Excessive perinea] pain is the hallmark symptom
° Change in vital signs disproportionate to the amount of blood loss should prompt a
gentle pelvic examination
0 Non-specific signs and symptoms may also present (e.g. pressure symptoms, swelling,
urinary retention, unexplained pyrexia)
C. Diagnosis
0 Other than the usual tests for bleeding and imaging may be helpful to confirm the
diagnosis when there is a suspicion for hematoma but the patient remains stable
0 Ultrasound, CT scan, or MRI:
• Mainly useful for diagnosing hematomas above the pelvic diaphragm
• Useful to assess any extension into the pelvis, particularly as bimanual examination
may not detect them until they become quite large and palpable
• Vaginal packing
• Balloon tamponade or blood pressure cuff tamponade
SCENARIO
I MANAGEMENT
Small, non-expanding • Can be managed conservatively (e.g., ice pack, pressure dressing
hematoma (<3 cm) and analgesia)
Large hematomas • Best managed with surgical evacuation, primary closure and
(;;,3cm) compression for 12-24 hours
• Additional surgical intervention is indicated (e.g.,ligation of the
Hematomas with
internal iliac artery, hysterectomy, selective arterial embolization)
intra-abdominal pelvic
extension • Embolization of the bleeding vessel may be a therapeutic if
bleeding is not life threatening
Source:CPGon ObstetricHemorrhage
2ndEdition.POGS,Inc;2014,2019
222
REFERENCES
l.Bailit JL, Grobman WA, Rice MM, et al: Morbidly adherent placenta treatments and outcomes. Obstet Gynecol 125(3):683,
2015
2.Belfort MA.Overview of postpartum hemorrhage. https://www.uptodate.com. Accessed June 14, 2021
3.Bonnar /. Baillieres Best Pract Res Clin Obstet Gynaecol 2000; 14:1
4.Callahan, Tamara L. (2013). Blueprints obstetrics & gynecology. Baltimore, MD :Lippincott Williams & Wilkins
S.Capitulo RB. Uterine Rupture. Philippine Obstetrical and Gynecological Society (Foundation), Inc. Clinical Practice Guidelines
on Obstetric Hemorrhage. November 2019.
6.Committee on Trauma, American College of Surgeons. Advanced trauma life support for doctors-student course manual. 8th
ed. American College of Surgeons, Chicago2008
7.Cummings K, Doherty DA, Magann EF, et al: Timing of manual placenta removal to prevent postpartum hemorrhage: is it
time to act? J Matern Fetal Neonatal Med 29(24):3930, 2016
8.Cunningham, F.G.. Leveno, K. J.. Bloom, S. L.. Spong, C.Y.,Dashe, J. S., Hoffman, B. L.,Sheffield, J. S. (2018). Williams obstetrics
(25th edition.). New York: McGraw-Hill Education.
9.Cunningham, F.G., Leveno, K. /., Bloom, S. L., Spong, C.Y.,Dashe, J. S., Hoffman, B. L.,Sheffield, J. S. (2018). Williams obstetrics
(25th edition.). New York: McGraw-Hill Education.
10. Dee MT.Retained Placenta. Philippine Obstetrical and Gynecological Society (Foundation), Inc. Clinical Practice Guidelines
on Obstetric Hemorrhage. November 2019.
11. Driessen M, Bouvier-Colle MH, Dupont C, et al: Postpartum hemorrhage resulting from uterine a tony after vaginal delivery.
Factors associated with severity. Obstet Gynecol 117(1):21, 2011
12. Festin, M. (2008). Manual of Obstetric and Gynecologic Emergencies. Manila: Publications Program. ■
13. Fro Iova Al, Stout MJ,Tuuli MG,et al: Duration of the third stage oflabor and risk of postpartum hemorrhage. Obstet Gynecol · -
127(5):951, 2016 ....
14. Hernandez-Quevedo MC. Uterine Inversion. Philippine Obstetrical and Gynecological Society (Foundation), Inc. Clinical •
Practice Guidelines on Obstetric Hemorrhage. November 2019.
15. Martel MJ.No. 115-Hemorrhagic Shock. J Obstet Gynaecol Can. 2018;40(12):e874-e882. doi:10.1016/j.jogc.2018.10.004
16. Norwitz ER, Park JS. Overview of the etiology and evaluation of vaginal bleeding in pregnant women. https://www.
uptodate.com. Accessed June 14, 2021
17. Oxorn H. Human labor and birth (5th ed). Norwalk, CT Appleton & Lange; 1986
18. Plotti I~ Di Giovanni A, Oliva C, Battaglia F, Plotti G (November 2008). "Bilateral ovarian pregnancy after intrauterine
insemination and controlled ovarian stimulation". Fertil. Steril. 90(5): 2015.e3-5
19. POGSCPG on Obstetric Hemorrhage. 2nd Edition. November 2019
20. POGSCPG on Third Trimester Bleeding and Postpartum Hemorrhage. 2nd Edition. November 2012
21. Practice Bulletin No. 183: Postpartum Hemorrhage.Committee on Practice Bulletins•Obstetrics. Obstet Gynecol.
2017;130(4):el68.
22. Quevedo, M.C. (2014). Clinical Practice Guidelines on Obstetric Hemorrhage. Quezon City: Philippine Obstetrical &
Gynecological Society (Foundation), Inc.
23. Reyes LO. Genital Tract Trauma. Philippine Obstetrical and Gynecological Society (Foundation), Inc. Clinical Practice
Guidelines on Obstetric Hemorrhage. November 2019.
24. Silver RM: Abnormal placentation: placenta previa, vasa previa, and placenta accreta. Obstet Gynecol 126(3):654, 2015a
25. Toral JA.Management of Ectopic Pregnancy: Expectant vs lnte,vention, Medical vs Surgical. Philippine Obstetrical and
Gynecological Society (Foundation), Inc. Clinical Practice Guidelines on Ectopic Pregnancy. November 2016.
223
ISSUES
OBSTETRIC
GENERAL
COMPLICATIONS
AND
SECTION ONE
PRETERM LABOR
OVERVIEW OF PRETERM LABOR
I. DEFINITION OF PRETERM LABOR
• Occurrence of regular uterine contractions associated with progressive cervical dilatation
and/or effacement before the completion of37 weeks AOG (term starts at 37 weeks)
CONCEPT I DEFINITION
• Refers to a fetus, pregnancy or neonate <37 weeks but is beyond the age
Preterm
of viability (20 weeks)
• Refers to a neonate that has the function expected of a newborn with age
of gestation less than 37 weeks
• It is best to use the AOG than the weight to determine if fetus is
Premature
premature or not ( a fetus may be large for gestational age, but is still
premature - also, a fetus may be small for gestational age and not be
premature)
II. ETIOPATHOGENESIS
■
A. Pathophysiology
0 Involves four (major) pathogenic processes that may overlap resulting in increased
contractility, membrane rupture and cervical ripening: '
• Activation of the hypothalamic-pituitary-adrenal (HPA) axis
• Infection and corresponding inflammatory response
• Decidual hemorrhage
• Pathologic uterine distention
227
III. CAUSESOF PRETERM LABOR
ETIOLOGY I REMARKS
• Early uterine distension acts to initiate expression of contraction-
Uterine
associated proteins (CAPs) in the myometrium
distension
• Examples: multifetal pregnancy, hydramnios
• Brought about by nutrient deficiency, obesity, maternal infection,
diabetes, psychological stress
Maternal-fetal
• Premature activation of the placental-adrenal endocrine axis increases
stress
placental-derived corticotropin-releasing hormone (CRH), leading to
early loss of uterine quiescence
Premature • Changes in the epithelial or stromal extracellular matrix
cervical
• Reduced mechanical competence of the cervix
changes
• Bacteria gain access to the uterine tissues through:
0 Transplacental transfer of maternal systemic infection
0 Seedings from the peritoneal cavity via the fallopian tubes
Infection 0 Accidental introduction during intrauterine procedures
0 Ascending infection with bacteria from vagina & cervix (most
common route)
III. OBSTETRICULTRASOUNDEXAMINATION
• Provides additional information:
0Determination of placental and fetal age
0Detection of fetal, placental, and maternal anatomic abnormalities
° Confirmation of fetal presentation
0Assessment of amniotic fluid volume
0Estimation of fetal weight
228
IV. TRANSVAGINALULTRASOUND
• Used to measure the cervical length and to check for the presence of cervical funneling
• Risk of preterm birth is higher if both a short cervical length and funneling are seen
A. Cervical Length
° Functional cervical length appears to be the best single cervical parameter to predict
spontaneous preterm birth
0A short cervix before 25 weeks AOG (length< 25 mm) indicates increased risk of
preterm birth
B. Cervical Funneling
0Defined as a protrusion of amniotic membranes into the internal cervical os by greater
than 5 mm from the shoulder of the original internal os
0Shape of the funnel indicates the degree of cervical dilation & effacement (see below)
• With amniotic
• No funneling membrane
• More ominous finding
• Normal cervical protrusion into the
• Indicates more advanced cervical ripening
shape internal os with a
closed external os
■
'
DIAGNOSTIC I REMARKS
• Glycoprotein expressed during pregnancy, localized at the
choriodecidual junction, uterus, and placenta
• Checked in selected cases (see algorithm on the next page) to
Fetal
distinguish true preterm labor from false labor
fibronectin
• Subclinical infection/inflammation, abruption, or uterine contractions
releases fetal fibronectin into cervicovaginal secretions, which is the
basis for its use as a marker for predicting spontaneous preterm birth
• To diagnose asymptomatic bacteriuria, which is associated with an
Urine culture
increased risk of preterm labor /birth
• Rectovaginal group B streptococcal culture [antibiotic prophylaxis
Others depends on the results)
• Testing for sexually transmitted infections (e.g., chlamydia, gonorrhea)
Source: LockwoodCJ. Pretermlabor.Uptodate
229
CONCEPTS IN THE MANAGEMENT OF PRETERM LABOR
I. OVERVIEW OF MANAGEMENT
• Determination of fetal age and EFW (e.g., review history, ultrasonography)
• Corticosteroid administration
• Maternal transfer to a tertiary perinatal center
• Communication with a neonatologist
• lntrapartum monitoring
• Management of pain
• Preterm labor inhibition
• Method of delivery
• Resuscitation of the neonate
No tocolysis or
antenatal
corticosteroids
Admit for delivery if in
Cervix ~3 cm Cervix <3 cm labor OR
Send home if
contractionscease
Fetal fibronectin
POSITIVE NEGATIVE
Source:Lockwood,
et al. PretermLabor.UpToDate:
2019
230
II. GOALS OF PRETERM LABOR INHIBITION
• Achieve a 24- to 48- hour delay in the preterm delivery to administer
Immediate antenatal corticosteroids to hasten fetal lung maturity
goals • Transfer antepartum patient to a tertiary care facility for a higher level of
neonatal intensive care
• Maintain a sustained labor suppression to enable the fetus to mature in
Long-term utero and reach a gestation age as close to term as possible
goals • Reduce duration of hospital stay and number of hospital admissions for
recurrent preterm labor
• Includes stratification of
Neonatal
neonates who are likely to
assessmentfor
thrive outside utero with X C C ✓
resuscitation
intensive neonatal management
• Given to decrease neonatal
respiratory morbidity,
Corticosteroid
■
therapy
intracranial hemorrhage, X X C ✓
necrotizing enterocolitis, and
death .
Magnesium • Administered to reduce
sulfate occurrence of cerebral palsy X X C ✓
• To provide short-term
prolongation of pregnancy
enabling administration of
Tocolysis
antenatal steroids, magnesium X X C ✓
sulfate as well as transport to a
tertiary facility if needed
Continuous • Close antenatal surveillance to
EFM rule out fetal distress X X C ✓
Group B
Streptococci • GBS prophylactic antibiotics to
(GBS) improve neonatal outcomes X X C ✓
prophylaxis
231
INDIVIDUAL COMPONENTS OF MANAGEMENT
I. TOCOLYTICAGENTS
• Drugs given to delay the delivery ofa fetus by inhibiting contractions ofmyometrial
smooth muscle contractions
• Given for at least 48 hours to permit completion of corticosteroid therapy
• Maintenance tocolysis is not associated with improved perinatal outcome and is therefore
not recommended routinely
TOCOLYTIC*
I EXAMPLES
I MECHANISM
I SIDE EFFECTS
• Nifedipine
• Tocolytic agent of
Calcium 30-40 mg/tab
first choice • Fetal: possible decrease in
channel (LD), then
• Inhibits the influx of uterine blood flow
blockers 30-160 mg/day
extracellular Ca2 •
in divided doses
;_c
• Monitor: urine output, deep
tendon reflexes, respiratory
• Not indicated as a rate.
• Magnesium primary tocolytic • Maternal: flushing, sensation
sulfate 4-6 g • Currently, more of warmth, nausea, emesis,
Neuro- slow IV over indicated for dizziness, nystagmus,
transmitter 20 minutes (LD), neuroprotection lethargy, pulmonary edema
blocker then infusion at • Reduces risk for • Antidote: Calcium
2 g/hourfor cerebral palsy gluconate 10 ml of10%
24-48 hours • Given between solution at bedside
24 - 32 weeks AOG • Fetal: nonreactive heart
rate, absent fetal breathing,
hypotonia, lethargy
• Terbutaline
• Maternal: hypotension,
5 mg PO Q4 or
tachycardia, arrhythmia,
0.25 mg SC for
pulmonary edema,
Beta- short-term use
• Reduces myometrial hyperglycemia,
adrenergic • Salbutamol
contractility hypokalemia
agonists 10 ug/min, up to
• Fetal: tachycardia,
45 ug/min
hyperinsulinemia with
• lsoxsuprine
hypoglycemia
• Ritodrine
• Maternal: flushing, nausea,
headache, dizziness,
palpitations, hypotension,
• Bind & inactivate
tachycardia
cyclooxygenase
• lndomethacin • Fetal: premature closure of
which regulates
50-100 mg (LD), ductus arteriosus with
Prostaglandin production of PGE2
then 25-50 mg consequent pulmonary
inhibitors to arachidonic acid
PO every 8 hours hypertension, persistent
• Category D if used
for 24-48 hours patent ductus arteriosus,
>48 hours or at
enterocolitis, intra-
>34 weeks AOG
ventricular hemorrhage,
oligohydramnios,
renal failure
• Inhibition of
Oxytocin
oxytocin receptors • Maternal: injection-site
receptor • Atosiban
antagonists in myometrium and reaction
decidua
*Somecontraindicationsto tocolyticsincludesevere preeclampsia,placentalabruption,intrauterineinfection,
advancedcervicaldilatation,or evidenceof fetalcompromiseor placentalinsufficiency
Source:ACOG,2016
232
II.STEROIDS
• Antenatal steroids should be given to patients at risk for preterm labor and delivery
between 26 and 34 weeks AOG
• Administration may also be considered in those at risk for preterm delivery >34 weeks to
36 617 weeks provided they were not given a previous course of antenatal steroids
• Regimens:
Betamethasone: 12 mg/IM every 24 hours for 2 doses, OR
• Dexamethasone: 6 mg/IM every 12 hours for 4 doses
III. PROGESTERONE:
• Recall that parturition involves progesterone withdrawal mediated by decreased activity
of progesterone receptors - therefore, giving progesterone may block preterm labor
• 17-Hydroxyprogesterone caproate (17-0HPC) given in weekly 250 mg/IM injections from
16-20 weeks through 36 weeks
• Micronized progesterone: daily 200 mg PO or per vagina (preferred route) from
24-34 weeks AOG
• Counteracts prostaglandin stimulatory activity, decreases myometrial oxytocin receptors
• PO route may cause nausea, headache, and sleepiness
Algorithm for Screening & Treatment of Singleton Pregnancies to Reduce Preterm Birth
■
l7 spontaneous preterm birth after 16 weeks J
• Cervical length is the best predictor of preterm birth (a history of spontaneous preterm
birth and short cervix are strong risk factors)
• Vaginal progesterone (either in capsular or in gel form), 170HPC, and cerclage can be
used to prevent the reoccurrence and the indications for such interventions should be
individualized
• For those with a short cervix in 2"" trimester without prior history of spontaneous
preterm birth, progesterone is the choice of treatment
• Cervical pessary use is an option, if available
• In multiple gestations, no intervention has been shown to effectively prevent preterm
labor
Source:Li, Chao.Maternal-Fetal
Medicine;
2020
233
IV. OMEGA-3LONGCHAIN POLYUNSATURATEDFATTYACIDS (LCPUFAs)
• Supplementation with Omega-3 LCPUFAs(>l gram per day) can significantly decrease
the risk of preterm delivery
• Best when given <20 weeks AOG
• Theories suggest that Omega-3 LCPUFAsare associated with downregulation of
inflammatory processes in the body by modulating prostaglandin synthesis and inhibiting
palmitate-induced inflammatory cascade leading to prolonged gestation
V. ANTIBIOTICS
• Antibiotics in the management of preterm labor depends on the presence of symptomatic
maternal infections like vaginitis or cervicitis, cystitis or pneumonia
• Antibiotics in idiopathic spontaneous preterm labor without clinical signs and symptoms
of infection does not significantly decrease the incidence ofpreterm birth
• GBSprophylaxis may be given in the following clinical situations:
Previous infant with invasive GBSdisease
GBSbacteriuria during any trimester
0 Positive GBScultures in late gestation during current pregnancy
Unknown GBS status PLUS:
• Preterm labor
• Ruptured membranes 2'18 hours
• lntrapartum temperature 2'39.0 'C
• lntrapartum nucleic acid amplification test (NAAT)positive for GBS
VI. CERCLAGE
• Refers to a variety of procedures to reinforce the cervix during pregnancy in women with
an incompetent cervix
• Offered to patients with prior preterm birth and short cervix (<2.5 cm) on ultrasound
• Approach maybe transvaginal, tranasabdominal or laparoscopic
• Multifilament/braided sutures such as Mersilene is used
234
PRELABOR RUPTURE OF MEMBRANES (PROM)
• Previously known as premature rupture of membranes
• Refers to the rupture of membranes at ;,,37 weeks AOG,before the onset of uterine
contractions
• Preterm prelabor rupture of membranes (PPROM) refers to the rupture of membranes at
<37 weeks AOG,before the onset of uterine contractions
I. ETIOPATHOGENESIS
A. Pathophysiology
0 Major etiologic factor is the presence of lower tract infection triggering a host-
inflammatory response, leadin to weakness & rupture in chorioamnionic membrane
• Infection
• Prolapse of the umbilical cord
• Premature births
• Prematurity
• Infection
• Respiratory distress syndrome
■
.
(complication of prematurity)
• Umbilical cord compression/prolapse
• Neonatal death
II. MANIFESTATIONS
• Sudden gush of fluid from the vagina, not associated with uterine contractions
• Speculum examination: pooling of amniotic fluid in posterior vaginal wall
• Internal exam: absence of membranes
III. DIAGNOSIS
• A correct diagnosis of PROM is of great importance
False-positive diagnosis may lead to a non-indicated intervention (e.g., early delivery,
surgical delivery)
False-negative diagnosis may place the infant and mother at increased risk of infection
which may be life threatening to one or both
A. Nitrazine Test
0 Amniotic fluid is normally alkaline (pH of 7.0 to 7.5)
0 It is done to determine the nature of vaginal fluid when PROM is suspected
Procedure: This test involves putting a drop of fluid sample from the vagina onto paper
strips containing nitrazine dye. The strips change color depending on the pH of the fluid
Interpretation:
• The strips will turn blue if the pH is greater than 6.0 due to alkalinity of fluid
• A blue strip is suggestive of membrane rupture
• False positive result may be due to contamination with blood, semen, bacterial vaginosis
and cervical secretions
235
B. Fern Test
0Vaginal secretions are inspected on microscopy for crystallization (i.e., ferning pattern
or arborization)
° Crystallization is due to an increased concentration of protein & electrolytes within fluid
0Vaginal secretions do not show the ferning pattern during pregnancy, but if amniotic
fluid is present, the fern pattern is seen
C. Immunoassays
° Fetal fibronectin
0 Placental alpha-microglobulin-1 (PAMG-1):most reliable method (not locally available)
0 Insulin-like Growth Factor Binding Protein-1 (!GFBP-1): Actim-PROM®1-step dipstick
IV. MANAGEMENT
• Determine the age of gestation by review of history and early ultrasound scan
• Management depends on the age of gestation at the time of rupture
• Patients with PROMwill usually deliver within 48 hours
236
INTRAAMNIOTIC INFECTION AND CHORIOAMNIONITIS
I. ETIOPATHOGENESIS
• Term used when clinical findings of infection resulting in
Intraamniotic
inflammation of any combination of the amniotic fluid, placenta,
infection
fetus, fetal membranes, or decidua is present
• Term used to denote histopathologic findings of inflammation of
Chorioamnionitis
the chorion, amnion, and/or umbilical cord
■
*Fever is the only reliable clinical indicator of chorioamnionitis
Source:PIDSOGandPOGS,CPGon ObstetricandGynecologic
Infectious
Diseases,
2ndEd;2015
Ill. DIAGNOSTICS
• The following laboratory tests support the diagnosis of intra-amniotic infection:
0Maternal leukocytosis
0Elevated CRP
0In mid-2"' trimester fetal losses, fetal autopsy plus placental biopsy may confirm if
chorioamnionitis was the cause of fetal death
IV. MANAGEMENT
A. General Approach to Prevent Adverse Maternal/Neonatal Sequelae
0 Deliver the baby regardless of age of gestation
Mode of delivery will depend on the usual obstetric indications
0
IV antibiotic therapy started immediately and continued until delivery (> 1 dose
0
for surgical site infection (obese, prolonged rupture of membranes, prolonged labor)
Administer paracetamol for maternal fever >38°C
0
B. Antibiotic Therapy
0 Benefits of antimicrobial treatment:
• Fewer women developed chorioamnionitis
• Fewer newborns developed sepsis, and
• Pregnancy was more often prolonged for 7 days
REGIMEN
I MANAGEMENT
• Benzylpenicillin (penicillin G) SM units loading dose, then
If with GBS infection or
2.5-3M units IV q4
history ofGBS
• If allergic to penicillin: give clindamycin 900 mg IV q8
For spontaneous • Ampicillin 2 g IV q6 AND
vaginal delivery • Gentamicin 1.5 mg/kg IVq8
• Clindamycin900 mg IVq8 until delivery OR
For Cesarean delivery Metronidazole 500 mg IVq8 AND
• Gentamicin 1.5 mg/kg IVq8
Source:PIDSOGandPOGS,CPGon ObstetricandGynecologic
InfectiousDiseases,2ndEd;2015
Cunningham
FG,et al. WilliamsObstetrics;
2018
237
SECTION TWO
FETAL DEMISE, POSTTERM PREGNANCY,
AND PROLAPSED CORD
I. CAUSES OF STILLBIRTHS
• Obstetrical complications (e.g., abruption, ruptured membranes at 20-24 weeks,
multifetal gestation)
• Placental abnormalities (e.g., uteroplacental insufficiency)
• Fetal malformations
• Infection involving the placenta or fetus
• Umbilical cord abnormalities
• Others: hypertensive disorders, diabetes, antiphospholipid antibody syndrome (APAS)
II. MANIFESTATIONS
• Changes noted immediately after fetal death: absent cardiac activity and fetal movement
(on real-time ultrasound findings)
• Suspected with loss of perceived fetal movement and lack of uterine growth
• After 20 weeks, diagnosis is confirmed by ultrasound (before 20 weeks, it is referred to as
an abortion)
ASPECT I CONFIRMATORY FINDING
Heart tones • Not detected by auscultation with a stethoscope or Doppler stethoscope
• Not detected by electronic fetal monitoring using an external
Cardiac activity
sonocardiogram or an internal scalp electrode
• Not detected by real time ultrasound
• There is no cardiac or great vessel vascular motion, which is 100%
Heart motion
accurate in diagnosing fetal demise
• Method of choice
lll. DIAGNOSIS
DIAGNOSTIC
I FINDINGS
• Robert sign (gas in the great vessels): caused by postmortem blood
degeneration
Radiologic • Spalding sign (overlapping skull bones): caused by collapse of the
(x-ray) fetal brain
• Angulation of the fetal spinal curvature: caused by loss of tone of
paraspinal muscles and ligaments
238
To determine the etiology:
WORK-UP I REMARKS
Infectious • TORCHstudies (fetal infection)
work-up • Listeria culture (fetoplacental infection)
Anticardiolipin Ab/
• Antiphospholipid antibody syndrome (APAS)
lupus anticoagulant
Fetal autopsy • Gross anomalies suggesting a syndrome
Karyotype • Abnormal fetal chromosomes
Total body fetal
• Osteochondrodystrophic disorders
radiograph
Maternal Kleihacuer-
• Fetomaternal bleed
Bettze test
Typical Ab titer • Maternal isoimmunization
75gramOGTT • Maternal diabetes mellitus
IV. MANAGEMENT
• This generally includes expeditious termination of the pregnancy
I
• Labor induction with prostaglandins or high-dose oxytocin if not yet in labor
• Cervical examination should be done to assess if cervix is favorable for labor & delivery
'
A. General Approach
• Labor can be induced, anticipating vaginal delivery
• Artificial rupture of membranes and IV-oxytocin infusion are
Favorable cervix
used to induce labor
• There is no benefit to delivering a dead fetus via cesarean section
• Use of the following should be considered:
Unfavorable cervix • Cervical ripening agents (e.g., dinoprost)
• Laminaria
I. ETIOPATHOGENESIS
A. Definition of Terms
TERM I DEFINITION
• Pregnancy that goes beyond 42 weeks AOGor greater than 294
Postterm or
days from the first day of the LNMP
prolonged
• Definition assumes that the last menses was followed by ovulation
pregnancy
and fertilization 2 weeks later
• Refers to the specific clinical fetal syndrome in which the newborn
has features indicating a pathologically prolonged pregnancy
Postmaturity • Wrinkled, patchy, peeling skin
syndrome • Long nails
• Long, thin body suggesting wasting
• Open-eyed, unusually alert, and appears old and worried
Source:ACOG,2016
B. Etiology
• Inaccurate aging
• Diminished levels of circulating estrogens (e.g., anencephaly, fetal adrenal hypoplasia,
and fetal pituitary hypoplasia)
• Genetic predisposition
• Irregular ovulation
BD tu ·ty S d V M
240
III. MANAGEMENT
• At 42 weeks -> labor induction
• Consider labor induction at 41 weeks
41 weeks
42 - 42 617weeks
Labor induction
DATE I MANAGEMENT
• Labor induction via IV oxytocin after negative contraction
IftheAOG is stress test
confirmed, and the • Continuous intrapartum fetal monitoring should be performed
cervix is favorable while watching for severe variable decelerations from cord
compression and late decelerations from fetal hypoxia
• Cervical priming agent given prior labor induction after
lftheAOG is
negative contraction stress test
confirmed, but the
• Continuous intrapartum fetal monitoring should be performed
cervix is unfavorable
while watching for severe variable decelerations from cord
(Bishop score S4)
compression & late decelerations from fetal hypoxia
• Request for (ultrasound) maturity indices
• Both the NST & AF! can be performed twice weekly while
If the dates are
waiting for spontaneous labor to occur
questionable
• Delivery should take place if the NST becomes non-reactive or
if the AF! <S cm
241
UMBILICAL CORD PROLAPSE
• Umbilical cord lies beside or below the presenting part
• Associated with a high fetal mortality rate and carries an increased maternal hazard from
the operative procedures used in treatment
I. ETIOPATHOGENESIS
A. Classification of the Prolapsed Cord
CLASSIFICATION I DESCRIPTION
Umbilical cord
• Membranes are intact
presentation
B. Etiology
0 Whenever the presenting part does not fit closely and fails to fill the inlet of the pelvis,
danger of prolapse of the umbilical cord exists
ETIOLOGY I CAUSES
• Abnormal presentation
• Prematurity
Fetal
• Multiple pregnancy
• Polyhydramnios
• Long cord
Cord and Placenta
• Low-lying placenta
• Artificial rupture of the membranes
• Disengaging the head
Iatrogenic
• Flexion of an extended head
• Version and extraction
B. Temporary Measures
0 Aim to lessen compression of the umbilical cord by:
• Push the presenting part up and away from the cord
• Place the patient in the knee-chest or Trendelenburg position, with the hips
elevated and the head low
• Oxygen support by mask is given to the patient
• Check fetal heart rate via transabdominal auscultation or palpation of the
umbilical cord
• Ascertain presentation, cervical dilatation, station of the presenting part, and
condition of the cord through vaginal examination
• Tocolytic drug can be given in an intravenous infusion to reduce pressure on the
umbilical cord from uterine contractions
242
C. Cervix Fully Dilated
° Cesarean section (CS) is the best treatment if it can be performed without delay
0 If CS cannot be carried out immediately the following procedures are indicated and
may be performed, as long as an experienced operator is available:
I
.
243
SECTION THREE
MULTIPLE GESTATIONS
MULTIPLE GESTATION
• Fueled largely by infertility therapy, rate and number of multifetal births increased
dramatically
• These rates of multifetal pregnancies may be associated with maternal and fetal complications
I. ETIOLOGIES
• Twin fetuses usually result from:
° Fertilization of two separate ova, which yields dizygotic or fraternal twins; or
° Fertilization of a single ovum that then divides to create monozygotic or identical
twins (less often)
• Mechanisms differentiating dizygotic and monozygotic twin pregnancy are as follows:
I DlZYGOTIC I MONOZYGOTIC
Also known • Double ovum, dizygotic or fraternal • Single ovum, monozygotic or
as twins identical twins
• Twins resulting from fertilization of • Twins arising from a single
two ova during a single ovulatory fertilized ovum that subsequently
Description cycle ( e.g., each twin will have its divides into two similar structures,
own chorion and amnion and two each with a potential to develop
placentas) into a separate individual
Fertilization • 2 sperms + 2 eggs • 1 sperm + 1 egg
Genetic
• Different between twins • Same between twins
make-up
FetaISex • Same or different sex • Same sex
• Depends on the time of division
Membranes • Dichorionic-diamnionic
(see table on next page)
Placenta • One fused or two separate • One or two
Incidence • Depends on race, heredity, age, parity • Constant (1 per 250 pregnancies)
Superfecundation • Fertilization of two ova within a period of time, but not at the same
coitus nor necessarily by sperms from the same partner
• Improved ultrasound technique can now detect twins early in the
1st trimester, allowing documentation of the absorption of an early
Vanishing Twin
fetal demise of a second of twin
• Incidence of twins is more during the first trimester, than at term
• A term used in obstetric imaging to describe a significant size or
weight difference between the two fetuses of a twin pregnancy
Twin
• Birth weight discordance= (larger twin weight• smaller twin weight)
Discordancy
larger twin weight x 100
• A discordancy of>25% is considered significant
Twin-to-Twin • Blood is transfused from the donor twin to its recipient
Transfusion • Donor becomes anemic and the recipient becomes polycythemic
syndrome • Significant mortality (70%) of one or both twins if left untreated
244
III. GENESIS OF MONOZYGOTICTWINS
• The outcome of the monozygotic t:\vinning process highly depends on the timing of division
• Sonographic determination of chorionicity is considered a recognized indication for first-
I I
trimester sonography
TIME OF
DIVISION I EVENTS
OCCURING OUTCOME ILLUSTRATION
amnion chorion
• Diamnionic,
dichorionic,
• Division occurs
monozygotic
before the inner
twins
1" 72 cell mass (morula)
• Two embryos
hours from is formed and
each in separate
fertilization outer layer of
amnionic and
blastocyst is not
chorionic sac
yet the chorion
• Placenta may be
t:\Vo or fused
• Diamnionic,
monochorionic,
• Division occurs
monozygotic
after the inner cell
4'"to 8 th
day from
fertilization
mass is formed
and cells destined
to be the chorion
has differentiated,
but those to be the
t\Vins
• Two embryos,
each in a separate
amnionic sac,
both covered
I
.
by a common
amnion have not
chorion & share a
placenta
chorion
• Monoamnionic,
monochorionic,
monozygotic
• Chorion t\Vins
8 th to 12 th
and amnion • Two embryos
day from
have already within a
fertilization
differentiated common
amnionic sac
and chorion and
share a placenta
• Cleavage is
incomplete
• Division occurs • Conjoined
After 12
when the embryos within
days from
embryonic disk is a common
fertilization
formed amnionic sac
and chorion and
share a placenta
Terminologies:
• Diamnionic:
twoseparate
amnionicsacs(innersac) • Monoamnionic:
oneamnionicsac
• Dichorionic:
twoseparate
chorionic
sacs(outersac) • Monochorionic:
onechorionic
sac
245
IV. ANTEPARTUM MANAGEMENT OF TWIN PREGNANCIES
A. Complications
FETAL I MATERNAL
246
V. INTRAPARTUM MANAGEMENT OF TWIN PREGNANCIES
A. Timing of Delivery
° Chorionicity and amnionicity of otherwise uncomplicated twin pregnancies determine
the timing of delivery
0 Below is a summary of suggested timing of delivery based on the chorionicity and
complications present in twin pregnancy:
• Uncomplicated
dichorionic
twins:38 weeks
• Uncomplicated
monochorionic twins:between34 and37 6n weeks
diamnionic
• Monoamnionictwins:32to 34 weeks
Source:BerghellaMaternal-Fetal
EvidenceBasedGuidelines,
Chapteron Multifetal
Pregnancy,3rdedition
AGOG;2016
C. Route of Delivery
0 Time interval of delivery between the first and the second of twin has no clinical
significance, but the remaining twin must be monitored closely
TYPE OF PREGNANCY
I ROUTE OF DELIVERY*
Monoamnionic-
monochorionic twin
• Cesarean delivery
If twin A is malpresented
Both twins are malpresented
• With EFW 1500-3500 g: may allow vaginal delivery**
Twin B is malpresented
• With EFW <1500 g: consider Cesarean delivery
Both cephalic presentation • May allow vaginal delivery
'In general,cephalicpresentation
ofthefirstfetusinlaboringwomenwithtwinsmaybe consideredforvaginaldelivery
"Vaginaldeliveryonlyperformed byan experienced obstetrician
oroperator,
withadequateanesthesia/analgesia
Source:AGOG;2016
247
SECTION FOUR
FETAL GROWTH DISORDER
FETAL GROWTH RESTRICTION (FGR)
I. ETIOPATHOGENESIS
• Compromised uteroplacental perfusion
• Fetus redirects blood flow to more vital organs
• This pattern of redistribution may be evident by a decreased diastolic flow in the
Umbilical artery Doppler studies
• Body fat, lean mass, and bone mineral content are reduced
A. Definition of Terms
1. Intrauterine Growth Restriction (IUGR)
• Term used to describe the size of the fetus in-utero
• Not synonymous to small for gestational age (SGA)
• EFW <10th percentile because of a pathologic process
• Diminished growth velocity documented by at least 2 intrauterine growth assessment
usually associated with abnormal Doppler findings of the umbilical arteries
TYPE
I DEFINITION
• Genetic abnormalities
• Aneuploidy
• Fetal infection [cytomegalovirus, toxoplasmosis, rubella, malaria, herpes
Fetus
simplex virus)
• Structural anomaly
• Multiple gestation
• Abruption
• Confined placental mosaicism
Placenta • Placenta accrete syndromes
• Chorioangioma
• Implantation abnormalities
• Maternal low prepregnancy weight, poor gestational weight gain,
malabsorption, poor nutritional status
I
• Short interpregnancy interval
• Extremes of maternal age
• Medical and obstetric conditions .
0Preeclampsia Uterine malformations
0
Ill. MANAGEMENT
• Review risk factors
• Evaluation of fetal anatomy, placenta, amniotic fluid ultrasound
• Assessment of the umbilical artery by Doppler
• Timing of delivery is individualized on the basis of established gestational age, Doppler
velocimetry studies, growth and biophysical testing
249
FETAL MACROSOMIA
• Macrosomia is defined as birthweights that exceed certain percentiles for a given population)
• Macrosomia is frequently defined based on mathematical distributions ofbirthweight
(see below)
I. ETIOPATHOGENESIS
• 5-10% are associated with maternal diabetes
• Fetal release of insulin, insulin-like growth factors, and growth hormone leads to
increased fetal fat deposition and, in turn, enhanced fetal size
A. Definition of Terms
Large for Gestational • Defined as a weight, length, or HC that lies above the 90th
Age (LGA) percentile for AOG
• BW ;,4,000 g irrespective of AOGor >90th percentile for a given
AOGafter correcting for neonatal sex and ethnicity
Macrosomia 0 Grade I: BW = 4000-4499 grams
MAJOR SYNDROMES
ASSOCIATED WITH MACROSOMIA
I MAJOR COMPLICATIONS OF
FETAL MACROSOMIA
• Pallister-Killian • Simpson-Golabi-Behmel • Increased risk of CS
• Weaver • Costello • Shoulder dystocia
• Sotos • Beckwith-Wiedemann • Clavicular fracture and damage
• Perlman • Macrocephaly-cutis marmorata • Brachia! plexus injury
• Berardinelli telangiectasia congenita (M-CMTC)
lipodystropia
III. DIAGNOSIS
• Ultrasound: abdominal circumference (AC) >35 cm is the most common and reliable
single UTZ parameter to assess risk of macrosomia
• Because current methods fail to accurately estimate fetal size, macrosomia cannot be
definitively diagnosed until delivery
IV. MANAGEMENT
• When macrosomia is suspected, pregnancy should be classified into uncomplicated,
gestational diabetes, prior cesarean delivery or history of shoulder dystocia
CLASSIFICATION
I MANAGEMENT
....
■
II. ASSESSMENT OF AFV
• AFV is routinely assessed during pregnancy because it is a marker of fetal health
• Qualitative or semiquantitative assessment of AFV is a standard component of every 2nd .
and 3rd trimester ultrasound examination
• Volume of amniotic fluid reflects the balance between "fluid production" and "fluid
movement out of amniotic sac"
B. Semiquantitative Analysis
PARAMETER I REMARKS
I INTERPRETATION
251
POLYHYDRAMNIOS (HYDRAMNIOS)
• Refers to an excessive volume of amniotic fluid
• Associated with an increased risk of adverse outcomes (e.g., preterm birth, placental
abruption, fetal anomalies)
• Generally from decreased fetal swallowing/diminished absorption or increased fetal
excretion of fluid
I. ETIOPATHOGENESIS
MECHANISM I EXAMPLES/REMARKS
Fetal (Congenital) 1Anom~alies(Structural Abnormalities or Genetic Syndromes)
Impaired • CNS anomaly: anencephaly, holoprosencephaly
swallowing • Craniofacial anomaly: cleft lip/palate, micrognathia
GIobstruction • Esophageal/duodenal atresia
Renaldisorders • Ureteropelvic junction obstruction (paradoxical), fetal Bartter syndrome
Other Causes JI
Increased • Maternal diabetes mellitus causes fetal polyuria from hyperglycemia
urine output and increased osmotic diuresis
(UO) • Fetal anemia can cause increased UO from increased cardiac output
Increased
transudation
• Placental tumors (e.g., chorioangioma)
from enlarged
vessels
• Fetal hydrops
• Congenital viral infection (e.g., TORCH)
Others
• Multiple gestation (e.g., twin-to-twin transfusion)
• Idiopathic
Source:BelooseskyR, Ross MG.Polyhydramnios:
etiology,diagnosis,and management.UptoDate
CunninghamFG,et al. WilliamsObstetrics;2018
II. MANIFESTATIONS
A. Presentation
Hydramnios is suspected if uterine size is large for gestational age (fundal height
0
B. Complications
° Fetal anomalies
0 Preterm birth and PROM
0 Macrosomia
0 Malpresentation
° Cord prolapse
0 Abruptio placenta
0 Increased primary CS rate
0 Uterine atony
252
III. DIAGNOSIS
A. Ultrasound Criteria
■
0
0 75gOGTT
.
IV. MANAGEMENT
• Treatment is directed to the underlying cause
• Severe hydramnios may result in early preterm labor or maternal respiratory
compromise. for which amnioreduction (i.e., large-volume amniocentesis) may be needed
AOG I SEVERITY I ANTENATAL SURVEILLANCE
• AFI <30 cm • AFI or SOP every 2-3 weeks
• AFI or SOP weekly to rule our hydrops
• AFI 2:30 cm • Weekly NST or Biophysical profile
23 to 38 6 17 • Consider amniocentesis
weeks
• AFI 2:35 cm • Amnioreduction to normalize AFV
• SOP 2:12 cm • NSAIDtherapy: indomethacin 75-200 mg per day given
• Maternal for 48 hours at <32 weeks AOG
symptoms • Antenatal monitoring beginning at diagnosis or 28 weeks
• Induction of labor and delivery with cautious amniotomy
.?39weeks for idiopathic polyhydramnios
• Cesarean delivery for obstetrical indications only
253
OLIGOHYDRAMNIOS
• Refers to amniotic fluid that is less than expected for gestational age, diagnosed by
ultrasound examination
• Anhydramnios refer to no measurable pocket of amniotic fluid
• Associated with an increased risk for fetal/neonatal death
I. ETIOPATHOGENESIS
• Pregnancies complicated by oligohydramnios include those in which:
AFV has been severely reduced since early 2nd trimester (i.e., fetal abnormality that
precludes normal urination or placental abnormality that impairs perfusion)
AFV was normal until near-term or even full-term (i.e., placental abnormality,
preeclampsia, maternal vascular disease)
• Ruptured membranes should be excluded
Common Etiologies of Oligohydramnios
• Congenital abnormalities, especially those with impaired urine production*
• Isolated/idiopathic form
• Uteroplacental insufficiency**
• Pulmonary hypoplasia
• Complication of multiple pregnancies (e.g., twin-to-twin transfusion)
• Iatrogenic (e.g. postchorionic villous sampling, exposure to ACE inhibitors & NSAIDs)
Source:Beloosesky
R, RossMG.Oligohydramnios:
etiology,diagnosis,andmanagement.
UptoDate
II. MANIFESTATIONS
A. Presentation
0 Oligohydramnios first suspected because uterine size (estimated by the fundic height)
is less than expected for AOG
B. Complications
During 1"
• Spontaneous abortion
trimester
• Fetal/neonatal death
During 2 nd • Preterm delivery
trimester • Anatomical & functional abnormalities (e.g. skeletal deformations,
contractures, and pulmonary hypoplasia
• Umbilical cord compression
During 3,• • Uteroplacental insufficiency
• Meconi um aspiration
trimester
• Low BW
• CS for non-reassuring fetal heart rate patterns
254
III. DIAGNOSIS
• Sonographic diagnosis (ultrasound criteria) of oligohydramnios is based on:
, SOP s2 cm (diagnostic method of choice), or
, AFI <5 cm
Source:AGOG,2016
IV. MANAGEMENT
.
• Question woman concerning PPROM
h Id d ocument norma Heta I k'd
Ultrasoun d SOU 1 nevs, bl a dd er, stomac h b u bbl e & ~eta we1g1
ht
• Amnioinfusion: if oligohydramnios (without PPROM) is detected just
before or in labor near or at term
Methods for • Maternal hydration:
increasing AFI ' IV hydration: Intravenous hypotonic versus isotonic solution
' Oral hydration: equally effective as IV hydration (allow mother
to drink 2 liters then reassess amniotic fluid)
• Trial of maternal hydration
Preterm
• If with persistent oligohydramnios, intensive surveillance (non-
with isolated
stress test plus SOP twice weekly) & delivery if with NRFS, abnormal
oligohydramnios
or biophysical profile
Term with • If BPS is reassuring, consider maternal hydration then repeat testing
isolated • With persistent oligohydramnios, consider labor induction versus
oligohydramnios expectant management with 2x weekly fetal surveillance
REFERENCES
I.American College of Obstetricians and Gynecologists: Intrapartum management of intraamniotic infection. Committee
■
'
255
MEDICAL
ISSUES
INPREGNANCY
SECTION ONE
OVERVIEW OF THE MEDICAL ISSUES IN PREGNANCY
GENERAL CONSIDERATIONS
• A pregnant woman is predisposed to the medical disorders that affect any woman of
child-bearing age
• Pregnancy-induced alterations in virtually all organ systems can amplify the existing
medical condition
• Conversely, the medical condition itself can affect the maternal physiological response to
pregnancy
• Obstetricians should have a working knowledge of the medical disorders common to
women of reproductive age
I. MEDICATIONS
• Most medications in the frequently encountered illness complicating pregnancy can be
safely given
• Some medications that have significant risk to the developing embryo/fetus include:
■
• Lead
• Bosentan • Tamoxifen
• Leflunomide, lenalidomide
• Carbamazepine • Tetracycline
• Lithium
• Chloramphenicol • Thalidomide
• Methimazole
• Cocaine • Toluene
• Mercury
• Corticosteroids • Topiramate
• Methotrexate
• Cyclophosphamide • Trastuzumab
• Misoprostol
• Danazol • Valproic acid
• Mycophenolate
• Diethylstilbestrol (DES) • Warfarin
Source:CunninghamFG,et al. W1ll1ams
Obstetrics;2018
II. RADIOGRAPHY
• Imaging modalities are used for the diagnosis and therapy during pregnancy (e.g.,
sonography, radiography, magnetic resonance imaging)
• Most diagnostic radiographic procedures are associated with minimal fetal risks, so some
guidelines would recommend to limit exposure through radiation safety practices
259
COMMON
CONCERNS
INPREGNANCY
CONDITION
I REMARKS
I REMEDY/MANAGEMENT
• Persists until 14-16 weeks AOG • Vitamin B6, doxylamine,
• Hyperemesis gravidarum: severe phenothiazine or Hl-receptor
Nausea and
vomiting causing dehydration, blocking antiemetics
vomiting
electrolyte & acid-base • Eating small meals at frequent
disturbances & starvation ketosis intervals
• Periodic rest with leg elevation, elastic
stockings
• Lower extremities varicosities • Surgery (injection, ligation or
stripping of veins) during pregnancy
generally is not advised unless severe
Varicosities • Fitted pantyhose, foam rubber pad
and • Vulvar varicosities suspended across the vulva by a belt
hemorrhoids to exert pressure on the dilated veins
• Topical anesthetics, hot sitz bath, and
stool-softening agents
• Hemorrhoids • Incision & removal of the clot under
local analgesia for thrombosed
external hemorrhoids
• Due to exagerrated lordosis • Reduced by squatting rather than
in pregnancy, exacerbated by bending when reaching down, using a
Backache
significant bending, lifting, or pillow back support when sitting and
walking by avoiding high-heeled shoes
• Results from upward • Small frequent meals & avoidance of
displacement and compression bending over or lying flat
Heartburn of the stomach by the uterus, • Antacids, aluminum hydroxide,
combined with relaxation of the magnesium trisilicate, or magnesium
lower esophageal sphincter hydroxide alone or in combination
• Craving for strange food
0 Pagophagia: craving for
nonfoods such as ice • Maintain a healthy, balanced diet
0 Amylophagia: craving for • Take prenatal multivitamins & iron
Pica
starch daily
0 Geophagia: craving for clay • Resist intake of non-food items
• May be triggered by severe iron
deficiency
• Eating small frequent meals
• Salivation sometimes appears to
• Chewing gum or sucking hard candies
Ptyalism follow salivary gland stimulation
• Taking small, frequent sips of water
by ingestion of starch
• Rinsing mouth frequently
I. PATHOPHYSIOLOGY
• Placental implantation with abnormal trophoblastic invasion of uterine vessels
• Immunologic maladaptive tolerance between maternal, paternal (placental), and fetal tissues
• Maternal maladaptation to cardiovascular or inflammatory changes of normal pregnancy
• Genetic factors including inherited predisposing genes and epigenetic influences
■
Obstetric and • History of preeclampsia
gynecologic Factors • Molar pregnancy
• Multiple pregnancies
• Immunologic habituation to paternal antigens through contact
between the sperm and the female genital tract
Paternal Factors: • New sexual partner will expose the mother to new paternal
Primipaternity antigens to which she may not be tolerant
• A man who has fathered a preeclamptic pregnancy in a different
woman
• Diabetes mellitus (DM)
Medical Conditions • Anti-phospholipid syndrome (APS or APAS)
• Systemic lupus erythematosus (SLE)
• Urinary tract infection (UTI)
Infection
• Periodontal disease
Source:CPGon Hypertension in Pregnancy.POGS;2015
CunninghamFG,et.al.WilliamsObstetrics25thEdition.2018
261
III. DEFINITION OF TERMS
TERM
I CRITERIA FOR DIAGNOSIS
• Hypertension known to predate conception or detected <20 weeks
of gestation & persists at least 12 weeks post delivery
Chronic 0 Blood pressure (BP) cut off is systolic blood pressure (SBP)
Hypertension of 2140, diastolic blood pressure (DBP) of 290, or both
0 Elevated BP should have been documented in at least twice and
measurements were done at least 4 hours apart
• New-onset BP elevations (SBP 2140, DBP 290, or both)
220 weeks of gestation in the absence ofproteinuria & features of
Gestational preeclampsia
Hypertension • BP levels return to normal by 12 weeks postpartum
• Failure of BP to normalize postpartum requires changing diagnosis
to chronic hypertension
• Diagnosis in women with HPN only in early gestation who develop
proteinuria 220 weeks of gestation, or women with proteinuria
<20 weeks of gestation who develop:
Chronic 1. Sudden exacerbation of HPN or need to escalate therapy
Hypertension with 2. New-onset signs/symptoms (increase in liver enzymes, RUQ
Superimposed pain, severe headache)
Preeclampsia 3. Platelet decrease to <100,000 umol/L
4. Pulmonary edema
5. Renal insufficiency
6. Sudden and sustained increase in protein excretion
• New-onset BP elevations (SBP 2140, DBP 290, or both)
220 weeks of gestation with proteinuria (2300 mg per 24-hour
urine collection), or protein:creatinine ratio 20.3, or urine dipstick
reading 2 + 1, OR
• In the absence of proteinuria, new onset hypertension with new
onset of any of the following
Preeclampsia 0 Impaired liver function (2x elevation ofliver transaminases)
0 Persistent cerebral/visual symptoms (e.g., headache, blurring of
vision)
• Pulmonary edema
Renal insufficiency (creatinine 97 µmol/L or 1.1 mg/dL or
"'
·.;
Q,
0
·.;
• Patient with preeclampsia presenting with any of the following
0 SBP 2160, DBP 2110, or both on 2 occasions at least 4 hours
Q, apart while a patient is on bed rest
E 0 Impaired liver function (2x elevation of liver transaminases)
"'
"Q Preeclampsia 0 Persistent cerebral/visual symptoms (e.g., headache, blurring of
'" with severe
... features
'"
0..
vision)
0 Pulmonary edema
0 Renal insufficiency (creatinine 97 µmol/L or 1.1 mg/dL or
doubling of creatinine in the absence of renal disease)
0 Thrombocytopenia (platelet count <100,000 umol/L)
• Development of seizures that cannot be explained by other causes
Eclampsia in a patient with preeclampsia
• Generally considered an indication for immediate delivery of the fetus
• Unique presentation of preeclampsia (Hemolysis, Elevated Liver
HELLP
enzymes, Low f!atelets)
Syndrome
• Generally considered an indication for immediate delivery of the fetus
Source:CPGon Hypertension ,n Pregnancy.
POGS;2015
Gestational
Hypertension
& Preeclampsia: ACOGPracticeBulletin.ObstetGynecol;2020
OnaDID.et al. 2020CPGfor the Management
of Hypertension
in the Philippines.
J ClinHypertens
(Greenwich)
2021.
262
Systolic BP • <160 mm Hg • 2'160 mm Hg
Diastolic BP • <110 mm Hg • 2'110 mm Hg
Glinical Manifestations
Gestational age • Late onset • Early onset
Headache
Visual disturbances
Upper abdominal pain
• Absent • Present
Oliguria
Convulsion (eclampsia)
Pulmonary edema
Labor:atorJ!Parameters
Serum creatinine • Normal • Elevated
Proteinuria
Thrombocytopenia
Serum transaminase
(<100,000/µL)
elevation
• None to positive
• Absent
• Mimmal
• None to positive
• Present
• Marked
I
•
SourceCunningham
FG,et al W1ll1ams
Obstetrics25thEd1t1on,
2018 :
CPGon Hypertensionin Pregnancy.
POGS;2015
2. Tennessee Classification
• This system proposed strict criteria for "true/complete" HELLP syndrome when all of
the findings in the platelet count and liver enzymes are found and "partial/incomplete"
HELLP syndrome when any one of the findings are noted
COMPLETE/TRUE I INCOMPLETE/PARTIAL
• Severe preeclampsia with any one of the following:
• Platelet< 100,000 0 Elevated liver enzymes, low platelet count
• AST >70 IU/L 0 Hemolysis, elevated liver enzymes
• LDH > 600 IU/L 0 Elevated liver enzymes
0 Low platelet count
Source:CPGon Hypertension in Pregnancy.
POGS;2015
Sibai,B.Obstetricsand Gynecology;
2004
Haram,K, et al. BMCpregnancyandchildbirth;2009
263
MANIFESTATIONS AND DIAGNOSIS OF HYPERTENSIVE DISORDERS
I. MANIFESTATIONS
Elevated BP prior
• No • Yes • No
to pregnancy
• <20 weeks AOG
Onset of BP
• ;,20 weeks AOG ( even before • ;,20 weeks AOG
elevation (AOG)
pregnancy)
• Headache
• Visual
Central nervous
• None • None disturbances
system findings
• Seizure (for
eclampsia)
• Right upper
quadrant
tenderness
due to liver
Gastrointestinal inflammation
• None • None
findings • Increased
intrahepatic
pressure and
stretching of the
Glisson capsule
• Arteriolar constriction
• Retinal
• Arteriovenous nicking
vasospasm
Ophthalmologic • Cotton wool spots
• None • Papilledema
findings • Yellow hard exudates
• Flame-shaped
(for longstanding
hemorrhages
hypertension)
Source: CPG on Hypertensionin Pregnancy.POGS:2015
CunninghamFG, et.al. WilliamsObstetrics25th Edition.2018
264
II. LABORATORYWORKUP AND PROCEDURES
LABORATORY I REMARKS
Ge.neral Wolik Up
Complete Blood Count • Check for presence of anemia & thrombocytopenia
• Check for presence of chamber enlargement (e.g., LVH),as
12LECG
a manifestation of chronicity
Blood Chemistry
• Sodium • Check for secondary causes of hypertension and
• Potassium comorbidities such as diabetes mellitus
• Creatinine • Check for end organ damage for chronic hypertension
• Blood urea nitrogen • Check for diagnosis of preeclampsia
• Albumin • Check for presence of features of severe preeclampsia
• Glucose level
Thyroid-stimulating
• Check for secondary causes of hypertension
hormone
• To evaluate presence of LVHamong patients with chronic
2D Echocardiography hypertension or possible structural heart disease in
patients presenting with pulmonary edema
,.,
Evalu!Jtion ofPreeclampsia-Eclampsia
• Check for diagnosis of preeclampsia
Liver enzymes {AST,ALT)
• Check for presence of features of severe preeclampsia
■
24 hour urine collection • Determination of creatinine clearance & protein excretion
• For calculating protein/creatinine ratio
Spot urine collection
• Dipstick for detection ofproteinuria
Chest radiograph with • Evaluate presence of pulmonary edema among patients
abdominal shield with preeclampsia with severe features
Cranial CT Scan/MRI of • Evaluation for other causes of seizure such as
the brain hemorrhage, mass or stroke
• Evaluate liver for patients with RUQpain and/or elevated
Abdominal Ultrasound
transaminases
Electroencephalography • Evaluation of recurrent seizure activity
Fetal monitoring • Monitor fetal activity and growth (fetal well-being)
265
MANAGEMENT OF HYPERTENSIVE DISORDERS IN PREGNANCY
I. PRINCIPLESIN THE MANAGEMENTOF HYPERTENSIONIN PREGNANCY
A. Factors to Take into Consideration
FACTORS I REMARKS
• Once 34 weeks AOGis reached, delivery may be recommended for
Age of gestation
maternal and fetal safety
• HELLP and eclampsia mandates delivery, regardless of AOG
• Severe preeclampsia patients are usually delivered once 34 weeks
Severity of
AOGis achieved
disease
• Conservative measures at <34 weeks in high-risk centers
• Preeclampsia without severe features can be managed as out-patient
• Regular monitoring of multiple-organ symptoms, vital signs, body
weight, input & output, laboratory tests.
• Close monitoring of women with gestational hypertension or
Maternal
preeclampsia without severe features:
evaluation
Daily assessment of symptoms and fetal movement
0
266
C. Timing of Delivery for Pregnant Patients with Hypertensive Disorders
DISORDER
I TIMING
Chronic hypertension • 38 weeks
Gestational hypertension • 37 weeks
Preeclampsia with non-severe features • 37 weeks
Preeclampsia with severe features • 34 weeks
Chronic hypertension superimposed preeclampsia • 37 weeks
Chronic hypertension superimposed preeclampsia with severe features • 34 weeks
Source:CPG on Hypertensionin Pregnancy.POGS;2015
Cunningham,FG, et al. WilliamsObstetrics25th Edition.2018
■
Source:ACOG.Task Force Recommendationon Hypertensionin Pregnancy,2013
GestationalHypertension& Preeclampsia:ACOGPracticeBulletin.Obstet Gynecol;2020
A. Pharmacologic Options
DRUG*
I DOSE AND ROUTE I MONITORING
• 10 to 20 mg IV,then
20 to 80 mg q20-30 mins • Adjust dose within the infusion rate
• Infusion rate: 1-2 mg/min range to achieve target BP
• Max dose: 300 mg
Labetalol
• Monitor BP at 10-minute intervals
• If BP uncontrolled after 10 mins,
• 20 mg IV over 2 minutes
give 40 mg IV over 2 minutes, and
consider referral to Cardiology
• Give 5 or 10 mg IV over
2 minutes • Monitor BP at 20-minute intervals
• ·If SBP 160 or DBP 110, • If BP uncontrolled after maximum
Hydralazine give another 5 or 10mg dose is given, give second-line
hydralazine up to a antihypertensive and consider
maximum cumulative dose referral to Cardiology
of20 mg in 24 hours
• 10 to 30 mg immediate • Given if IV access is not yet available
release capsule, every 20 • If BP uncontrolled after 50-60 mg of
Nifedipine** minutes for up to 3 doses immediate release nifedipine, give
• Immediate release capsule another antihypertensive ( usually
given per orem (not sublingual) hydralazine)
• 10 mg+ 90 cc D5W
• Infusion rate: 1 mg/hr
• Adjust dose to achieve target BP, c/o
Nicardipine** • Titrate every hour with
IM/Cardiology
increments of 1 mg/hr
• Max dose: 10 mg/hour
'Caution ifwithMgS04
.. The first-lineof treatmentis IVhydralazineand labetalol.IVnicardipineis consideredas a second-lineoption.
Extendedrelease oral nifedipinemay also be consideredas first-linetherapy,particularlywhen IVaccess is not
available.
Source:Committeeon ObstetricPractice.Obstetricsand gynecology;2015;AGOG;2015.
RobertsJM,et al. Hypertension;2003
CPG on Hypertensionin Pregnancy.POGS;2015
268
IV. MANAGEMENTOF PREECLAMPSIA
A. Prevention of Preeclampsia
Universal Screening for Preeclampsia
• All pregnant women should be screened for between 11 weeks to 13 617 weeks using:
0 Maternal risk factors
0 Biomarkers (mean arterial pressure, uterine artery Doppler, serum placental growth factor)
• If resources are limited, routine screening for preeclampsia should include maternal risk
factors and mean arterial pressure
Women at High Risk for Preeclampsia should be given:
• Aspirin prophylaxis ("'150 mg at night) starting at 11-14 weeks gestation (or <16 weeks) until
36 weeks AOG,when preeclampsia is diagnosed
• For women with low calcium (Ca2 ') intake (<700 mg/d), give Ca'· replacement
(;el g elemental Ca'' /day) or supplementation (1.5-2 g elemental Ca''jday)
Source:PoonLCet al. International
Journalof Gynecology
& Obstetrics;2019
■
• Deliver*
• Daily NST
Source:AGOG;2020;
Clinicalpracticeguidelineson Hypertension
in Pregnancy.POGS;2015
CunninghamFG,et.al.WilliamsObstetrics25thEdition.2018
270
4. Monitoring for Magnesium Toxicity:
MANIFESTATIONS
:
• Calcium gluconate IV (10 mL of 10% solution)
271
V. MANAGEMENTOF ECLAMPSIA
• Hospitalize patient
General • Control seizures & prevent recurrence
• Control BP
• Induce labor if cervix is favorable
• CS is reserved if:
Delivery 0 Vaginal delivery does not appear easy and imminent
° Failure to progress after induction
° Fetal compromise
• Anticonvulsant therapy continued at least 24 hours after delivery
Post-Delivery
• Ensure good BP control
Sources:Quillamor,
et al. POGSCPGon Hypertension
in Pregnancy;2015
MarianoD,et al. POGSCPGon Hypertensive
Complications
of Pregnancy;2010
WHORecommendations. WHO;2011
AOG I MANAGEMENT
<24weeks
• Delivery be undertaken shortly after initial maternal stabilization
(non-viable)
• Delay delivery for 24-48 hours once maternal and fetal conditions are
24to 33 6/7
stable to complete course of corticosteroids for fetal benefit
2e 34weeks • Deliver promptly, soon after maternal stabilization
'Promptdeliveryis indicatedat anyAOGifthereis DIC,liverinfarctionor hemorrhage,renalfailure,pulmonary
edema,suspectedabruptioplacenta,or non-reassuring fetalstatus
'Vaginaldeliveryis desirableforwomenin laboror withrupturedmembranesand vertex-presenting fetus,regard-
less ofgestationalage
'Cesareandeliveryis suggestedforgestationsless than30 - 32 weekswithan unfavorable cervixto avoida paten-
tiallylonginduction.However, cesareandeliveryis performedforthe usualobstetricalindications
Source:Acu,ML.POGSCPGon Hypertension in Pregnancy3rd Ed;2015
in Pregnancy:Obstetrics& Gynecology;
ACOGTaskForceon Hypertension 2013
PooleJH.MCN ClinicalIssues;1997
Sibai,B.Obstetricsand Gynecology;
2004
MagannE, et al. ClinObstetricsand Gyncology;
1999
272
SECTION THREE
HEMATOLOGIC & IMMUNOLOGIC DISORDERS
AC ·t . f A I p b WHO d US CDC
TRIMESTER
273
IRON DEFICIENCY ANEMIA (IDA) IN PREGNANCY
• Second most common cause of anemia in pregnancy (after physiologic anemia)
• Common in reproductive-age, even in nonpregnant women
I. ETIOPATHOGENESIS
• Primarily caused by expansion of plasma volume without normal expansion of
hemoglobin
B. Iron Status for Women During Pregnancy and the Postpartum Period
IRON
IRON
I IRON
SUFFICIENCY I DEFICIENCY
WITHOUT
DEFICIENCY
II. MANIFESTATIONS
A. Signs/Symptoms
0 Easy fatigability
0 Pallor
0 Shortness of breath
0 Weakness
III. DIAGNOSIS
TEST
I REMARKS
274
IV.MANAGEMENT
A. Considerations in Management of IDA
0 Objective is to correct the deficit in hemoglobin mass & replenishment of iron stores
0 Transfusion is not necessary, unless there is hypovolemia
I PREVENTION OF IDA*
I TREATMENT OF !DA**
Target • All pregnant adolescent & adult • All pregnant women diagnosed
group women with IDA
,-
Source: POGS CPG on IronDeficiencyAnemia;2015
PREPARATION
Ferrous fumarate
I IRON COMPOUND
(mg per tablet)
200
I ELEMENTAL IRON
(mg per tablet)
66
V.COMPLICATIONS
OF IDA
• Increased risk of infertility
• Increased risk of preterm birth, low-birth weight, and perinatal mortality
• Associated with poor maternal nutrition
• Maternal hypoxia leads to compensation: increased placental size or placental
hypertrophy to increase 02 extraction and to compensate for the low hemoglobin
275
MEGALOBLASTIC ANEMIA
I. ETIOPATHOGENESIS
• Inhibition of DNAsynthesis leads to inadequate DNAfor mitosis, which in turn leads to
unbalanced red blood cell growth
• Usually seen in women with low intake offolate-containing food (e.g., green leafy
vegetables and animal protein)
• May develop from:
0 Hyperemesis gravidarum
0 Excessive alcohol intake
II. MANIFESTATIONS
• Similar to iron deficiency anemia
III. DIAGNOSIS
• Hypersegmented neutrophils and newly formed RBCs
• Hallmark: macrocytosis (increased MCV)
• Leukothrombocytopenia
• Nucleated RBCs
IV. MANAGEMENT
A. Prevention
If with history offolic acid deficiency: folic acid 4.0 mg daily preconception and during
0
V. COMPLICATIONS
• Premature births
• Fetal neural tube defects
• Cleft palate
I. ETIOPATHOGENESIS
• Can be primary or secondary in the presence of systemic lupus erythematosus (SLE)
• Anti-phospholipid (aPL)-binding plasma protein antibodies places patients in a
prothrombotic state
• Infections, oxidative stress, surgery and discontinuation of anticoagulant treatment may
induce disease exacerbation by triggering induction of antibodies to PL-binding proteins
II. MANIFESTATIONS
• Manifestations represent direct and indirect expression of venous or arterial thrombosis
and/or pregnancy morbidity
• APASshould be suspected among patients with any of the following:
0 Unexplained venous or arterial thrombotic events in young patients
Pregnancy related morbidity including fetal death after 10 weeks gestation, premature
birth due to severe eclampsia or placental insufficiency
0 Unexplained thrombocytopenia or prolongation of blood coagulation parameters
276
MANIFESTATIONS I SPECIFIC EXAMPLES
• Deep vein thrombosis or pulmonary embolism
Venous thrombosis & • Livedo reticularis
related consequences • Superficial thrombophlebitis
• Thrombosis in various other sites
• Stroke, transient ischemic attack, myocardial ischemia
• Leg ulcers/digital gangrene
Arterial thrombosis and
• Retinal artery thrombosis (amaurosis fugax)
related consequences
• Avascular necrosis of bone
• Multi-infarct dementia
Neurologic • Migraine, epilepsy
manifestations • Chorea, cerebellar ataxia, transverse myelopathy
• Renal artery /vein thrombosis
Renal manifestations
• Fibrous intima hyperplasia
Osteoarticular • Arthralgia
manifestations • Arthritis
• Pre-eclampsia, eclampsia
Obstetric manifestations • Recurrent miscarriage
• Preterm delivery
• Fetal loss/death
Fetal manifestations
• Premature birth or fetal-growth restriction
■
Hematologic
• Thrombocytopenia, autoimmune hemolytic anemia
manifestations
Source:Harrison'sPrinciplesof InternalMedicine.19thed1t1on.
2015.
CunninghamFG,et al. Williams obstetrics;2018
Ill. DIAGNOSIS:
A. Diagnostics
0 Who to screen: women with clinical criteria for APAS
, Tests include (if detected, testing should be repeated in >12 weeks):
• Anticardiolipin antibodies (aCL) lgG & IgM
• Lupus anticoagulant (LA)
• Anti-beta-2-glycoprotein-1 antibodies (P2GP1) IgG & lgM
Anticoagulation:
'"
Has the patient had an
APAS-definingpregnancy Antepartum: Therapeutic-dose
I
Postpartum: Warfarin indefinitely I
No [
I '"
Antithrombotic management: Type of APS-defining
Antepartum: Low-dose ASA pregnancymorbidity?
Postpartum
After vaginaldelivery: •
~1 fetal losses at
•
?1 preterm deliveriesof a
Intermittent pneumatic
~.10 weeks AOG morphologicallynormal infant
compressionand low-dose
ASAwhile in hospital; OR before 34 weeks AOG due to
'Low-doseaspirin(ASA):80-100mg
Anticoagulation•
• Low molecular weight heparins (LMWH)are generally preferred (e.g.,enoxaparin, tinzaparin)
• Dose (prophylactic versus therapeutic) depends on the indication for anticoagulation
(see algorithm above)
I PROPHYLACTIC DOSE
I THERAPEUTIC DOSE
Enoxaparin • 40 mg SC once daily • 1 mg/kg every 12 hours
Tinzaparin • 4500 units SC once daily • 175 units/kg once daily
Unfractionated
• 5,000 units every 12 hours SC • Varies per protocol
heparin (UFH)
'Anticoagulation
can generallybe resumed4-6 hoursaftervaginaldeliveryor 6-12hoursafterCS (unlesswith
significant
riskof bleeding,activebleeding,or previousneuraxialanesthesia).Directoralanticoagulants
(e.g.,
rivaroxaban)shouldnotbe used.
B. Fetal Surveillance
Early ultrasound for accurate pregnancy
0 dating
Detailed fetal anatomic scan (congenital
0 anomaly scan)
Ultrasound every 4-6 weeks for growth,
0 amniotic fluid and Doppler studies if indicated
° Fetal surveillance tests (e.g., biophysical profile) starting at 32 weeks or earlier
depending on fetal condition
D. Timing of Delivery
° Consider at 39 to 39 ,;, weeks AOGto control timing of anticoagulation discontinuation
If clinically indicated, consider delivery at early term
0
On regional anesthesia:
0
■
• If on LMWH: may use 2'24 hours after the last dose
279
SECTION FOUR
ENDOCRINOLOGIC DISORDERS IN PREGNANCY
GESTATIONAL DIABETES MELLITUS (GDM)
I. ETIOPATHOGENSIS
• Diabetes mellitus (OM) recognized during pregnancy should now be classified as either:
0 Gestational diabetes mellitus (GDM)
0 Overt diabetes mellitus
• Insulin resistance in pregnancy is mediated by placental section of growth hormone,
corticotropin-re!easing hormone, placental lactogen (chronic somatomammotropin),
prolactin and progesterone
• GDMoccurs when pancreas in pregnant women cannot overcome the pregnancy-induced
insulin resistance
A. Definition of Terms
TERM I DEFINITION
Pregestational
• OM diagnosed in a woman even before pregnancy
DM
• Diagnosed in the 2nd and 3rd trimester of pregnancy that is not
clearly overt OM
Gestational
• The word "gestational" implies that diabetes is induced by pregnancy
DM(GDM)
• Most important perinatal correlate is excessive fetal growth
(primary effect attributed to GDMis macrosomia)
• Pregnant woman who meets the standard non-pregnant criteria for
OvertDM
diagnosis of OM
280
II. DIAGNOSIS(One-Step Strategy)
A. Screening for GDM:
0 Universal screening for GDM is recommended for Filipino gravidas
0At the first prenatal visit, determine if the gravid is high risk or not based on historical
and pregnancy risk factors
■
• All Filipino gravidas are considered "high risk" by race or ethnic group (Pacific Islander)
• All should be screened for type 2 DM in the first prenatal visit (FBS, HbAlc, or RBS)
• For Filipino gravidas with no other risk factors aside from race or ethnicity and the
initial test (FBS, HbAlc or RBS) is normal, screening for GDMshould be done at 24-28
weeks using a 2-hour 75 gram OGTT.If there are other risk factors identified, screening
should proceed immediately to 2-hour 75 gram OGTTat first consult
POGSCPGon DiabetesMellitusin Pregnancy,November2011
281
C. Procedure for the 75 g OGTT:
0 Ask the patient to have at least 3 days of unrestricted carbohydrate intake (>150 g
carbohydrate daily)
0 Perform the test in the morning (7-9 am) after an 8-14 hour overnight fast (water is
allowed). Smoking or physical activity are not permitted during the test.
0 Extract the initial fasting blood glucose (FBS) sample.
0 Give the patient a standard 75 g glucose solution in 250-300 mL of water, to be
ingested within 5 minutes.
0 Extract blood samples after 1 hour post-prandial glucose (PPG) and 2 hours PPG of the
glucose load
, The test should not be done during acute illness
R d d D ·1 C 1 . I t k d ™. ht G .
,;30% fats
0
Lifestyle Changes
• Advise against alcohol consumption and smoking
• If without contraindications, maintain sufficient level of physical activity & exercise
B. Monitoring
Women with GDM on diet treatment alone: monitor capillary blood glucose levels 4x a
0
day (fasting blood glucose once a day and postprandial blood glucose 3x a day)
Women on pharmacological therapy may monitor 4 to 6 times a day and include
0
preprandial values
MODE I CONDITIONS
period criteria
0 Havelifelongscreening for the development of DMat least every 3 years
II. MANIFESTATION
• Recall that normal pregnancy simulates some findings similar to thyroxine excess
• Suggestive findings of thyrotoxicosis include tachycardia that exceeds that usually seen
with normal pregnancy, thyromegaly, exophthalmos, and failure to gain weight
284
III. DIAGNOSIS
• Diagnosis made based on clinical manifestations and thyroid function tests
• Confirmatory findings for hyperthyroidism:
, Markedly depressed TSH
, Elevated serum FT4 or FT3
Trimester-Specific Reference Values For Thyroid Function Tests In Pregnant Filipino Women
TEST I 1ST TRIMESTER I 2ND TRIMESTER I 3RD TRIMESTER
TSH (uIU/mL) 0.05 - 4.24 0.13 - 3.95 0.20 - 3.00
FT4 (pmol/L) 9.80 - 21.88 9.10 -18.95 9.16-18.64
FT3 (pmol/L) 2.40 - 6.20 2.77 - 5.00 2.09 - 3.70
Source:Patal,P; et al. JAFES2016
IV. MANAGEMENT
• Maintain persistent but mild hyperthyroidism to prevent maternal complications and
fetal hypothyroidism
• Pharmacologic treatment for those with moderate to severe hyperthyroidism
DRUGS I REMARKS
• Preferred treatment for overt hyperthyroidism in the first trimester
Propylthiouracil
• May be shifted to methimazole in the 2nd trimester if patient cannot
(PTU)
tolerate PTU or has an adverse response to it
■
• Started during the 2nd trimester, but associated with embryopathy if
Methimazole used in the first trimester
• Other side effects: esophageal or choanal atresia, aplasia cutis
Beta-Blockers
• Used to treat tachycardia and tremors
(Metoprolol or
• Avoid long term use in pregnancy (not more than 2 to 6 weeks)
Propranolol)
285
V. THYROID STORM
A. Etiopathogenesis
Life-threatening condition that develops in cases of untreated thyrotoxicosis
0
B. Manifestations
° Fever, tachycardia disproportionate to fever, mental status alterations, vomiting,
diarrhea, dehydration, cardiac arrhythmias, congestive heart failure
Rarely seizures, shock, stupor and coma
0
C. Diagnosis
° Clinical testing with confirmatory testing show increased FT4 (or increased FT3) and
very lowTSH
D. Management
0 Refer to IM/Endocrinology for further evaluation and management
Therapeutic options:
0
E. Obstetric Management
Thyroid storm is not an absolute indication for delivery
0
HYPOTHYROIDISM IN PREGNANCY
• Women should ideally achieve euthyroidism before conception
• Thyroid function should be evaluated immediately after pregnancy confirmation and
every 4 weeks during the first half of pregnancy, which may be decreased to every 6-8
weeks after 20 weeks' gestation
I. ETIOPATHOGENESIS
• Changes in the immune system, leading to the onset, exacerbation, or amelioration of an
underlying autoimmune thyroid disease
• Increased thyroid hormone metabolism by the placenta
• Increased urinary iodide excretion
II. MANIFESTATIONS
SIGNS I SYMPTOMS
• Bradycardia • Blurred vision
• Coarse, brittle, straw-like hair • Cold intolerance
• Coarse facial features • Constipation
• Dull facial expression • Decreased appetite
• Goiter (simple or nodular) • Decreased perspiration
• Hoarseness • Dry skin
• Hyporeflexia with delayed relaxation • Depression, emotional !ability, forgetfulness
• Macroglossia • Fatigue, lethargy, sleepiness
• Pericardia! effusion • Hair loss
• Periorbital puffiness • Inability to concentrate
• Pitting edema of lower extremities • Sleepiness
• Weight gain
286
III. DIAGNOSIS
• Diagnosis made based on clinical manifestations and thyroid function tests
• Thyroid function tests compatible with hypothyroidism:
0High TSH
0 Low FT4
IV.MANAGEMENT
• Goal TSH: <2.5 m!U/L for the first trimester and <3.0 m!U/L for the second and third
trimesters
• Separate intake oflevothyroxine from prenatal vitamins and iron supplements by at least
4 hours
• Thyroid hormone requirements are increased by up to 50% during pregnancy
• Daily iodine intake of at least 250 ug is recommended during pregnancy
■
C. Monitoring of Treatment
0 Monitor TSH and FT4 every 4 weeks until 20 weeks: adjust LT4 dose to maintain
TSH <2.5 in the first trimester
0 Obtain TSH and FT4 between 26-32 weeks: adjust LT4 dose to maintain TSH <3.0 in
the 3rd trimester
0 Obtain TSH and FT4 at 6 weeks postpartum
FG,et al.WilliamsObstetrics25thEdition;2018
Source:Cunningham
CPGon MedicalComplicationsin Pregnancy.POGS;2015
V. COMPLICATIONS
SPECTRUM I COMPLICATIONS
• Maternal: gestational hypertension, preeclampsia, increased
Overt placental weight
Hypothyroidism • Fetal: cretinism, low birth weight, fetal demise, spontaneous
abortion, IUGR
• Miscarriage
Subclinical • Placental abruption
hypothyroidism • Preterm delivery
• Low IQ at age 7-9
• Spontaneous miscarriage
Complications • Recurrent miscarriage
associated with
• Preterm delivery
TPO (+)
• Placental abruption
Source:Stagnaro-Green, et al, JAMA,1990
FG,et al.WilliamsObstetrics25thEdition;2018
Cunningham
Negro,et al.J ClinEndocrinol Metab.2006
287
SECTION FIVE
LUNG DISORDERS AND INFECTIONS IN PREGNANCY
BRONCHIAL ASTHMA IN PREGNANCY
I. ETIOPATHOGENESIS
• Hallmarks: reversible airway obstruction from bronchial smooth muscle contraction,
vascular congestion, tenacious mucus, and mucosa! edema
• Asthma is an obstructive lung disease characterized by limitation of airflow that is more
marked during expiration (obstruction is reversible)
• Decreased functional residual capacity (FRC) and increased effective shunt make the
pregnant patient more susceptible to hypoxia and hypoxemia
II. MANIFESTATION
• Expected physiologic changes - rule of 1/3:
• 1/3 of patients will worsen, 1/3 of patients will improve, 1/3 of patients will remain
controlled
• Peak of asthma exacerbation is in the 2nd trimester
• Reasons for poor control and exacerbations during pregnancy:
• Mechanical/hormonal changes
• Cessation or reduction of maintenance medications because of maternal or health
provider concerns about the potential ill effects to the fetus
Increased susceptibility to respiratory viral infection (e.g., influenza)
III. MANAGEMENT
A. General Principles
, Advantages of actively treating asthma in pregnancy markedly outweigh any potential
risks of usual controller and reliever medications
, Using medications to achieve good symptom control and prevent exacerbations is
justified even when their safety in pregnancy has not been unequivocally proven
C. Acute Exacerbations
• Inhaled corticosteroids (JCS) prevent exacerbations of asthma during pregnancy
• Bronchoconstriction may be induced by hyperventilation during active labor, and
should be managed with a short-acting beta agonist (SABA)
• During acute exacerbation, aggressive treatment with SABA,oxygen & systemic
corticosteroids prevent fetal hypoxia
288
IV. MONITORING
• Monthly monitoring (e.g., symptom frequency, nocturnal asthma, interference with daily
activities, exacerbations, and medication use), lung auscultation, and pulmonary function
• Spirometry should be done at baseline, with peak expiratory flow (PEF) measurement on
follow-up
• Respiratory infections should be monitored and treated promptly
• Balancing risks and benefits, refrain from stepping down !CS & long-acting
bronchodilating agent (LABA) until after delivery
V. COMPLICATIONS
MATERNAL I FETAL
• Preeclampsia • Premature birth
• Gestational hypertension • Congenital abnormalities
• Preterm labor • Fetal growth restriction
• Postpartum hemorrhage • Low birth weight
Source:PedersenS, et al. GlobalInitiativeforAsthma;2017
BusseWW,et.al.ManagingAsthmaduringPregnancy;2004
CunninghamFG,et al. Williamsobstetrics;2018
PNEUMON~INPREGNANCY
I. ETIOPATHOGENESIS
• Special consideration in pregnancy state:
0Decreased immune status
■
0 Reduced ability to expectorate
• Most common etiologic agent: Streptococcus pneumoniae
• Most common cause of influenza pneumoniae: Influenza A and B
II. MANIFESTATION
Cough followed by at least 2 symptoms:
Temp ;,38°C
0 Rigors
0
RR ;,20 breaths/min
0 ° Chills or dyspnea
HR;, 100 bpm
0 Auscultatory findings (e.g., localized crackles, rhonchi)
0
III. DIAGNOSIS
• Chest X-ray with abdominal shield
• Arterial blood gas (ABG) especially in cases where CO2 retention is suspected
• Sputum Gram stain, culture, and sensitivity studies
IV. MANAGEMENT
ETIOLOGY I MANAGEMENT
• Require hospitalization for work up and management
• Paracetamol may be given to control fever
• Antibiotics:
Bacterial 0 Macrolide: initial monotherapy (e.g., azithromycin)
° For more severe cases: 8-lactams (co-amoxiclav) + azithromycin
° For beta-lactam allergy: may use clindamycin + azithromycin
V. COMPLICATIONS
• Premature rupture of membranes (most frequent)
• Low-birthweight infants
• Possible intubation & mechanical ventilation
289
URINARY TRACT INFECTION (UTI) IN PREGNANCY
I. ETIOPATHOGENESIS
UTls are the most frequent bacterial infections complicating pregnancy
• Asymptomatic bacteriuria is the most common type
• Symptomatic infection includes cystitis or pyelonephritis
• Escherichia coli strains: most common etiologic agent for UT!
• Treatment is indicated to
• Screening is done between reduce risk of:
9th -17th week AOG, • Acute cystitis &
• Persistent, actively preferably on the 16th week pyelonephritis in
multiplying bacteria • Urine culture & sensitivity pregnancy
within urinary tract in (C/S) test for screening is • Low birth weight &
asymptomatic women recommended preterm infants
• May be associated with • If culture unavailable, • Choice of antibiotic is based
preterm or low-birth pyuria (>10 WBC/HPF) or on urine C/S
infants gram stain (> 2 organisms/ • Follow-up culture should be
OIF) in 2 consecutive done 1 week after treatment
midstream samples is used • Monitoring is done every
trimester until delivery
Acute Uncomplica{eil Cyst[tis (AUC)in Pregnancy
• Treatment indicated to
• Diagnosis made by utine C/S prevent spread of infection
• In the absence of urine C/S: • Start empiric antibiotics
• Urinalysis: significant immediately, then adjust
• Lower UT!may develop
pyuria (>8 pus cells/mm 3 using urine Gram stain or
without antecedent
in uncentrifuged urine urine C/S
bacteriuria
or >5 pus cells/HPF in • Post-treatment culture 1-2
• Presents with dysuria,
centrifuged urine) weeks after completion
urgency, and frequency
0 Dipstick: positive of therapy to document
• Pyuria and bacteriuria
leukocyte esterase and eradication of bacteria
are usually found
nitrite test • 7-day treatment with oral
• Pre-treatment urine culture antimicrobial agent safe
is needed for pregnancy (1 day for
fosfomycin)
Acute Uncomplicated Pyelonephritis (AUP) in Pregnancy
"
• One of the most
frequent serious medical
complications of • Consider admission if with
signs of preterm labor
pregnancy • Urinalysis & urine Gram
• Post-treatment urine C/S
• More frequent in the stain or C/S
to confirm resolution of
2nd trimester • Blood culture not routinely
infection
• Unilateral and right- done, unless septic
sided in most • Monitor with monthly urine
cultures until delivery
• May have abrupt fever/
chills & flank tenderness
290
III. ANTIBIOTICSFOR UTI IN PREGNANCY
• Nitrofurantoin
maybe givenduringthe 2ndtrimesteruntil32 weeks.AvoidTMP-SMX
AvoidCo-amoxiclavin the2ndtrimesterdueto the riskof necrotizing
enterocolitis
in the 1stand3rdtrimesters.
(NEC)in theneonate
.. IVtherapymaybe shiftedto oraloncepatientis 48 hoursafebrile,witha recommended
(in theabsenceof urineC/S,empirictherapyshouldbe basedon localsusceptibility
.
durationof 14days
patternsof uropathogens
-
I
primaryoptionis ceftriaxone
IV)
"' Whenurinegramstainshowsgrampositiveorganisms
Source:TaskForceon UrinaryTractInfections,
PPGG-IO
PSMID;2013-2014
291
SEXUALLY TRANSMITTED INFECTIONS IN PREGNANCY
I. VAGINITIS
MANAGEMENT
MANAGEMENT
I MATERNAL EFFECTS
I PRINCIPLES
B ac t er,a lVia9mos1s (BV)
• Options (for 7 days):
• Increased risk of other
0 Metronidazole 500 mg BID
sexually transmitted
0 Metronidazole 250 mg TIO
infection
° Clindamycin 300 mg BID
• Increased risk of
• BV is sexually associated rather than • None
PROM,preterm birth,
transmitted
intraamniotic infection
• Routine screening is not recommended
and postpartum
• Routine treatment of sex partners not
endometritis
recommended
,-- ,,,.
Trichom_gniasis n ~-
292
II. MUCOPURULENT
CERVICITIS
• Uncomplicated infections
in pregnancy**:
° Ceftriaxone 500 mg IM
single dose, OR
° Cefixime 400 mg PO
293
lll. GENITAL ULCERS
Syphilis
MANAGEMENT
I MATERNAL
EFFECTS I FETAL/NEWBORN
EFFECTS
Herpes Simplex
• Localized to eye or
• Routine screening for HSV is not
mouth
recommended
• CNS disease with
• Acyclovir 400 mg TID for 7-10 days appears
encephalitis,
to be safe for use in pregnancy (>36 weeks
lethargy, irritability,
with recurrence)
tremors, temperature
• Cesarean delivery is indicated for women
dysregulation, bulging
with active genital lesions or prodromal • Preterm labor
fontanelle
symptoms
• Disseminated disease
• Women with HSV may breastfeed, if there
with multiple major
are no active HSV breast lesions
organ involvement:
• Valacyclovir and acyclovir may be used
coagulopathy, liver
during breast feeding
dysfunction, pulmonary
• Symptomatic partners should be treated
failure, death
Chancroid
• Soft chancres:
painful,
• Azithromycin lg PO as single dose, OR
• Erythromycin 500 mg PO TID x 7 days, OR
nonindurated
genital ulcers . None
• Ceftriaxone 25 mg IM single dose • Painful
suppurative
inguinal nodes
294
NON-SEXUALLY TRANSMITTED INFECTIONS IN PREGNANCY
I. VIRALINFECTIONS
CLINICAL
MANIFESTATIONS I MANAGEMENT I MATERNAL
EFFECTS
I
FETAL/NEONATAL
EFFECTS
Varicella zoster
- IL "Sc
Rub.eola (measles)
• Koplik spots
• Fever
• Coryza,
conjunctivitis,
cough (3 C's]
• Vaccine not
recommended
Breastfeeding
allowed
• Serum lg IM
• Pneumonia
•
•
•
•
Diarrhea
Abortion
Preterm delivery
Low birthweight
• Not teratogenic
• Neonatal infection I
Mu'!'ps
-
-
• Infection of salivary • Vaccine not
gland, gonads, recommended • Spontaneous • Not teratogenic
meninges, pancreas, • Breastfeeding abortion • Fetal infection rare
etc. allowed
295
II. BACTERIALINFECTIONS
FETAL/
CLINICAL MATERNAL
MANIFESTATIONS
Clostridium perfringens
I MANAGEMENT
I COMPLICATIONS
I NEONATAL
EFFECTS
• Fever
• Intravascular
• Tachycardia out of
hemolysis,
proportion to the
• Penicillin G jaundice,
fever • Fetal demise
• Clindamycin hemoglobinuria,
• Uterine discharge
hypotension and
and marked
renal shutdown
leucocytosis
Clostridium tetani
• Infant tetanus:
symptoms may
or may not
be apparent
immediately
• Respiratory
after birth
• Tetanus Immunization failure and
• Trismus or lockjaw because
• Tetanus lg (Passive) convulsive
incubation
seizures
period can be
as short as
24 hours & as
long as 16-30
days
Group B Streptococcus (GBS)
• Universal rectovaginal
GBSscreening culture
at 35-3 7 weeks
• Intrapartum
prophylaxis*:
• Meningitis
0 Recommended:
• Neonatal
Penicillin G (IV) • Preterm labor
• May present with sepsis
SM U initial dose, • PROM
UT! or pneumonia • Fetal death
then 2.5-3M U q4 • Chorioamnionitis
• Respiratory
until delivery
distress
0 Alternative:
Ampicillin (IV)
2 g IV initial dose,
then 1 g IVq4 until
delivery
296
III. PROTOZOALINFECTIONS
FETAL/
CLINICAL MATERNAL
MANAGEMENT NEONATAL
MANIFESTATIONS
I I COMPLICATIONS
I EFFECTS
Toxoplasma gondii
• Acquired from: raw/
undercooked meat • Routine screening
• Low birthweight
infected with tissue not recommended
• Hepato-
cysts or cat feces • Spiramycin: reduce
splenomegaly
with oocysts (litter, risk of congenital
• Jaundice
soil or water) infection given • Mostly
• Anemia
• Risk of infection during acute subclinical
• Neurologic
increases with infection in early • Initial infection
disease
duration of pregnancy confers
• Micro- or
pregnancy • Pyrimethamine, immunity
hydrocephaly
• Manifestations: sulfonamides &
• Learning
feve1; headache, folinic acid: eradicate
disabilities
muscle pain, fatigue, parasites in placenta
maculopapular rash, & fetus
lymphadenopathy
-
Malaria_
• Most common • Mostly
human parasitic asymptomatic
■
• Chloroquine or
disease • For those with
hydroxychloroquine:
• From female symptoms,
treatment of
anopheline the classic
choice for sensitive
mosquito manifestations • Stillbirth
Plasmodium species
• Infected of malaria are • Preterm birth
• Chloroquine-
erythrocytes typical • Low birthweight
resistant
accumulate in • Anemia and • Miscarriage
(P. falciparum):
placenta jaundice
mefloquine,
• Flu-like symptoms: • Kidney failure,
quinine sulfate with
fever, chills, coma and death
clindamycin
headaches, myalgia, (P.falciparum
and malaise infections)
Amebiasis (Entamoeba histolytica)
• Asymptomatic
intestinal or vaginal
carrier state can
be converted to
clinically overt • Metronidazole or • 68% of fatal
disease tinidazole: drug of cases of
• Most are choice for amebic amebiasis in
• None
asymptomatic colitis & invasive females were
• Amebic dysentery: disease in pregnant associated with
fever, abdominal patients pregnancy
pain and bloody
stools
• Hepatic abscess:
worst prognosis
297
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300
TOPATIENTS
APPROACH
INGYNECOLOGY
OVERVIEW OF THE APPROACH TO PATIENTS IN GYNECOLOGY
• Gynecology is branch of medicine that specializes in the reproductive health of females
• Any condition that affects the reproductive system, such as the cervix, uterus, ovaries,
fallopian tubes, vagina, and vulva are treated under the care of gynecologists
Basic Examination
Well woman visit
Height, weight, • Annually
&BMI
Blood pressure • Annually • Annually
• Every 3-5 years
screening
Clinical breast
• Every 1-3 years
exam
Pelvic/speculum
• As indicated /periodically
exam*
1--0_t_h_er_E_xa_m_i_n_a_t,_·o..,n
...
s~~~---.a..,.----------.----~~~~-----1 .;_. :
• Discontinue screening
0 2:3 negative cytology
tests within the past
10 years, with the
• Every 3 years most recent Pap smear
Pap Smear (sta1t at 25 • Every 3 years within the past 3 years
years old} • After hysterectomy:
discontinue screening if
without history of CIN2+
or cervical cancer in the
past 2 0 yea rs.
• May offer starting
40 years old
• Annually after 45
Mammogram • If indicated • Annually
years old
• Start not later than
50 years old
Screening
for diabetes • If indicated • Every 3 years
mellitus
• Screen at 45 years
Screening for old
• If indicated • Every S years
dyslipidemia • If normal, repeat
every S years
303
• If with risk factors, • Start screening at
Osteoporosis
• N/A start screening at 65 years old then
screening
50 years old every 2 years
• Influenza yearly
• Influenza yearly • Influenza yearly
• Td every 10 years
• Td every 10 years • Td every 10 years
Immunizations • TDaP once
• TDaP once • TDaP once
• Herpes zoster once
• MMR, HPV • Pneumococcal once
(>59 years)
• Annually with
nucleic acid
amplification tests
(NAAT) in sexually
Chlamydia/ active 13-24 years
• As indicated
gonorrhea old
• Annually in
women >24 years
old with increased
risk of infection
HIV • Offered routinely
•Pelvicexaminations shouldbe performed Thedecisionto perform
whenindicatedby medicalhistoryor symptoms.
a pelvicexaminationshouldbe a shareddecisionbetweenthepatientandherobstetrician-gynecologist.
at 45 yearsold
.. Startcoloncancerscreening
Source:AGOG.ObstetGynecol;2018
BaturP,et al.AmJ Med;2020
Oncologists
Societyof Gynecologic (SGOP),3rdedition,2019
of the Philippines
USPreventiveServicesTaskForce.JAMA;2018,2020,2021
AmericanFamilyPhysician. Am FamPhysician;2009
CPGon Immunization for Women;POGS,2017
304
OVERVIEW OF THE GYNECOLOGIC HISTORY
I. GENERAL IDENTIFYING INFORMATION SHOULD INCLUDE:
INFORMATION I REMARKS
Last normal
menstrual • Establishes a baseline for evaluating subsequent complaints
period (LNMP)
• Describes the total number of confirmed pregnancies, regardless of the
gestational age when the pregnancy ended
• Gravidity can be confirmed by:
Gravidity • Positive pregnancy test
• Sonogram showing gestational sac or embryo
• Embryo / fetus that was passed
• Pathology report showing trophoblastic villi
Parity • Describes pregnancies continuing 2:20 weeks gestation
Abortions • Pregnancies that are terminated before 20 weeks gestation
■
• D.uration of each monthly cycle/number of days during which
menses occurs
Menstrual • Amount of flow
History • Symptoms (e.g., dysmenorrhea)
• LNMPand previous menstrual period (PMP)
• For postmenopausal patients:
• Age of last menses
• History of hormone replacement therapy
• Presence of postmenopausal bleeding
• Patient would be asked to list all pregnancies including abortions,
molar and ectopic pregnancies.
• For deliveries, the following should be obtained;
• Date of delivery
• Gestational age at delivery
• Type and place of delivery (e.g.,normal or operative vaginal delivery,
Previous
cesarean section)
Pregnancies
• Infant birth weight
• Any complications that may have occurred
• For all other pregnancies
• Circumstances of which they took place
• Method used (e.g.,dilatation & curettage, history of methotrexate therapy)
• Complications
Vaginal/pelvic • History of sexually transmitted infections (STls), vaginitis, and pelvic
infections inflammatory disease (PID)
• Date of last human papilloma virus (HPV) typing± Pap smear
Cervical
• Frequency of screening
cancer
• Abnormal tests and treatment
screening
• HPV vaccination status
305
• Methods used, including length and time they have been used
Contraceptive
• Effectiveness of the method
History
• Complications and adverse reactions noted
• Age at first sexual contact
Sexual
• Number of lifetime sexual partners
History
• Sexual dysfunction (e.g., dyspareunia or anorgasmia)
• Note all surgical procedures including office procedures, with particular
Gynecologic
focus on gynecological procedures (uterine, cervical, vulva1;vaginal biopsy)
surgical
procedures Date and type of procedure, diagnoses, complications
0
lll. COMMONGYNECOLOGIC
COMPLAINTS
COMPLAINT
I REMARKS
• Normal discharge (clear, white, or light yellow) is composed ofmucoid
secretions with desquamated vaginal epithelium & normal bacteria
Vaginal
• Ask patient about the following
discharge
0 Onset, duration, frequency, colo1; consistency, volume, and odor of
and/or itching
the discharge
0 Onset, duration, and frequency of itching
• Vaginal bleeding most often represents uterine bleeding
• Pregnancy should be excluded in any patient of reproductive age
Abnormal
• Ask patient about amount, duration, and frequency
bleeding
• It is abnormal when bleeding is associated with a change in the normal
menstrual pattern or occurs after menopause
• Defined as failure to conceive after:
0 12 months of regular intercourse without contraception in women
Infertility <35 years old, OR
0 6 months of regular intercourse without contraception in women
;,,35 years old
• Location, timing, quality, radiation, intensity and duration of symptoms
• Factors that increase, decrease or subside pain intensity
Abdomino-
• Associated triggers, signs and symptoms
pelvic pain
• Relationship of pain to the menstrual cycle and association with other
events such as coitus or bleeding, bladder and bowel symptoms
Source:LoboRA,et al. Comprehensive 7thedition;2016
Gynecology.
CarusiDA,et al. Thegynecologic
historyand pelvicexamination.Uptodale.
306
OVERVIEW OF THE GYNECOLOGIC PHYSICAL EXAM
I. PATIENT PREPARATION
• Use hospital gown that ensures comfort and modesty
• Offer option of a chaperone
• Equipment: good light sources, gloves, speculum, water-soluble lubricant
• Patient positioning:
0 Lying supine on an office examination table with the knees flexed, and with the feet
in supporting stirrups (dorsal lithotomy position)
0 The patient's head is often elevated with a pillow, or by slightly elevating the head
of the examining table
STEPS I REMARKS
■
b. Arms over head A B
1
c. Arms pressed against hips
d. Leaning forward
• Observe for skin changes,
symmetry, contours and
retraction.
C D
307
III. ABDOMEN
• Perform inspection, auscultation, percussion, and palpation
• Many gynecological tumors enlarge and occupy the abdomen; an undisclosed
pregnancy may be present as well
• Be certain that the bladder is empty
• Advise patient to inform you if she feels any discomfort during the examination
I. SPECULUM EXAMINATION
• Inspect for lesions
• Assess vaginal discharge and cervical mucus
• Usually, a light source may be required to aid visualization
A. The Speculum
A speculum is an instrument which may be made of metal or plastic; it is hinged and
0
duck-bill shaped.
It is inserted into the vaginal canal, and blades are separated in order to visualize
0
Types of Speculum
PEDERSON SPECULUM I GRAVES SPECULUM
308
B. Speculum Examination
0Done to visualize the vagina canal and cervix
0Most commonly utilized are the Graves and Pederson specula, with each available in
several sizes corresponding to the width and length of the blades (small, medium, large or
extra large)
• Warm the speculum (via warming device or warm water); if necessary, a water-based
lubricant may be used. Hold the speculum with the non-dominant hand
• Two fingers of the dominant hand apply downward pressure on the introitus to relax
the vagina. The speculum is inserted with the transverse diameter of the blades in the
anteroposterior position (or at a 45 degree angle) with the tips pointing downward
• Once inserted, speculum should be turned so that the transverse axis of the blades is in
the transverse axis of the vagina. Blades should be inserted to their full length
• Open the blades to adequately visualize the cervix and lock the speculum in place
• Inspect the vaginal walls for lesions or discharge. Fluid discharge should be collected for
wet mount and potential culture
■
• Inspect the cervix. Any lesion should be noted & biopsy should be performed as needed
II. BIMANUALPELVICEXAMINATION
• Allows physician to palpate the uterus and adnexa
• Only if indicated in asymptomatic, non pregnant adult women
EXAMINATION OF THE UTERUS I EXAMINATION OF THE ADNEXA
Top view
• Insert the gloved index and middle fingers of the dominant hand in the vagina and place the
non-dominant hand in the lower abdomen. Water-based lubricants may be used if needed
• Palpate the vagina, cervix, uterus, adnexa and surrounding structures by using the
abdominal hand to sweep the pelvic organs downward, while the vaginal hand is
simultaneously elevating them
• Assess for size, shape, location, consistency, mobility, and tenderness of the uterus
• Assess for adnexal masses; note their size, consistency, mobility and tenderness.
• Assess the posterior cul-de-sac and utero-sacral ligaments also for masses and nodularities
309
III. RECTOVAGINALEXAMINATION
• A rectovaginal examination allows for optimal palpation of the cul-de-sac and uterosacral
ligaments, as well as the uterus and adnexa
• Performed as indicated based on symptoms or findings from pelvic examination
• Useful if:
0 Bimanual examination has been insufficient to assess the pelvic anatomy properly
0 Suspected endometriosis or pelvic mass
Symptoms involving the rectal area
310
SECTION TWO
PROCEDURES IN GYNECOLOGY
2 mm 3 mm 4 mm 5 mm 6 mm 7 mm
0
■
0 0
• Skin and subcutaneous tissue are infiltrated with local anesthetic using a small
needle and wait 5-10 minutes for anesthesia to take effect
• Press a 3- or 4-mm Keyes punch biopsy instrument against the skin to be biopsied
and gently rotate the instrument 360' to get a nice cylindrical sample
• The small core of skin and subcutaneous tissue separated by the instrument is elevated
by small tooth tissue forceps and trimmed off the base with curved Iris scissors
• No need to suture the hole that is left but make sure to apply pressure to the biopsy
site, with the base cauterized with silver nitrate sticks
311
II. VAGINALSMEARS
• Usually done in patients complaining of vaginal discharge
• Requires three glass slides, binocular microscope, normal saline solution (NSS) and
10% potassium hydroxide (KOH)
• Three most common infections:
° Candidiasis
0 Trichomoniasis
0 Bacterial vaginosis
312
PAP (PAPANICOLAOU) SMEAR
• Procedure to obtain cells from the cervix for cervical cytology
• Screening tool for cervical intraepithelial lesions and cervical cancer
• Goal: collect cells from the transformation zone of the cervix
Area of metaplastic
squamous epithelium • The transformation zone
Area of columnar (squamocolumnar junction) is
epithelium where most cervical precancer
and/or cancer lesions occur
(due to constant wear and tear/
repair)
Old SCJ
New SCJ+---1----'---+=-·<r:_7~
Transformation
zone
• Normal columnar epithelium
is replaced by squamous
epithelium
• New squamocolumnar junction
is found near the cervical os
I:.·.• :
WHO 2021 Guidelines for Screening and Treatment of Cervical Pre-Cancer Lesions for
Cervical Cancer Prevention
<30years
old, general • No screening
population
• HPV DNAdetection in a screen-and-treat approach starting at the age of
30 with regular screening every 5 to 10 years
• HPV DNAdetection in a screen, triage, and treat approach starting at the
30-50 years
age of 30 yeas with regular screening every 5 to 10 years
old
• Where HPV DNAtesting is not yet operational, WHO suggests a regular
screening interval every 3 years when using VIA or cytology as the
primary screening test
• WHO suggest screening is stopped after two consecutive negative
After SO
screening results consistent with the recommended regular screening
years old
intervals among both the general population and women living with HIV
• HPV DNA detection in a screen, triage, and treat approach starting at the
age of 25 years with regular screening every 3 to 5 years
Women
• Where HPV DNAtesting is not yet operational, WHO suggests a regular
with HIV
screening interval every 3 years when using VIA or cytology as the
primary screening test
WHO2021Guideline
forScreeningandTreatmentof CervicalPre-cancerLesionsforCervicalCancerPrevention
313
ACS 2020 Cervical Cancer Screening Recommendation
<2 5 years old • No screening
• Primary HPV test alone every 5 years (preferred)
• Use an FDA approved HPV test for primary screening
~ 25 to 65 years old
• Acceptable options: co-testing (HPV testing in combination
with cytology) every 5 years or cytology alone every 3 years
> 65 years old with
• Discontinue cervical cancer screening with any modality if
• no history of CIN grade
with adequate negative prior screening*
2 or a more severe
• Individuals aged >65 years without documentation of prior
diagnosis within the past
screening should continue until criteria for cessation are met
25 years, and
• documented adequate
negative prior screening*
in the 10 year period
before age 65 years old
• Follow age-specific screening recommendations (same as
After HPV vaccination
unvaccinated individuals)
• Satisfactory
Specimen • Unsatisfactory (not ideal sample):
Adequacy • No cells on the slide
0Too much inflammation/blood that obscures the sample
• Negative for intraepithelial lesion or malignancy
General
• Epithelial cell abnormality
category
• Other malignant neoplasms
• Trichomonas vaginalis
• Fungal organisms (e.g., Candida spp)
Organisms • Shift of flora consistent with bacterial vaginosis
• Bacteria morphologically consistent with Actinomyces spp
• Cellular changes consistent with HSV
• Automated review
• Ancillary testing
• Interpretation/result (negative or diagnosis)
Others
• Organisms (e.g., Trichomonas, Candida, Actinomyces, Bacterial Vaginosis,
Herpes Simplex)
• Other findings (e.g., inflammation, atrophy, reactive inflammation with IUD)
314
IV. OBTAININGSAMPLESFOR CYTOLOGY
• Samples for cervical cytology and HPV testing are obtained during the speculum
examination
• Sample secretions from:
0
Ectocervix (i.e., external surface of the cervix]
0 Endocervical canal to evaluate the transformation zone (squamocolumnar
junction)
0 Sample the vaginal wall (optional)
• Two methods for sample collection and preparation include:
I
0
V. PATIENT PREPARATION
• Refrain from tampons, birth control foams, or vaginal creams 2-3 days before test
• No douching for 2-3 days before the test
• No sexual intercourse for 2 days before the test
• The best time is at least 5 days after the menstrual period stops
315
VI. SAMPLE COLLECTION
Ayer spatula
Cervical broom
c~
~!/!fl~
Detach head
and place in ~:
medium
A. Collection is done with patient in dorsal lithotomy position with the speculum inserted into
the vagina so that the cervix can be clearly seen. Sampling the ectocervix before the endocervix
will minimize bleeding [i.e., obscuring blood in the sample interferes with the interpretation)
B. Spatula is used to circumferentially scrape the ectocervix, while the cervical broom for
liquid-based cytology is inserted into the endocervix and rotated 180 degrees to obtain sample.
C. For conventional cytology, the Ayer spatula is smeared on a slide, while the brush head of the
cervical broom is detached and submerged in the liquid-based cytology medium.
316
Vil. INTERPRETATION
A. Negative for lntraepithelial Lesion or Malignancy
0 No signs of cancer or precancerous changes or other significant abnormalities were
found
0 Other findings may be unrelated to cervical cancer (e.g., infection)
0 Some cases may also show reactive cellular changes that are responses of cells to
irritation
317
COLPOSCOPY
• Diagnostic technique involving visual inspection of the cervix and other areas of the
lower genital tract with a low power (3-lSx) binocular scope
• The surface contour, vascular pattern and staining pattern of changes seen with dilute
acetic acids and Lugo! iodine reflect the severity and extent of cervical abnormality and
help the clinician to select a location for biopsy confirmation
I. INDICATIONS
• Suspicious looking cervix
• ASC-H/HSIL/SCCA/ AGCon cytology
• Persistent low grade abnormalities on cytology
• Unsatisfactory quality on repeated cytology
• Infection with oncogenic HPV
• Acetopositivity on visual inspection with acetic acid (VIA)
• Positive on visual inspection with Lugo! iodine (Schiller Test)
IMMATURE
CIN &
SQUAMOUS
PRECLINICAL INFLAMMATION
METAPLASIA &
EARLY INVASIVE AND HEALING
REGENERATING
CANCER
I I EPITHELIUM I
• Less pale, thin, • Distributed widely
• Dense, thick opaque
Appearance translucent (not restricted to
• Well-defined borders
• Indistinct margins the transition zone)
Disappearance of • Quickly disappears • Quickly disappears
• 2 to 4 minutes
acetowhitening within 30 seconds within 30 seconds
Source:LoboRA,et al. ComprehensiveGynecology.7th edition;2016
HandaVL,et al. OperativeGynecology12thedition;2019
318
III. PRINCIPLES
I PURPOSE I FINDINGS
• Transformation zone (light pink):
smooth translucent epithelium with a
pinkish tinge after application of NSS
Normal • Used for moistening and
• Original squamous epithelium
saline cleaning
(more pink): No vascular patterns
solution • Helpful for evaluating blood
(NSS) are often seen
vessels and leukoplakia
• Columnar epithelium (dark red):
with a sea anemone tentacle-like
villous appearance
• To detect & evaluate any abnormal • Normal squamous epithelium: little
areas or transformation zone coagulation occurs in the superficial
• Causes swelling of epithelial layers
3-5% acetic tissue, columnar, & any abnormal • Areas ofCIN undergo maximal
acid squamous epithelial areas coagulation due to their higher
• Causes reversible coagulation content of nuclear protein (in
or precipitation of the nuclear contrast to the normal squamous
proteins and cytokeratins epithelium)
• High glycogen: normal squamous
epithelium
• No glycogen: normal columnar
epithelium
• Little or no glycogen: suspicious
• Iodine solution confers a
squamous epithelium
Lugol's mahogany brown or nearly black
0 Immature squamous metaplasia
iodine squamous cells which contain
I
0 Regenerating epithelium
stores of glycogen
0 Inflammatory and congenital
transformation zone
° Condyloma
0 Abnormal transition zones (CIN or
invasive cancer)
• Applied to the light source to increase the contrast of the red blood vessels
Green filter
and help clarify any vascular changes
• Suspected areas of cervical lesions should be sent for histopathologic studies
Cervical
• Can be undertaken using special instruments such as the Tischler,
biopsy
Kevorkian, Younge, or Gaylord biopsy forceps
319
ENDOMET~ALSAMPLING
• Endometrial sampling allows for histologic evaluation of endometrium (see indications)
either through an office endometrial biopsy or through an endometrial curettage
B. Contraindications
ABSOLUTE I RELATIVE
• Pregnancy • Cervical stenosis
• Acute pelvic inflammatory disease • Clotting disorder or coagulopathy
• Acute cervical infection
• Acute vaginal infection
• Cervical cancer
320
lll. ENDOMETRIAL CURETTAGE
• Both diagnostic and therapeutic in cases of abnormal uterine bleeding
• Dilatation of the cervix and endometrial curettage
A. Indications
THERAPEUTIC INDICATIONS I DIAGNOSTIC INDICATIONS
• Therapeutic abortion* • Endometrial hyperplasia or cancer
• Late postpartum hemorrhage • Infertility
• Retained placental tissues
• Abnormal uterine bleeding
•mega!in the localsetting
B. Procedure
INSTRUMENTS I PROCEDURE
• Vaginal retractor • Place patient in lithotomy position under anesthesia
• Tenaculum forceps • Aseptic technique
• Hysterometer • Empty bladder via straight catheterization
• Hegar dilators • Sterile draping of the perineum
• Ovum forceps • Bimanual exam to evaluate uterine size and position
• Uterine curettes • Adequately expose the cervix with open-sided or weighted
speculum
• Assess the depth of uterine cavity using a hysterometer
• Dilatate cervix using Hegar dilators
• Curettage of anterior, lateral, and posterior uterine walls
using an appropriately sized curette
■
• Reassess the depth of the uterine cavity using a hysterometer
C. Complications
0 Acute hemorrhage
0 Trauma to the uterus and adjacent structures
° Cervical laceration
321
OTHER COMMON PROCEDURES IN GYNECOLOGY
• Gynecologic procedures are varied and some are done as office procedures while others are
done in the operating room
• Diagnostic procedures: colposcopy, transvaginal ultrasound, hysterosalpingography, saline
infusion sonography
• Therapeutic procedures: oophorocystectomy, salpingectomy for ectopic pregnancy, salpingo-
oophorectomy, hysterectomy
322
PROCEDURE I REMARKS
Ther,apeutic
-
• Use of refrigerant gas (carbon dioxide or nitrous oxide)
to ablate abnormal lesions
Cryotherapy
• Tissue is cooled to -20°C to cause crystallization of
intracellular water and destroy the lesion
• Also known as thermal cautery
• Direct or alternating current is passed through a wire
Electrocautery
electrode to generate heat
• Applied in living tissue to achieve hemostasis
• A form of coagulation attained by arcing or spraying of
"sparks" to tissue surface using high voltage, damped, or
interrupted function with active electrode not touching
Fulguration
tissue
• This is used to coagulate bleeding vessel or for treatment
of endometriosis
• Surgical removal of the uterus (total hysterectomy)
• Supracervical hysterectomy (or subtotal hysterectomy);
Hysterectomy removal of the uterine fundus, transecting the upper
portion of the cervix below the level of the uterine
vessels (cervix is left in situ)
• Surgical removal of an ovary
• Prophylactic oophorectomy: surgical removal of clinically
Oophorectomy
normal ovaries at the time of hysterectomy to reduce risk
of ovarian and, possibly, breast cancer
Oophorocystectomy
• Surgical removal of an ovarian cyst without removing the
ovaries
• Reapproximation of perinea! connective tissue including
I
Perineorrhaphy the bulbocavernosus and transverse perinea! muscles to
restore the perinea! body
Salpingectomy • Surgical removal of a fallopian tube
Salpingooophorectomy • Surgical removal of the ipsilateral oviduct and ovary
• Operative opening made in the oviduct that is used to
Salpingotomy remove an unruptured tubal pregnancy then the tube is
closed by primary intention
• Operative opening made in the oviduct that is used to
remove an unruptured tubal pregnancy then the tube is
allowed to close by secondary intention
Salpingostomy
• Can also refer to salpingoneostomy; creation of a new
stoma in an oviduct with a completely occluded distal
end such as in cases of hydrosalpinx
323
REFERENCES
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2018 Oct;132(4):1080-1083. doi: 10.1097 /AOG.0000000000002896. PMID: 30247359.
Z.ACOG Committee Opinion No. 755: Well-Woman Visit. Obstet Gynecol. 2018 Oct;132(4):e181-e186. doi: 10.1097 /
AOG.0000000000002897. PMID: 30247364
3.ACOGPractice Bulletin - Clinical Management Guidelines for Obstetrician-Gynecologists: No. 140: Management of Abnom1a\
Cervical Cancer ScreeningTest Results and Cervical Cancer Precursors. Committee on Practice Bulletin. Obstet Gynecol.
2013;122(6):1338-136 7.
4.American College of Obstetricians-Gynecologists (ACOG).Practice bulletin no.122: Breast cancer screening. Obstet Gynecol.
2011;118(2 Pt 1):372-382.
S.American Family Physician. U.S.Preventive Se1vices Task Force screening for lipid disorders in adults: recommendation
Statement. Am Fam Physician. 2009 Dec 1;80(11):1273-1274.
6.Batur P,Phipps M, Qaseem A The Women's Preventive Services Initiative Well-Woman Chart: A Helpful Tool for the Practice
of Internal Medicine. Am J Med. 2020 Oct;133(10):1122-1125. doi: 10.1016/j.amjmed.2020.05.011. Epub 2020 Jun 18.
PMID: 32565259.
7.Bickley, L, Szilagyi, P.and Hoffman, R., 2017. Bates' guide to physical examination and history taking. 12th ed. Philadelphia:
Wolters Kluwer
8.Carusi DA,et al. The gynecologic history and pelvic examination. Uptodate.
9.Clinical Practice Guideline on Immunization for Women (2017). Philippine Obstetrics and Gynecologic Society
10. Colposcopy and treannent of cervical intraepithelial neoplasia: a beginners' manual, Edited by J.W. Sellars and R.
Sankaranarayanan Chapter 6: Colposcopic appearance of the normal cervix (https://screening.iarc.fr /colpo.php)
11. Handa, Victoria L.;Van Le, Linda (2019) Te Lindes Operative Gynecology 12th edition Lippincott Williams & Wilkins
12. Handa, Victoria L; Van Le, Linda (2019) Te Lindes Operative Gynecology 12th edition Lippincott Williams & Wilkins
13. Lefevre ML; U.S. Preventive Services Task Force. Screening for Chlamydia and gonorrhea: U.S. Preventive Services Task
Force recommendation statement. Ann Intern Med. 2014 Dec 16;161(12):902-10. doi: 10.7326/M14-1981. PMID:
25243785.
14. Lobo RA, Gershenson DM, Lentz GM,Valea FA Comprehensive gynecology. 7th edition. Elsevier, 2016
15. Massad LS, Einstein MH, Huh WK. et al. 2012 updated consensus guidelinesfor the management of abnormal cervical
cancer screening tests and cancerprecursors. J Low Genit Tract Dis. 2013;17(5 Suppl 1):Sl-S27.
16. Practice Bulletin No. 179 Summary: Breast Cancer Risk Assessment and Screening in Average-Risk Women. Obstet
Gynecol. 2017 Jul;130(1):241-243. doi: 10.1097 /AOG.0000000000002151. PMID: 28644328.
17. Society of Gynecologic Oncologists of the Philippines (SGOP) Clinical Practice Guidelines for the Obstetrician-Gynecologist.
3rd Ed.; July 2019.
18. US Preventive Setvices Task Force, Curry SJ, Krist AH, Owens DK. Barry MJ,Caughey AB, Davidson KW,Doubeni CA.Epling
JW Jr, Kemper AR, Kubik M, Landefeld CS, Mangione CM, Phipps MG,Pignone M, Silverstein M,Simon MA,Tseng CW,Wong
JB.Screening for Osteoporosis to Prevent Fractures: US Preventive Services Task Force Recommendation Statement. JAMA
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19. US Preventive Services Task Force, Krist AH, Davidson KW, Mangione CM, Bany MJ, Cabana M, Caughey AB, Donahue
K, Doubeni CA, Epling JW Jr, Kubik M, Landefeld S, Ogedegbe G, Pbe1t L, Silverstein M, Simon MA, Tseng CW. Wong JB.
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CA. EplingJW Jr, Kubik M, Landefeld CS,Mangione CM, Pbert L, Silverstein M, Simon MA,Tseng CW,Wong JB. Screening for
HIV Infection: US Preventive Se,vices Task Force Recommendation Statement. JAMA.2019 Jun 18;321(23):2326-2336.
doi: 10.1001/jama.2019.6587. PMID: 31184701.
21. US Preventive Services Task Force. Screening for Colorectal Cancer: US Preventive Services Task Force Recommendation
Statement. JAMA.2021;325(19):1965-1977. doi:10.1001/jama.2021.6238
22. Zweitig S, Noller K. Reale F,et al. Neoplasia associated with atypical glandularcells of undetermined significance on cervical
cytology. Gynecol Oncol.1997;65:314-318.
324
BENIGN DISEASES
GYNECOLOGIC
SECTION ONE
BENIGN DISEASES OF THE VULVA AND VAGINA
DERMATOLOGIC DISEASES
• Broad spectrum of atrophic and hypertrophic conditions characterized by skin changes
due to variety of etiologic agents
• Pruritus (single most common gynecologic problem): intense itching with an associated
desire to scratch and rub the affected area
MANIFESTATIONS &
ETIOPATHOGENESIS MANAGEMENT
DIAGNOSIS
Liche!.'Simplex <thronicus
- .
327
MANIFESTATIONS &
ETIOPATHOGENESIS
Contact Dermatitis'·
I DIAGNOSIS
I MANAGEMENT
328
BENIGN CYSTS & TUMORS
• Occlusion ofpilosebaceous ducts, sebaceous ducts and apocrine sweat glands
• Treatment is only needed if lesions become symptomatic or infected
ETIOPATHOGENESIS
I MANIFESTATIONS I DIAGNOSIS I MANAGEMENT
Epidermal Inclusion Cysts (EiC)
• Most common small • Multiple cysts, • Simple examination • If infected: local
vulvar cyst majority <l cm in • Biopsy in some heat application,
• Skin invagination with diameter cases incision and
keratinized epithelial • Asymptomatic • Transperineal drainage
lining, stratified unless secondarily ultrasound • For recurrent
squamous epithelium infected infection or
with a center of cellular pain: excision
debris that grossly when acute
resembles sebaceous inflammation
material. has subsided
• Most epidermal cysts
do not have sebaceous
cells or sebaceous
material
Sebaceous, Cyst
- - -
• Most common tumor • Often multiple and • Biopsy • Incision &
of the vulva (together asymptomatic • Transperineal drainage
with EiC) • Sebum accumulates ultrasound
• Due to occlusion of within the cyst
sebaceous duct • May become super-
infected with local
flora
Apocrine Sweat Glarfd Cyst t
• Fox-Fordyce disease:
microcystic disease
• Hidradenitis
suppurativa: multiple
infected abscesses
• Pruritic and foul
smelling
• Biopsy
• Transperineal
ultrasound
• Wide local
excision
• Incision &
drainage
• Overlying
I
• Due to occlusion of cellulitis:
apocrine gland ducts antibiotics
in the mans pubis and
labia majora
Paraurethral Gland Cyst
• Skene duct cyst • Maybe • Biopsy • Incision &
• Due to chronic superinfected • Transperineal drainage
inflammation of ultrasound
the gland causing
obstruction of the duct
GattnerDuctCyst •s
• Dysontogenic cyst • Usually • Biopsy • Excision
• Remnants of asymptomatic • Transperineal • IYP& cystoscopy
mesonephric ducts of • Tense palpable ultrasound performed
the Wolffian system cyst that may bulge preoperatively
• Submucosal along below vaginal wall • Yasopressin
anterior or lateral wall • May present during perioperatively
of the upper vagina adolescence with
dyspareunia
or difficulty in
inserting tampons
329
ETIOPATHOGENESIS I MANIFESTATIONS I DIAGNOSIS I MANAGEMENT
Bartholin Duct e.r,st and Abscess
• Due to obstruction of • Usually • Transperineal • No treatment
Bartholin gland (for asymptomatic ultrasound for 1-2 cm &
cyst) or polymicrobial • Unilateral, round, • Biopsy if indicated asymptomatic
infection or STDs (for fluctuant/tense (2:40 years old) • Sitz bath: for
abscess) usually in the pain relief &
• Bartholin gland: inner aspect of reduced healing
located entrance of the inferior labia time
the vagina at 5 & 7 majora or lower • Marsupialization:
o'clock position vestibule entire cyst
• Most common large • Pressure or abscess is
cyst of the vulva symptoms, local incised & edges
pain, dyspareunia, are sutured to
difficulty in vaginal mucosa
walking • Excision biopsy
• May be associated (2:40 years old)
with cellulitis • Word catheter
• Antibiotics
Urethral Carunclel: _ ~
- -
• Outgrowth of distal • Majority are • Biopsy (caruncle • Avoidance of
edge of urethra asymptomatic is com posed of irritation
• Due to chronic • Often secondarily transitional and • Estrogen (oral
irritation or infection infected, producing stratified squamous or topical)
• Mostly seen in ulceration & epithelium with a • Cryosurgery,
prepubertal and bleeding loose connective fulguration,
postmenopausal • Point tenderness tissue. Often the excision
women after contact with submucosal layer
• Associated with undergarments or contains relatively
hypoestrogenism during intercourse. large dilated veins)
• Ulcerative lesions • Voiding
usually produce cystourethrography
spotting on contact • Cystourethroscopy
Urethral Diverticul-qm
• Permanent • 3 D's of • Voiding • Excision if
epithelialized sac-like diverticulum: cystourethrography symptoms are
projection 0 Dysuria • Cystourethroscopy persistent or
, Dyspareunia with recurrent
0 Dribbling infection
Nevus II
• Commonly referred to • Benign nevus: • Excisional biopsy: should be adequate
as a "mole" flat, elevated, in width and depth, with ~5-10 mm of
• Localized nest sharp borders, normal skin surrounding the nevus and
or cluster of even color, and underlying dermis included
melanocytes symmetrical
• One of the most • Dysplastic: 6-20
common benign mm with diffuse
neoplasms in females margins, speckling
of color, and
asymmetrical
330
ETIOPATHOGENESIS I MANIFESTATIONS I DIAGNOSIS I MANAGEMENT
Hemangioma -
• Rare malformations • Mostly • Biopsy • Resection or
of blood vessels rather asymptomatic excisional
than true neoplasms • Usually single, biopsy
1-2 cm in diameter, • Cryosurgery or
flat, and soft, and argon laser
they range in color
from brown to red
or purple
Fibroma
-
-
• Most common benign • Smaller fibromas • Biopsy • Operative
solid tumor of the are asymptomatic • Transperineal removal if
vulva • Pressure symptoms ultrasound symptomatic,
• Low-grade potential • Acute pain during grows larger,
for becoming degeneration and for
malignant • Smooth surface cosmetic
and a distinct reasons
contour
• Most commonly
found in the labia
majora
Lipoma
• Second most frequent • Asymptomatic • Biopsy • Excision for
type of benign vulvar (unless extremely • Transperineal large tumors
mesenchymal tumor large) ultrasound
• Slow-growing, • CT scan
circumscribed • MRI
■
tumors of fat cells
arising from the
subcutaneous tissue
of the vulva
Source:Lobo,et al. Comprehensive
Gynecology.
7thed. 2017
331
BENIGN DISEASES OF THE CERVIX, UTERUS,
AND FALLOPIAN Tl'.JBES
332
ENDOMETRIAL POLYP
I. ETIOPATHOGENESIS
• Localized overgrowths of the endometrial glands and stroma projecting beyond the
endometrial surface
• Has three histological components:
, Endometrial glands
0Endometrial stroma
Central vascular channels
III. MANAGEMENT
• Removal by hysteroscopy via transcervical resection of the polyp (TCRP)
LEIOMYOMA (MYOMA)
I. ETIOPATHOGENESIS
• Benign tumors of smooth muscle cell origin
• The most frequent pelvic tumor and the most common tumor in women
Highest prevalence at the 5th decade of woman's life
• Found in 30-50% of perimenopausal women
A. Risks Factors:
, Increasing age
, Early menarche
Low parity
0
, Tamoxifen use
, Obesity
,..B_.
0
_T...._ ■
_:_:g_:_f_f:~t._:_i:_t_a..,_b_as_e_d_o_n_l_o_ca_t_io_n-',_r_.e._e_r_to_C_h_a._t_e_r_l_6.,_or_th_e_F_I_G_O_S'-u-b_c_la-'s_s1._
,_·c_at_i_on......__~
Submucous
TYPE OF
DEGENERATION
I REMARKS
II. MANIFESTATIONS
• Usually asymptomatic but may include bleeding, pressure symptoms, pain, and infertility
• Symptomatic leiomyomas are the primary indication for approximately 30% of all
hysterectomies
• Pelvic examination: uterine size, as assessed by bimanual examination, correlates well
with uterine size and weight at pathologic examination, even in most obese women
III. DIAGNOSIS
DIAGNOSTICS
I REMARKS
• Typically used to confirm the diagnosis of myomas
• Complementary transabdominal ultrasound evaluation may be of
value in selected cases such as large volume myomas
TransvaginaI • Sonohysterography or saline infusion sonography (SIS)
Ultrasound (TVS) • Color Doppler with SIS: may be useful in distinguishing polyp
from submucosal myomas based on the vascularity of the lesions
0 Polyps: a single feeding vessel
0 Myoma: several vessels
Hystero-
• Mandatory in the evaluation of infertility
salpingography
• Diagnostic hysteroscopy & SIS are equivalent diagnostic tools for
Hysteroscopy
the detection of submucous myomas and polyps
• MRI is more accurate for exact myoma mapping and should be
preferred when such mapping is important
• Recommended for preoperative evaluation when extensive
MRI
surgery is planned especially for those who want to preserve
fertility
• MRI is superior to TVS for ruling out adenomyosis
334
IV. MANAGEMENT
• Myomas that are asymptomatic may be managed expectantly regardless of size & location
• Treatment is aimed at symptom reduction and/or preservation of fertility
• Medical therapy is usually targeted to symptoms of heavy menstrual bleeding
• Surgery is best for submucous myoma presenting with heavy menstrual bleeding, and
myomas causing bulk symptoms, pain, and infertility
A. Medical Management
■
Levonorgestrel endometrial stroma and acts on the
releasing • Irregular bleeding and
uterine vasculature and the receptors
intrauterine spotting, cramping
in myometrium that results in
system • Hepatotoxicity
(LNG-IUS) decrease in bleeding
• Some studies have shown decrease
in myomas volume with LNG-lUS
• Blocks the peripheral conve'rsion
• Hot flushes, vaginal
Aromatase of androgens to estrogen in the
dryness, musculoskeletal
inhibitors ovaries and peripheral tissues, thus
pain
decreasing estrogen
•AsofSeptember2020,the EuropeanMedicines Agency'sRiskAssessmentCommittee has recommendedthe
revocationof PharmacovigilanceMarketing Authorityforthe 5 mgoraltabletsofulipristal
acetate(UPA)generics
after5 cases ofsevereliverinjuryneedinglivertransplantwerereported
Source:ReesV,et al. EMAsafetycommittee.
EuropeanPharmaceutical
Review;2020
DonnezJ, DolmansMM.Uterinefibroidmanagement.
HumReprodUpdate;2016
335
B. Surgical Management
I DESCRIPTION
I REMARKS
C. Others
I DESCRIPTION I REMARKS
• Minimally invasive option for • Ideal for those with heavy
management of myoma related menstrual bleeding or
symptoms dysmenorrhea caused by
Uterine artery
• Percutaneous angiographic intramural myoma, who are
embolization
procedure performed with premenopausal, and who have
(UAE)
video fluoroscopic imaging no desire for future pregnancy,
with injection of embolic agents and who are poor surgical risk
into the uterine artery patients
High intensity • Ideal for patients who would
• Utilizes high intensity
frequency want to retain their uterus,
ultrasound energy to induce
ultrasound with myomas <10cm in
(HiFU) coagulative necrosis of myomas
maximal dimension
PARATUBAL CYSTS
I. ETIOPATHOGENESIS
• Para tubal cysts may be of mesonephric, mesothelial, or paramesonephtic orgin
• When paratubal cysts are pedunculated and near the fimbrial end of the fallopian tube,
they are called hydatid cysts of Morgagni
II. MANIFESTATIONS
• Asymptomatic (majority)
Symptoms
• When para tubal cysts are symptomatic, they usually present with dull pain
• Large and rapidly growing cysts may present with abnormal enlargement
• On physical examination, it is difficult to differentiate a paratubal cyst
Signs
from ovarian cysts
• If present, they may present as movable adnexal masses
III. DIAGNOSIS
• On transvaginal ultrasound, they are visualized as adnexal masses which are separate
from the ovaries
IV. MANAGEMENT
• If asymptomatic, expectant management is recommended
• In pregnancy, they may grow rapidly and cause torsion; in these cases, treatment is
simple excision
336
ENDOMETRIOSIS
• Presence and growth of the glands and stroma from the endometrial lining of the uterus
in an aberrant or heterotopic location
• The classic symptom of endometriosis is cyclic pelvic pain
I. ETIOPATHOGENESIS
A. Theories in Etiology
• Implantation of endometrial cells shed during menstruation
Retrograde
gaining access to the peritoneal cavity through the fallopian tubes,
menstruation
growing as homologous grafts under hormonal influence
• Endometriosis is transplanted via lymphatic & vascular system
Lymphatic • Best explains endometrial implants found in remote sites.
and vascular Hematogenous dissemination of endometrium is the best theory
dissemination to explain endometriosis of the forearm and thigh, as well as
multiple lesions in the lung
• Endometriosis arises from metapiasia of the coeiomic epithelium
Metaplasia
or proliferation of the embryonic rests
• Endometrial glands and stroma are implanted during surgical
Iatrogenic
procedure (e.g., endometriosis on abdominal incision site)
Genetic • Incidence of endometriosis in relatives of women with the disease:
predisposition 7x increase
• Those who develop endometriosis have more peritoneal
Immunologic macrophages that are larger
changes • These hyperactive cells secrete multiple growth factors and
cytokines that enhance the development of endometriosis
Iliac
vessels I
section
Cardinal
ligament
Uterus
Fallopian
tube
Round
ligament
Pelvic
peritoneum
'Blackshapesindicate
Ovary implants
endometrial
• Majority are located in the dependent portions of the female pelvis
• Ovaries (most common): ovarian endometrioma are called "chocolate cysts" due
to accumulation of old blood
• Pelvic peritoneum over the uterus and fallopian tube
• Anterior and posterior cul-de-sac
• Uterosacrai, round, and broad ligaments
• Rectovaginai septum
• Rectosigmoid
337
II. MANIFESTATIONS
• Classic symptoms: cyclic pelvic pain and infertility
• Common symptoms: pelvic heaviness, dyspareunia
• Abnormal bleeding
Symptoms
• GI and urinary tract symptoms: cyclic abdominal pain, intermittent
constipation, diarrhea, dyschezia, urinary frequency, dysuria, hematuria
• Rare: Catamenial hemothorax (thoracic endometriosis) and as cites
• Classic pelvic finding: Fixed retroverted uterus, with scarring and
tenderness posterior to the uterus
• Tenderness of the pelvic structures, nodularity of the uterosacral
ligaments and cul-de-sac
Signs
• Advanced cases: extensive scarring and narrowing of the posterior
vaginal fornix
• Ovaries may be enlarged and tender and are often fixed to the broad
ligament or lateral pelvic sidewall
'
III. DIAGNOSIS
• Pathognomonic symptoms: pelvic pain, dysmenorrhea, dyschezia, dyspareunia, and
infertility can often pinpoint to a diagnosis of pelvic endometriosis (supported by
findings of a retroverted uterus, adnexal masses, and nodularities in the cul de sac)
• Experts are advocating non-invasive means of diagnosing endometriosis
• Other diagnostic modalities: transvaginal ultrasound, MRI,and laparoscopy
DIAGNOSTICS I REMARKS
• Characteristic ultrasound findings: a unilocular cyst with homogenous
low level echogenicity
• Presence of soft markers such as absence of sliding sign may also be
Transvaginal
noted (involves using gentle probe pressure to assess whether the
or transrectaI
ultrasound
anterior rectum & sigmoid colon glide freely across the posterior
aspect of the upper uterus, cervix, and vaginal wall)
• May be able to visualize endometriotic nodules on the rectosigmoid
and uterosacral ligaments
I
• May be used in the diagnosis of deep infiltrating endometriosis
MRI
• Limited value in diagnosing superficial endometriosis
• Gold standard for diagnosis: allows for tissue biopsy which shows
endometrial glands, stroma, and hemosiderin laden macrophages
Laparoscopy • Allows for an accurate visual diagnosis and staging of disease
• Invasive procedure and should not be a prerequisite to starting
medical therapy (can treat empirically, especially for young patients)
338
IV. MANAGEMENT
• Short term goals: relief of pain and address infertility
• Long term goal: prevent progression or recurrence
CONDITION I DEFINITION
I MANAGEMENT
I
SIDE
EFFECTS
• State of androgen excess • Anti-estrogen, • Acne, weight
Pseudo- that sends negative hyperandrogenic gain, hot
virilized feedback to the brain effect (danazol* 400 flashes,
state and disrupts ovulation & to 800 mg/day for 6 deepening of
induces amenorrhea months) voice
• Hormonal state • Hot flahes,
where in there is no • GnRH agonist vaginal
Pseudo- production of estrogen (leupro!ide 3.75mg IM dryness,
menopause & progesterone from per month or insomnia&
state ovaries due to absence 11.25 mg IM for decrease in
of gonadotropins as an 3 months) mineral bone
effect of GnRH agonists density
• Monophasic combined • May cause
• The constant hormonal
OCP (1 pill daily for at irregular
levels supplied by
Pseudo- least 6 months) bleeding
OCPs or progesterone-
pregnancy • Progesterone-only • May cause
only therapy disrupts
state contraceptives (DMPA bloating,
ovulation & induces
150mg IM every 3 headaches,
amenorrhea
months) nausea
'Has fallenoutof favordue to severityof sideeffects
B. Surgical Management
0
Indications ■
erapy d
• AFailedmedical thf1 .:
• cute rupture o arge en ometriomas
• Deep infiltrating endometriosis (ureteral obstruction, compromised large bowel
function]
• Endometriotic cysts of >3 cm associated with pain & non-responsive to medications
• Endometriotic cysts of>4 cm if for assisted reproductive procedure
• Adnexal enlargements of more than >8 cm
• Patient no longer desirous of future pregnancies
339
ADENOMYOSIS
I. ETIOPATHOGENESIS
• Derived from aberrant glands of the basalis layer of the endometrium (compared to
endometrosis which is derived from the functionalis layer)
• Associated with aromatase expression and higher levels of tissue estrogen
• Break down between the endometrium and myometrium
• Standard histologic criterion: Presence of endometrial glands and stroma more than one
low-powered field (2.5 mm) from the basal is layer of the endometrium
PRESENTATION I HISTOPATHOLOGY
Symmetrical
• Diffuse involvement of the anterior and posterior walls of the uterus
(diffuse
adenomyosis)
resulting in a uniformly enlarged uterus (most common)
Asymmetrical
• Focal areas of adenomyotic lesions resulting in an asymmetric or an
(focal
adenomyosis)
irregular shaped uterus (often referred to as adenomyoma)
II. MANIFESTATIONS
• Asymptomatic (majority)
• Classic symptoms: dysmenorrhea & heavy menstrual bleeding
• Pain may be due to bleeding & swelling of endometrial islands
Symptoms
confined in myometrium
• Heavy menstrual bleeding is related to the increased endometrial
surface of the enlarged uterus
• Classic findings in the uterus on pelvic exam
0 Diffusely enlarged usually 2 to 3x normal size
Signs
0 Globular
, Mobile
III. DIAGNOSIS
DIAGNOSTICS I REMARKS
• A transvaginal ultrasound is the first line imaging modality
• Ultrasound findings:
0 Asymmetrical thickening of the myometrium (with the
Transvaginal posterior myometrium typically thicker)
Ultrasound 0 Presence of myometrial cysts
0 Linear striations radiating out from the endometrium
0 Loss of clear endomyometrial border
0 Increased myometrial heterogeneity
• Reserved for cases wherein it is important to distinguish diffuse and
focal adenomyosis from leiomyomas
MRI
• Allows for a quantification of the thickening of the junctional zone,
I with > 12 mm generally considered diagnostic of adenomyosis
Source:ReinholdC, et al. Radiographies;
1999
IV. MANAGEMENT
• No satisfactory medical management (e.g., GnRH agonist, cyclic hormones, prostaglandin
synthetase)
• Definitive treatment: hysterectomy
340
ENDOMETRIOSIS VERSUS ADENOMYOSIS
• Endometriosis and adenomyosis are clinically different diseases
• The only common feature is the presence of ectopic endometrial glands and stroma
I ENDOMETRIOSIS
I ADENOMYOSIS
• Presence & growth of the glands
and stroma of the endometrial
Definition
lining of the uterus in an • Endometrial glands and stroma
aberrant or heterotopic location more than one low-powered field
• Endometrial glands (2.5 mm) from the basalis layer of
• Endometrial stroma the endometrium
Histology
• Hemosiderin-Iadenmacrophages
(confirmatory)
• Aberrant location or outside the • Myometrium at least 2.5 mm from
Location
uterus the basalis
• Retrograde menstruation
• Metaplasia
• Derived from aberrant glands
• Lymphatic and vascular spread
Etiology of the basalis layer of the
• Immunologic change
endometrium
• Genetic predisposition
• Iatrogenic dissemination
• Does not respond to cyclic
• Responds to cyclic changes in
Cyclic changes changes in ovarian hormone
ovarian hormone production
production
Prevalence • Nulliparous women • Multiparous women
Symptoms • Dysmenorrhea and infertility • Dysmenorrhea and menorrhagia
• Fixed retroverted uterus with
I
• Diffuse symmetric enlargement of
posterior tenderness
Signs the uterus, 2-3 times the normal
• Nodularities at uterosacrals
size
• Ovarian cysts
• Ultrasound
• Laparoscopy
• Confirmed following histologic
Diagnosis • Confirmed following histologic
examination of the uterus after
examination of implants
hysterectomy
• Pain relief
Goals of • Pain relief • Preservation of fertility
Management • Preservation of fertility • Control abnormal uterine
bleeding
• Medical management may be less
than satisfactory
Management • Medical and Surgical
• Hysterectomy (definitive
treatment)
341
SECTION THREE
BENIGN DISORDERS OF THE OVARIES
I. GENERALCLASSIFICATION
FUNCTIONAL CYSTS I BENIGN CYSTS/TUMORS
• Follicular cysts • Dermoid cyst (mature teratoma)
• Corpus luteum cysts • Endometriomas
• Theca-lutein cysts • Fibroma
• Brenner tumor (transitional cell tumors)
• Adenofibroma & cystadenofibroma
I BENIGN
I MALIGNANT
Mobility • Mobile • Fixed
• Solid or mixed
• Cystic
• Multilocular
• No solid components
Consistency • Multicystic
• No septations
• Nodular; papillary
• Smooth, thin capsule & septa
• Irregular, thick capsule & septa
Tumor surface • Smooth • Irregular
Lat:'erality • Unilateral • Bilateral
Size • <8 cm • >8 cm
• Ascites
Associated • Peritoneal masses
• Calcifications
features
• Lymphadenopathy
342
FUNCTIONAL CYSTS OF THE OVARIES
DIAGNOSIS*
ETIOPATHOGENESIS MANIFESTATIONS OBSERVATION**
(Ultrasound)
Follicular Cyst
• Most frequent cystic • Most are • Usually <8 cm • Repeat
structures in the asymptomatic • Unilateral, simple ultrasound
normal ovaries • Translucent and and unilocular in after 6-8 weeks
• Persistence of thin walled structure
dominant follicle, or • Filled with clear,
• Failure of a follicle to watery to straw
rupture during the colored fluid
follicular maturation
phase
-
Corpus Luteum Cyst
• Failure of the corpus • Halban triad: • Larger • Repeat
luteum to regress • Spotting with • Simple, unilateral ultrasound
during the luteal delay in menses and unilocular in after 6-8 weeks
phase • Unilateral pain structure
• Clinically more • Small, tender,
important than adnexal mass
follicular cysts • Smooth, red to
brown
• Gray-white if
chronic
Theca Lutein Cyst
• Least common of the • Almost always • Multicystic • Theca Lutein
three physiologic bilateral (partially solid/ will regress
ovarian cysts
• Prolonged or
excessive stimulation
by endo/exogenous
gonadotropins (e.g.,
• Massive ovaries
(;elO cm)
• Hypereactio
luteinalis (multiple
luteinized
partially cystic)
• Bilateral
after pregnancy
I
hCG) follicular cysts)
• Increased sensitivity • Honeycomb
to gonadotropins appearance
• Straw colored fluid
'Diagnosticsto request:pregnancytest, vaginalultrasound
"Laparoscopyis donefor:
• Adnexalmasses aftermenopauseor beforepuberty
• Solidadnexalmass regardlessof age
• Cysticmasses >8 cm
• Cysticmasses 5-8cm persisting>8 weeksin a menstruatingwoman
343
BENIGN OVARIAN TUMORS
I. ETIOPATHOGENESIS
~ ·,.
Egltheltal Tlimod
"' - -· -
Serous • Most frequent ovarian epithelial tumors
cystadenoma • Resembles the fallopian tubes
• Can reach enormous size
Mucinous
• Multilocular with mucoid substance within
cysadenoma
• Resembles cells of en do cervix or intestinal epithelium
• Transitional cell tumor
• Solid mass or nests of epithelial cells & a surrounding fibrous stroma
Brenner tumor
• Epithelium similar to transitional epithelium of the urinary bladder
• Epithelial cells have "coffee bean"-appearing nucleus
...
Germ Cell Tumors
• Dermoid cysts/ Mature teratoma: involve all 3 germ layers
• 80% occur in reproductive life
Benign cystic • Most common neoplasm in prepubertal female
teratoma • Rokitansky protuberance: site where most varied tissue types are
found; most common location also of malignant transformation
• Monodermal teratoma made up of thyroid tissue: struma ovarii
,~
Stromal Tumor ow ,.
• Most common benign solid tumor of the ovary
• Extremely slow growing and unilateral
• Whorled pattern on cross section
Fibroma • Meig Syndrome:
1. Ovarian Fibroma
2. Ascites
3. Hydrothorax
344
GENERAL APPROACH TO ADNEXAL MASSES
I. APPROACHTO ADNEXAL MASSES IN PREMENARCHEALCHILDREN
• A complete pediatric examination should include a complete history and thorough
inspection and palpation of the involved sites and possible related areas
• Transabdominal ultrasonography: first-line imaging modality
• Children with simple ovarian cyst <10 cm with no malignant features should be
manage expectantly (otherwise, surgery is preferred)
• Laparoscopy is preferred over open surgery in benign ovarian tumors
• For malignant diseases, surgical staging is recommended but with preservation of the
uterus and contralateral ovary even in advance disease.
Serum Markers
Dysgerminoma + - + -
Endodermal Sinus Tumor - + - -
Choriocarcinoma + - - -
Immature Teratoma - + + +
Embryonal Carcinoma + + - -
Source:LawrenceAE,et al. J PediatrSurg;2020
■
Simple cysts <5 cm after a few menstrual cycles
• Repeat ultrasound during the first half of the follicular
phase (days 4-6) after 3 cycles may be done
• >50% are functional and will resolve within 2-3
menstrual cycles, repeat ultrasound after 3 months
Asymptomatic with simple • If ovarian cyst is still present at 6 months, CA-125 may
cysts 5-7 cm be requested
• lfCA-125 is <200 IU/mL and there are no suspicions
for malignancy, may opt to observe
• No consensus of cut-off size
Persistent asymptomatic
• Some recommend that a persistent asymptomatic cyst
cysts
>6 cm may be offered surgical management
Syt,lptomatic '
Symptomatic ovarian cysts
that peresent with pain or • Surgical management
pressure symptoms
~ ·111
With Suspicion of Malignancy
"' -
Any size with non-benign
ultrasound findings and/
or elevated tumor markers • Surgical management
that are highly suggestive
of malignancy
Source:lrabonI. et al. POGS;2018
345
B. Surgical Management
0 Benign masses may be removed laparoscopically or through laparotomy
0 Ovarian cystectomy if:
• Preoperative suspicion for malignancy is low
• Mass appears benign intraoperatively
• No evidence of metastatic disease
0 Aspiration of ovarian cyst should not be done
REFERENCES
!.Clinical Practice Guidelines for the Obstetrician-Gynecologist. Society of Gynecologic Oncologists of the Philippines
(Foundation), Inc. Third Edition. July 2019
2.Donnez J, Dolmans MM. Uterine fibroid management: from the present to the Future. Hum Reprod Update. 2016
Nov:22(6):665-686. doi: 10.1093/humupd/dmw023. Epub 2016 Jul 27. PMID: 27466209; PMCID:PMC5853598.
3.lrabon, I. Manaement of adnexal masses in reproductive-aged women. Clinical Practice Gudelines on Adnexal Masses.
PhilippineObstetricaland Gyneocological Society,Inc. November 2018
4.Kumar,R.,Ellenson,H, Ronnett, L., Brigette.M.. Blaustein'sPathologyof the FemaleGenitalTract. New York:Springer,2019.
$.LawrenceAE, FallatME, Hewitt G,et al. Understandingthe Valueof Tumor Markers in PediatricOvarianNeoplasms.)Pediatr
Surg. 2020;55(1 ):122-125. doi:10.1016/i.jpedsurg.2019.09.062
6.Lobo RA,GershensonDM, Lentz GM, Valea FA.ComprehensiveGynecology. 7th edition. Elsevier,2017
7.MomenimovahedZ, Tiznobaik A, Taheri S, SalehiniyaH. Ovarian cancer in the world: epidemiologyand risk factors.Int J
Womens Health. 2019;11:287-299. Published 2019 Apr 30. doi:10.2147 /IJWH.Sl 97604
8.Munro MG,CritchleyHOD,Fraser IS,FIGOMenstrual DisordersCommittee.The tvvoFIGOsystemsfor normal and abnormal
uterine bleeding symptomsand classificationof causesof abnormal uterine bleeding in the reproductiveyears: 2018
revisions. In J Gynaecol Obstet 2018; 143:393.
9.PhilippineObstenicaland Gynecological Society.ClinicalPracticeGuidelineson Myoma and AdnexalMasses,2010
10. PhilippineSocietyfor ReproductiveMedicine.ClinicalPracticeGuidelineson Endometriosis,2014
11. PhilippineSocietyfor ReproductiveMedicine.ClinicalPracticeGuidelinesfor Uterine Leiomyomas,2017
12. QuickReferenceManual on ReproductiveEndocrinologyand Infertility: 1st ed.,Diliman,QuezonCity: PhilippineSocietyof
ReproductiveEndocrinologyand Infertility, Inc.,2012
13. Rees,V.(2020, September8). EMA safetycommitteerecommendswithdrawal of ulipristalacetatemarketingauthorization.
European Pharmaceutical Review. Retrieved from: https://www.europeanpharmaceuticalreview.com/news/127776/
ema-safety-committee-recommends-withdrawal-of-ulipristal-acetate-marketing- authorisation/
14. Reinhold C,Tafazoli F, Mchio A, Wang L,Atri M, Siegelman ES, Rahaman L. Radiographies. 1999;19 Spec No:Sl47.
346
INFECTIONS
TRACT
GENITAL
SECTION ONE
OVERVIEW OF THE GENITAL TRACT INFECTIONS
OVERVIEW OF GENITAL TRACT INFECTIONS
• Infections of the female genital tract may include:
Sexually transmitted diseases
Endogenous infections
Iatrogenic infections
I
(HSV-2) • Prematurity
Human papilloma virus • Congenital laryngeal
• Genital warts
(HPV) papillomatosis
Source:BrunhamRC,et al. PlenumPress;1992
349
ENDOGENOUS INFECTIONS
• These are infections that arise when commensal or endogenous bacteria that possess
pathogenic prerequisites attain replicative dominance
• Caused by overgrowth of organisms normally present in the genital tract of healthy
women (e.g., bacterial vaginosis or vulvovaginal candidiasis)
IATROGENIC INFECTIONS
• Refer to infections caused by low-virulence organisms introduced to the genital tract by
medical procedures such as dilatation and curettage or JUD insertion during childbirth
• Includes infections from improperly performed procedures (e.g., unsafe abortion or poor
childbirth practices)
350
SECTION TWO
LOWER GENITAL TRACT INFECTIONS
BARTHOLIN GLAND CYST AND ABSCESS
• Bartholin glands (or the greater vestibular glands) located in the entrance of the vagina
(at 5 and 7 o'clock positions) secrete mucus to lubricate vulva
• Most common Bartholin masses (when the glands are obstructed) are cysts or abscesses
I. ETIOPATHOGENESIS
• Infection, trauma, mucus changes, or congenitally narrowed ducts may cause obstruction
of the Bartholin duct leading to cystic dilation of the Barthol in duct (Bartholin Cyst)
• When Bartholin cysts become infected (usually E.coli), they form a Bartholin abscess
II. MANIFESTATIONS
• Found in the labia majora and duct orifices are at the base of the labia
Location
minora just distal to the hymen (5 and 7 o'clock positions)
Size •l-Bcm
Laterality • Often unilateral but may be bilateral
• Tense cystic mass • Develops rapidly (2-4 days)
Signs
• Clear/white fluid • Erythema, tenderness, edema
• Acute vulvar severe pain
• Usually non-painful
Symptoms • Dyspareunia
• May be asymptomatic
• Pain during walking
Source:Lobo,et al. Comprehensive
Gynecology.
7thed. 2017
■
III. DIAGNOSIS
Differential diagnoses: mesonephric cyst, epithelial inclusion cyst
• Diagnostics:
° CBC,urinalysis, transperineal ultrasound, GS/CS of abscess
Biopsy of capsule wall for patients ;,40 years old and/or recurrent abscess
0
IV. MANAGEMENT
MANAGEMENT I INDICATION
Marsupialization • Bartholin gland abscess
(I&D) • Bartholin gland cyst in a patient less than 40 years old
• Bartholin gland cyst in a patient " 40 years old
Excision
• Recurrent abscess and/or persistent deep infection
Antibiotics
with anaerobic • Barthol in gland abscess
coverage
Source:Lobo,et al. Comprehensive
Gynecology.
7thed.2017
351
VULVAR INFECTIONS
PATHOGENESIS I MANIFESTATIONS I DIAGNOSIS I MANAGEMENT
pt
Pedicu osis (hh irus pu bis o_rera bl ouse
·- -
• Most • Confined to hairy • Direct • Recommended: permethrin
contagious of areas of vulva microscopy 1% cream rinse OR
all STDs • Pubic pruritus pyrethrin with piperonyl
• Direct • Eggs (nits), lice & butoxide
transmission pepper grain feces • Alternative: malathion 0.5%
(e.g. sexual in pubic hair lotion OR ivermectin 250
contact) µg/kg body weight orally,
repeated in 7-14 days
Scab(flS(Sareop'te/scabei)
,.
-
~
I. SYPHILIS
A. Etiopathogenesis
° Chronic complex systemic disease caused by 'lreponema pallidum (anaerobic, elongated,
tightly-wound spirochete which can penetrate the skin or mucous membrane)
0 Highest risk: women from lower socioeconomic groups, adolescents, early-onset
sexual activity, multiple sex partners
° Contagious during the primary, secondary & probably the 1st year of latent phase
0 In pregnant patients, transplacental transmission is most common
B. Manifestations
STAGE I MANIFESTATIONS
• Ulcers or chancre at the infection site
• Chancre: hallmark lesion; solitary, painless ulcer with raised, rounded
Primary
borders and uninfected base in the cervix, vagina, vulva, mouth, anus
• Usually heals spontaneously but may undergo secondary infection
• Systemic disease, skin rash, mucocutaneous lesions, lymphadenopathy
• 6 weeks to 6 months after chancre appears
Secondary • Maculopapular rash over the palms of the hands and the soles of the feet
• VuIvar lesions: mucous patches & condyloma lata associated with
painless adenopathy
• Follows secondary stage
Latent
• Positive serology without symptoms or signs of the disease
• Seen in untreated syphilis that may appear up to 20 years after
• Potentially destructive effects on the central nervous, cardiovascular,
and musculoskeletal systems
Tertiary
• Optic atrophy, tabes dorsalis, generalized paresis, aortic aneurysm
I
• Gummas: similar to a cold abscess with a necrotic center and the
obliteration of small vessels by endarteritis
C. Diagnosis
• VDRL(Venereal Disease Research Laboratory) test
Screening*
• RPR (Rapid Plasma Reagin) test
• Treponema Immobilization Test
Confirmatory • FTA-ABS(Fluorescent Treponemal Antibody-Absorption)
Tests • MHA-TP(Micro-hemagglutination Treponema pallidum)
• Darkfield microscopy: shows thin, silvery spiral motile organism
'Bothtests abovemeasureanticardiolipin
antibodies,causingpotentialfalse-positive
resultsfromotherconditions
353
D. Management
Parenteral penicillin G is the preferred drug for all stages of syphilis
0
Treatment for latent and tertiary syphilis require a longer duration of therapy
0
STAGE
I RECOMMENDED
I ALTERNATIVES*
II. CHANCROID
A. Etiopathogenesis
0 Bacterial STD caused by Haemophilus ducreyi (highly contagious small gram-
negative rod, "school of fish" in microscopy)
0 Sexually transmitted, acute, ulcerative disease of the vulva
B. Manifestations
Soft chancre: painful and tender ulcers with ragged edges
0
D. Management
Azithromycin 1 g PO in a single dose, OR
0
Sources:CDCST!TreatmentGuidelines,2021
Lobo,et al. ComprehensiveGynecology.
7th ed. 2017
354
Ill. GENITALHERPES
A. Etiopathogenesis
0 Most prevalent genital ulcer disease
° Chronic, life-long viral infection caused by herpes simplex virus (HSV) 1 or 2, which
can enter sensory nerve endings
• HSV-1: genital herpes can be caused by oral-genital sexual practices
• HSV-2: causes primarily genital lesions
0 Recurrent, highly contagious
0 More severe in women compared to men
B. Manifestations
0 Paresthesia of the vulvar skin
0 Papule and vesicle formation
0 Severe vulvar pain, tenderness and inguinal adenopathy
0 General malaise and fever
0 Recurrence may be related to the onset of menstrual period or emotional stress
0 Prodrome: sacroneuralgia, vu Ivar burning, tenderness and pruritus for a few hours
to 5 days before vesicle formation
0 HSV resides in a latent phase in the dorsal root ganglia of S2, S3 and S4
C. Diagnosis
0 Viral culture positive in primary episodes
0 Nucleic acid amplification test (NAAT): most accurate and sensitive
0 Western blot assay for antibodies to HSV: most specific method for diagnosing
recurrent, unrecognized or subclinical herpes
0 HSV culture, ELISA and lmmunoblot test
D. Management
INDICATION
I VALACYCLOVIR
I ACYCLOVIR
I FAMCICLOVIR
First clinical • 1000 mg BID x 7-10 • 400 mg TID x 7-10 • 250 mg TID x 7-10
episode days days* days
• 125 mg BID x 5
I
• 800 mg BID x 5 days, OR
• 1000 mg daily x 5
Recurrent days, OR • 1000 mg BID x 1
days, OR
episodes • 800 mg TID x 2 day, OR
• 500 mg BID x 3 days
days** • 500 mg once then
250 mg BID x 2 days
355
IV. LYMPHOGRANULOMA VENEREUM (LGV)
A. Etiopathogenesis
0 STD characterized by skin lesions followed by regional lymphadenopathy in the groin
° Chronic infection of lymphatic tissue, mostly affecting the vulva
° Caused by Chlamydia trachomatis
B. Manifestations
0 Most common manifestation among heterosexuals is tender inguinal and/or femoral
lymphadenopathy that is typically unilateral (buboes)
PHASE I DESCRIPTION
Primary • Shallow painless ulcer of the vestibule or labia, which resolves
Infection spontaneously
Secondary • Bubo: painful adenopathy in inguinal and perirectal areas
Infection • Groove sign: enlarged lymph node, tender and matted
• Formation of multiple draining sinuses and fistula
Tertiary • Extensive destruction of external genitalia & a no rectal region leading
Infection to extensive scarring which can lead to elephantiasis, multiple fistulas,
stricture formation of the anal canal and rectum
C. Diagnosis
° Culture, direct immunofluorescence or nucleic acid detection of C. trachomatisofpus
or aspirate from an infected node
° Complement fixation antibody titer >l:64 is indicative of infection
D. Management
0 Doxycycline 100 mg BID x 21 days
0 Alternative:
• Azithromycin 1 gram PO once weekly for 3 weeks (then do test of cure with C.
trachomatisNAAT 4 weeks after completion of treatment), OR
• Erythromycin base 500 mg QID x 21 days
B. Manifestations
0 Initially appears as asymptomatic nodule which ulcerates (beefy red ulcer with fresh
granulation tissue), coalesce, and eventually destroy the normal vu Ivar architecture (if
untreated)
0 Subcutaneous involvement (i.e., pseudobubo)
0 Secondary bacterial infection
C. Diagnosis
0 Microscopy using silver stain: Donovan bodies (clusters of dark-staining bacteria with
a bipolar or safety-pin appearance)
D. Management
0 Azithromycin 1 gm orally once weekly, OR 500 mg once daily for at least three weeks
and until all lesions completely heal
0 Alternative regimens (minimum treatment duration 3 weeks and until lesions have
completely healed)
• Doxycycline 100 mg BID
• Erythromycin base 500 mg QID
• Trimethoprim-sulfamethoxazole 800 mg/160 mg BID
Source:CDC.STITreatment
Guidelines,
2021
356
- -
_ ULCERS
LYMPHOGRANULOMA
CHANCROID GENITAL HERPES
VENEREUM (LGV)
mapallidum • Haemophilus ducreyi • HSVl/ HSVZ • Chlamydia trachomatis (Ll, LZ,L3) • Klebsiell,
1, non-
• Purulent • Serous, erythematous • Variable • Red and,
It
• Antigen detection by
Id direct • Direct lmmunostaining ELISA • Giemsas1
• Gram Stain • lmmunoperoxide
>florescence rapid Assay • Tissuesn
staining and ELISA
-
VAGINITIS
Overview of Differentials for Vaginitis based on Vaginal Discharge*
FEATURE
I NORMAL
I
BACTERIAL
VAGINOSIS
I
TRICHOMONIASIS ICANDIDIASIS
I. BACTERIALVAGINOSIS(BV)
A. Etiopathogenesis
0 Polymicrobial syndrome resulting from replacement of the normal hydrogen peroxide
producing Lactobacillus spin the vagina with high concentrations of anaerobic bacteria
(e.g., Gardnerel/a vagina/is)
0 BV is sexually associated rather than transmitted
0 Routine treatment of sexual partner(s) not recommended
B. Manifestations/Diagnosis:
0 BV is the most prevalent cause of vaginal discharge or malodor
° Can be diagnosed using a clinical criteria or Gram stain
2. Gram Stain
• Considered the gold standard laboratory method for diagnosing BV
• Used to determine the relative concentration of the following organisms:
• Lactobacilli (i.e., long Gram-positive rods) are decreased
• Gram-negative and Gram-variable rods & cocci (i.e., G. vagina/is, Prevotel/a,
Porphyromonas, and peptostreptococc,)
• Curved Gram-negative rods (i.e., Mobiluncus)
C. Management
358
II. TRICHOMONIASIS
A. Etiopathogenesis
0 Due to Trichomonas vagina/is (tetra flagellated motile protozoan)
0 Most prevalent nonviral STD
B. Manifestations
0 Most are asymptomatic (70%)
0 Green-yellow frothy vaginal discharge with offensive odor
0 "Strawberry" cervix or colpitis macularis (punctate hemorrhages)
0 Dyspareunia
0 Vulvovaginal soreness and itching
, Dysuria and frequency
C. Diagnosis
0 NAAT(Nucleic Acid Amplification Test): the new gold standard
° Culture (previously considered as the gold standard)
0 Trichomonads seen on wet mount: most common method because of convenience
D. Management
Trichomoniasis among women: metronidazole 500 mg PO BID x 7 days
0
B. Manifestations
Pruritus (primary symptom)
0
C. Diagnosis
0 Hyphal elements on KOH smear (wet preparation)
0Gram stain with yeast hyphae or pseudohyphae
° Culture with Nickerson or Sabouraud
~~~~----1
~- Management: Recommended Re,qimen for Vulvova,qinal Candidiasis
Over-the-Counter Intravaginal Agents
• Clotrimazole 1% cream 5 g intravaginally daily for 7-14 days, OR
• Clotrimazole 2% cream 5 g intravaginally daily for 3 days, OR
• Miconazole 2% cream 5 g intravaginally daily for 7 days, OR
• Miconazole 4% cream 5 g intravaginally daily for 3 days, OR
• Miconazole 100 mg vaginal suppository one suppository daily for 7 days, OR
• Miconazole 200 mg vaginal suppository one suppository for 3 days, OR
• Miconazole 1,200 mg vaginal suppository one suppository for 1 day, OR
• Tioconazole 6.5% ointment 5 g intravaginally in a single application
Uncomplicated
vvc Prescription Intravaginal Agents
• Butoconazole 2% cream (single-dose bioadhesive product) 5 g
intravaginally in a single application, OR
• Terconazole 0.4% cream 5 g intravaginally daily for 7 days, OR
• Terconazole 0.8% cream 5 g intravaginally daily for 3 days, OR
• Terconazole 80 mg vaginal suppository one suppository daily for 3 days
Oral Agent
• Fluconazole 150 mg orally in a single dose
Sources:Source:CDC.STITrealment
Guidelines,
2021
Lobo,et al. Comprehensive
Gynecology.
7thed.2017
359
.
Complicated VVC u ..
y
CERVICITIS
I. ETIOPATHOGENESIS
• Refers to inflammation of the uterine cervix, which primarily affects the columnar
epithelial cells of the endocervical glands or the squamous epithelium of the ectocervix
• Sexually transmitted disease
• Typical pathogens of cervicitis include:
• Chlamydia trachomatis
• Neisseria gonorrhea
• In most cases, no organism is isolated
• Cervicitis can ascend and cause endometritis or pelvic inflammatory disease (PIO)
II. MANIFESTATIONS
• Frequently asymptomatic, but some complain of vaginal discharge/bleeding, dyspareunia,
or an edematous/hypertrophic cervix
• Two major diagnostic signs characterize cervicitis:
• Purulent or mucopurulent endocervical exudate visible in the endocervical canal or on
a endocervical swab specimen
Sustained endocervical bleeding easily induced by gentle passage of a cotton swab
through the cervical os
IV. DIAGNOSIS
• Leukorrhea (>10 WBC/high-power field (hpf) on microscopy of vaginal fluid: associated
with chlamydia! and gonococcal infection of the cervix
• Gram negative intracellular diplococci on gram stain: specific for gonococcal cervicitis
• Nucleic acid amplification testing (NAAT) for testing for chlamydia & gonorrhea
■
Alternative x 7 days
• Azithromycin 2 g orally SD, OR
regimens • Pregnant: Azithromycin 1 g orally
• Cefixime 800 mg orally SD
SD, OR Amoxicillin 500 mg orally
TID x 7 days
•1fchlamydia!infectionhas not been excluded,providersshouldalso treat forchlamydiawithdoxycycline100 mg
orally2 times/dayfor 7 days
.. For persons weighing2'150kg, 1 g ceftriaxoneshouldbe administered
Source:CDC.STITreatmentGuidelines,2021
361
SECTION THREE
PELVIC INFLAMMATORY DISEASE
OVERVIEW OF PELVIC INFLAMMATORY DISEASE (PID)
• PID refers to infection in the upper genital tract (e.g., uterus, fallopian tubes, ovaries) not
due to pregnancy or intraperitoneal pelvic operations
• Sexually transmitted
• Although some are asymptomatic, others are not diagnosed because patient or health-
care provider fails to recognize implications of even mild symptoms (e.g., infertility)
I. ETIOPATHOGENESIS
A. Pathophysiology
B. Pathophysiology
• Results from ascending infection from the bacterial flora of the vagina
Acute PID
and cervix
(<30 days)
• Mostly commonly secondary to N.gonorrhea and C. trachomatis.
ChronicPID • Associated with Mycobacterium tuberculosis or Actinomyces
C. Risk Factors
0 History of STDs and PIO 0 Multiple sexual partners
0 Early age at first coitus 0 IUD use
0 Young age <25 years old (sexually active) 0 Induced abortion
0 Lack of barrier contraception use 0 lmmunocompromised state
D. Etiologic Agents
0 Majority are due to sexually transmitted infections (e.g., N. gonorrhea, C. trachomatis)
0 Microorganisms of the vaginal flora (e.g., anaerobes, G. vagina/is, H. influenzae, enteric
Gram-negative rods, Streptococcus agalactiae)
0 Others: cytomegalovirus, M. hominis, U urealyticum, M. genitalium
II. MANIFESTATIONS
362
III. DIAGNOSIS
I CRITERIA
Minimum criteria • Uterine tenderness or
(presumptive • Adnexal tenderness or
diagnosis)* • Cervical motion tenderness
MANAGEMENT OF PIO
• Regimens must provide empiric, broad spectrum coverage of likely pathogens
• All regimens used should be effective against N. gonorrhea & C. trachomatis because
negative endocervical screening for these does not rule out upper genital infections
Treatment should be initiated as soon as the presumptive diagnosis has been made
I. MEDICALMANAGEMENT
ROUTE
I RECOMMENDATION
Intramus~ular/Qral Regimen*
• Ceftriaxone 500 mg IM in a single dose (SD)** PLUS doxycycline 100 mg PO BID x 14 days
■
with metronidazole 500 mg PO BID x 14 days, OR
• Cefoxitin 2 g IM as SD & probenecid 1 g PO concurrently as SD PLUS doxycycline 100 mg
PO BID x 14 days with metronidazole 500 mg PO BID x 14 days, OR
• Other parenteral 3rd-generation cephalosporins (e.g., ceftizoxime or cefotaxime) PLUS
doxycyc!ine 100 mg PO BID x 14 days with metronidazole 500 mg PO BID x 14 days
-
fareqteral Regimen***
• Ceftriaxone 1 g IV every 24 hrs PLUS doxycycline 100 mg PO or IV
every 12 hrs PLUS metronidazole 500 mg PO or IV every 12 hrs, OR
Recommended • Cefotetan 2 g IV every 12 hrs PLUS doxycycline 100 mg PO or IV every
regimen 12 hrs, OR
• Cefoxitin 2 g IV every 6 hrs PLUS doxycycline 100 mg PO or IV every
12 hrs
363
II. CRITERIA FOR HOSPITALIZATION
• Surgical emergencies (e.g., appendicitis) cannot be excluded
• Tuboovarian abscess
• Pregnancy
• Severe illness, nausea and vomiting, or high fever
• Unable to follow or tolerate an outpatient oral regimen
• No clinical response to oral antimicrobial therapy
III. SURGICALMANAGEMENT
• Considered if there is clinical deterioration or no improvement after 24-48 hours of
antibiotics & is restricted to life-threatening infections, ruptured tuba-ovarian abscesses,
or persistent and symptomatic masses.
• Options include:
0 Ultrasound-guided aspiration of abscess
0 Laparoscopic-guided drainage of abscess cavities or salpingo-oophorectomy or
salpingectomy (goal: uterine & ovarian preservation to maintain fertility)
0 Pelvic clean up (i.e. THBSO): for completed family size
IV. FOLLOWUP
• Clinical improvement should be apparent within 72 hours of initiation of therapy
• If patient is responding, she should be examined 4-6 weeks after therapy to assess
resolution of clinical symptoms and establish a posttreatment baseline
• If no improvement within 72 hours after outpatient IM/oral therapy, hospitalization,
assessment of the antimicrobial regimen & consideration of diagnostic laparoscopy for
alternative diagnoses or for definitive surgical management are recommended
• All diagnosed with chlamydia! or gonococcal PIO should be retested 3 months after
treatment
REFERENCES
1.Workowski KA, Bolan GA. Sexually transmitted diseases treatment guidelines, Centers for Disease Control and Prevention,
2015. MMWR Recomm Rep 2015;64
2.Amsel R, Totten PA, Spiegel CA, et al. Nonspecific vaginitis. Diagnostic criteria and microbial and epidemiologic associations.
Am J Med 1983;74:14-22
3.SchwebkeJR.Hillier SL, Sobel JD, et al. Validity of the vaginal gram stain for the diagnosisof bacterial vaginosis.Obstet
Gynecol 1996;88(4 Pt 1):573-6.
4.Powell AM, Nyrijesy P.Acute cervicitis. Uptodate. Available online https://www.uptodate.com/contents/acute-cervicitis.
Accessed on July 4, 2021
5.Brunham RC, Embree JE. Sexually transmitted diseases: current and future dimensions of the problem in the third world.
In: Germain A, Holmes KK, Piot P.Wasserheit JN,editors. Reproductivetract infections:global impact and priorities for
women's reproductivehealth. New York: Plenum Press;1992
6.Lobo RA,GershensonOM, Lentz GM, Valea FA.Comprehensivegynecology.7th edition. Elsevier,2016
7.Bryan Larsen, Gilles R. G. Monif. Understandingthe Bacterial Flora of the FemaleGenital Tract
8.Clinical Infectious Diseases, Volume 32, Issue 4, 15 February 2001, Pages e69-e77, https://doi.org/10.1086/318710
9.Centers for Disease Control and Prevention. SexuallyTransmtiied Infections Treatment Guidelines, 2021. \V\.,,,...,.cdc.gov.
Accessed September 23, 2021
10. Holmes KK.Mardh PA,Sparling PF,et al. Sexually transmitted diseases, 2nd ed, New York: McGraq-Hill; 1990
364
PELVIC
FLOOR
SECTION ONE
OVERVIEW OF ANATOMY & PHYSIOLOGY OF PELVIC FLOOR
-..-..-..---;,,1+- Coccygeus
Puborectalis
lliococcygeus
I
Levator
ani
~"':::-77---- Pubococcygeus
• Pelvic diaphragm
o Levator ani (pubococcygeus, puborectalis, iliococcygeus)
o Coccygeus
• Perinea! membrane
• Deep perinea! pouch
■
Vaginal cuff
Uterosacral ligament
Sacrospinousligament
Obturator internus
Arcustendineus
Levell~
Level 2
'-'~c:
Level 3 ,~~';:•;"'''""
Symphysis
pubis
Vesical
neck
• There are three integrated levels of vaginal support (discussed on the next page)
• These supports may be affected by congenital anatomic weaknesses, stresses of
childbearing, injury, surgical damage, and straining
367
• Uterosacral ligament • Loss of support contributes
Apical
I Support
(strongest uterine support) to prolapse of uterus and/or
• Cardinal ligament vaginal apex
• Anterior: pubocervical or • Loss of support contributes to
Midvaginal
II Support
pubovesical fascia anterior vaginal wall prolapse
• Posterior: rectovaginal fascia (cystocele)
• Anterior: pubourethral
Distal • Loss of support results in distal
III Support
ligament
rectocele or perinea! descent
• Posterior: perinea! body
Source:Stepp,KJ,et al.A MosbyElsevier,Philadelphia
2007
I. PATHOPHYSIOLOGY
• The descent of one or more of the pelvic organs:
Anterior compartment prolapse: cystocele, urethrocele
0 Posterior compartment prolapse: rectocele, perinea! descent
Apical compartment prolapse: uterine prolapse, enterocoele, vaginal vault prolapse
Posterior
• Posterior vaginal wall has descended
from its original anatomical position
o Rectocoele (descent of the rectum):
■
Compartment defect of rectovaginal fascia
Prolapse o Perinea! descent: detachment
of the perinea! body from the
rectovaginal fascia
III. MANIFESTATIONS
A. Symptoms of POP:
B. Physical Examination
0 The unequivocal diagnosis or pelvic organ prolapse can only be made on physical
examination
0 Each compartment of the vagina (anterior, posterior, and apex) must be inspected and
evaluated separately to define the true nature and degree of prolapse
370
A. Locations of the Six Defined Points when Prolapse if Fully Reduced:
gh
POINT
I DESCRIPTION
Anterior Vaginal Wall
• Point at the midline of the anterior vaginal wall 3 cm proximal to the
external urethral meatus
PointAa
• Position of Point Aa relative to the hymen may be -3 (indicating no
anterior vaginal POP) to +3 cm (indicating a full prolapse)
• Point that refers to the most superior location of the front vaginal wall
Point Ba 0 Can coexist with Aa (-3 cm) in a woman with no anterior prolapse
0 Can coexist with point Cina woman with full prolapse
Upper Vagina
• Lowest edge of the cervix or the vaginal cuff
Pointe
• This location identifies if the cervix is descending
PointD • It is the topmost point of the posterior vaginal wall
Posterior Vaginal Wall
- - -
■
• Point located in the midline of the posterior vaginal wall 3 cm
PointAp proximal to the hymen.
• Position of Point Ap relative to the hymen is -3 to +3 cm
• Point at the most distal position of any part of upper posterior vaginal
PointBp
wall (between vaginal cuff or posterior vaginal fornix and Point Ap)
371
STEP 3: RECORD THE MEASUREMENTS
Anterior Anterior Cervix or
wall wall cuff
Ap Bp D
1980 1996
Measuring POPStaging
• POP-Qemploysthehymenas the pointof referenceandassigneda valueof 0
• Pointsabovethe hymenaredesignated(-)measuredin cm
• Pointsbelowthe hymenaredesignated(+)measuredin cm
POPis consideredsymptomaticwhenthe leadingedgeof theprolapseis at or beyondthelevelof thehymen(i.e.,
~stage2 POP-Q).
Source:HaylenBT,et al. Int Urogynecol
J, 2010andMadhuC, et al. NeurourolUrodyn,2018
372
MANAGEMENT OF POP
I. CONSERVATIVEMANAGEMENT
• Diet (i.e. increase fluid and fiber intake)
• Non-weight bearing exercises
Lifestyle
• Weight loss
modifications
• Avoid activities that can increase intra-abdominal pressure
• Control medical co-morbidities (i.e. chronic cough, constipation, obesity)
• Also called "Kegel Exercises"
• Involves isolation and repetitive contraction of pelvic floor muscles
Pelvic floor over a period of time
muscle training • There is no consensus regarding the frequency and number of pelvic
(PFMT) floor contractions but the usual advice is as follows:
8-10 contractions, 10 seconds per contraction, 3x a day
• Ideally coached by physiotherapist for symptomatic women
II. SURGICALMANAGEMENT
• Goals are for symptom relief, treatment of pelvic support defects, maintenance of
bladder /bowel and sexual function, and prevention of recurrence
TYPE OF
PROLAPSE
Anterior·Compdrtmept Prolapse
• Cystocoele • Anterior colporrhaphy • Burch colposuspension
• Urethrocoele • Transvaginal mesh interposition • Sacrocolpopexy with anterior
• Cystourethrocele mesh interposition
. "'
Posterior Compartment Prolapse -
• Rectocoele • Posterior colporrhaphy • Sacrocolpopexy
• Perinea! descent • Transvaginal mesh interposition
Apical Compar.tmen~Prolapse
• Bilateral Ileococcygeal Fascia • Sacrohysteropexy
(BICF) or prespinous fixation • Sacrocolpopexy
• Uterine prolapse • Sacrospinous ligament fixation • Uterosacral fixation/
• Enterocoele
• Vault prolapse
• Uterosacral ligament fixation/
suspension
• McCalls culdoplasty
• Obliterative (i.e. Colpocleisis)
suspension
• Culdoplasty (Moschowitz/
Halban)
II
373
III. VAGINALPESSARY
• Made of soft PVCor silicone material
• May be offered to all women regardless of site or severity of prolapse
• Two types: support pessaries and space-occupying pessaries
Choice is usually based on experience and trial and error
A. Support Pessaries
Lie along the vaginal axis providing a supportive shelf for the descending pelvic organs
0
Generally easier to insert, allow sexual intercourse and are associated with less
0
• For all types and stages of • For cystoceles and • ·For mild cystoceles in
prolapse (usually for 1st rectoceles with or without woJTienwith a narrow
and 2nd degree) uterine descent pubic arch
• Usually first choice • For correcting a
because of ease of retroverted uterus
insertion and removal
B. Space-Occupying Pessaries
CUBE PESSARY I DONUT PESSARY I GELHORN PESSARY
374
SECTION THREE
URINARY INCONTINENCE
OVERVIEW OF URINARY INCONTINENCE
• Involuntary loss (or leakage) of urine that is objectively demonstrable and is a social or
hygienic problem
• Risk factors include increasing age, obesity, high parity, history of vaginal delivery, and
family history
375
II. MANIFESTATIONS
TYPE I MANIFESTATIONS
Stress • Urine loss during coughing, laughing, sneezing
Incontinence • There is no urge to urinate prior to the leakage
• Frequent, small volume voids that keeps the patient up at night
Urgency • Symptoms may worsen after taking a diuretic
Incontinence • Patient may have a strong urge to void with an inability to make it to the
bathroom in time
• Presents with continuous urinary leakage or dribbling in the setting of
incomplete bladder emptying
Overflow • Due to detrusor muscle underactivity: loss of urine with no warning and
Incontinence occurs with a change in position
• Due to bladder outlet obstruction: often with stress or urgency
symptoms with a sensation of incomplete emptying
Ill. DIAGNOSIS
DIAGNOSTIC I REMARKS
• Urinalysis and culture when appropriate
• Kidneys/ureters/bladder (KUB) ultrasound
Basic tests
• Pelvic floor ultrasound
• KUB-intravenous pyelogram (to diagnose genito-urinary fistula)
• Position patient in the lithotomy position with a moderately full bladder
Cough stress
• Tell tlie patient to cough / bear down
test
• Observe for urine loss per urethra
• Objective measurement of severity of urinary leakage by measuring the
Pad test number of pads used over a certain period of time
• Does not determine the type of urinary leakage
• Measures the pressure volume.relationship of the bladder
• Examples of different urodynamic studies:
Urodynamic
Office cystometry
0
studies
Multi-channel urodynamic studies
0
Video urodynamics
0
-
• Visualization of the urethral lumen using a fiber optic-illuminated rigid
Urethroscopy
scopes
• Visualization of the urinary bladder cavity using a fiber optic-
Cystoscopy
illuminated rigid scopes
• Aids in determining the location of the fistula
• First dye: take rifampicin PO 4-6 hours or inject indigo carmine IV prior
to the procedure
• Second dye: insert 3 gauze pads inside the vagina and methylene blue
introduced retrograde in to the urethra thru a Foleycatheter until the
Two-Dye Test sense of urgency is felt
• Interpretation of tests:
0Proximal and/or middle gauze turns blue: vesicovaginal fistula
0Proximal gauze turns orange: ureterovaginal fistula
0Distal gauze turns blue: urethrovaginal fistula or spillage of the dye
thru the urethral meatus
376
MANAGEMENT OF URINARY INCONTINENCE
I. BASIC MANAGEMENT
DIAPPERS
• Delirium
• Infection
Modification • Atrophic urethritis and/or vaginitis
of transient • Pharmaceuticals (i.e. antihistamines, decongestants, ACE-inhibitors,
causes of diuretics)
incontinence • Psychologic disorders
• Excessive urine output (i.e. hyperglycemia)
• Restricted mobility
• Stool impaction
• Dietary changes
Lifestyle
• Smoking cessation
modification
. • Weight loss
• Topical vaginal estrogen: for peri- or postmenopausal women with
vaginal atrophy in the presence of concomitant stress or urgency
Estrogen incontinence
• Oral estrogen +/- progestin: for peri- or postmenopausal women with
vaginal atrophy, in the presence of other systemic climacteric symptoms
TYPES OF
INCONTINENCE
I REMARKS
■
and during a cough
0 Bladder training: timed voids (i.e. every 2-3 hours)
0 Pessary
• Primary treatment is medical
0 Anticholiner.gics
0 p3-adrenergic receptor agonists
Urgency
• Kegel exercise
Incontinence
• Bladder training
• Biofeedback: pressure sensors are placed inside the urethra, vagina
and rectum
Mixed Urinary
• Address the more pressing symptom
Incontinence
Overflow • Address the cause of the detrusor underactivity or the bladder
Incontinence obstruction
Functional • Modify the physical environment (i.e. grab bars in bathroom, bedside
Incontinence commodes)
-
Extra-urethral • Prolonged catheterization for the smaller genito-urinary fistula
Incontinence • Surgical repair for genito-urinary fistula
377
REFERENCES
1.Abrams P, Andersson KE, Apostolidis A, Birder L, Bliss D, Brubaker L, et al. 6th International Consultation on Incontinence
Recommendations of the International Scientific Committee: Evaluation and treatment of urinary incontinence, pelvic
organ prolapse, and faecal incontinence. Neurourol Urodyn 2018 Sep;37(7):2271·2272.
2.Bent AE, Cundiff GW, Swift SE. Ostergard's Urogynecology and Pelvic Floor Dysfunction. 6th Ed. Philadelphia: Lippincott
Williams & Wilkins (LWWJ; 2007.
3.Culbertson S, Davis AM, Nonsurgical Management of Urinary Incontinence in Women. JAMA.2017 Jan;317(!):79-80.
4.DuBeau CE, Kuchel GA,Johnson T 2nd, et al. Incontinence in the frail elderly: report from the 4th International Consultation
on Incontinence. Neurourol Urodyn. 2010;29(1):165.
S.DuBeau CE, Kuchel GA, Johnson T, et al .. Incontinence in the frail elderly. In: Incontinence, 4th ed., Abrams P, Cardozo L,
Khoury S, Wein A. (Eds), Health Publications Ltd, Paris 2009. p.961.
6.Effective Health Care Program. Nonsurgical Treatments for Urinary Incontinence in Adult Women: Diagnosis and
Comparative Effectiveness. Agency for Healthcare Research Quality 2012. Available at: http://effectivehealthcare.ahrq.
gov /ehc/products/169 /1021/CER36_Urinary-lncontinence_execsumm.pdf (Accessed on November 19, 2012).
7.Haylen BT,De Ridder D, rreeman RM, et al. An International Urogynecological Association (IUGA)/lnternational Continence
Society (ICS) joint repo1t on the terminology for female pelvic floor dysfunction. Int Urogyneco\ ]. 2010;21:S-26
8.Haylen BT, Maher CF, Barber MD, et al. Erratum to: An International Urogynecological Association (IUGA)/lntemational
Continence Society (ICS) joint report on the terminology for female pelvic organ prolapse (POP). Int Urogynecol J.
2016;27:655-684
9.Haylen BT, Maher CF,Barber MD, Camargo SFM, Dandolu V, Digesu A, Goldman HB, Huser M, Milani A, Moran P.Schaer GN,
Withagen Ml. International Urogynecological Association (IUGA) / International Continence Society (!CS) Joint Report on
the Tem1inology for pelvic organ prolapse (POP). Int Urogynecol ).2016, 27(2):165-194; Erratum,2016, 27(4): 655-684;
Neurourol Urodyn,2016,35(2):137-168.
10. Lobo RA, Gershenson OM, Lentz GM,Valea FA Comprehensive Gynecology. 17th Ed. Philadelphia: Elsevier; 2017.
11. Madhu C, Swift S, Moloney-Geany S, Drake MJ. How to use the pelvic organ prolapse quantification (POP-Q) system?
Neurourol Urodyn 20!8;37:S39-43
12. POGSClinical Practice Guidelines on Rcconstructive and Reproductive Surgery in Gynecology. (2013)
13. Prodigalidad-Jabson L1; Amin-Ong A], Jose JB, Ocampo MS, Chan LL, Luna MTC and Sison JM, POGS Clinical Practice
Guidelines on Urogynecology. !st Ed. (2010).
14. Richter HE, Burgio KL, Brubaker L, Nygaard IE, Ye W. Weidner A. Bradley CS, Handa VL, Borello-France D, Goode PS,
Zyczynski H, Lukacz ES, Schaffer ], Barber M, Meikle S, Spino C, Pelvic Floor Disorders Nenvork Continence pessary
compared with behavioral therapy or combined therapy for stress incontinence: a randomized controlled trial. Obstet
Gynecol. 2010;115(3):609.
15. Scott Farrell, editor. Pessaries in clinical practice.London: Springer-Verlag; 2006.
16. Stepp, KJ, Walters, MD. Anatomy of the lower urinary tract, rectum, and pelvic floor. In: Urogynecology and
Reconstructive Pelvic Surgery, 3rd ed., Walters, MD, Karram, MM (Eds), Mosby Elsevier, Philadelphia 2007
378
CONGENITAL
ANOMALIES
OFTHE
FEMALE
REPRODUCTIVE
TRACT
0 CONGENITAL ANOMALIES
1. AFS Class I: Agenesis
OF THE UTERUS
I. INCIDENCE
• Actual incidence is unknown due to underreporting or misreporting
• Incidence reported to be generally around 0.1-3.5%
• Mean incidence of uterine malformations was 4.3% for the general population
• Incidence of Mullerian duct anomalies in women with reproductive problems is 3 to 6%
0 Women with recurrent abortions have an incidence of 5-10%
0 Women having third-trimester miscarriages have a higher incidence ofMullerian defect
II. EMBRYOGENESIS
A. Formation of the Uterus and Vagina
0Mullerian ducts (paramesonephric ducts) & the urogenital sinus are the embryonic
precursors of the female reproductive tract
• Upper 1/3 of the paired Mullerian ducts become the bilateral fallopian tubes
• Lower 2/3 fuse & form the uterine corpus, cervix, and superior aspect of vagina
• Lower vagina differentiates from the primordial urogenital sinus
0Normal development of the female reproductive tract involves a series of processes
of differentiation, migration, fusion, & canalization of the Mullerian system
0Mullerian ducts are believed to embryologically merge in a caudal-cranial direction
Fallopian tube
Uterine
I
Mullerian
(paramesonephrlc)
duct caudal tip
Urogenital
sinus
381
B. Consequential Mullerian Anomalies Upon Interruption of these Processes
PROCESS AFFECTED
I DEFECT
• Aplasia/agenesis
Organogenesis defects • Hypoplasia
• Unicornuate uterus
• Bicornuate uterus
Fusion defects
• Uterine didelphys
Resorption/canalization • Septate uterus
defects • Arcuate uterus
III. PATHOGENESIS
• Etiology of Mullerian tract anomalies is unknown
• Multifactorial patterns of inheritance and teratogens (e.g., diethylstilbestrol) have
been implicated
• Other congenital abnormalities have been associated with Mullerian duct defects
• Urinary tract anomalies
• Skeletal abnormalities
• Cardiac defects
• Auditory deficits
IV. MANIFESTATIONS
• Obstructive anomalies present earlier with menstrual disorders
• Non-obstructive types may manifest later with fertility and obstetric difficulties
V. DIAGNOSIS
• Asymptomatic patients are diagnosed incidentally
• Diagnostic imaging & minimally invasive procedures are needed for diagnosis
DIAGNOSTIC
I REMARKS
• Keytool to differentiate between a septate & a bicornuate uterus
Ultrasound • Determines presence/absence of a cervix
• Evaluate kidneys of patients with Mullerian anomalies
• Provides better information about interior contour of the
Hysterosalpingography uterine cavity (but not the external contour)
(HSG} • Determines patency of fallopian tubes
• Cannot distinguish between septate and bicornuate uteri
• Accurate delineation of both internal and external uterine
Magnetic resonance contours
imaging (MRI) • Differentiates septate from bicornuate uteri
• Determines presence/absence of a cervix
382
SECTION TWO
CONGENITAL ANOMALIES OF THE UTERUS
• Various degrees of
hypoplasia/agenesis of the
Class I:
upper reproductive tract
Hypoplasia/
agenesis (the uterus, cervix, and
upper two-thirds portion
of the vagina)
Tubal Combined Complete
• Characterized by arrest in
development of one of the
Class II:
Miillerian ducts, resulting
Unicornuate
in either a present or
absent rudimentary horn
Non•communicating No horn
■
Complete Partial
Class V:
Septate
T ~
~
1/,
• Failure of resorption of
midline septum
Class VI:
Arcuate ~ I , • Mild endometrial
indentation along the
uterine fundus
• Combination of
features post-exposure
Class VU: to diethylstilbestrol
DES-related (hypoplasia, T-shaped
uterine cavity, abnormal
cervical forms)
Source:TheAFSclassifications.
FertilSteril1988
383
CONGENITAL ANOMALIES OF THE UTERUS
• Congenital uterine anomalies (CUA's) may cause pelvic pain, abnormal bleeding at time of
menarche, recurrent pregnancy loss, or preterm delivery
• MRI is the gold standard for the diagnosis of these abnormalities
• General pathogenesis
0 Hypoplasia/agenesis (AFS I) and unicornuate (AFS 11):failure of one or both MUllerian
ducts to develop
Didelphys [AFS Ill) and bicornuate (AFS IV): failure ofmidline fusion
Septate (AFS VJand arcuate (AFS VI): failure of resorption of the midline septum
384
PATHOGENESIS I MANIFESTATIONS I DIAGNOSIS
I MANAGEMENT
385
PATHOGENESIS I MANIFESTATIONS I DIAGNOSIS
I MANAGEMENT
AFS Class IV: Bicomuate Uterus ~
386
PATHOGENESIS
I MANIFESTATIONS
I DIAGNOSIS
I MANAGEMENT
387
SECTION THREE
CONGENITAL ANOMALIES OF THE VAGINA AND VULVA
Pathogenesis
• Membrane resulting
from the fusion between • Urogenital sinus fails
• Urogenital membrane
the vaginal plate and to canalize to form the
that fails to develop an
the caudal aspect of the inferior one-third of the
opening.
Mullerian ducts fails to vagina.
resorb
388
PATHOGENESIS IMANIFESTATIONS I DIAGNOSIS
I MANAGEMENT
Imper/orate Hymen
• The urogenital • Often is not • Note of thin • Hymenotomy:
membrane that diagnosed until bluish membrane incision without
failed to develop an adolescent that bulges out suturing
an opening. reports primary of the vagina on ° For infants with
• Obstruct the amenorrhea examination of the mucocolpos
vaginal canal and cyclical introitus • Hymenectomy:
causing fluid hypogastric pain • Suprapubic membrane excised
accumulation • Retrograde ultrasound: fluid with edges sutured
amd bulging of menstruation filled vagina , For post-
the hymen out • Sequela: extending to the menarcheal girls
of the introitus endometriosis uterine cavity
into a thin-walled • May present with
protuberance mucocolpos in
infants
Microperforate Hy1tien
• The opening is • Periodically, • Examination of the • Hymenotomy or
much smaller menstrual flow introitus hymenectomy
than the normal escapes • Pelvic ultrasound
hymenal orifice • Hematocolpos may may be needed
also develop
• May complain
of foul-smelling
vaginal discharge
Labial Hypertrophy
• No clear cause • Labial hypertrophy • Examination of the • Asymptomatic: no
• Some are born usually affects the vulva treatment
with large labia, labia minora • Reassurance that it
while others • May be unilateral is a normal variant
develop it in the or bilateral • Labiaplasty: if
reproductive age • Mostly with discomfort
asymptomatic or is pulled into
but may cause the vagina during
irritation and pain intercourse
• Usual complaint:
aesthetic
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32:40-46
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390
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Vagina. Geburtsh U Frauenheilk 1987; 47: 650-3
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2014
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29. Rock JA,Jones HW Jc The clinical management of the double uterus. Fertil Steril. Aug 1977;28(8):798-806.
30. Rock JA,SchlaffWD. The obstetric consequences of uterovaginal anomalies. Fertil Steril. May 1985;43(5):681-92.
31. RockJA. Surgery for anomalies of the mullerian ducts. In: Tompson JD, Rock JA,eds. TeLind's Operative Gynecology. 9th ed.
Philadelphia, Pa: JB Lippincott Williams & Wilkins; 2003:705.
32. Sarto, GE, Simpson, JL. Abnormalities of the Mullerian and Wollfian Duct systems. Birth defects Orig Articles Series
1978;14:37-54
33. Scott Chudnoff. Uterine anomalies. Fertil Steril 2002; 78:899·915
34. Simon C, Martinez L, Pardo F, et al. Mullerian defects in women with normal reproductive outcome. Fertil Steril. Dec
1991;56(6):1192-3.
35. Stassart JP. Nagel TC, Prem KA, Phipps WR. Uterus didelphys, obstructed hemivagina, and ipsi\ateral renal agenesis: the
University of Minnesota experience. Fertil Steril. Apr 1992;57(4):756-61.
36. Strassmann EO. Fertility and unification of double uterus. Fertil Steril. Mar-Apr 1966;17(2):165-76
I :
37. Tanaka YO,Kurosaki Y,Kobayashi T, Eguchi N, Mori K, Satoh Y.Uterus didelphys associated with obstructed hemivagina and • .
ipsilateral renal agenesis: MR findings in seven cases. Abdom Imaging. Jul-Aug 1998;23(4):437•41.
38. The American Fertility Society classifications of adnexal adhesions, distal tubal occlusion secondary to tubal ligation, tubal
pregnancies, Miillerian anomalies and intrauterine adhesions. Fertil Steril 1988;49:944
39. Tridenti G, Bruni V, Ghirardini G. Double uterus with a blind hemivagina and ipsilateral renal agenesis: clinical variants in
three adolescent women: case report and literature review. Adolesc Pediatr Gynecol. 1995;8:201.
40. Valle RF.Sciarra Jj. Hysteroscopic treatment of the septate uterus. Obstet Gynecol. Feb 1986;67(2):253-7.
41. Williams EA, Congenital absence of the vagina - a simple operation for its relief. I Obstet Gyneco\ Br Commonw. Aug 1964;
71:511-2.
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study. Br J Radio!. Mar 1978;51(603):161-70.
391
PEDIATRIC
AND
ADOLESCENT
GYNECOLOGY
■
SECTION ONE
OVERVIEW OF PEDIATRIC/ADOLESCENT GYNECOLOGY
REPRODUCTIVE TRACT OF CHILDREN & ADOLESCENTS
• The reproductive tract in children and adolescents differ from that of adult females
• Physicians must be aware of the differences, so that the approach is accurate and appropriate
Illustration
vr: Vt
• Responds to
:~
• Genital organs
1.0
cm
• External • Internal/external
cm
OS
cm
Uterine/
• 0.25-0.5 • 0.5-1.0 • 1.0-1.5 • 1.5-2.0
cervix ratio*
Labia • Approaches adult
• Bulbous • Flatter • Denser
majora appearance
• Extremely thin
Labia • Thick& • Appear as an • Become • Considerable
minora protruding extension of rounded variation
clitoral hood
• Large but has a • Clitoris begins • Approaches adult
• Less
Clitoris normal index** of to increase in size: width <l cm
prominent
0.6 cm' or less size & length 1.5-2.0 cm
■
• As estrogen
declines, .
endometrial • Corpus becomes
• Regresses in • Starts to
Uterus lining sheds twice as large as
size enlarge in size
• Vaginal bleeding the cervix
occurs which
stops within 7-10
days after birth
• Uterus/cervixratio is defined as the ratio of the length of the uterine corpus to the length of the cervix.The uterus
increases in size with hormonalstimulation.
"The clitoralindex refers to the productof the sagittal and transverse diameters of the glans of the clitoris.
Source: BeiberEJ. Physiologyof the uterus and cervix.Online
395
PUBERTY
• Process by which a sexually immature individual becomes capable of reproduction
• Encompasses a series of neuroendocrine and physiologic changes largely as the result
of the maturation of the hypothalamic-pituitary-ovarian axis, which result in the
ability to ovulate and menstruate
• As a rule, breast development, cornification of the vaginal mucosa, and the growth of
genital hair precede menstruation by 2 years
I. CHANGESIN PUBERTY
• Overview of changes include:
o Development of secondary sex characteristics
o Growth spurt
o Achievement of fertility
• Ratio of fat to both total body weight (TBW) and lean body weight (BW) is the most
relevant factor for onset of puberty and menstruation (obese women have earlier
onset of menarche)
AGE*
EVENT
I (in years)
• 6-8 years
I HORMONE
• Increase in adrenal androgen production • Peaks
Adrenarche • DHEA-S
derived from the zona reticularis between
13-15
• Activation of the HPO axis
• Involves pulsatile GnRH secretion
stimulating the anterior pituitary to • GnRH
Gonadarche • 9-10 years
release FSH & LH, which trigger the • FSH, LH
ovary to produce estrogens and effect
cyclical ovulation
• First sign of puberty
Thelarche • 10-11 years • Estradiol
• Breast development
• Appearance of axillary/pubic hairs-and
Pubarche • 10-12 years • Androgens
development of the pilo~ebaceous unit
• GH
• Substantial portion of adult height, about
Maximal • IGF-1
17-18% is gained during puberty
growth • 11-12 years • TSH
• Peak height velocity is attained 6 months
velocity • Sex
before menarche
steroids
• First menstruation
Menarche • Last sign of puberty (usually occurs 2-3 • 11.5-13 years • Estradiol
years after thelarche
•Averageage and age range forthe onset of the majorphysicalchanges associatedwithpuberty
DHEA-S:dihydroepiandrostenedione sulfate
GH:growthhonmone
IGF-1:insulin-like
growthfactor-1
396
GYNECOLOGIC EXAMINATION
I. POSITIONS USED TO EXAMINE THE PEDIATRIC PATIENT
POSITION I REMARKS
• Most common
Frog-leg • Child has direct view of examiner
and herself
~
• Lateral and downward traction of
the labia improves visualization
into the vaginal canal
~
Sources:SantillanesG, et al. Harwood-Nuss'clinicalpracticeof emergencymedicine,6th edition
ZinnsL, et al. Vaginalbleeding.Online
I NEWBORN
I PREPUBERTAL
• Epithelium: uncornified, redder, thinner
• 4-6 cm long
• Labia majora: puffy
• Labia majora: lose fullness
• Labia minora: thickened
Vulva • Labia minora: become thinner and do not fully
• Redundant hymenal folds
and cover the vaginal vestibule
• Mucosa: pink & moist
vagina • Perineum & perivaginal tissues: rigid/inelastic
• Vaginal pH: acidic
• Vaginal pH: is neutral or slightly alkaline
• Discharge: mucoid
• lntroitus: more anterior
• Often crescent-shaped
• Hymen is redundant
• May protrude upon straining
Hymen • Estrogenized
( until 10 years old)
(thick & elastic)
• Clitoris: 1-2 cm (prominent)
397
III. EXAMINATIONOF BREAST DEVELOPMENTAND BODY HAIR DISTRIBUTION
• Stages of development of secondary sexual features in females has been described by
Marshall and Tanner as follows:
I
DEVELOPMENT GROWTH
I r:-,v~
A· ·1' I U/
K~
• Papillae
elevated
(preadolescent)
• No breast
buds
• None
?url ~
• Breast buds • Sparse,
II f!v~
Ao of_ I
and papillae
slightly
elevated
straight,
slightly
pigmented
A'~~1'I ~U!
r!il~ 1~
• Breast
• Darker,
and areola
III confluent,
coarser,
curly
V elevated
• Areola and
IV
t\fj r >ur
i~ papillae
projected
above breast
• Adult-type
pubis
~~/ )U!i~
ffv~ • Papillae • Lateral
V projected distribution
398
SECTION TWO
DISORDERS OF SEXUAL MATURATON
I. ETIOPATHOGENESIS
• Precocious or advanced sexual maturation is due to:
o An abnormally early hypothalamic-pituitary-ovarian (HPO) activity; or
o Stimulation by estrogens of exogenous or endogenous origins
I GnRH-DEPENDENT
I GnRH- INDEPENDENT
• Production of sex hormones at
• Activation of HPO axis high levels (without activation
Pathology of the HPO axis)
• Central or true precocious puberty • Peripheral precocious puberty
'Labor:atory'Rindings "'
FSH, LH l
i
Estradiol (EZ) i
i
Testosterone i i
■
DHEAS
i i .
GnRH response Pubertal Flat
399
II. SPECIFICETIOLOGIES
ETIOLOGY I PATHOGENESIS I FEATURES
GnRH-Depeni!entll
• Seen nearing age of menarche
• No abnormalities except early
development of the secondary
sexual characteristics which
progress in an orderly
• Due to early maturation and
sequence
Idiopathic activation of the HPO axis
• Future menstrual pattern and
(80%) • Random LH > 0.3 lU/L
fertility are expected to be
normal
• May have decreased adult
height due to an accelerated
bone maturation and early
closure of the epiphyses
• Lesions at hypothalamus near the
3rd ventricle, tuber cinereum, or
mamillary bodies • Early sexual development may
CNSLesions • Associated CNS diseases include be due to an early activation of
TB, encephalitis, trauma, the HPO axis
hamartomas, craniopharyngioma,
hydrocephaly
• Primary thyroid insufficiency (e.g.,
Hashimoto thyroiditis ), leads to
• Girls aged 6 and 8 years
increase TSH and gonadotropins
• Precocious puberty is a rare
or Van Wyk-Grumbach syndrome
complication of prolonged
Primary • Exact mechanism is unknown
primary hypothyroidism
hypothyroidism (low thyroid hormone levels may
• Bone age is retarded: unique to
lead to compensatory production
hypothyroidism
ofTRH which may cross react with
GnRH in the pituitary because
they share the same alpha-subunit
GnRH-lndepende4f" ~ "'' •
• Tumors of the ovary that produce
estrogen or stimulate estrogen
production: granulosa cell tumor
(most common), thecoma,
• Estrogen-secreting tumors can
luteoma, teratoma, follicular cyst
Sex steroid cause breast development and
• Tumors of the ovary that produce
producing vaginal bleeding
tumors androgens: Sertoli-Leydig tumors
• Androgen-secreting tumors can
• Extragonadal tumors may also be
cause virilizing features
hormonally functional and able to
produce or induce the production
of sex hormones (e.g., adrenal
adenomas and hepatomas)
• May have feminizing
(isosexual) or virilizing
• Both adrenal tumors and
(contrasexual) effects
late onset congenital adrenal
• If treated during neonatal
hyperplasia can cause virilization
Adrenocortical period, normal puberty ensues.
• Diagnosed using adrenal imaging,
• If treated late, feminizing
21- or llB-OHase or 3B-ol
features appear.
dehydrogenase
• If untreated, develops virilizing
features
400
ETIOLOGY
I PATHOGENESIS
I FEATURES
• Vaginal bleeding (first sign)
• Mutation in G3 protein activating • Complex genetic disorder
adenylate cyclase affecting the bone, skin and
McCune • Constant stimulation of FSH, LH, endocrine systems
Albright TSH & GH • It is characterized by:
syndrome • The prognosis is unfavorable: precocious puberty,
most patients have menstrual polyosthotic fibrous dysplasia,
abnormalities and are infertile and irregular cutaneous
pigmentation (cafe-au-lait spots)
III. MANIFESTATIONS
• History: Life threatening causes like neoplasms of ovary, adrenal or CNS
• Physical exam: Premature appearance of secondary sexual characteristics
• Early growth spurt with resultant shorter adult height
• In GnRH-dependent precocious puberty, the bone growth is also advanced for age
• Exception: primary hypothyroidism ( only cause of GnRH dependent precocious puberty
where bone age is retarded)
GnRH-
GnRH Dependent Syndromes* lndependent
Syndromes*
FINDINGS
McCune
Idiopathic CNS Tumors Hypothyroidism Albright
Syndrome
Breast
Yes Yes Yes Yes
enlargement
Pubic hair Yes Yes Unusual Yes
Vaginal
■
bleeding
Yes Yes Yes Yes
.
"rili i g s·g s No No No No
Bone age Advanced Advanced Normal or retarded Advanced
Neurologic
No Yes No Yes
deficits
Abdominopelvic Occasional
findings Occasional bloating,
No No
masses constipation,
and/or ascites
·In GnRHdependentprecociouspuberty,physicalchangesare typically
thoseof normalpuberty,withthe exceptionof the
"ageof onser. InGnRH-independent
syndromes,physicalchangesare markedlydiscordantfromnormalpuberty
Source:Loboet al.,Comprehensive
Gynecology,
7th Edition,2016.
401
IV. DIAGNOSIS
A. Indications for Evaluation of Precocious Puberty:
o <6 years of age with breasts OR pubic hair
o <8 years of age with breasts AND pubic hair
o <8 years of age with breasts OR pubic hair (warrant careful history and PE, bone
age, and close follow-up to determine linear growth rate)
o Those with increased risk for intracranial pathology (onset of puberty <6 years old,
rapid pubertal progression, symptoms of headache, seizures, or neurologic deficits)
C. Other Diagnostics
o Brain imaging, EEG's
o Ultrasound, CT or MRI of abdomen
o Serum FSH, LH,TSH, PRL, E2, testosterone, DHEA-S,hCG, androstenedione, 17-OH
progesterone, T3 and T4
o Genetic testing
V. MANAGEMENT
• Reduce gonadotropin secretions
• Reduce or counteract the peripheral actions of sex steroids
Goals of therapy
• Reduce the growth rate to normal
• Slow down skeletal maturation to allow maximal adult height
• Indications for medical therapy:
0 Menarche <8 years old
0 Progressive thelarche & pubarche
0 Bone age >2 years of chronological age
• Depending on etiology
Medical therapy
0 GnRH dependent: GnRH agonist (leuprolide - drug of choice,
goserelin, triptorelin)
0 GnRH independent: estrogen antagonist therapy (e.g., aromatase
inhibitors - letrozole or anastrazole) or estrogen receptor
antagonist (e.g., fulvestrant)
Surgical therapy • Removal of tumor or lesion producing excess hormones
402
VI. INCOMPLETESEXUAL PRECOCITY
• Occasionally due to unknown reasons, only one sign of pubertal development will be
individually present (breast development, pubic hair growth, or menstruation).
• This is possibly the result of:
o Transient elevation of circulating steroid hormones
o Extreme sensitivity of the end organs to the low prepubertal levels of sex hormones
o Variant of normal puberty
• Usually self-limiting (treat or remove underlying cause, if any)
ETIOLOGY/
DISORDER
I FEATURES
I MECHANISMS
• Isolated development of the breast prior to
the age of 8 years
0 Breast buds enlarge (often asymmetric)
0 Nipple development is absent
• Transient ovarian
0 No axillary or pubic hair development
follicular activity
0 Somatic growth pattern is not
Premature • Exogenous source
Thelarche accelerated
(e.g., environment or
0 Normal linear growth & bone age, adult
height is not affected diet)
0 Smears of the vagina fails to show estrogen
effect
0 Benign, self-limiting; biopsy of the breast
tissues is unnecessary
• Isolated development of pubic hair before
• These may be signs
the age of 8 years without other signs of
of excess androgen
precocity
0 Non-progressive, no clitoral hypertrophy
production due to:
Premature 0 Some with abnormal EEGwithout neuro
0 Enzymatic
Pubarche deficiency
disease
(congenital adrenal
0 Bone age not advanced, adult height is not
hyperplasia)
affected
0 Tumors (Leydig
o -Increased androgen (DHEA & DHEA-S)by
cell tumor)
adrenal glands
• Isolated development of axillary hair before
the age of8 years without other signs of
precocity • May evolve into
Premature
0 Bone age not advanced, adult height is polycystic ovary
Adrenarche
not affected syndrome
0 Increased androgen (testosterone and
17-0H progesterone)
• Denotes the occurrence of cyclic vaginal
■
bleeding in prepubertal girls without other
Premature.,,, sighs of secondary sexual development • Cause is unknown,
Menarche
0 Bon(!age not advanced, adult height is not
idiopathic
affected
0 Resultant menstrual pattern is normal
0 Fertility potential is ~nimpaired
403
DELAYED SEXUAL MATURATION
• Defined as the absence of normal pubertal changes at an age 2.5 SD from the mean
• The absence of thelarche by age 14 or of menarche by age 16 is an indication for investigation
I. HYPOGONADISM
Cause of Lack
I HYPERGONADOTROPIC
HYPOGONADISM*
• Due to primary ovarian failure (two
I HYPOGONADOTROPIC
HYPOGONADISM
• Due to the lack of pubertal
of Gonadal intact X chromosomes are needed maturation of the hypothalamus
Function for normal ovarian function) and pituitary
Gonadotropin
• Elevated • Low
Levels
• Hypoestrogenism
Manifestations • Undeveloped breasts and little or no pubic hair
• Atrophied cells on smear of the vaginal walls
• Turner syndrome: gonadal
dysgenesis due to X chromosome • Reversible causes:
deletion (See Section 3) 0 Weight loss/fat loss
• Ovarian failure with normal sex 0 Marked protein deficiency
chromosomes (46XX)due to: 0 Cranial tumors (e.g., pituitary
Examples
0 Mumps adenoma, craniopharyngioma)
0 Infiltrative disease • Irreversible causes:
(e.g., TB of ovary) 0 GnRH deficiency
0 Autoimmune diseases 0 Hypopituitarism
0 Environmental agents
II. EUGONADISM
• Estrogen levels are sufficient with timely appearance of secondary sexual characteristics.
• Most have well-formed female body configuration with developing breasts.
• Menarche does not occur because of absent ductal elements or obstruction of the
menstrual outflow tract
• Congenital anomalies of the paramesonephric (Mullerian] structures:
o Responsible for most eugonadal patients with amenorrhea or cryptomenorrhea
o Most frequent defect is the absence of the uterus and vagina
• Other causes: imperforate hymen, transverse vaginal septum, agenesis/atresia of vagina
• For obstructive causes, corrective surgery is indicated
Ill. VIRILISM
• Virilization may delay development of normal secondary sexual characteristics in girls:
o Small breasts
o None or irregular menstrual cycles
• Masculinization may be manifested by all or a combination of the following:
o Enlarged clitoris
o Acne formation
o Deepening of voice
o Excessive facial hair and male-pattern baldness
• Virilization at puberty is the result of elevated androgens from adrenal or gonadal
sources (may be the result of an enzyme deficiency as in late-onset congenital adrenal
hyperplasia or neoplasm as in Sertoli-Leydig cell tumor]
• Management is the removal or treatment of underlying cause
404
SECTION THREE
DISORDERS OF SEXUAL DEVELOPMENT (DSD)
TERM
I DEFINITION
Genetic or • Defined by the sex chromosome, typically XXor XY
chromosomal sex
• Defined by the direction of gonadal differentiation into ovaries or
Gonadal sex
testes, as directed by genetic sex
• Defined by the appearance of external genitalia and the secondary
Phenotypic sex sexual characteristics that develop at puberty as controlled by the
hormonal environment directed by gonadal sex
ETIOLOGY
I PATHOGENESIS
I FEATURES
■
resulting from a defective cortisol degrees of virilization .
and aldosterone biosynthesis • Genital ambiguity: clitoral
brought about by an enzyme enlargement, labial fusion and
deficit (usually 21-hydroxylase abnormalities of the urethra
deficiency) and the vagina
Mu[lerian Agenei1s(or ~ayer-Rolflta_nsk~-Kuste~ Hauster Synclr-;,,rie)
• Due to • Failure of the uterus and the • Primary amenorrhea,
chromosomal vagina to develop properly in normal breast and pubic hair
translocations women who have normal ovarian development, and no vaginal
function and normal external canal
genitalia
405
II. 46XY DISORDERSOFSEXUALDEVELOPMENT(INCOMPLETELY MASCULINIZED MALES)
• May be secondary to disorders of testicular development, disorders of androgen
synthesis, disorders of androgen action, LH receptor defects, or disorders of AMH and
its receptors
406
III. SEX CHROMOSOME DISORDERS OF SEXUAL DEVELOPMENT
• Results from defective gametogenesis, often non-disjunction
• Chromosomes fail to separate (non-disjunction) therefore both go to one of the daughter
cells during meiosis, the other has none
ETlOPATHOGENESlS
I FEATURES
1, Turner Syndrome - -- --
• Complete absence of one • Commonly presents with short stature, absence of
sex chromosome: leads to sexual development, a webbed neck, low set ears
monosomy X (45XO) genotype and posterior hairline, widely spaced nipples (shield
chest), short fourth metacarpals, and cubitus valgus
• May have renal, cardiac, and ocular anomalies
• Presents at adolescence with primary amenorrhea
and absence of pubertal development
Klinefelter5yndrome
--- ,, X
• Results from meiotic • Habitus exhibits long arms and legs, due to both
nondisjunction that leads to a a long bone abnormality and the influene of
47XXYgenotype testosterone deficiency, and a short trunk
• Most common congenital cause • Presents with testicular atrophy, gynecomastia, and
ofhypogonadism in males female hair distribution
Mixid (:onadal Dysgenesis
• 45XO/ 46XY is the most • Asymmetrical gonadal dysgenesis, where one gonad
commonly associated can be identified as a testis and the other is a streak
karyotype gonad or absent altogether
• Phenotype in MGDcan vary • Genitalia are typically ambiguous, but can also be
widely, reflecting the relative female or male
proportions of 45XO and 46XY • Incidence of gonadal tumors is relatively high (25%)
in the gonadal ridge
APPROACH TO MANAGEMENT
• Karyotyping
Diagnostic
• Other tests to support diagnosis and management of specific
work-up
causes (e.g., ultrasound, enzyme assays)
• Individuals with DSDs should be allowed to develop a gender
Gender
identity for him or herself with the help of the parents and the
assignment
guidance of a child and adolescent psychologist
■
Hormonal&
• Applicable hormonal replacement may be given to achieve the .
desired secondary sexual characteristics
other medical
• Medical treatment of associated co-morbidities should be given as
treatment
indicated
1,, • Removal of the gonads is performed on a phenotypic female with a
Y chromosome as prophylaxis against gonadoblastoma before age
Surger;y 19 years of age
• Gender assignment surgeries are put off until the individual with
DSD is of legal age to decide for themselves
Assisted • Often infertile or even sterile, reproductive efforts sometimes
reproductive
involve third-party ART* (e.g., ovum and/or sperm donation,
techniques
surrogacy, etc.)
(ART)
'Not practicedinthe localsetting
407
SECTION FOUR
MENSTRUAL DISORDERS
ABNORMAL UTERINE BLEEDING (AUB)
• Vaginal bleeding is one of the most common problems in the adolescent female
I. ETIOPATHOGENESIS& MANIFESTATIONS
• Physiologic immaturity of the HPO feedback mechanism
• Blunting of the LH surge resulting in anovulation
• Excessive endometrial stimulation by estrogen
• Absence of the formation of the corpus luteum that brings about an inadequate
production and withdrawal of progesterone
• Excessive proliferation of the endometrium and non-uniform sloughing in different
areas of the endometrial lining.
II. MANAGEMENT
• Observation and reassurance
Minimal
• May resolve in time by itself with the maturation of the HPO axis
bleeding
• Iron supplementation
• Acute bleeding
• Hospitalization may be needed to administer of high doses of
estrogen to facilitate re-epithelialization of the endometrial lining
over the denuded areas
Severe 0 Once bleeding stops, progesterone is added to stabilize the
bleeding endometrium and to ensure uniform sloughing upon withdrawal
° Fibrinolytics and hematinics may be given
• Chronic bleeding: cyclic regulation of the menses for the next 3-6
months may be achieved by giving cyclic progesterone or combined
contraceptive pills, after which a period of observation follows
PRIMARY DYSMENORRHEA
I. ETIOPATHOGENESIS
• Development of painful menstruation in the absence of an organic cause
• Prostaglandin theory: most accepted theory to explain occurrence of dysmenorrhea
• Prostaglandins released during menstruation induces uterine muscle and vascular
contraction that causes uterine contractions and ischemia respectively
II. MANIFESTATIONS
• Tightness of the internal os has been implicated with the observation that symptom
improves with menstrual egress
III. MANAGEMENT
• Primarily directed towards reassuring the patient and the mother that such condition
will disappear or resolve with time
• Menstrual cramps may be alleviated by giving analgesics with prostaglandin
synthetase inhibiting properties (e.g., NSAIDS)
408
SECTION FIVE
OTHER 01SORDERS IN PEDIATRIC GYNECOLOGY
VULVOVAGINITIS
I. ETIOPATHOGENESIS
• Most common gynecologic disorder/complaint in children
• The child is susceptible to this kind of infection because of the following reasons:
o Lack of estrogen (which makes the vaginal mucosa thin and atrophic)
o Possibly immature immune mechanisms in the vagina
o Contamination by stool and other debris (poor perinea! hygiene)
• Organisms: group A or B beta-hemolytic streptococcus, H.injluenzae, Enterobius vermicularis
II. MANIFESTATIONS
• Area of redness/soreness limited to perineum or may extend to thighs and/or anus
• Acute vulvovaginitis may:
o Denude the thin vulvar and vaginal mucosa
o Have varying vaginal discharge from scant to copious
o Have bleeding, but usually minimal
• The irritating discharge often causes the child to scratch the area to the point of bleeding.
Ill. DIAGNOSIS
CLASSIFICATION I REMARKS
IV. MANAGEMENT
• Lifestyle modification:
o Good perinea! hygiene (front-to-back wiping) and avoid harsh soaps
o Frequent change of cotton underwear to absorb discharge
o Wear loose fitting clothes
o Urination with legs spread apart to separate the labia
• Infection: broad spectrum antibiotics (e.g., amoxicillin), antivirals, or antihelminthics
as indicated
• Pruritus: antihistamines or low potency topical corticosteroids for the pruritus
• In recurrent infections refractory to treatment or associated with a foul-smelling,
bloody discharge, it is necessary to exclude foreign body or tumor
.;;;.U..;_R=E;.,;;.T..;_H"'"RA"-=L;...;;P....;;R..;;,.O;;_L=A-"P;_S=E=--------------------1
I. ETIOPATHOGENESIS
• Urethral mucosa protrudes through the urethral meatus which forms a hemorrhagic,
sensitive vulvar mass due to lack of estrogen
II. MANIFESTATIONS
• Prepubertal bleeding (most common symptom)
• Red mucosa! circumferential mass prolapses out of the urethral opening after coughing
III. MANAGEMENT
• Small lesion without impairment of urination: expectant management, often resolves in time
• Small lesion with mild impairment of urination: short course of daily topical application
of estrogen cream
• Large and necrotic lesion with or without urinary retention: resection of the prolapsed
tissue and submit tissue for biopsy to rule out malignancy; insertion of indwelling catheter
409
FOREIGN BODIES
I. ETIOPATHOGENESIS
• Foreign bodies in the vaginal canal induce an intense inflammatory reaction and
result in blood-stained, foul-smelling discharge
II. MANIFESTATIONS
• Foul-smelling, bloody vaginal discharge (classic symptom)
• Partially buried or embedded object in vagina
• Examine child in the knee-chest position to better visualize foreign objects within the
vaginal canal
III. DIAGNOSIS
• Not always a reliable imaging technique to visualize foreign
Radiographs
objects within the vagina, since most objects are not radioopaque
Vaginoscopy • To identify and remove obje~ and exclude other causes of bleeding
IV. MANAGEMENT
• Proper care and hygienic instructions to the mother and child are indicated
• Management consists mainly of the removal of the foreign material:
LABIAL ADHESION
• Fusion of the labia minora at the midline (i.e., the two labia minora are "stuck" together)
• Pathognomonic sign is the presence of a mid line vertical line in between the labia minora
I. ETIOPATHOGENESIS
• Common in prepubertal girls
• Due to irritation/inflammation of "unestrogenized" epithelium with adhesions
forming during the healing process
• Related to low levels of estrogen
o Skin covering the labia is extremely thin, and local irritation induces scratching,
which may denude the labia
o Labia minora then adhere in the midline and stick to each other in the process of healing
o Re-epithelialization occurs with the labia minora remaining fused to each other
II. MANIFESTATIONS
• Asymptomatic: incomplete labial adhesions
• Important to differentiate this condition from congenital absence of the vagina
• Symptoms are usually related to obstruction in urine flow or accumulation of urine
behind the filmy adhesion
• Cardinal symptoms: dysuria, and recurrent vulvar & vaginal infections
• Recurrence is common until puberty because of low estrogen
III. MANAGEMENT
Asymptomatic to
• Need not be treated
minimal/moderate
labial fusion
• Often separate naturally in time
·•Estrogen cream applied twice daily for 7-10 days or until the
Symptomatic fusion is released spontaneously
labial fusion • For tenacious adhesions: simple midline incision along the fusion
,, line l:o separate the labia minora
410
LICHEN SCLEROSUS
I. ETIOPATHOGENESJS
• Hypotrophic dystrophy of the vulva
• Most common in prepubertal & postmenopausal age groups
• Histologically, the findings are:
o Flattening of the rete pegs
o Hyalinization of the subdermal tissues
o Keratinization
II. MANIFESTATIONS
• Presents with flat ivory papules that may coalesce into plaques that, in extreme cases,
involve the entire vulva
• Usually, does not extend laterally beyond labia majora nor does it encroach into vagina
• Clitoris is frequently involved as well as the posterior fourchette and anorectal area
• Symptoms consist ofvulvar irritation, dysuria and pruritus.
• Scratching is common leading to an increased tendency to bruising, formation of
bloody blisters, and secondary infections
Ill. DIAGNOSIS
• No known malignant potential if only hypoplastic dystrophy is present
• Histologic confirmation may be necessary in postmenopausal women, but not always
indicated in children
• Resolution of the condition with a clinical trial of daily application with estrogen
cream eliminates the need for a biopsy
• If the lesion appears to be lichen sclerosus to the experienced observer, histologic
confirmation is usually not necessary
JV.MANAGEMENT
• Topical estrogen
• Hydrocortisone cream
• Improved perinea) hygiene
VAGINAL BLEEDING
• Vaginal bleeding at any time may be due to trauma or tumors
• Differentials for bleeding, depending on the onset of menarche is summarized below:
·.
BLEEDING BEFORE MENARCHE I BLEEDING AFTER MENARCHE
411
SECTION SIX
GYNECOLOGIC TUMORS
I. EPIDEMIOLOGY
Although rare, every type of genital neoplasm reported in adults has also been found
in girls under 14years of age
• Benign tumors of the vulva and vagina are rare in childhood, and may seldom cause
bleeding
• Ovarian tumors account for the majority of tumors in pediatric adolescent patients (in
contrast to adults)
412
TUMORS OF THE OVARIES
I. ETIOPATHOGENESIS
• Ovarian tumors of all varieties (except for Brenner tumors) have been reported in
premenarcheal children, with benign cystic teratoma accounting for at least 30%
• Incidence of malignant degeneration of the neoplasms is higher in children than in the
adolescent or adult women
II. MANIFESTATIONS
• Two most common manifestations: abdominal pain & mass
Symptoms • Hormone-producing ovarian tumors may cause vaginal bleeding
and early appearance of secondary sexual characteristics
• The small pelvic cavity of the child causes most ovarian tumors to
Signs
rise above the pelvic inlet and present abdominally
III. MANAGEMENT
• Management in premenarcheal children varies from that of older patients
• Continued ovarian function is needed to complete sexual & somatic maturation in children
• Fertility sparing surgery is the standard of care
REFERENCES
LBeiber EJ. Physiology of the uterus and cervix. Abdominal key. Available online: https://abdominalkey.com/physiology-of-
the-uterus-and-cervix/#F3-3. Accessed June 23, 2021
2.Lobo RA,GershensonDM, Lent'l GM, Valea FA.Comprehensivegynecology. 7th edition. Elsevier,2016
3.Philippine Obstetrical and Gynecological Society (Foundation), Inc. Clinical Practice Guidelines on Pediatric and Adolescent
Gynecology.First Edition. November 2012.
4.QuickReferenceManualon ReproductiveEndocrinologyand Infertility; 1st ed., Diliman,QuezonCity: PhilippineSocietyof
ReproductiveEndocrinologyand Infertility,Inc.,2012
S.SantillanesG,Gausche•HillM. Harwood·Nuss'clinical practiceof emergencymedicine.6th edition. Availableonline: https:/ /
doctorlib.info/medical/clinical•practice•emergency•medicine/288.html.AccessedJune23, 2021
6.Taylor HS, Pal Land Seli E (eds.) Speroff's Clinical Gynecologic Endocrinology and Infertility, 9th edition. Philadelphia: ■
Wolters Kluwer; 2020. · "'
7.Zinns L, Chuang J.Posner JC,ParadiseJ.Vaginal bleeding. Anesthesiakey. Available online: https://aneskey.com/vaginal· ~ •
bleeding-4/. Accessed June 23, 2021 ·
413
REPRODUCTIVE
GYNECOLOGY
SECTION ONE
AMENORRHEA
OVERVIEW OF AMENORRHEA
• The absence of menstrual bleeding is a common gynecologic complaint seen in clinics
• Amenorrhea is a normal feature in prepubertal, pregnant, and postmenopausal females
• In the absence of pregnancy, the exact cause of amenorrhea must be determined
• May be primary or secondary, based on whether patient already had her menarche
I. DEFINITIONOF TERMS
TERM
I GENERAL DEFINITION
• Defined as the absence of menstrual bleeding, which may be
Amenorrhea
primary or secondary
• Condition caused by anatomic disorders interfering with the outflow
Cryptomenorrhea
of menses (e.g.,imperforate hymen, transverse vaginal septum)
Primary Versus Se~ondary Amenorrhea
Primary • Failure of menarche to occur when expected in relation to the
amenorrhea onset of pubertal development
• Cessation of menses for an arbitrary period (usually >6 months)
Secondary
sometime after menarche has occurred
amenorrhea
• Most common cause is pregnancy (should always be ruled out)
Source:GershensonOM,et al. Comprehensive
Gynecology;
2022
■
• Hyperprolactinemia, prolactinoma
Pituitary
• Infiltrative disorders: sarcoidosis
• Drugs: antidepressants, antihistamines, opiates, cocaine
• Sheehan syndrome, Simmonds syndrome
• Gonadotropin deficiency: Kallmann syndrome
• Infections: meningitis, tuberculosis, syphilis
Hypothalamic
• Metabolic disorders: functional gastrointestinal malabsorption, rapid
weight loss, eating disorder, stress (e.g. competitive physical activity)
• Thyroid disease, polycystic ovary syndrome (PCOS),ovarian tumors
Other endocrine • Constitutional delay of puberty
gland disorder • Adrenal disease, androgen-secreting tumor, adult-onset adrenal
hyperplasia
417
PRIMARY AMENORRHEA
• Failure of menarche to occur when expected in relation to the onset of pubertal development:
• No menarche by age 15, or within 5 years after initial secondary sexual characteristic
development at age 10
• Problem may be endocrinologic or anatomic
Yes
Secondarysexualcharacteristicspresent?
Measure
FSHand LH
Hypogonadotropic Hypergonadotropic
hypogonadism hypogonadism
46XX 45XO
Premature Turner
ovarian failure syndrome
Do ultrasonography
of the uterus
No Outflow Yes
obstruction
Imperforate
hymen or
transversevaginal
46XY
septum
Evaluatefor
Androgen Mullerian secondary
insensitivity agenesis amenorrhea
t • t •
• 17,20 desmolase deficiency • Androgen resistance
• Agonadism • Uterovaginal agenesis
• 17a-OHase deficiency (46XY)
WITHOUT
UTERUS
d d
CATEGORY! CATEGORY4
• Hypothalamic failure • Hypothalamic/pituitary/
• Pituitary failure ovarian/uterine causes
• Gonadal failure • Outflow tract obstruction
* Treat as secondary amenorrhea
WITH
UTERUS
419
I. CATEGORY 1: UTERUS PRESENT AND BREASTS ABSENT (Most Common)
• Phenotypically female with absent secondary sexual maturation characterized by
markedly underdeveloped breasts
• Lack of breast development means low estrogen production, check FSH levels to establish
etiology
Pituitary Gonads
!GnRH
___ _.. , ...;.
USH
__ .,.
!LH 0 , ____. ! Estrogen
Pituitary Gonads
A..
tFSH
_G_n_R_H_.,.~ ....;t_L_H
_ _.. 00 ____.
! Estrogen
420
II. CATEGORY2: UTERUS ABSENT AND BREASTS PRESENT
• Phenotypically female with absent uterus and variable vaginal length
• Breast development means estrogen is present
• Karyotyping should be done to differentiate the possible causes
° Complete vaginal agenesis (Mayer-Rokitansky-Kiister-Hauser)
0 Androgen insensitivity syndrome (historically, "testicular feminization")
COMPLETE VAGINAL
AGENESIS ANDROGEN INSENSITIVITY
(Mayer-Rokitansky-Kuster- SYNDROME
I Hauser Syndrome) I
• Lack of androgen receptors
• Vaginal agenesis and no uterus
in target organs: no
Pathophysiology • Second most common cause of
differentiation of male external
primary amenorrhea
and internal genitalia
Karyotype • 46XX • 46XY
I
level
.
• Creation of neovagina • Gonads are removed as
( see Section 1 of Chapter 14) prophylaxis against germ cell
• Can have biological children tumors (at around 18 years
with ART+ surrogacy or uterine old to allow time for full breast
transplantation development & epiphyseal
Management
• Uterine transplant from a closure)
compatible donor has been • Creation of neovagina if
done successfully resulting in patient decides to continue
livebirths of biological offspring. on as female, (see Section 1 of
Chapter 14)
421
III. CATEGORY 3: UTERUS ABSENT AND BREASTS ABSENT (Rare)
• Reduced or absent levels of both gonadal and adrenal sex hormones result in sexual
infantilism and ambiguous genitalia in 46XYpatients
• Low estrogen and (+) MIF: check karyotype
• Conditions include:
17, 20-desmolase enzyme deficiency (46XY)
17-alpha-hydroxylase enzyme deficiency (46XY)
0Agonadism/vanishing testes syndrome (46XY)
SECONDARY AMENORRHEA
• Absence of menses for an interval of time equivalent to a total of at least 3 previous cycles
or no menses over a 6-month period in women who have menstruated previously
ETIOLOGY
I CONDITIONS
• CNStumor & infections
• Drugs, stress, exercise, weight loss
CNS- Hypothalamic
• PCOS
• Functional hypothalamic amenorrhea
Pituitary
• Neoplastic:chromophobe adenoma, ACTHand GHsecreting adenomas
(Hypoestrogenic
amenorrhea)
• Non-neoplastic lesions: Sheehan syndrome and Simmonds disease
II. MANIFESTATIONS
• Absence of menses, hot flashes, decrease in breast size, vaginal dryness
• Manifestations related to underlying causes and co-morbidities, risk of intrauterine
adhesions, current drug use (e.g., OCP), diet, weight loss, stress, exercise, etc.
422
III. DIAGNOSIS
• A stepwise approach to the work-up of secondary amenorrhea will systematically
facilitate diagnosis of its underlying cause as follows:
DIAGNOSTICTEST I REMARKS
• Pregnancy must be ruled out since it is the most common cause of absence
Pregnancy Test
of menstruation in a previously menstruating woman
Progesterone • To differentiate ovulatory from anovulatory causes by inducing
Challenge Test withdrawal bleeding from estrogen-primed endometrial lining
• Includes estradiol (E2), FSH, LH,prolactin (PRL), TSH,
Hormonal Titers
dihydroepiandrostenedione (DHEAS)
• Ultrasound, CTscan, or MRI
Imaging
• Hysteroscopy
Withdrawalbleeding occurs
(PositivePCT)
Anovulation
Get LHlevels
Normal or low LH J
Get TSHlevels PCOS
Hypothalamicpituitary
Hyperprolactinemia
dysfunction
DIFFERENTIALS DESCRIPTION
I No withdrawal bleeding I
(Negative PCT)
I
I Get FSHlevels
I
I
Normal or Low FSH ! 1 High FSH{>30 mlU/mL)
IDoEstrogen+ Progesterone I
Challenge*
Premature Ovarian
Insufficiency
I
No bleeding I l With bleeding I
Cervicalstenosis I I Get LHlevels I Do karyotypingif
I Asherman syndrome <30 years old
Narmo/LH !
IJ towLH
Checkfor
Hypothalamic Ruleout CNStumors autoimmune disease
I amenorrhea I I (i.e., do MRI) I if >30 years old
DIFFERENTIALS I DESCRIPTION
• Formation of scar tissues obliterating the endometrial cavity that
Asherman prevents the occurrence of normal menstrual periods
Syndrome • Occurs most frequently after a vigorous scraping during curettage
• Endometrial tuberculosis
• Can occur after a cone biopsy or loop electrosurgical excision procedure (LEEP)
Cervical
• Although ovulation and estrogen production is present, iatrogenic
Stenosis
outflow tract obstruction results in a negative PCT
IV. MANAGEMENT
• Management depends on the etiology of secondary amenorrhea
• Objectives of treatment may vary and some etiologies may or may not be correctable
424
SECTION TWO
MENSTRUAL ABNORMALITIES
DYSMENORRHEA
• Suprapubic pain which may occur before, during, and even after the menstrual flow
• Often accompanied by other symptoms (e.g., sweating, tachycardia, headache, nausea)
I. ETIOPATHOGENESIS
A. Pathogenesis
0 There is a close association between dysmenorrhea and elevated prostaglandin F2a
(PGF2a) levels
0 During menses, myometrial contractions decrease uterine blood flow and cause
ischemia and sensitization of pain fibers
■
Age • Almost always occurs in
years old (but may occur in those
predilection women <20 years old
younger)
• No obvious abnormalities
• Structural abnormalities on
except a generalized
Examination bimanual examination and pelvic
tenderness throughout the
ultrasound
pelvis
• In endometriosis: dyschezia and
dyspareunia
Associated • Nausea, vomiting, and
• Other associated symptoms vary
Symptoms headache
with the etiology of the secondary
dysmenorrhea
425
II. APPROACH TO DIAGNOSIS
APPROACH I REMARKS
• Diagnosis is made predominantly by history and physical examination
• Typical complaint is midline, crampy, lower abdominal pain which begins with
History the onset of menstruation and gradually resolves over 12-72 hours
• Pain does not occur at times other than menses and only occurs in ovulatory
cycles
• Oral contraceptives
Other therapies • Other analgesics
• Transcutaneous electrical nerve stimulation (TENS)
426
2. Pain Control
• NSA!Ds (e.g., mefenamic acid, ibuprofen, diclofenac, naproxen): analgesics of choice
because of its anti-prostaglandin properties
3. Conservative/Definitive Surgery
ETIOLOGY I MANAGEMENT
• Laparoscopic fulguration of endometriotic mplants
• Oophorocystectomy
Endometriosis • Presacral neurectomy
• Hysterectomy: reserved for those refractory to medical
treatment and conservative management, or fertility not desired
• Removal of adenomyotic lesions (Osada technique),
Adenomyosis
hysterectomy
Pelvic adhesions • Laparoscopic adhesiolysis
Cervical stenosis • Dilation of the cervix
I. ETIOPATHOGENESIS
• Unknown cause, but is likely multifactorial (physiologic and psychological)
• Women with PMS and PMDD may have an abnormal response to normal hormonal changes
• Syndrome is likely attributed to estrogen excess
TERM I DEFINITION
Premenstrual • Group of mild/moderate symptoms that occur in the second half of
Syndrome (PMS) the menstrual cycle
• More severe disorder
• With marked behavioral and emotional symptoms
• PMDD (in contrast to PMS) has the following characteristics:
Premenstrual , More severe
Dysphoric 0 Must have one severe affective symptom ( e.g., markedly
Disorder (PMDD) depressed mood or hopelessness, anxiety or tension, affective
]ability, or persistent anger) which occurs regularly during the
last week of the luteal phase
0 Substantial impairment in personal functioning
Source:Gershenson
DM,et al. Comprehensive
Gynecology;
2021
II. MANIFESTATIONS
■
• Irritability, anxiety, depression
• Symptoms are followed by a period entirely free of symptoms
Symptoms
• PMDD and PMS are similar in that symptoms manifest in the luteal
phase of the menstrual cycle and resolve during menses
Signs • Breast tenderness, bloating, headache
Source:Gershenson
DM,et al. Comprehensive
Gynecology;
2022
427
III. DIAGNOSIS (CRITERIA)
• Symptoms must occur in the 2 weeks prior to menstruation and resolve following onset
of menses
• There must be at least a 7-day symptom-free interval in the first half of menstrual cycle
• Symptoms must occur in at least t'No consecutive cycles for the diagnosis to be made.
IV. MANAGEMENT
428
SECTION THREE
ABNORMAL UTERINE BLEEDING
• Light □
Flow volume
(patient • Normal □
determined)
• Heayy □
• None □
Intermenstrual
Bleeding (1MB) 1,• Random □
Bleeding between
• Early Cycle □
cyclically regular • Cyclic (predictable) • Mid Cycle □
onset of menses
• Late Cycle - □
■
Unscheduled • Not applicable (not on gonadal steroid medication) □
Bleedin~on
Progestm +/- • None (on gonadal steroid medication) □
Estroi:en Gonadal
Stermds** • Present □
'Usingthesecriteria,thenormalrange(shortest
to longest)
varieswithage:
18-25yearsofage:,:;gdays
0 26-41yearsofage:$7 days
0 42-45yearsofage:,:;gdays
"Progestin+/-estrogen gondalsteroids
mayincludebirthcontrolpills,rings,patches,
orinjections)
429
FIGO (PALM-COEIN) CLASSIFICATION SYSTEM OF AUB
• Classification system with a standardized nomenclature intended to be used worldwide
by researchers/clinicians investigating & treating women of reproductive age with AUB
• There are nine main categories, arranged according to the acronym PALM-C0EIN
l
~ l
IStructural I INon-structural I
1 1
!'_olyp !; oagulopathy
~ denomyosis Q vulatory dysfunction
~eiomyoma ;_ ndometrial
• Components of the PALMgroup are discrete (structural)entities that can be measured visuallywith
imaging techniques and/or histopathology
• The COEIN group is related to entities not defined by imaging/histopathology(non-structural)
I. STRUCTURAL AUB
ETIOPATHOGENESIS
I MANIFESTATIONS I MANAGEMENT
Ed 1 (AUB-P)
n omet r,a IP oyp ~
430
II. NON-STRUCTURAL AUB
ETIOPATHOGENESIS
I MANIFESTATIONS
I MANAGEMENT
Coagulopathy (APB·C)
-
• Encompasses a spectrum
• As seen in systemic disorders such
of systemic disorders of • Treatment of
as von Willebrand disease and
hemostasis that may be underlying cause
prothrombin deficiency
associated with AUB
Ovul;,t'ory Dysfunction, (AUB-O) .,
""
• Includes ovulatory disorders at
extremes of reproductive age • Oligomenorrhea
• Cyclic
• May be secondary to alterations in • lntermenstrual bleeding
progesterone
neuroendocrine function (e.g., PCOS, • Heavy menstrual
• Combination OCPs
hypothyroidism, prolactinemia, obesity, bleeding
mental stress, extreme exercise)
Primary Endometriill l)isorder (:AUJ!·EJ
• Excessive uterine production • Primary disorder of the
ofprostacyclin, a vasodilatory endometrium when AUB • LNG-IUSmay be
prostaglandin that opposes platelet occurs in a predictable & helpful
adhesion and may also interfere cyclic manner, typical of • NSAIDs
with uterine contractility ovulatory cycles
A
Iatrogenic (AUB•I)
• Due to medications such as SERMs,
GnRH analogues, anti-coagulants,
• Tailored to the
risperidone and other antipsychotics • Depending on cause
specific cause
• Uterine perforation or laceration
associated with surgical procedures
!Jot other~ise clas~ified fAUB·N)
-
• Abnormal bleeding not classified in
the previous categories • Tailored to the
• Depending on cause
• Examples of such conditions may specific cause
include foreign bodies or trauma
Source:MunroMGet al IS IntJ GynecolObstet2018
431
The FIGOSystem Categories of Myomas
• This is the FIGO
leiomyoma
subclassification
system that includes a
tertiary classification
ofmyomas
• It further categorizes
submucous and
subserous myomas
based on the ratio of
the myoma located
intramurally
0 Pedunculated intracavitary
SM-SUBMUCOUS 1 <50% intramural
2 ;,SQ% intramural
UNCLASSIFIED 3 Contacts endometrium; 100% intramural
4 Intramural
5 Subserous ;,50% intramural
0 -OTHER 6 Subserous <50% intramural
7 Subserous pedunculated
8 Other (specify e.g., cervical, parasitic)
Submucous and subserous, each with less than half the
2-5 diameter in the endometrial and peritoneal cavities,
respectively
HYBRID
'Twonumbersare listedseparatedbya hyphen.Byconvention, the firstrefersto the
relationship
withthe endometriumwhilethe secondrefersto the relationship to the
serosa.Oneexampleis above.
Source:MunroMG.et al. J GynaecolObste;2018
432
APPROACH TO ABNORMAL UTERINE BLEEDING
I. DEFINITION OF ABNORMAL UTERINE BLEEDING (AUB)
• Includes any significant deviation from normal menstrual bleeding patterns attributed to
the uterine corpus
• AUBmay include (with or without any recognizable pathology):
Short or long (but regular) cycles
, Irregular cycles
Heavy /light periods
, lntermenstrual bleeding
, Premenarcheal or postmenopausal bleeding
• Heavy menstrual bleeding is defined as excessive menstrual blood loss which interferes
with the physical, emotional, social and quality of life, and which can occur alone or in
combination with other symptoms
ONSET I DEFINITION
• An episode of heavy bleeding sufficient in quantity to require immediate
AcuteAUB
intervention to prevent further blood loss
• Present for the majority of the past 6 months
ChronicAUB
• Usually does not require immediate intervention
II. DIFFERENTIALS
ONSET OF MENORRHAGIA I PROBABLE DIAGNOSIS
• Immediately after menarche • Physiologic: anovulation, perimenopausal
• Late 40s & SOs transition
• Since onset of medication
• Medication-induced
• Soon after medication
• Weight gain or symptoms of hyperandogenism • Anovulation (e.g., PCOS)
• Gradual increase over months or sudden & • Myoma
noncyclic • Hyperplasia or carcinoma
• Increasing disability from systemic disease • Chronic disease
III. DIAGNOSIS
DIAGNOSTIC I REMARKS
• Pregnancy test or sensitive ~-hCG assay
• CBCand coagulation profile (adolescent & older women)
• Thyroid function tests (TSH, FT3, FT4)
Basic tests
• Pap smear
• Screening for ST!
• Serum ferritin
• Ultrasonography: first-line diagnostic tool
Imaging
• Saline infusion sonography (SIS): accurate evaluation tool for
studies
intracavitary lesions
■
• Postmenopausal woman with bleeding or premenopausal woman with
heavy /irregular vaginal bleeding
EndometriaI • Postmenopausal women with endometrial cells on pap smear
biopsy • Premenopausal women with atypical glandular cells on pap smear
• Breast cancer patients on tamoxifen with abnormal vaginal bleeding
• Women who are still "menstruating" after 52 years of age
• Gold standard
Hysteroscopy • Both diagnostic & therapeutic
• Targeted biopsy more accurate than D&C
Sources:NICEguidelinesfor heavymenstrualbleeding,2007
MunroMGel al. IntJ GynecolObstel2018
CPGonAbnormalUterineBleeding,POGS,Inc.:2017.
433
IV. MANAGEMENT
• In general, structural etiologies for AUB (PALMfrom the PALM-COEINSystem) generally
require surgical correction
• Therapy for non-structural causes of AUB (COEINfrom the PALM-COEIN System) should
be tailored to address the specific underlying cause when a cause is identifiable
434
A. Long-term Management for AUB {depends on underlying cause)
~
UNDERLYING
CAUSE
Structural Causes .
Polyps --- • Polypectomy
• GnRH agonist
• Adenomyomectomy
Adenomyosis • Levonorgestrel intrauterine
• Hysterectomy
system (LNG-IUS)
• Hormonal suppression • Myomectomy
• GnRH agonist • Uterine artery embolization
Leiomyomas • Selective progesterone • MRI guided focused
receptor modulator* ultrasound
• Tranexamic acid • Hysterectomy
• Hysteroscopy with
endometrial curettage
Endometrial • Extrafascial hysterectomy
• Progestin therapy
hyperplasia with bilateral salpingectomy
(EHBS) ± bilateral
oophorectomy
• lfyoung and desirous of
• Extrafascial hysterectomy
fertility, provided early stage
with bilateral
and satisfies criteria** for
salpingooophorectomy
Endometrial cancer conservative management
(EHBSO)+ lymph node
• May give high dose
dissection
progestins and LNG-IUSwith
• Chemotherapy /radiotherapy
close surveillance
Non-structural Causes
- -
• Thyroid hormone replacement for hypothyroidism
Thyroid disorder
• Anti-thyroid medications for hyperthyroidism
Hyperprolactinemia • Dopamine agonists: bromocriptine, cabergoline
• Combined estrogen/progestin pills, patch, or ring
Anovulation • Cyclic progestin
• LNG-IUS
Primary
endometrial • NSAIDs
disorder
'As of September2020,the EuropeanMedicines Agency'sRiskAssessmentCommittee· (PRAG)has
recommended the revocationof PharmacovigilanceMarketing Authority
forthe 5 mgoraltabletsof ulipristal
■
acetateafter5 cases of severeliverinjuryneedinglivertransplantwerereported
"Criteriaforconservativemanagement:
0Well-differentiated
tumor(Grade1, endometrioidtype)
0Nomyometrial invasion,
cervical,
adnexal,parametrial
andvaginalinvolvement
onMRI
0Nosuspicious retroperitoneal
lymphnodesor noevidenceoflymphnodemetastasis
0NegativePFC
0Nolymphovascular space invasion(LVSI)
0Nocontraindications formedicalmanagement
435
SECTION FOUR
POLYCYSTIC OVARY SYNDROME
I. ETIOPATHOGENESIS
• Previously known as the Stein-Leventhal Syndrome
• Most common endocrinologic disorder among women of reproductive age
A. Risk Factors
0Associated conditions: diabetes, obesity, heart disease, endometrial cancer
B. Pathophysiology
0 Poorly understood
, Primary problem may lie in the hypothalamus, the pituitary, the adrenals, the ovaries,
or even the adipose tissues
MECHANISM I EFFECTS
• Results in increased production of LHby the pituitary
• Constant elevation of LH in turn prevents the occurrence of an LH surge
Increased that promotes anovulation, leading to:
frequency of 0 Incomplete follicular development resulting in the polycystic ovarian
GnRH pulsatility morphology and increased androgen production by ovaries
0 Elevated estrogen milieu and an absence of the physiologic
production and withdrawal of progesterone
• Androgen brings about insulin resistance that leads to a compensatory
insulin hypersecretion:
Insulin 0 Promotes further androgen output by the ovaries and adrenals
Resistance 0 Suppress hepatic production of sex hormone binding globulin
(SHBG),which exacerbates hyperandrogenemia by increasing the
proportion of free circulating androgens and estrogens
Source: SperoffL, et al. ClinicalGynecologicEndocrinology 2011
and Infertility;
II. MANIFESTATIONS
A. Features of PCOS
0 Manifestations include menstrual disorders, androgen excess, and difficulties in conceiving
0 Presents with hirsutism, virilization, anovulation, amenorrhea, and obesity
FEATURES I REMARKS
• For the ovaries to be labelled polycystic, 12 or more cystic follicles
Polycystic Ovaries measuring 2-9 mm in diameter or an ovarian volume of>l0 cm3 will have
to be documented by transvaginal or trans rectal ultrasound
• Majority (68-85%) have abnormal menstruation
Anovulation
• Oligomenorrhea and amenorrhea: most frequently experienced
• Clinical manifestations may include hirsutism, acne, alopecia, truncal
obesity, and acanthosis nigricans
• Biochemical abnormalities for androgen excess:
Hyperandrogenism
Elevated serum free testosterone
0
Decreased SH8G
0
436
B. Androgen Excess(Hyperandrogenism) in Females
0 Hirsutism (60%): primary clinical indicator of androgen excess
0 Virilization: characterized by masculinizing and anti-estrogenic effects of testosterone
0 Other manifestations ofhyperandrogenism include acne and androgenic alopecia
I HIRSUTISM I VIRILIZATION
• Mild forms: upper lip & chin
• Characterized by masculinizing
• More severe forms: cheeks,
and anti-estrogenic effects of
intermammary, chest,
testosterone
abdomen, thighs, back,
• Temporal balding, clitoral
Features intergluteal areas
hypertrophy
• May have normal ovulatory
• Reduced breast size
menses
• Vaginal dryness
• Usually have oligo or
• Increased muscle mass
amenorrhea
Onset • Gradual • Abrupt
Severity of
• Normal, or mild to moderately • Marked elevation of circulating
Androgen
excess elevated (<1.5 ng/mL) testosterone (>2 ng/mL)
Ill. DIAGNOSIS
• There are three Consensus Diagnostic Criteria for PCOS
• Some women with PCOSmay not have menstrual irregularity, so the Rotterdam criteria
emerged, which is most widely used for PCOS
• The Rotterdam Criteria is used locally to guide in the diagnosis of PCOS
437
Ferriman-Gallwey Scoring System:
(helpful in evaluating and quantifying the pattern and extentofhirsutism in PCOS)
•
Upper
lips @-
~
~ (0-·®-·
,,.,, tt> c,r,, ,,<t>
;;;:
a., ,.~
0,
(0~®- ®··- ®.:.
<$'-, ,~
e$
- ~- a.,
::.
,.-i, a.,
::.
,11;> <T>,,•.._.
.:;;:.
<t•• ,,,c,
:;;:.
ch·in
1 2 3 4 1 2 3 4
Che~ fV:W,
v/v~v~,
1 2 3 4
~:::~.f
1 2 3 4
rlitlf
+1
;~;:~.,t\f 1 2 3 4
Back f'f'ffi\::
1 2 3 4
Acms il I\ I\f'
1 2 3 4
Thighs wwww 1 2 3 4
438
B. Diagnostic Considerations For Adolescents
For adolescents, polycystic ovarian morphology and anovulatory symptoms may not
be enough to make a diagnosis of PCOSsince these may be normally seen in the early
period of reproductive maturation
Diagnosis of PCOSin this age group may be established based on:
• Oligomenorrhea, AND
• Clinical and/or biochemical evidence of androgen excess
Ultrasound is not recommended in diagnosis in patients <8 years post menarche
l
If no clinicalhyperandrogenism
Test for biochemicalhyperandrogenism Menstrual
(excludeother causes) ➔ diagnosis irregularities
l
If ONLYirregular cycles ORhyperandrogenism PCOS PCOS
(B) (O)
PCOS
Adolescent: ultrasound not indicated ➔ (A)
consider at risk of PCOSand reassess later
PCOS
Androgens (C) Ultrasound
Adults: request ultrasound for PCOM
If positive (oxcludeother causes) ➔ diagnosis
l
Classifythe phenotype
Phenotypization
PhenotypeA:has all 3 criteriaof Rotterdam.
PhenotypeB:has 2, menstrualirregulari!ies and hyperandrogenism (clinicalor biochemical)
PhenotypeC: has 2, hyperandrogenism (clinicalor biochemical)
and polycystic ovarieson ul!rasound
PhenotypeD:has 2, menstrualirregularities and polycysticovarieson ul!rasound
IV. MANAGEMENT
With the problem probably lying primarily on the hormonal regulation by the
hypothalamus plus the involvement of many other organs, it should be considered a
multisystemic disorder
• Treatment depends in the particular symptoms and the desires of the patient
■
• Management goals consist of: .
Restoration of normal menstruation
Improvement of fertility
, Lowering of insulin resistance levels
Treatment of hirsutism, alopecia or acne
, Prevention of endometrial hyperplasia, DM, and cardiovascular disease
0 Regular exercise
439
B. Interventions Based on Symptomatology
DESIROUS OF
SYMPTOM
Abnormal
I PREGNANCY I NOT DESIROUS OF PREGNANCY
441
SECTION FIVE
INFERTILITY
OVERVIEW OF INFERTILITY
I. DEFINITION OF TERMS
• Applied only to an individual who has some absolute factor preventing
Sterility
pregnancy
• The inability of a couple to achieve pregnancy after one year of regular
Infertility
unprotected coitus
Primary • Refers to a woman who has never conceived despite unprotected
infertility coitus for at least 12 months
Secondary • Refers to a woman who has previously conceived but unable to
infertility conceive again despite unprotected coitus for at least 12 months
Fecundity • Ability to achieve a live birth in one menstrual cycle
• The probability of achieving pregnancy within a menstrual cycle (25%
Fecundability
in normal couples)
442
EVALUATION AND DIAGNOSIS OF INFERTILITY
I. HISTORY AND EXAMINATION
• Any pregnancy complications
• Previous pelvic surgery of any type or procedures to treat cervical
abnormalities
Medical • Significant dysmenorrhea
history • Dyspareunia or sexual dysfunction
• Abnormal cervical cytology
• Medical co-morbidities and use of medication
• Symptoms suggestive of endocrine disorders (e.g.,weight change, skin change)
• Genetically related illnesses
Family History • Birth defects
• History of age of menopause in female family members
• Occupational hazards
Social History
• Smoking, drinking, and drug use
Sexual History • Risks for sexually transmitted infections
• Extremes of body mass
• Skin changes, hirsutism
• Thyroid size
Physical exam • Secondary sexual characteristics
• For males: inspection of the penile shaft and urethra, palpation & ocular
inspection of the testicles
• For females: inspection of vagina & cervix & internal/bimanual examination
■
• Tubal ligation
Tubal Environmental • Radiation
• Pelvic adhesions
disorders • Heat
• Endometriosis
• Klinefelter syndrome
• Congenital malformation Genetics
• Immobile cilia syndrome
• Submucosal fibroids
Uterine • Uterine Polyps • Erectile dysfuction
Sexual
• Asherman's syndrome • Ejaculation failure
dysfunction
• Luteual phase defect • Retrograde ejaculation
• Cervical stenosis • Varicocele
Structural
Cervical • Cervicitis • Vasectomy
defects
• Unfavorable mucuous • Testicular torsion
443
APPROACH TO FEMALE FACTOR INFERTILITY
I. EVALUATIONOF FEMALEFACTORINFERTILITY
• Work-up should carefully exclude ovulatory dysfunction, pelvic factor, tubal facto,; and
uterine factors
A. Establishing Ovulation
Regular menstrual cycles, midcycle pain, and menstrual molimina are strong evidences
of ovulation that can be gathered based on careful history taking
0 Other methods of documenting ovulatory cycles include the following:
OVULATION
ASSESSMENT
I REMARKS
444
C. Evaluation of Cervical Factor
1. Billing Method
I PRE-OVULATORY I POST-OVULATORY
Dominant hormone • Estrogen • Progesterone
Ferning • Good • None
Spinnbarkeit • Thin, watery, copious • Thick, viscous, scanty
2. Post-Coital Test
• Done at time of ovulation to assess penetrability of the cervical mucus by sperms
• Taken 6 to 12 hours after coitus
• A good result would show 10 or more progressive motile sperm per high-power
field (HPF)
• No longer routinely done with the availability of in vitro fertilization (IVF) and
intrauterine insemination (JUI)
DIAGNOSTIC I REMARKS
• Visualizes significant pathology such as
° Fibroids
0 Adenomyosis
0 Endometriosis
Transvaginal 0 Uterine septum
Ultrasound 0 Polyps
0 Ovarian masses
• A baseline ultrasound is best done on Day 2-5 of menses,
when endometrium is thin in order to visualize endometrial
pathology
• Tubal patency determined by the opacification of tubal lumen
and spillage of transcervically introduced radio opaque dye into
the pelvic cavity; done under fluoroscopy or X-ray guidance
Hysterosalpingography • Scheduled during the week following the end of menses to
(HSG) avoid irradiating a possible pregnancy
• Contraindications:
0 History of salpingitis in the recent past
0 Tenderness on pelvic exam
• Similar to HSGbut done under ultrasound guidance
• Tubal patency determined indirectly by the accumulation
Sonohysterogram of fluid in the cul de sac when media is introduced into the
uterine cavity spills into the peritoneal cavity thru one or
both fallopian tubes
• Visual evaluation of the reproductive tract
• May be done by laparoscopy, hysteroscopy, and falloposcopy,
■
where available
Endoscopy
• May establish tubal patency by chromopertubation of
methylene blue intracervically and visualization of spillage
into the peritoneal cavity during laparoscopy.
445
II. MANAGEMENTOF FEMALEFACTORINFERTILITY
A. Timed Intercourse
0 This is the scheduling of coitus during days in the menstrual cycle when achieving
pregnancy is at its highest, usually on the day of ovulation and two days before & after
0 Use of LH kit, serum progesterone monitoring, or follicle monitoring to determine best
time for coitus
B. Management of Specific Cause
ETIOLOGY
I INTERVENTION
• Intrauterine adhesions (IUA): hysteroscopic lysis of adhesions
Uterine factor
• Leiomyoma: myomectomy
Ovulatory
• Ovulation induction (see table below)
dysfunction
• Tubal surgery may be appropriate for selected cases of distal tubal disease
but if pregnancy has not occurred within 12 months of tubal surgery, in
vitro fertilization (IVF) should be discussed
Tubal factor
• IVF should be considered as the first line treatment for moderate to severe
proximal or distal tubal disease
• TB ("pipe-stem" tube): anti-Koch's treatment
Pelvic factor • Endometriosis: fulguration of implants, cystectomy, !VF,IUI
• Controlled ovarian stimulation (COS)+ JUI or IVF
• COSshould be performed with either clomiphene citrate or human
menopausal gonadotropin (HMG)
Unexplained
• The following should proceed directly to IVF because of reduced efficacy of
Infertility
COS in such women:
• Women >36 years old after failed treatment
• Women >42 years old
446
APPROACH TO MALE FACTOR INFERTILITY
I. EVALUATION OF MALE FACTOR INFERTILITY
Normal Abnormal
results Semen analysis x2 results
Female evaluation
Normal Abnormal
Eliminate Hormone
gonadotoxins evaluation
No improvement With improvement
Oligospermia,
Lowvolume Azoospermia
asthenospermia
■
Sperm count • Number of sperm in ejaculate • >39 million
Sperm concentration • Number of sperm per volume • >15 X 10 6/mL
Total motility • Proportion of sperm that can swim • 2!40%
Progressive motility • Sperm swimming in one linear direction • ;,32%
447
B. Vasogram
0 Will evaluate ductal system in the absence of fructose in the ejaculate, as in:
• Seminal vesicle aplasia
• Vas deferens aplasia
C. Testicular Biopsy
0 Will distinguish obstructive azoospermia from the following non-obstructive causes:
• Sertoli only cells
• Peritubular fibrosis
• Germinal hypoplasia
INTRAUTERINE INSEMINATION
• Concentrated washed sperm preparation is deposited directly into the uterine cavity
around the time of ovulation
• Rationale: bypass cervical factor; remove seminal plasma; initiate sperm capacitation;
increase conception rates by increasing the density of motile sperm with a high
proportion of normal forms that will reach the site of fertilization
• Requires at least one healthy fallopian tube
Indications:
• Male factor infertility • Mild endometriosis
• Unexplained infertility • Cervical factor infertility
Indications:
• Tubal factor infertility
0 Bilateral hydrosalpinx or distal tubal obstruction and tubal reconstruction is not possible
0 If no pregnancy one year after tubal reconstruction
• Severe endometriosis
• Severe male factor infertility
0 Severe oligospermia (total motile count (TMC] < 1 million after semen preparation)
0 Azoospermia
, Ejaculatory disorders
• Ovarian Factor
0 Ovarian failure and diminished ovarian reserve
0 Ovulatory dysfunction (PCOS, chronic anovulation)
• Unexplained infertility in patients who have tried other treatments
• Fertility preservation
448
I. SPERM COLLECTION
• Ejaculation is the usual method for semen collection
• Microsurgical sperm collection: because of the limited number of sperms collected, these
procedures are reserved only for planned lntracytoplasmic Sperm Inseminations (ICSls)
in relation with doing In-Vitro Fertilizations and Embryo Transfers (IVF-ETs)
449
SECTION SIX
MENOPAUSE
OVERVIEW OF MENOPAUSE
• Cyclical ovulation continues for almost 40 years between menarche and menopause
• Genetically predetermined physiologic event
I. DEFINITIONOFTERMS
TERM I DEFINITION
• Permanent cessation of menstruation due to loss of ovarian
follicular activity
Menopause
• 12 months of amenorrhea after the LNMP with no attributable cause
• Body goes through changes that no longer allow her to get pregnant
• Years prior to menopause that encompass the change from normal
Perirnenopause
ovulatory cycles to cessation of menses.
(Menopausal
• Skipped periods, or longer intervals ( 40-60 days), is the hallmark of
Transition)
perimenopause
• Period of time when a woman passes from reproductive age to
non-reproductive age
Climacteric • Includes perimenopause, menopause and postmenopausal years
• Because cessation of menses is variable, and related symptoms may
occur prior, there is no precise timing to this event
II. EPIDEMIOLOGY
OF MENOPAUSE
PERIOD I TIMELINE*
Perimenopause
• Mean age: 45.1 (39 to 51 years old)
(Menopausal
• Mean duration: 5 years
Transition)
• Average age of menopause worldwide is 51 years old
Menopause • Mean age (Filipinos): 48 years old
• Age range: 44 to 56 years old
'Modernwomenare spendinga greaterportionof theirlivesaftermenopause(becauselifeexpectancyis
increasingoverthe years)
I
0
Menopause
uterus causes pelvic relaxation that causes uterine prolapse
, Decrease in the collagen content of the endopelvic fascia causes
cytocoele and rectocoele
0 Atrophic changes in the urinary tract lining and loss of ureteral tone
causes urinary urge incontinence & frequent urinary tract infections
• A complex interaction involving several factors that culminates in
decreased interest in sex among elderly women:
Sexual , Body changes
Dysfunction , Vasomotor symptoms
0 Effects of atrophy (e.g. painful sex from dryness)
0 Decreased libido secondary to decreased testosterone levels
451
• Osteoporosis: bone formation does not keep pace with bone resorption
Diagnosed by bone mineral density assessment by DEXA
0
° Financial insecurities
Emotional
Empty nest syndrome
0
Lability
Death in the family
0
Medical problems
0
MANAGEMENT OF MENOPAUSE
I. OVERVIEW OF MANAGEMENTOPTIONS
• Low dose estrogens +/- progestins
• Hormonal
• Tibolone
• Phytoestrogens
Alternative Therapy
• Traditional medicine
SYMPTOM I OPTIONS
• Estrogen is the best therapy for the hot flash
Vasomotor • Clonidine
flashes • Selective serotonin reuptake inhibitors (SSRI) (i.e., paroxetine)
• Others: vitamin-E, black cohosh, gabapentin
Vaginal • Lubricant
atrophy • Vaginal estrogen
• Calcium and vitamin-D supplementation
Osteoporosis
• Bisphosphonates, calcitonin, tamoxifen, raloxifene
(to improve
bone density)
• Weight bearing exercise
• Reduction in smoking, caffeine, and alcohol intake
Cardiovascular • Improvement of lifestyle and diet
risk • Optimal blood pressure control
452
III. HORMONEREPLACEMENTTHERAPY (HRT)
• Most effective means of treatment of menopause
, Not given to asymptomatic women interested exclusively for cardiovascular protection or
neurocognitive protection
• Prerequisites prior to H RT:
Do clinical history, PE and labs to identify indications & contraindications
0 Recommended work-up: pelvic ultrasound, Pap smear, lipid profile, mammogram, DEXA
Estradiol • EE 10 mcg tablet typically used daily for the first two weeks; then
I
Vaginal twice a week
Tablets • Not helpful with vasomotor symptoms
•• Topical estrogen replacement therapy (ERT) hardly reaches systemic levels. Does not
require concomitant progesterone administration. Use of topical preparations alone should
be primarily considered if hormonal treatment is solely for vulvovaginal symptoms
E2: estradiol
GEE:conjugatedequine estrogen
DRSP:drospirenone
EV:estradiolvalerate
EE: ethinylestradiol
MPA:medroxyprogestetroneacetate
NETA:norethisteroneacetate
MicroP:micronizedprogesterone
LNG:levonorgestrel
Source: InternationalMenopauseSociety,2016
PSCMCPG on Care for the MenopausalWoman,2017
453
B. Benefits ofHRT
0 HRT will address and minimize symptoms mostly linked to the vasomotor and
atrophic effects of menopause
• Proven benefit for: vasomotor symptoms, genitourinary syndrome of menopause,
bone health
• Cardiovascular benefits when given within 10 years of the onset of menopause, but
must not be given exclusively for the prevention of coronary heart disease
• Inconclusive benefit for dementia
0 The benefits of HRT may be maximized while minimizing its deleterious effects by
giving the hormones:
• At the lowest effective dose
• Early, when it is expected to be most helpful
• No longer than necessary
• Based on the symptom of concern
C. Contraindications to HRT
° Current, past, suspected breast cancer
° Known or suspected estrogen dependent malignant tumors (e.g., endometrial cancer)
0 Undiagnosed genital bleeding
0 Untreated endometrial hyperplasia
0 History of venous thromboembolism
0 History of arterial thromboembolism
0 Untreated hypertension
0 Active liver disease
0 Hypersensitivity to active substances or HRT excipients
0 Porphyria cutanea tarda
Source:PracticalRecommendations
for HRTfor the Peri-and Postmenopause,
2004.28
B. Lifestyle Modification
0 Efforts to modify the climacteric's lifestyle and environment may be resorted to when
medical options are contraindicated
General • Age-appropriate make-over and preference for cooler clothing
Modifications • Environmental modification
Diet • Avoiding alcohol, caffeine and spicy food
• Weight-bearing exercises
Activities
• Relaxation techniques
• Optimize foreplay
Sexual • Use water-based lubricants
Modifications • Engage in non-coital activities with partner
• Regular sexual activity to maintain vaginal health
454
~4 iiii·l~►i#ii~---
I_ - - FERTILITY PRESERVATIO_N___ ~---
MANAGEMENT OPTIONS
I. OVERVIEWOF MANAGEMENT
455
II. BRIEF DESCRIPTIONOF EACHMETHOD
METHOD I REMARKS
Sperm • Involves freezing and banking sperms collected through
cryopreservation ejaculation, epidydimal aspiration, or testicular sperm extraction
• Requires time for ovarian stimulation and harvesting of ova prior
to cancer treatment
Embryo
• Ideal for married patients
cryopreservation
• Harvested eggs are fertilized & frozen for transfer after cancer
treatment
• Requires time for ovarian stimulation and harvesting of ova prior
Oocyte to cancer treatment
cryopreservation • An option for female patients without partners because sperms
are not needed
Ovarian tissue • Ovaries cryopreserved or ovarian cortex frozen in thin slices
cryopreservation • Potential option for prepubertal girls; presently experimental
Testicular tissue • Freezing of testicular tissue for re-implantation after treatment
cryopreservation • Potential option for prepubertal boys; presently experimental
• For hysterectomized women in countries where surrogacy is
restricted or prohibited
Uterine • Has already resulted in livebirth with:
transplantation 0 Immunosuppressant therapy all throughout pregnancy
0 Assisted reproductive technology
° CS-hysterectomy after completion of family size
III. MULTIDISCIPLINARYAPPROACH
• Ideally, the decision about who is a candidate for fertility preservation should be
rendered by a team including the following: oncologist, ART specialist, pathologist,
psychologist, and bioethicist
• The oncologist plays a special role in:
Prognosticating the long-term survival of the patient
0 Informing patients about the risk that their cancer treatment will permanently impair
fertility
Referring to psychosocial providers
0 Referring interested patients to reproductive specialist
4S6
ASCORecommendations on Fertility Preservation in People Treated for Cancer
Source:ASCO,2018
REFERENCES
I.Albanese A, Stanhope R. Investigation of delayed puberty. Clin Endocrinol (Oxf) 1995;43:105-10.
2.American Society of Clinical Oncology Recommendations on Fertility Preservation in People Treated for Cancer (ASCO),
2006
3.Avis NE, Brambilla D, McKinlay SM et al. A longitudinal analysis of the association between Menopause and depression:
results from the Massachusetts women's health survey. Ann Epidemic!. 4:212-214; 1996.
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460
FAMILY
PLANNING
SECTION ONE
OVERVIEW OF FAMILY PLANNING
FAMILY PLANNING
• With the ever-increasing population, there is definitely a need for us to find ways of
sustaining its growth
• With the limited resources available to man, controlling the population growth may be
more feasible
• Contraception remains to be a viable option
• There are two major types: temporary and permanent planning methods
I. TEMPORARYPLANNINGMETHODS
METHOD DESCRIPTION
■
• Latex or polyurethane sheath that forms a physical barrier and keeps
Condom sperm out of the vagina
• For males and females
• Thin, dome-shaped membrane of latex rubber or silicone that creates
Diaphragm a mechanical barrier between the vagina and the cervix
• Should be used with spermicides
Spermicidal • Immobilizes or kills sperm on contact by destroying the sperm cell
foam or gel membrane
463
II. PERMANENTPLANNINGMETHODS
METHOD I DESCRIPTION
• Occlusion, transection, or removal of the fallopian tubes; prevents the egg
Female
from reaching the uterus and also keeps the sperm from reaching the egg
sterilization
• Includes bilateral tubal ligation (BTL), bilateral salpingectomy
Male
• Occlusion of the lumen of the vas deferens that prohibits sperm from
sterilization
(vasectomy) passing into the ejaculate
Intrauterine systems
T
(Levonorgestrel 0.1-0.4%
intrauterine system) • After the
procedure,
Intrauterine device little or
0.8%
(copper IUD) nothing
to do or
1 remember
HIGHLY
EFFECTIVE • For
Vasectomy 0.15% vasectomy,
use another
method for
the first 3
months
~
Injectable suspensions • Get repeat
(e.g., Depo-
Medroxyprogesterone
/(1) 4%
injections.
every 3
acetate (DMPA]) months
• Take a pill
~
Oral contraceptives
2 7% on time each
pills (OCP)
VERY day
EFFECTIVE • Replace
Contraceptive patch
0 7%
weeklyx 3
weeks per
month
• Keep ring in
Vaginal ring
\) 7%
place for 3
weeks per
month
464
Unintended I How to
TIER
I METHOD
IPregnancy
wothon 1"
year of use
Make your
Method Most
Effective?
Diaphragm
0 . .
17%
• Use correctly
every time
you have sex
3
Withdrawal method 22%
EFFECTIVE
Spermicides 21%
• Abstain or use
Fertility awareness-
23% condoms on
based methods
fertile days
■
Tier2: 4-7pregnancies
per100womenin thefirstyearof use
Tier3: >13pregnancies
per100womenin thefirstyearof use
Long-acting reversible
contraceptives (LARCS},likethe injectables,
implants,andthe intrauterine
devices,areless
user-dependent andarethereforemorereliableevenwithtypicaluse.Requiringlessconscious effort,compliance
is
easierfor the userthusfacilitatingproperusage
Sources:TrussellJ, et al. Contraceptive
technology;
2018
WHO.FamilyPlanning:
A GlobalHandbook for Providers;
2018
465
MEDICAL ELIGIBILITY
• Reversible contraceptives are designed for the protracted use of preventing pregnancies
• The risk:benefit ratio for contraceptives must be individually ascertained, especially for
women with medical co-morbidities
• The World Health Organization (WHO) through its Medical Eligibility Criteria (MEC)
provides recommendations for safe prescription of contraception for all medical
conditions a potential user might possibly have
• Based on the latest clinical and epidemiological data, depending on the medical condition,
the WHO MECcategorizes each type of medical contraceptive as follows:
Where resources for clinical judgment are available, the medical contraceptive may be
categorized WHO MEC 1 to 4. For example, for ischemic heart disease:
ISCHEMIC HEART DISEASE
Where resources for clinical judgment are limited, such as in community-based services,
the four-category classification framework can be simplified into two categories ("Yes"
if WHO MEC 1 or 2 and "No" if WHO MEC3 or 4). For example, for ischemic heart disease:
ISCHEMIC HEART DISEASE
NATURAL(FERTILITYAWARENESS-BASED) METHODS
• The use of natural means of avoiding pregnancy may be safe, but are the least reliable of
the options
• Involves identifying the fertile days of the menstrual cycle using a combination of cycle
length and manifestations of ovulation (e.g., change in cervical secretion) and then
avoiding sexual intercourse on those days
8. Relative Contraindications
o Irregular cycles
o Inability to track physiologic changes
o Lack of supportive partner
Ill. METHODS
• Sexual abstinence
• Coitus interruptus
• Fertility awareness methods
SEXUALABSTINENCE
• Avoidance of vaginal intercourse
• Simple and 100% effective with perfect use
• Easier said than done
• Needs strong discipline and an even stronger will power and determination
-=-C-=-0..:....:IT'--=U;..;:S:....:l:...:.NT..:...;E=-:Rc...:.:Rc...:.cU::..:P-'T:....:U:....:S:....._
_______________ _
• "Withdrawal method" or the practice of withdrawing the penis from the vaginal canal
before ejaculation
• 74% effective at best
• Many males do not know when or may not have the will power to pull out in time
• Small amount of pre-ejaculate on erect penis for lubrication can still expose to infections
or a possible pregnancy
467
FERTILITY AWARENESS-BASED METHODS
• A technique of identifying fertile and infertile phases in a woman's menstrual cycle by
observing signs and symptoms
• Least effective even with perfect use
• Complex and tedious
• Needs strong motivation
Needs cooperation of the partner
• Ovulation may occur irregularly
I. CERVICALMUCUSMETHOD (BILLINGMETHOD)
• Based on the observation of changes in the cervical mucus and sensation of wetness and
dryness in relation with day of the menstrual cycle
• Near ovulation, mucus production increases and it becomes thinner in consistency
• Fertile period begins when watery mucus is noted and sensation of wetness is felt after
menses and ends 3 days after the last day of slippery mucus
• Refrain from vaginal intercourse once presence of clear, wet, and slippery mucus
secretion is observed until the 4th day after her peak day of wetness
Billing Method: insert finger into vagina and get some mucus & stretch it using the thumb
and middle/index finger. The following may be observed:
• For thin mucus (predominantly estrogen), • For thick & viscid mucus (predominantly
do not have sexual contact during this time progestin), may have unprotected sexual
(woman is fertile) contact
1:::=-•·.··~···~
----- UNSAFEPERIOD ------ SAFEPERIOD--
Ovulation occurs
III. TWODAYMETHOD®
• Helps women determine whether they are fertile at any given day
• Based on the presence or absence of cervical secretions
• If a woman notices secretions, the couple should refrain from vaginal intercourse on that
day and the day after
468
I~SYMPTOTHERMALMETHOD
• Combination of cervical mucus and BBT methods and observation of certain symptoms
• Changes in cervical mucus ( onset of fertile period]
• Changes in BBT (end of fertile period)
• Refrain from vaginal intercourse when the woman senses cervical secretions, until both
the 4 th day after peak cervical secretions and the 3rd full day after the rise in BBT
• lfthere is disparity in the application of rules of both methods, the more conservative
rule will be followed
V. CALENDARRHYTHM METHOD
• Requires recording of the length of 6 previous menstrual cycles
Formula:
• Shortest cycle minus 18 is the first day of fertile period
• Longest cycle minus 11 is the last day of fertile period
• Do not have sexual contact during the computed fertile period
Example: A patient's shortest cycle is 28 days and her longest cycle is 32 days
• 28 - 18 = 10; Day 10 is the first day of fertile period
• 32 - 11 = 21; Day 21 is the last day offertile period
• Therefore, avoid unprotected coitus from Days 10 to 21
469
SECTION THREE
HORMONAL CONTRACEPTION
OVERVIEW OF HORMONAL CONTRACEPTION
• Use is independent of sexual intercourse (does not interfere)
• Can be carried out without partner's knowledge
• The choice between combined oral contraceptives (COCs) and progestin-only
contraceptives is the biggest issue that needs to be hurdled
'"Increase in cervicalcancer riskis associated withthe change of the susceptibilityof cervicalcells to persistent
infectionwithhigh-riskHPVtypes
Hormone Components
HORMONE I REMARKS
• Most combined oral contraceptives (COC) contain ethinyl estradiol as
estrogen component with an average dose of20-35 mcg (i.e., low dose)
Estrogen • Creates a negative feedback mechanism to prevent follicular
development, which is necessary for ovulation
• P,·events follicle maturation by suppressing FSH release
Extended cycle • Active pills are taken for 12 weeks followed by a one-week pill-free
preparations period for withdrawal bleeding ( e.g. 30 mcg EE+ 0.15 mg LNG)
Continuous COC • Active pills taken for 365 days a year (e.g. 20 mcg EE + 0.09 mg LNG)
EE:ethinylestradiol EV:estradiolvalerate
LNG:levonorgestrel DNG:dienogest
2 pills missed in a row • Take the last missed pill and the pill due for the day,
or new pack started 2 then continue taking the rest as scheduled.
days late • No back-up required
• Take the last missed pill and the pill due for the day,
3 pills missed in a then continue taking the rest as scheduled.
row in the 1st and
• Use back up for the next 7 days
2nd week or new pack
• If with intercourse in the past 5 day, may use
started 3 days late
emergency contraception
• Discard current pack and start new pack right away
3 pills missed in a row • Use back-up method for the next 7 days
in the 3rd week •ff with intercourse in the past 5 days, may use
emergency contraception
I
471
B. Safety
o COCsdo not disrupt an existing pregnancy
o COCs do not cause birth defects and will not harm the fetus even if the woman
becomes pregnant while taking the pills or accidentally starts the pill when she is
already pregnant
ABSOLUTE CONTRAINDICATIONS I RELATIVE CONTRAINDICATIONS
• History of vascular disease • Smokers (<35 years old)
• Systemic diseases affecting vascular • Migraines
system • Undiagnosed cause of amenorrhea
• Smokers >10 cigarette sticks per day • Depression
• Uncontrolled hypertension • Prolactin-secreting macroadenomas
• Existing breast and endometrial cancer
• Undiagnosed uterine bleeding
• Elevated triglycerides
• Pregnancy
• Functional heart disease
• Active liver disease
CONTRACEPTIVE CONTRACEPTIVE
I TRANSDERMAL PATCH
I VAGINAL RING
• Sustained-release delivery system in
the form of a flexible plastic ring
• Medicated adhesive • Produces a consistent concentration
Description patches containing EE and of the circulating contraceptive
norelgestromin hormones that prevent the daily
fluctuations associated with the use
of COCs
• 20 mcg EEand 150-mcg • 15 mcg EE and 120 mcg etonogestrel
Dose
norelgestromin per 24 hours per 24 hours
• One patch weekly for 3 weeks • One ring every 3 weeks
Administration
• Followedby patch-free week • Followed by ring-free week
Availability • Not available locally • Not available locally
472
PROGESTIN-ONLY CONTRACEPTIVES
• Contain only the hormone progestin
• Examples include progestin-only pills (POP), injectables, subdermal implants, and
LNG-IUS(discussed under IUD)
• Mechanisms of action:
o Thickening of cervical mucus and retardation of sperm passage
o Suppresses LH, blunting the LH surge
o Since there is no estrogen, there is no suppression FSH
B. Administration
o Should be taken at the same time every day ( or at least within 3 hours of usual
schedule) with no break between packs of pills; If taken 4 hours late, use of back-up
method ( e.g., condom, abstinence) for the next 48 hours
ADVANTAGES I DISADVANTAGES
• Can be given to breastfeeding mothers as it • May induce changes in menstrual
does not interfere with milk production bleeding and prolongs/causes heavy
• No estrogen side effects (nausea) menstrual bleeding in some
• Promotes compliance in pill taking (i.e.,women • Need to be taken at the same time every
take one pill every day with no break) day to be an effective contraceptive
• May help prevent benign breast disease, as thickening of cervical mucus from
endometrial/ovarian cancer, and pelvic progesterone effect only lasts ~24 hours
inflammatory disease from last intake
• May benefit patients with endometriosis • Headache, breast tenderness
as progestin-only pills have been shown to
suppress endometriotic lesions
DOH.The PhilippineClinicalStandardsManualon FamilyPlanning;2017
B. Administration
o Initial injection should be given within the first 5 days of menses
o If certain not to be pregnant, the patient can be injected the initial dose at any time
during the menstrual cycle but a backup contraceptive method is required for 7 days if
given after the 7th day of menses.
o Return of fertility after 6 months to 1 year from last dose of DMPA
473
C. Side Effects
o Irregular bleeding patterns ("breakthrough bleeding")
o Weight changes
o Headaches
o Mood changes
o Bone Loss
A. Dose
o The initial serum concentration of etonogestrel (ENG) is about 800 pg/mL, decreasing
to 150 pg/mL by the end of the third year of use
o The required level to inhibit ovulation is ~90 pg/mL and implant is meant for only 3
years of use
B. Administration
o Ideally inserted within 5 days of menses
o If certain not to be pregnant, the implant may be placed at any time during the
menstrual cycle but a backup contraceptive method is required for 7 days if given after
the 7th day of menses.
Source:ErkkolaR,et al.ActaObstetricia;
2005
474
SECTION FOUR
INTRAUTERINE DEVICES
OVERVIEW OF INTRAUTERINE DEVICES (IUD)
An IUD is a small plastic device inserted into a woman's uterine cavity to prevent pregnancy
• Contains copper or releases a hormone ( e.g., levonorgestrel)
• Induces a local inflammatory reaction of the endometrium, creating an environment that
is hostile to sperm so that fertilization of the ovum does not occur
TYPES OF IUD
TYPE
I MECHANISM
I REMARKS
• Intense local endometrial
• Labeled for use up to 10 years but
inflammatory response
has been proven to be effective up to
• Cellular and humoral components
12 years.
of this inflammation are
• Adverse effects: heavy menstrual
Copper IUD expressed in endometrial tissue
bleeding, may be treated with
and in fluid fillingthe uterine
antifibrinolytic agents and
cavity and fallopian tubes leading
nonsteroidal anti-inflammatory
to decreased sperm and egg
drugs.
viability
• Releases LNGdirectly into the
uterine cavity at an initial rate of
20 mcg per day followed by slow,
• Local inflammatory reaction
sustained systemic release for
Levonorgestrel- • Progestin component (thickens
5 years
containing cervical mucus, impeding sperm
• It affords hassle-free, long term
intrauterine penetration and access to the
effects similar to implants, but with
system upper genital tract)
ease of discontinuation when so
(LNG·IUS) • Blunts LH surge, prevents
decided
ovulation
• Non-contraceptive benefits: reduces
heavy menstruation, dysmenorrhea,
and endometriosis
■
II. TIMING OF INSERTION
• The IUD can be safely inserted in any of the following scenarios:
o On any day of the cycle provided the woman is not pregnant
o During menstruation
o Immediately post-abortion
o Immediately postpartum (vaginal or Cesarean section delivery)
• Immediate postpartum insertion carries a higher risk of IUD expulsion, particularly in the
case of an LNG-IUS following vaginal delivery
, Postpartum IUD insertion is usually not done >48 hours to 4 weeks post-partum because of the
higher risk of IUDexpulsion compared to immediate post-partum and interval IUD insertion
475
III. COMPLICATIONS OF IUD
COMPLICATION
I DESCRIPTION
I MANAGEMENT
IV. CONTRAINDICATIONS
• Pregnancy or suspicion of pregnancy
• Genital bleeding of unknown origin
• Known or suspected uterine or cervical malignancy
• Postpartum endometritis or infected abortion
• Acute PIO
• Testing for gonorrhea and chlamydia should be performed and IUD insertion delayed if
there is a clinical suspicion of infectious endocervicitis, or the patient has two out of three
of the following:
o Purulent vaginal discharge
o Adnexal tenderness
o Cervical motion tenderness
476
SECTION FIVE
BARRIER METHODS
DESCRIPTION
I ADVANTAGES
I DISADVANTAGES
■
on contact by destroying • May be inserted 1 hour spontaneity of sexual
the sperm cell membrane) before intercourse intercourse if not inserted
• Spermicides need to be • No systemic effects before hand
placed into the vagina • User controlled • May produce vaginal or
before each coital act • Easily initiated and penile irritation
discontinued
• Good for infrequent
contact
477
SECTION SIX
STERILIZATION
FEMALE STERILIZATION
• Being permanent in nature, this is only recommended for women who have completed
their desired family size or have serious contraindications to having another
pregnancy
• Patient must first be a good surgical risk without predisposition to bleeding, infection,
and anesthetic complications
• Accomplished by occlusion, transection, or removal of the fallopian tubes
ADVANTAGES I DISADVANTAGES
• Highly effective (0.5 pregnancies • Must be considered permanent (success of
per 100 women during first year reversal cannot be guaranteed)
of use) • Patient may regret later (highest before age 30)
• Effective immediately • Risk of surgical complications such as bleeding
• Worry-free and infection
• Does not interfere with intercourse • Short-term discomfort and pain following
• Good for patient if pregnancy procedure
would pose a serious health risk • Requires trained physician (gynecologist or
• No long-term side effects surgeon for laparoscopy)
• No change in sexual function (no effect • Increased risk of ectopic pregnancy
on hormone production by ovaries)
478
2. Other Methods
PARKLAND METHOD I IRVING METHOD
• A 2-cm segment of the mid-portion • After excision of a mid-segment of each
of each tube is ligated proximally and fallopian tube, the proximal part is tied to
distally with delayed absorbable sutures the backside of the uterus and the distal
• Segment between the sutures is excised part is buried in the mesosalpinx
• Due to the enlarged uterus and the • With the non-pregnant uterus barely
consequently higher location of beyond the pelvis, the approach to the
the fallopian tubes, the transverse fallopian tubes is made through a transverse
minilaparotomy incision is made just minilaparotomy incision just above the
below the lower border of the umbilicus upper border of the symphysis pubis
V
II. STERILIZATIONVIA LAPAROSCOPY
• Tubal occlusion done by using Hulka Clips or Falope Rings applied to the tubes using
specialized laparoscopic operative instruments
• Bipolar cautery and transection of the fallopian tube may also be employed
III. BILATERALSALPINGECTOMY
• In selected cases, bilateral salpingectomy may be done for surgical sterilization and at the
same time prophylaxis against some types of ovarian carcinoma
• May be performed via laparoscopy or in relation with a laparotomy for another procedure
• Couples must be advised that this procedure as a means of sterilization is permanent
with no prospects of reversal
I.PROCEDURE
• Vas deferens of each side is blocked (tying and cutting) to prevent sperms admixing with
ejaculated semen
• lncisional vasectomy: both vas deferens are identified individually through a scrotal
incision, ligated, and transected
• No scalpel vasectomy: same as traditional vasectomy, but reaches the vas through a
puncture on the scrotum instead of through an incision
• Complete expulsion of sperms stored in the reproductive tract beyond the interrupted vas
deferens takes:
o 3 months (one cycle ofspermatogenesis)
o 20 ejaculations (to empty vas deferens distal to the vasectomy)
o Needs semen analysis to confirm azoospermia
• The vas deferens can be accessed • Each vas is individually pulled through the
either through a mid line incision or incision until it forms a loop
puncture made into the skin of the • Two non-absorbable ligatures are placed
scrotum 1 cm apart
• Segment between the two ligatures is then
excised
Source:OblepiasVR,et al. Contraceptionby Surgery;1977
Adaptedfrom the illustrationby Dr.AugustoM. Manalo
480
SECTION SEVEN
EMERGENCY CONTRAGEPTION
Source:TrussellJ. Emergency
contraception:
WHOTaskForceStudy;1998
K.Contraception;
Sources:Gemzel-Danielsson 2010
FinePM.AdvTher;2011
Ill. MANNEROF INTAKE
A. Oral hormonal contraceptives
o May be taken up to 5 days after unprotected vaginal intercourse, but is most effective if
taken as soon as possible within 72 hours of coitus
o For two-dose regimens, the second dose must be taken 12 hours after
o Vomiting is common with oral EC use:
• Vomiting within 2 hours of intake: repeat dose
• Vomiting after 2 hours: no need to repeat dose
• If with continuous vomiting, anti emetics may be taken
• Cannot tolerate oral doses: pills can be inserted vaginally into the posterior fornix
• For two-dose regimen, if the woman experiences nausea and/or vomits with the first
dose, she can take anti-emetics 30-60 minutes prior to intake of the second dose
o The woman should refrain from unprotected coitus after EC until onset of menses
o Advise follow-up and pregnancy test if next expected menstruation is 7 days late
o Start or re-start contraception after emergency contraception use:
• immediately (no need to wait for next menstruation)
• anytime if it is reasonably certain she is not pregnant
• while abstaining from unprotected sex or using a back-up method (e.g., condom, etc.)
for the first 7 days on the chosen contraceptive method
B. IUD
o May be inserted up to 5 days after unprotected vaginal intercourse, but is most ■
effective if inserted as soon as possible within 72 hours of coitus
o Appropriate for patients who would like to start using a highly effective, long-acting, ·:
and reversible contraceptive method
o Effectivity: >99%
Source:WHOContraecptiveFactSheet,2018
481
PILL TYPE AND HORMONE
Dedicated ECPPr(),ducts
I
FORMULATION
- -
~ -- " -- ,-
1.5 mg LNG* 1 0
Progestin-only
0,75 mg LNG* 2 0
Ulipristal acetate 30 mg 1 0
Qra! co"ntrat;eptiv":Pills Usedfor,,_Em(!.r-oency
Contraception
0,02 mg EE+ 0,1 mg LNG 5 5
0,03 mg EE+ 0.15 mg LNG 4 4
Combined (estrogen- 0.03 mg EE+ 0.125 mg LNG 4 4
progestin) oral
contraceptives 0.05 mg EE+ 0.25 mg LNG 2 2
0.03 mg EE+ 0.5 mg norgestrel 4 4
0.05 mg EE+ 0.5 mg norgestrel 4 4
Forinformation
onbrandsof ECPSandoralcontraceptivepills,see:TheEmergency Contraception
Website(http:/
ec.princeton.edu)
andthe International
Consortium
for Emergency Contraception
(http:/www.cecinfo.org).
REFERENCES
1.Bonnar J. Coagulation effects of oral contraception. Am J Obstet Gynecol.1987;157(4 Pt 2):1042-1048. doi:10.1016/s0002-
9378[87]80129-1
2.Department of Health. The Philippine Clinical Standards Manual on Family Planning (2014 Edition), Manila, Philippines:
DOH,2014. 437 pages
3.Erkkola R, LandgrenBM. Roleofprogestins in contraception.Acta Obstetriciaet GynecologicalScandinavica,2005.Available
on line: https:/ /obgyn,onlinelibrary.wiley.com/ doi/full/10.1111/j,0001-6349,2005.00759.x
4,Fine PM. Updates on emergency contraception, Adv Ther 2011;28(2):87-90)
S.Gemzel-Danielsson K Mechanism of action of emergency contraception. Contraception 2010;82:404-409
6.Jennings V. Fertility awareness-based methods of pregnancy prevention. Uptodate. Available online https://www.uptodate.
com/contents/fertility-awareness-based-methods-of-pregnancy-prevention.Accessed on June24, 2021
7.0blepias YR, et al. Contraception by Surgery, 1977
a.PhilippineObstetricaland GynecologicalSociety in collaborationwith the PhilippineSociety for FamilyPlanning (2nd ed.),
ClinicalPracticeGuidelineson FamilyPlanning;2017
9.PhilippineSocietyof ReproductiveEndocrinologyand Infertility,Inc.QuickReferenceManualon ReproductiveEndocrinology
and Infertility: 1st ed,, Oiliman, Quezon City:, 2012
10. SuvisaariJ,Lahteenm3kiP.Detailedanalysisof menstrualbleeding patternsafterpostmenstrualand postabortalinsertionof
a copper IUD or a levonorgestrel-releasing intrauterine system. Contraception. 1996;54( 4):201
11. Sumpaico, et al (eds), Philippine Textbook of Obstetrics, 3rd ed., Quezon City: Association of Writers of the Textbooks of
Obstetrics & Gynecology, Inc., 2008.)
12. Trussell J. Emergency contraception: WHO Task Force Study. Lancet 1998;352(9135);1222-3
13. TrussellJ,AikenARA,MicksE,GuthrieKA.Efficacy;safety,and personal considerations.In:HatcherRA,Nelson AL,Trussell
J,Cwiak C, Cason P, Policar MS, Edelman A, Aiken ARA, Marrazzo J, Kowal D, eds. Contraceptive technology. 21st ed. New
York, NY:Ayer Company Publishers, Inc., 2018. Available online:https://www.cdc.gov/mmwr /pdf/rr /rr62e0614.pdf
14. World Health Organization Department of Reproductive Health and Research (WHO/RHR) and Johns Hopkins Bloomberg
School of Public Health/Center for Communication Programs (CCPJ, Knowledge for Health Project Family Planning: A
Global Handbook for Providers (2018 update), Baltimore and Geneva: CCP and WHO, 2018
15, World Health Organization. Medical eligibility for contraceptive use, 5th ed. WHO, 2015
16, Wilcox A, et al. Post-ovulatory aging of the human oocyte and embryo failure. Hum Reprod 1998; 12:394.
482
GYNECOLOGIC
ONCOLOGY
SECTION ONE
INTRAEPITHELIAL NEOPLASIA OF THE LOWER GENITAL TRACT
ETIOPATHOGENESIS
I. PERSISTENT HIGH RISK HUMAN PAPILLOMAVIRUS
• All cases of cervical cancer are caused by persistent infection with high-risk types of
human papilloma virus (HPV)
• Double-stranded DNA virus that replicates within epithelial cells
• HPV is the most common sexually transmitted disease (STD):
0 Develop significant preinvasive disease in 3-5% of women
0 Develop invasive cancer in <l % of women
• More than 120 types with ~40 types known to infect genital tracts of men and women
• Approximately 12 types are considered high-risk, with types 16 & 18 being responsible
for 70% of cervical cancers
Condylomata acuminata 6, 11
High-grade squamous intraepithelial neoplasia & 16,18
invasive carcinomas of the anogenital tract
Bowenoid papulosis, erythroplasia ofQueyrat 16
Buschke-Lowenstein tumor 6, 11
Laryngeal papillomatosis 6, 11
Heck disease 13, 32
'Otherthancervicalcancer,HPVcanalsocausecancersin theoropharynx,
anus,penis,vulva,vagina
II. PATHOGENESIS
• High-risk HPV causes neoplastic cellular changes when viral DNA becomes integrated
into the host cell genome leading to loss of repressor areas of the viral genome
• Allows expression of the viral E6 and E7 genes leading to the production of oncoproteins
resulting to inactivation of the p53 and retinoblastoma tumor suppressors ➔ cell
immortalization and rapid cell proliferation (Le. loss of apoptosis or programmed cell death)
• Majority of cases associated with infection of one or more types of HPV
• Cervical cancer develops in 15 to 20 years in women with normal immune systems vs 5 to
10 years in women with weakened immune systems (Le untreated HIV infection) ■
485
LSIL HSJL
,~ ____ c_1N_1
___ ~I J CIN 2 I LI ____ c_,N_3
___ ~
III. RISKFACTORS
• Compromised immune system (genetic, iatrogenic, infectious)
• Increased risk for acquiring HPV infection:
Early age of first sexual intercourse (<14 years old)
0 Early age at first full term pregnancy ( <17 years old)
Lifetime number of sexual partners (<!2partners)
History of and/or co-infection with other sexually transmitted infections (e.g., herpes
simplex, chlamydia and gonorrhea)
Long-term use of oral contraceptive pill (OCP) (>5 years)
History ofvulvar or vaginal dysplasia
Smoking (Squamous Cell CA,not Adena CA)
0 Uncircumcised male partner
486
PREVENTION OF INTRAEPITHELIAL NEOPLASIA
• Cervical cancer is a preventable disease, with excellent tools for prevention (i.e.,
vaccination) and screening (i.e., Pap and human papillomavirus testing)
I. PRIMARY PREVENTION
A. Education and Counseling
• Sexual abstinence
• Lifetime monogamous sexual relationship
• Delay in onset of sexual intercourse
• Use of barrier contraceptive methods (e.g., condom)
B. HPV Vaccination
• Bivalent vaccine or Cervarix® (targets HPV types 16,18)
• Quadrivalent vaccine or Gardasil® (targets HPV types 6,11,16,18)
• Nonavalent vaccine or Gardasil-9® (targets HPVtypes 6, 11, 16, 18, 31, 33, 45, 52, and 58)
HPV6/11/16/18/
HPVTypes HPV 16/18 HPV 6/11/16/18
31/33/45/52/58
Sex&Age
Indication Female I :e15y/o
Female
Male
I 14-45 y/o
I 14-26 y/o
Female
Male
I
I
"15 y/o
Sex&Age
Female 19-14 y/o
Female I 9-14 y/o Female I 9-14y/o
Indication Male I Male I
Dosage 0, 5-13 months 0, 6 or 0,12 months 0, 5-13 months
MODALITY I REMARKS
• Most widely used screening test
• Has low sensitivity, but widespread testing has reduced
Cervical cytology
incidence of cervical cancer by 50- 70%
testing
• Performed by placing a speculum into the vagina and scraping
(Pap smear)
cervical cells using a spatula and endocervical brush
• Cells are sampled from the transformation zone
• May be more sensitive than Pap smear, but co-testing with HPV is
PrimaryHPV also recommended
testing • Preferred screening method in countries where Pap smear is not
feasible and HPV testing is available
Gynecology17thEd; 2017
LoboRA.Comprehensive
I
487
B. Guidelines for Cervical Cancer Screening
WHO 2021 Guidelines for Screening and Treatment of Cervical Pre-Cancer Lesions for
Cervical Cancer Prevention
<30years
old, general • No screening
population
• HPV DNA detection in a screen-and-treat approach starting at the age of
30 with regular screening every 5 to 10 years
• HPV DNA detection in a screen, triage, and treat approach starting at the
30-50years
age of 30 yeas with regular screening every 5 to 10 years
old
• Where HPV DNA testing is not yet operational, WHO suggests a regular
screening interval every 3 years when using vaginal inspection with
acetic acid (VIA} or cytology as the primary screening test
• WHO suggest screening is stopped after two consecutive negative
After 50
screening results consistent with the recommended regular screening
years old
intervals among both the general population and women living with HIV
• HPV DNA detection in a screen, triage, and treat approach starting at the
age of 25 years with regular screening every 3 to 5 years
Women
• Where HPV DNA testing is not yet operational, WHO suggests a regular
with HIV
screening interval every 3 years when using VIA or cytology as the
primary screening test
488
CERVICAL CYTOLOGY REPORTING: THE 2014 BETHESDA SYSTEM
• First part states whether the sample is satisfactory or unsatisfactory
• Next part indicates whether cellular material is normal
• Abnormalities are divided into squamous and glandular
• Other comments may also include evidence of infection (e.g., yeast, bacterial vaginosis)
SPECIMEN ADEQUACY
- Satisfactory for evaluation (describe presence or absence of endocervica/lrransformation
zone component and any other quality indicators, e.g., partially obscuring blood,
inflammation, etc.)
D Unsatisfactory for evaluation ... (specif.i•reason)
J Specimen rejected/not processed (speciji• reason)
J Specimen processed and examined, but unsatisfactory for evaluation of epithelial
abnormality because of (specify reason)
INTERPRETATION/RESULT
NEGATIVE FOR INTRAEPITHELIAL LESION OR MALIGNANCY
(When there is no cellular evidence of neoplasia, state this i11the General Categorizatio11 above
and/or in the lnrerpretation!Result section of the report - whether or not there are organisms or
other 11011-neoplasticfi11di11gs)
Orga11isms
□ Trichomonas vagina/is
7 Fungal organisms morphologically consistent with Ca11didaspp.
'.J Shift in flora suggestive of bacterial vagjnosis
J Bacteria morphologically consistent with Actinomyces spp.
□ Cellular changes consistent with herpes simplex virus
■
D Cellular changes consistent with cytomegalovirus
OTHER
J Endometrial cells (in a woman ;,45 years old)
(Specify if '11egativefor squamous i11traepithelial lesion)
489
Page 2 of2
EPITHELIAL CEU ABNORMAL/TIES
Squamous Cell
□ Atypical squamous cells
0 Of undetermined significance (ASC-US)
D Cannot exclude HSIL (ASC-H)
□ Low-grade squamous intraepithelial lesion (LSIL)
(encompassing HPV!mild dysplasia/C!N I)
□ High-grade squamous intraepithelial lesion (HSIL)
(encompassing moderare and severe dysp/asia, CIS; CIN 2 and CIN 3)
□ With features suspicious for invasion (if invasion is suspected)
□ Squamous cell carcinoma
Glandular Cell
□ Atypical glandular cells
0 Endocervical cells (NOS or specify in commenls)
□ Endometrial cells (NOS or specify in commenrs)
□ Glandular cells (NOS or specify in comments)
□ Atypical glandular cells
□ Endocervical cells, favor neoplastic
□ Glandular cells, favor neoplastic
□ Endocervical adenocarcinoma in situ
0 Adenocarcinoma
0 Endocervical
0 Endometrial
0 Extrauterine
0 Not otherwise specified (NOS)
ADJUNCTIVE TESTING
Provide a brief descriprion of rhe res/ method(s) and report rhe result so thar ii is easily
understood by the clinician.
490
II. DESCRIPTIONAND MANAGEMENTOF SPECIFICABNORMALITIES
PAP SMEAR
OR CYTOLOGY
FINDINGS
I REMARKS
I MANAGEMENT*
HPV 16 or 18 positive
0
postpartum
• Atypical squamous
cells, cannot exclude • Refer for colposcopy** regardless of HPV
a higher-grade lesion status
(ASC-H)
• Indicates more
High-grade • Immediate Loop Electrosurgical Excision
severe dysplasia or
squamous Procedure (LEEP), except if patient is
CIN 2/3
intraepithelial pregnant or age 21-24, OR
lesion (HSIL) • 20% may progress
• Refer for colposcopy**
to cervical cancer
Glandular,Cell Abnormalities
• Plus any subcategories: atypical
endocervical cells or atypical glandular cells
(except atypical endometrial cells):
Refer for colposcopy** and endometrial
0
• May be classified
Atypical sampling (if>35 y/o or <35 y/o and at
by the site of origin
glandular cells risk for endometrial neoplasia: obesity,
(e.g., endometrium,
(AGC) abnormal uterine bleeding, or conditions
endocervix, ovary)
suggesting chronic anovulation.)
• Plus atypical endometrial cells:
Endometrial and endocervical biopsy
0
■
"Colposcopyis oftenthefirststepin evaluation
of womenwithabnormalcytology.Colposcope (lightedmagnified
instrument)
is usedto examinethecervix,placedjust outsidethevaginaaftera speculumis inserted.Thisis
performed
by a certifiedOB-GYNColposcopist.
Source:AmericanSocietyof Colposcopy
andCervicalPathology
(ASCCP);2012;2019
LoboRA.ComprehensiveGynecology
17thEd;2017
491
III. LOW-GRADESQUAMOUSINTRAEPITHELIAL LESION(LSIL}CYTOLOGY
• Management varies based on previous and current HPV status, previous cytology result,
and previous biopsy result
HPVRESULT
(Current)
~ RECOMMENDATION
Unknown -
Negative
Follow-up after 1
Negative ASCUS
year
Negative Negative LSIL
Positive NILM
Follow-up after 1
- - CIN 2 or 3 year, if previously
treated
Unknown Refer for colposcopy
Negative - - Follow-up after 1
Negative ASCUS - year
Positive Negative LSIL
Refer for colposcopy
Positive NILM
Refer for colposcopy,
- - CIN 2 or 3
if previously treated
AdaptedfromASCCP2019
492
CERVICAL INTRAEPITHELIAL NEOPLASIA (CIN)
• CIN is the precancerous lesion of the squamous epithelium of the cervix
• It is a histologic (versus cytologic) diagnosis, based on tissue examination of a cervical
biopsy specimen
• Graded 1, 2, or 3 (depending on how much of the epithelial layer contains atypical cells)
■
With inadequate colposcopy, recurrent CIN2,3 or ECCis CIN2, 3
• CIN2: Observation for up to 12
months using both colposcopy
• Diagnostic excisional procedure
and cytology at 6 month intervals
• CIN3: Ablation or Excision
Source:AmericanSocietyforColposcopyand CervicalPathology;2013
493
CERVICAL ADENOCARCINOMA IN SITU
• Adenocarcinoma in situ (A!S) is a premalignant precursor to cervical adenocarcinoma
• The glandular architecture of the endocervical glands are preserved in A!S, but the glands
are lined by atypical columnar epithelial cells
I. ABLATIVEAND EXCISIONAL
PROCEDURES
II. FOLLOW-UP
• Rate of recurrent or persistent disease following excisional or ablative treatment for C!N
2/3 is 5-17%, with no significant differences in outcomes between the different treatments
• Co-testing with cervical cytology and HPVat 12 and 24 months:
If both co-tests are negative, the woman can return to routine screening
0
494
VULVAR ATYPIA
ETIOPAlHOGENESIS I MANIFESTATIONS I DIAGNOSIS I MANAGEMENT
Liche11.Sclerosus
• 5%-15% ofpostmenopausal • Pruritus • Biopsy • High potency
women • Diffuse whitish topical steroids:
• Cumulative incidence of skin 0.05% Clobetasol
squamous cell carcinoma of the • Skin appears thin proprianote
vulva~ 6.7% • May have ointment
• Latency period between scarring, • Topical calcineurin
diagnosis and subsequent vulvar contracture, inhibitors (TCls)
cancer~ 3 years fissuring and/or • Testosterone cream
• Standard incidence ratio of excoriation • Progesterone cream
developing vulvar cancer= 33.6
• Epithelium markedly becomes
thinned with loss or blunting
of the rete ridges; thickening or
hyperkeratosis of surface layers;
inflammation present
Squamous Cell Hyperplasia (formerly called hyperpla~tic dystrophy without atypici)
• Hyperplasic dystrophy • Chronic pruritus • Biopsy • Medium potency
• Elongation & widening of rete • Whitish lesions topical steroids:
ridges, which may be confluent • Thickened skin Triamcinolone
• Focal or acetonide or
multifocal rather Fluocinolone
than diffuse acetonide
■
epithelium
• VIN 3: Severe dysplasia
(atypia) - more than 2/3 of the
epithelium; Carcinoma-in-situ -
full thickness of the epithelium
Sources:vanderLindenet al. PagetDiseaseof theVulva,CntRevOneHem,2016
Gershenson et al. Comprehensive
Gynecology,
8thEd,2022.
495
*Wilkinson Classification of Vu/var Puget's Disease (VPD)
496
SECTION TWO
CERVICAL CARCINOMA
CERVICAL CARCINOMA
• Cervical carcinoma is the third most frequent malignancy of the lower female genital tract
(after endometrial and ovarian cancer)
• It is the 2nd most frequent cause of death (after ovarian cancer)
I. RISK FACTORS
• Persistent high risk HPV type (necessary cause of cervical cancer)
• Parity of 7 or more
• 0CP use >S years with HPV
• Current smokers & younger age at smoking
• Co-infected with Chlamydia or HSV-2
• HIV
• Early age at sex <14 years old
• Lifetime number of sexual partners 2:2
• First pregnancy <17 years old
• No cervical cancer screening
• Low socio-economic status
• Poor access to healthcare services, poor nutrition, etc.
■
• Neuroendocrine tumors
Other (mixed)
epithelial tumors --- • Carcinoid
0 Atypical carcinoid
carcinoma
• Undifferentiated carcinoma
497
MANIFESTATIONS AND STAGING
I. SIGNSAND SYMPTOMS
• Irregular spotting or light bleeding between periods in women of
reproductive age
Symptoms in
• Postmenopausal spotting or bleeding
the early stages
• Bleeding after sexual intercourse
• Increased vaginal discharge (sometimes foul-smelling)
• Persistent back, leg and/or pelvic pain
• Weight loss, fatigue, loss of appetite
Symptoms in • Foul-smelling vaginal discharge and discomfort
the late stages • Swelling of a leg or both lower extremities
• Other severe symptoms may arise at advanced stages depending on
which organs cancer has spread
• Visible and/or palpable cervical lesion/mass
Exophytic growth or cauliflower-like
0
Signs
Endophytic growth or barrel-shaped
0
498
II. THE UNION FOR INTERNATIONALCANCERCONTROL (UJCC) TNM AND FJGO 2018
STAGINGCLASSIFICATIONOF CERVICALCANCER
T I
FIGO
CATEGORY STAGE
I DEFINITION
■
t1/ • The carcinoma has extended beyond the true pelvis or has involved
IV (biopsy proven) the mucosa of the bladder or rectum. A bullous
edema, as such, does not permit a case to be allotted to Stage IV
T4
IVA • Spread of growth to adjacent organs
IVB • Spread to distant organs
499
Notes on Cervical Cancer Staging
'Imagingandpathology canbe used,whenavailable,to supplement
clinicalfindingswithrespectto tumorsizeand
extent,in all stages.Pathological
findingssupercede
imagingandclinicalfindings
of vascular/lymphatic
'The involvement spacesshouldnotchangethestaging.Thelateralextentof the lesionis no
longerconsidered
'Addingnotationof r (radiologic
or sonographicimaging)andp (pathology)
to indicatethefindingsthatareusedto
allocatethecaseto stageIIIC.Exampleif imagingindicatespelviclymphnodemetastasis, stageallocation
would
be stageIIIC1rand if confirmedby pathologic
findings,casewouldbe stageIIICp.Typeof imagingmodalityand
pathologictechniqueusedshouldalwaysbe documented
Source:8theditionof the Unionfor International
CancerControl(UICC)TNMclassification of malignant
tumours;2016
RevisedFIGOstagingfor carcinomaof thecervixuteri.IntJ GynaecolObstet2019
MANAGEMENT
STAGE I MANAGEMENT
• Desirous of pregnancy with no Lymphovascular Space Invasion (LVSI)
0 (-) margins: observe
0 ( +) margins: repeat cone biopsy or do trachelectomy
+ PALS± BO
NOTE:Forpatientswhowillundergoa surgicalintervention,
postoperative will be dependent
chemoradiation onthe
presenceof surgicopathologic
factors. e
500
ENDOMETRIAL HYPERPLASIA
I. ETIOPATHOGENESIS
• Endometrial hyperplasia results from an excess of estrogen or an excess of estrogen
relative to progestin (such as occurs with anovulation)
• Two important separate categories:
Atypical hyperplasia
0 Hyperplasia without atypia
I Benign endometrium I
Unopposedestrogen TP53
(irregular ovulation/ I mutations
anovufotion, obesity)
II. PATHOLOGY
A. Pathologic Features
PATHOLOGY I CHARACTERISTIC
• Irregularity in the shape of glands with cystic alterations
• Abundant stroma between glands
• Glands cystically dilated with occasional outpouchings and
Simple hyperplasia
focal crowding
• Lined by pseudostratified tall columnar epithelium
• Glands separated by abundant cellular stroma
• Loss of polarity
■
• Increased nucleus:cytoplasm (N:C) ratio
Atypia* • Irregular size and shape
• Prominent nucleoli
• Thick nuclear membrane
'Cytologicatypia in endometrialhyperplasiais the most importantfactor in determiningmalignantpotential
501
B. Endometrial Intraepithelial Neoplasia (EIN) Criteria
EIN CRITERIA I COMMENTS
• Benign
endometrial
hyperplasia
• Simple
non-atypical
endometrial
• Low level
hyperplasia
of somatic
• Complex
mutations
non-atypical • Weakly pre-
in scattered
Hyperplasia endometrial malignant
glands with
without hyperplasia • <1% • Relative risk
atypia
morphology
• Simple (RR):
on HE
endometrial 1.01-1.03
staining
hyperplasia
showing no
without
changes
atypia
• Complex
endometrial
hyperplasia
without
atypia
• Many of
the genetic
changes
• Complex typical for
atypical endometrial
endometrial cancer • Complex
Atypical hyperplasia (endometrioid atypical
hyperplasia / • Simple type) are hyperplasia
Endometrial atypical present, • 25-33% has the
Intraepithelial endometrial including • 59% greatest
Neoplasia hyperplasia microsatellite malignant
(EIN) • Endometrial instability; potential
intraepithelial PAXZ • RR: 14-15
neoplasia inactivation;
(ElN) mutation of
PTEN,KRAS
and CTN NB1
(~-catenin)
502
III. DIAGNOSIS
DIAGNOSTIC I REMARKS
• Types include:
0 Hysteroscopic-targeted biopsy
Endometrial biopsy 0 Ultrasound-guided biopsy
0 Office biopsy
0 Endometrial curettage
Pelvic Ultrasound with
• Primary tool for evaluation of abnormal uterine bleeding
Dopplers using the IETA
IV. MANAGEMENT
I POSTMENOPAUSAL
HISTOLOGIC
TYPE I PREMENOPAUSAL
WOMEN
• Levonorgestrel-releasing Intrauterine System
WOMEN
or Leuprolin
acetate500mgweeklyx 3-6monthsPLUS
• Goserelin3.6 mgor Leuprolin3.75mgor Triptorelin
11.25mgor Triptorelin
3.75mgevery28 daysx 6 monthsORGoserelin10.8mg
11.25mgdepotevery3 monthsx 6 monthsORTriptorelin
22.5mgsingle
I
dose
503
ENDOMETRIAL CANCER
• Endometrial carcinoma is the most common malignancy of the female genital tract
• Adenocarcinoma of the endometrium affects women primarily in the perimenopausal
and postmenopausal years (most frequent in the ages of SO to 65 years)
I. ETIOPATHOGENESIS
INCREASES THE RISK I DIMINISHES THE RISK
• Unopposed estrogen stimulation of the • Monthly ovulation and menstruation
endometrium • Progestin therapy
• Unopposed menopausal estrogen • Combination oral contraceptive pills
replacement therapy ( 4-Bx) • Menopause before 49 years
• Menopause after 52 years (2.4x) • Multiparity
• Obesity (2-Sx) • Smoking
• Nulliparity (2-3x)
• Diabetes (2.Bx)
• Insulin resistance
• Estrogen secreting ovarian tumors
• Polycystic ovarian syndrome (PCOS)
• Tamoxifen therapy for breast cancer
• Lynch syndrome
Ill. DIAGNOSIS
• Biopsy of the endometrium
• WHO histological classification of tumors of the uterine corpus:
• Endometrioid adenocarcinoma
• Endometrioid adenocarcinoma with squamous differentiation
• Clear cell carcinoma
• Serous carcinoma
• Secretory carcinoma
• Mucinous carcinoma
Squamous carcinoma
0 Mixed carcinoma
• Undifferentiated carcinoma
• Carcinosarcoma
IV.MANAGEMENT
• Surgery is the primary treatment modality for patients with endometrial carcinoma
• Standard management of endometrial cancer includes the following surgical procedures:
• Peritoneal fluid cytology (PFC)
Extrafascial hysterectomy (EH)
Bilateral salpingo-oophorectomy (BSO)
Bilateral pelvic lymph node dissection (BLND)
Para-aortic lymph node sampling (PALS)
• Exceptions to surgical approach
Poor surgical risk: should undergo primary complete radiotherapy with or without
·:
chemotherapy
Non-resectable disease: should undergo primary complete radiotherapy with or
without chemotherapy
• Well-differentiated lesion and contraindications to anesthesia and unsuited for
radiotherapy - may use high-dose progestins ■·
• Patients desirous of future fertility who have all the following criteria:
• Well-differentiated tumor (Grade 1, endometrioid type)
• No myometrial, cervical, adnexal, parametrial and vaginal involvement on MRI
• No suspicious retroperitoneal lymph nodes or no evidence of lymph node metastasis
• Negative PFC
• No lymphovascular space invasion (LVSI)
• No contraindications for medical management
505
STAGE I
I SURGICO-PATHOLOGIC
STAGING I ADJUVANTTREATMENT
Surgery: PFC, EHBSO, BLND ± PALS (indicated for Stage 1Band/orG3 tumors)
Gl, G2 Observe
IA
G3 Brachytherapy
Gl,G2 Brachytherapy
1B
G3 EBRT ± Chemotherapy*
Gl, G2 Brachytherapy
V. FOLLOW-UP
• Every 3-6 months for 2 years, then every 6-12 months thereafter
• Pap smear is not routinely indicated
• PET-CT Scan, CT Scan, MRI and/or Bone Scan if suspicious for tumor recurrence
• Annual chest x-ray is not recommended for early detection of recurrent disease in
asymptomatic patients
• Serum CA-125 monitoring every 3 months for selected patients (i.e. advanced stages
[Stages III-IV], poor histologic type [serous or clear cell] and/or an elevated pre-
treatment CA-125 level)
506
SECTION FOUR
OVARIAN CANCER
ETIOPATHOGENESIS
• Ovarian cancer is the second most common malignancy of the female lower genital tract
• Most frequent cause of death from gynecologic neoplasms
• Major contributing factor to the high death rate is the frequent detection of the disease
after metastasis
• Theories on pathogenesis:
I. TYPESOF OVARIANCARCINOMAS
EXPLAININGTUMORHETEROGENEITY
CHARACTERISTIC
I TYPE 1
I TYPE 2
• 25% of ovarian malignancies • 75% of ovarian malignancies
Epidemiology
• 10% of deaths • 90% of deaths
• Low-grade serous • High-grade serous
• Low-grade endometrioid • High-grade endometrioid
Histology • Clear cell • Undifferentiated
• Mucinous • Carcinosarcoma
• Brenner • Transitional cell
• Cystadenoma
• Serous tubal intraepithelial
Early lesion • Borderline Cystadenoma
carcinoma (STIC)
• Endometriosis
Morphological
• Identified • Not identified
precursors
Presentation
and transition to • Indolent, slow, gradual • Rapid growth, abrupt
malignancy
• Multifocal distribution, • Mesothelial lined surfaces of
Spread pattern distant recurrence, systemic the ovary, fallopian tube, and
spread peritoneum
Stage of diagnosis • Early • Advanced
Prognosis • Good • Poor
• Genomic stability
■
• Genomic instability
• Frequent mutations: KRAS,
Genomic profile and • p53 mutation,
BRAF,ERBBZ,PTEN,
mutations BRCAl/2 inactivation,
B-catenin, PIK3CA,CTNNBl,
CCNEl multiplication
ARIDlA
Sources:Rescigno et al. BiomedResInt,2013.
Aggarwalet al.The Obstetrician
andGynaecologist, 2016.
507
II. WHO HISTOLOGICALCLASSIFICATIONOF TUMORS OF THE OVARY
• Serous • Clear cell (Mesonephroid)
Epithelial (65%) • Mucinous • Brenner
• Endometrioid
Serous Tumors
• Most frequent ovarian epithelial tumors
• Resembles fallopian tubes
508
MANIFESTATIONS AND DIAGNOSIS
I. MANIFESTATIONS
• Early disease is nearly always almost asymptomatic
• Vague pelvic pressure
Signs & Symptoms
• Abdominal fullness and bloating
(non-specific)
• Dyspepsia
• Advanced disease may present with ascites
Abdominopelvic Exam • Predominantly solid, fixed, irregular abdominopelvic mass
findings with or without ascites
PET-CT Scan, MRI or CT • Determine origin of the tumor, extent of the disease and
Scan with contrast probability of achieving optimal cytoreductive surgery
• 80% of patients with epithelial ovarian cancer have elevated
Tumor markers
CA-125
'InternationalOvarianTumorAnalysis-Assessment
of DifferentNEoplasiasin the adneXa(IOTA-ADNEX)
TYPE
I AGE I TUMOR
MARKERS
I HISTOLOGY
• 1 or 2 ovaries or
FTs with any of
• 1 ovary or FT the following:
• 2 ovaries or FTs
only • Cl: surgical spill
• No tumor on
• No tumor on
ovarian or FT • CZ:ovarian
• Confined to ovarian or FT capsule or FT
surface
ovaries or surface
I fallopian tubes • No malignant
• No malignant serosa ruptured
cells in the before surgery or
(FT) cells in the tumor on ovarian
ascites or
ascites or
peritoneal surface
peritoneal
washings • C3:malignantcells
washings
in the ascites or
peritonealwashings
• 1 or 2 ovaries or
FTswith • Extension and/
• Extension to
• Pelvic extension or implants on
other pelvic
II (below pelvic the uterus and/
intraperitoneal
---
brim) or or FTs and/ or
tissues
• Primary ovaries
peritoneal cancer
•Ali:(+)
retroperitoneal
• Macroscopic • Macroscopic
LN metastases
peritoneal peritoneal
510mm
metastasis metastasis
in greatest
beyond pelvis,;; beyond pelvis
• Stage II PLUS dimension
2 cm in greatest > 2 cm in greatest
• Cytologically or
• Alii: (+) dimension, dimension,
histologically
retroperitoneal with or without with or without
confirmed
LN metastases positive positive
spread to the
> 10mm retroperitoneal retroperitoneal
III peritoneum
in greatest LNs LNs
outside the
dimension • Includes • Includes
pelvis and/or
extension of extension of
metastases to the • A2: (+) tumor to liver tumor to liver
retroperitoneal microscopic and/or spleen and/or spleen
LNs extrapelvic capsule without capsule without
(above the pelvic parenchymal parenchymal
brim) peritoneal involvement of involvement of
involvement+/- either organ) either organ)
positive retro-
peritoneal LNs
• Parenchymal
metastasis (liver
• Distant and/or spleen)
metastases & metastasis to
• Pleural effusion
IV excluding
with(+) PFC
extra-abdominal ---
peritoneal organs (including
surfaces inguinal LJ':!sand
LNs outside of the
abdominal cavity)
VII. MANAGEMENT
• First line post-operative/adjuvant management, if indicated, is usually platinum-based
chemotherapy± targeted therapy:
GERM CELLTUMORS
25-25% of all ovarian tumors
BENIGN TUMORS ..
95% ----- MALIGNANT
~5%
Mostly benign cystic teratoma
(mature teratoma/ dermoid tumor)
....._.._ lk sac- endodermal
'- - chorfocarci
e-immatu
II. MANIFESTATIONS
• Pelvic pain due to rapid growth, hemorrhage, and necrosis
• Pressure symptoms on the bladder or rectum
• 85% will have abdominal pain and pelvic mass
III. DIAGNOSIS
GERM CELL TUMOR TUMOR
(MALIGNANT)
I HISTOLOGY
lymphocytes
Dysgerminoma • LDH
• 10% are bilateral
• Analogous to seminoma of the testes
Endodermal sinus tumor • Schiller-Duval bodies - numerous hyaline
• AFP
or Yolk sac tumor droplets
• Hemorrhagic
Choriocarcinoma • Highly malignant cytotrophoblast and • ~-hCG
syncytiotrophoblast (dimorphic pattern)
• Consists of immature embryonic structures
Immature teratoma • AFP
admixed with mature elements
IV.MANAGEMENT
• If fertility is desired: PFC, USO+ Complete Surgical Staging (IO, RPB, BLND,PALS)±
Tumor Debulking
■
• No desire for fertility: PFC, TAHBSO,JO, RPB, BLND,PALS± Tumor Debulking
511
OVARIAN TUMOR: SEX CORD
I. ETIOPATHOGENESIS
• Sex cord stromal tumors are functioning tumors meaning these tumors secrete either
estrogen (granulosa cell) or testosterone (Sertoli-Leydig)
• May manifest with symptoms attributable to the excess hormone production (i.e.
precocious puberty, abnormal uterine bleeding, virilizing symptoms)
I GRANULOSA CELL
TUMOR(75%)
• Sex Cord: Granulosa
I SERTOLI LEYDIG CELL
TUMOR
• Sex Cord: Sertoli
Component
• Strama: Theca • Strama: Leydig
• Granulosa cells have grooved "coffee
bean" nuclei and are arranged in small
Microscopic • Resemble fetal testes
clusters around a central cavity
(Call-Exner bodies)
• Functionally
Hormones • Functionally estrogenic
testosterogenic
• Virilization
• Premenarcheal: precocious puberty
• Hirsutism
Symptoms • Premenopausal: menstrual irregularities
• Temporal recession
• Postmenopausal: bleeding
• Deeper voice
• Desirous of pregnancy: PFC, USO+ Complete Surgical Staging
Management • Not desirous of pregnancy: PFC, THBSO,IO, RPB, BLND,PALS
± Tumor Debulking
Tumor marker • lnhibin, AMH
512
SECTION FIVE
VULVAR CANCER
ETIOPATHOGENESIS
• Accounts for approximately 4%-5% of female genital tract malignancies
• Occurs less often than uterine, ovarian and cervical cancers
• More than 80% of patients are older than 50 years at the time of diagnosis
• 90% of primary vulvar malignancies is squamous cell carcinoma (SCCA)
CHARACTERISTIC
I TYPE! I TYPE II
Age group • 35-65 years of age • 55-85 years of age
• Human papillomavirus • Vulvar non-neoplastic
Etiology
(HPV) infection epithelial disorders (VNED)
• Lichen sclerosus
Precursor lesion • LGSIL-HGSIL(VIN 1-3) • Lichen planus
• Squamous hyperplasia
• Sexually transmitted
Other predisposing diseases (STDs)
• "Itch-scratch cycle"
factors • Low socioeconomic status
• Nicotine use
Somatic mutation --- • TP53
Source:Gershenson
et al. Comprehensive Gynecology,
8th Ed.2022
Alkatoutet al. Int J WomenHealth,2015.
II. RISK FACTORS
INCREASES THE RISK I DECREASES THE RISK
• Human Papilloma Virus infection • HPV vaccination
• Tobacco smoking • Prompt treatment of lichen sclerosus,
• Untreated vulvar dermatoses lichen planus and squamous hyperplasia
• Presence of anogenital warts • Cessation of smoking
• History ofvulvar atypia
• History ofpreinvasive disease or invasive
cancer of the cervix and/or vagina
• Alcohol consumption
CLINICAL MANIFESTATIONS
SYMPTOMS I SIGNS
• Long history ofvulvar pruritus • Vulvar lump or mass
• Vulvar bleeding ° Fungating or ulcerated
• Vulvar discharge ° Fleshy or warty
• Vulvar pain 0 Leukoplakic
• Dysuia • Palpable groin node(s)
·:
• Dyschezia • Leg edema
Source:Alkatoutet al. Int J WomenHealth,2015.
DIAGNOSIS
• Punch or incision biopsy at the peripheral edge of the tumor using a Tischler or Keyes ■·
biopsy instrument
0Include underlying stroma
0Avoid necrotic center of the tumor
• Pap smear and colposcopy to rule an associated lesion on the cervix and vagina
• Imaging: PET-CTScan, CT Scan, MRI, ultrasound
• Endoscopy: cystoscopy, proctosigmoidoscopy
Source:CPGfor the Obstetrician-Gynecologist,
3rd Ed,SGOP,2019
513
WHO2020 Classification of Tumors of the Vulva
• Squamous cell carcinoma
HPV-associated
0
HPV-independent
0
NOS
0
Malignant
0
Eccrine adenocarcinoma
0
• Tumor of any size fixed to bone, or fixed, ulcerated lymph node metastases, or
IV
distant metastases
IVA • Disease fixed to pelvic bone, or fixed or ulcerated regionaJbJymph node metastases
'Criteriafor SentinelLymphNode(SLN)Mapping:
1) Tumorsize,; 4 cm
2) > 1 mminvasion
3) Noclinicallysuspiciouslymphnodes
4) Nopreviousgroinnodedissection
5) Nopriorgroinirradiation
6) Notfor multifocaldisease
7) Notgrosslyinflamedprimarytumor
8) Notfor recurrentdisease
Sources:ClinicalPracticeGuidelines,SGOP,20181
van der Zee et al. J ClinOneal,2008. : :
515
REFERENCES
l.Abhatla N,Aoki D, Sharma D, etal. Cancer of the cervix uteri. IntJ Gynaecol Obstet 2018;143:22-36; Corrigendum to "Revised
FIGO staging for carcinoma of the cervix uteri". Int J Gynaecol Obstet 2019;147:279-280.
2.Aggarwal IM, Lim YH and Lim TYK.The Fallopian Tube as the Origin of Non-Uterine Pelvic High-Grade Serous Carcinoma.
The Obstetrician & Gynaecologist 2016:18:143-152.
3.Alkatout I, Schubert M,Garbrecht N,Weigel MT,Jonat W, Mundhenke C and Gilnther V.Vulvar Cancer: Epidemiology,Clinical
Presentation and Management Options. Int J of Women's Health. 2015:7:305-313.
4.Emons G, Beckmann MW, Schmidt D, Mallmann P and for the Uterus Commission of the Gynecological Oncology Working
Group (AGO). New WHO classification of endometrial hyperplasias. Geburtsh Frauenheilk 2015 Feb:75(2):135-136.
5.Fontham ETH, Wolf AMO, Church TR. Etzioni R. Flowers CR, Herzig A, et al. Cervical Cancer Screening for Individuals at
Average Risk: 2020 Guideline Update from the American Cancer Society. CA CANCERJ CLIN 2020;70:321-346.
6.Gershenson OM, Lentz GM, Valea FA, Lobo RA. Comprehensive Gynecology. 8th Ed. Philadelphia: Elsevier; Inc.; 2022.
7.Handisurya A, Schellenbacher C, Kirnbauer R. Diseases caused by human papillomaviruses (HPV). JDDG 2009;7:453-466.
8.Herbst AL. The epidemiology of ovarian carcinoma and the current status of tumor markers to detect disease. Am J Obstet
Gynecol.1994;170(4):1099-1105
9.Lobo RA, Gershenson OM, Lentz GM, Valea FA.Comprehensive Gynecology. 17th Ed. Philadelphia: Elsevier; 2017.
10. Melnikow J, Henderson JT.Burda BU,Senger CA,Durbin S, Souls by MA.Screening for Cervical Cancer With High•Risk Human
Papillomavirus Testing: A Systematic Evidence Review for the U.S. Preventive Services Task Force. Evidence Synthesis No.
158. AHRQ Publication No. 17-05231-EF-1. Rockville, MD: Agency for Healthcare Research and Quality; 2018.
11. Nayar Rand Wilbur DC.The Pap Test and Bethesda 2014. Acta Cytologica 2015;59:121-132.
12. Olawaiye AB, Cotler J, Cuello MA, Bhatia N, Okamoto A, Wilailak S et al. FIGO Staging for Carcinoma of the Vulva: 2021
Revision. Int J Gynecol Onstet. 2021:155;43-47.
13. Perkins RB, Guido RS, Castle PE, Chelmow D, Einstein MH, Garcia F,et al. 2019 ASCCP Risk-Based Management Consensus
Guidelines for Abnormal Cervical Cancer Screening Tests and Cancer Precursors. J Low Genit Tract Dis 2020;24: 102-131.
14. Rescigno R. Cerillo I, Ruocco R, Condello C, De Placido Sand Pensabene M. New Hypothesis on Pathogenesis of Ovarian
Cancer Lead to Future Tailored Approaches. Biomed Research International Volume 2013: Article ID 8522839;13 pages.
15. Schorge JO, Modesitt SC, Coleman RL, Cohn DE, Kauff ND, Duska LR, Herzog TJ. SGO White Paper on ovarian cancer:
etiology, screening and surveillance. Gynecol Oneal. 2010
16. Society of Gynecologic Oncologists of the Philippines (SGOP) Clinical Practice Guidelines for the Obstetrician•Gynecologist.
3rd Ed.; July 2019.
17. Society of Gynecologic Oncologists of the Philippines (SGOP) Clinical Practice Guidelines. 8th Ed.; July 2018.
18. Soslow RA, Tornos C, Park KJ, Malpica A. Matias-Guiu X., Oliva E., et al.. Endometrial Carcinoma Diagnosis: Use of FIGO
Grading and Genomic Subcategories in Clinical Practice: Recommendations of the International Society of Gynecological
Pathologists. Int J Gynecol Pathol Jan 2019:38(1) Suppl 1: S64-S74.
19. Union for International Cancer Control (UCC).Bth edition of the UICCTNM classification of malignant tumours (2016).
20. WHO Classification of Tumours Editorial Board. Female Genital Tract Tumours. Lyon (France). International Agency for
Research on Cancer, 2020. (WHO Classification of Tumours series, 5th ed: vol 4). https://publications.iarc.fr/592.
21. van der Linden M, Meeuwis KAP,Bulten J,Bosse T, van Poelgeest MIE and de Hullu JA. Paget Disease of the Vulva. Critical
Reviws in Oncology/Hematology. 2016:101;60-74.
22. Van der Zee AG, Oonk MH, De Hullu JA, Ansink AC, Vergote I, Verheijen RH, et al. Sentinel node dissection is safe in the
treatment of early stage vulvar cancer. J Clin Oncol 2008;26(6):884-9.
516
GESTATIONAL
TROPHOBLASTIC
DISEASE
ANDNEOPLASIA
SECTION ONE
OVERVIEW OF GESTATIONAL TROPHOBLASTIC DISEASES
I. CLINICALCLASSIFICATION
HYDATIDIFORM MOLE I GESTATIONAL TROPHOBLASTIC
NEOPLASIA (GTN)*
• Invasive mole**
• Complete hydatidiform mole • Choriocarcinoma
• Partial hydatidiform mole • Placental site trophoblastic tumor (PSTT)
• Epithelioid trophoblastic tumor (ETT}
'Malignantformsof GTDare termed GTN. Otherterms for GTNare malignantgestationaltrophoblasticdisease
and persistentgestationaltrophoblasticdisease.
"Invasive moleis deemed malignantdue to its markedpenetrationintoand destructionof myometriumand its
abilityto metastasize.
Source:WHOClassificationof GTD
II. PATHOLOGY
• Most GTD produces the beta-subunit of human chorionic gonadotropin (P-hCG)
• Assessment of DNA content enhances the diagnostic accuracy of histologic diagnosis
• With excess paternal genes, there is excessive placental or trophoblastic proliferation
(because paternal genes have more control over placental growth)
519
■
SECTION TWO
BENIGN GESTATIONAL TROPHOBLASTIC DISEASES
I. ETIOPATHOGENESIS
• H-mole is categorized as complete or partial mole
• They occur after an aberrant fertilization
I COMPLETE H-MOLE
(DIANDRIC, DIPLOIDY)
I PARTIAL H-MOLE
(DIANDRIC, TRIPLOIDY)
• 1 maternal (23X) and 2 paternal
• Paternal chromosome only plus
chromosomes (23X, 23Y)
empty ovum
• Maternal chromosome gives rise
• Gives rise to generalized
to fetal component
Pathogenesis swelling of placental villi
• Paternal chromosome causes
with marked trophoblastic
focal swelling of placental villi
proliferation and absent fetal
and milder form oftrophoblastic
component
invasion
Homozygous
~--0--®)
Triploid partial mole
Empty ovum
Heterozygous
complete mole
~
23, Y
Oispermy
Illustration ~
520
B. Risk Factors
RISK
I REMARKS
Extremes in • Two-fold risk for those <15 years old, 36-40 years old
maternal age • Ten-fold risk for those >40 years old
Paternal age • >45 years old increases risk for complete but not partial mole
OB history • Previous molar pregnancy
Racial factors • Asians, Hispanics, American-Indians
Diet and Nutrition • Decreased dietary carotene & animal fat
'Strongest riskfactorsare age and a priorhydatidiform
mole
II. MORPHOLOGY
AND MANIFESTATIONS
Uterine size • Larger than AOG • Same size or smaller than AOG
13-hCGLevel • >100,000 mlU/mL • <100,000 mlU/mL
Theca Iutein • Common (25-30%): due to LH,
• Rare
cysts FSH stimulation
• Hyperemesis, preeclampsia: due
to high 13-hCG
• Hyperthyroidism: due to
Medical thyrotropin-like effects of the
• Rare
complications 13-hCG
• Respiratory insufficiency: due to
trophoblastic deportation
• DIC:from profuse vaginal bleeding
Malignant
• 15-25% (higher) • 0.4-5.0%
transformation
Source:E1felPJ,et al. Gynecotog,c 200611
Cancer;
521
III. DIAGNOSIS
A. Serum Jl-hCGMeasurements
0 In complete molar pregnancy, Jl-hCGare elevated (more marked elevation in those
with more advanced moles)
0 In partial moles, Jl-hCGmay be significantly elevated, but more commonly
concentrations fall into ranges expected for gestational age (see below)
GESTATIONAL GESTATIONAL
AGE
I MEDIAN (RANGE)
I AGE
I MEDIAN (RANGE)
8. Sonography (Ultrasound)
0 Mainstay oftrophoblastic disease diagnosis (but not all cases are confirmed initially)
0 Most accurate non-invasive imaging modality
0 Most common mimics: incomplete or missed abortion
I FlNrnNGS
• Snowstorm-like pattern: echogenic uterine mass with numerous
Complete
anechoic cystic spaces (grape-like or hydropic villous change)
mole
• No fetus or amniotic sac seen
Partial • Thickened, multicystic placenta along with a fetus or at least fetal tissue
mole
C. Histologic Diagnosis
0 Provides a definitive diagnosis
0 lmmunostaining with P57KIP2: protein product of paternally imprinted but
maternally expressed gene CDKNIC
• Negative in CHM
• Positive in PHM
° Karyotyping (diploid, triploid)
522
IV. MANAGEMENT
B. Chemoprophylaxis
, First line: methotrexate (second line: actinomycin DJ
' Given to patients with high risk for persistent disease & with the following features:
• Maternal age ;,40 years
• Uterine size larger than gestation by >6 weeks
• Serum f3-hCGtiter ;,100,000 mlU/mL
• Theca lutein cyst(s) ;,6 cm
• Medical complication arising from increased trophoblastic proliferation (e.g.
preeclampsia, thyrotoxicosis, DIC, pulmonary insufficiency)
• Recurrent H. mole
• Documented H. mole with a coexisting normal twin (given after delivery of the twin)
' May be given for those with probable poor compliance to follow up
C. Follow-up
• 1 week after surgical evacuation
Post-evacuation
• Every 2 weeks until f3-hCGbecomes normal for 2 consecutive tests
f3hCGmonitoring
• Every 1 month for first 6 months
• Avoid pregnancy during monitoring period
Follow-up advice • Ideal to use low-dose OCP for contraception
• Pregnancy allowed 6 months after normal f3hCG
• Do early ultrasound to rule out molar pregnancy
For succeeding
• Perform quantitative serum f3-hCG6 weeks postpartum
pregnancies
• Placenta submitted for histopathologic exam
Source:PSSTDCPG,2016
523
■
SECTION THREE
GESl'.AlilONAL TROPHOBLASTIC NEOPLASIA (GTN)
I. ETIOPATHOGENESISAND PATHOLOGY
II. MANIFESTATIONS
• Persistent or irregular vaginal bleeding after a molar pregnancy (most common
presentation)
• Failure of uterine involution
• Signs and symptoms which may be referrable to the site of metastases
Lung: hemoptysis, dyspnea
0 Brain: headache, loss of consciousness, seizures
0 Gastrointestinal: melena, acute abdomen, abdominal pain
• Manifestations may be seen immediately or after years of antecedent pregnancy
• Metastasis is via the hematogenous route
• Most common site of metastasis: lungs which show "cannonball" lesions on radiologic
imaging
524
III. DIAGNOSIS
• High index of suspicion
• Histopathology is not necessary for the diagnosis of GTN
• Clinical manifestations (e.g., abnormal bleeding or amenorrhea, pelvic pain)
• High levels of P-hCG
• Ultrasonography with Doppler studies
• Histopathologic findings if hysterectomy is performed
A. Anatomical Staging
STAGE
I EXTENT
I • Disease confined to the uterus
II • GTN extends outside the uterus but is limited to the genital
structures (adnexae, vagina, broad ligament)
III • GTN extends to the lungs with or without genital tract involvement
Antecedent
pregnancy
Mole Abortion Term ---
Interval months
from index <4 4-6 7-12 >12
pregnancy
Pretreatment
1,000 to 10,000 to
serum 13-hCG <l,000 .>100,000
<10,000 <100,000
(mJU/mL)
Largest tumor
size (including <3 cm 3-4cm ;,S cm ---
uterus)
Site of
metastasis* --- Spleen, kidney Gastrointestinal Liver, brain
Interpretation:
• Lowrisk:<7 (suggests lowriskof resistance to single-agentchemotherapy)
• Highrisk:;, 7 (predictsa high riskof resistance to single-agentchemotherapy)
525
■
VI. MANAGEMENT
A. Chemotherapy (cornerstone of treatment)
STAGE I MANAGEMENT
• Single agent chemotherapy (methotrexate or actinomycin DJ
I • ± hysterectomy
B. Consolidation Therapy
0Given after reaching normal P-hCG titers (i.e., ,;;S mIU/mL) to ensure eradication of
every viable trophoblast cells which may no longer be detected by the P-hCG assays
0Number of therapies:
• Low risk: 2 consolidation therapies
• High risk: 3 consolidation therapies
526
PLACENTAL SITE TROPHOBLASTIC TUMOR (PSTT) AND
EPITHELIOID TROPHOBLASTIC TUMOR (ETT)
• Both have lower 13-hCGlevels compared to invasive mole and choriocarcinoma
I. ETIOPATHOGENESIS
• Usual antecedent pregnancy: term pregnancy
• Behavior is generally unknown due to rarity of conditions
PLACENTAL SITE EPITHELIOID
I TROPHOBLASTIC TUMOR I TROPHOBLASTIC TUMOR
• Rare tumor • Rare tumor
Pathogenesis • Arises from intermediate • Develops from chorionic-type
trophoblasts at the placental site intermediate trophoblast
• Main site of involvement is the
Pathology • Main site of involvement is the uterus
placental implantation site
II. MANIFESTATIONS
• Abnormal vaginal bleeding or manifestations referrable to the metastatic site
• Interval from the antecedent pregnancy is variable
• Serum 13-hCG:usually <2,000 mlU/mL, even with disseminated disease
• Staging: all patients are staged using the FIGO 2000 Staging System (the WHO prognostic
scoring system is not applicable)
III. MANAGEMENT
• Surgery is the primary mode of treatment
• Chemotherapy: EMACO
• Follow up: same as invasive mole and choriocarcinoma
REFERENCES
1. FIGO Committee on Gynecologic Oncology: Current FIGO Staging for Cancer of the vagina, fallopian tube, ovary, and
gestational trophoblastic neoplasia. Int) Gynaecol Obstet 2009 Apr;lOS(l):3-4
2. PhilippineSocietyfor the Study of TrophoblasticDiseases(PSSTD)Clinical PracticeGuidelinesfor the Diagnosisand
Managementof GestationalTrophoblasticDisease.3rd Ed.;2016,
3.Cunningham FG, Levene K, Bloom S, Spong C, Dashe), Hoffman 8, Casey 8. Williams Obstetrics. 25th Ed. New York:
McGraw-Hill Education Medical; 2018.
4. Lobo RA, Gershenson DM, Lentz GM,Valea FA.Comprehensive Gynecology. 17th Ed. Philadelphia: Elsevier; 2017.
5. EifelPJ,GershensonDM, KavanaghJI,SilvaEG.GynecologicCancer.New York:Springer-Verlag;2006:230.
527
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BOARD
CORRELATES
SECTION ONE
OBSTETRICS
531
I
.
EARLY PREGNANCY COMPLICATIONS
Most common site of implantation • Ampulla (70%), isthmus (12%), fimbriae (11%)
532
PRENATAL SCREENING
Most common cause of
• Trisomy 21
Down syndrome
• FORCEPS
Criteria for forceps
• Fully dilated, Operator experienced, Ruptured membranes,
delivery
CPD absent, Empty bladder, Position definite, Station at least+ 2
533
I
.
ANTEPARTUM HEMORRHAGE
• Occurs when a velamentous cord insertion
Vasa previa causes the fetal vessels to pass over the
internal cervical os
Most frequent indication for
• Uterine atony
peripartum hysterectomy
• Circumvallate - membranes double back
over the edge of the placenta
• Velamentous - vessels insert between
Circumvallate vs velamentous vs amnion and chorion away from placental
succenturiate placenta margin
• Succenturiate - extra placental lobe
implanted away from the rest of the
placenta
• Painless vaginal bleeding, with a sentinel
Classical sign of placenta previa
bleed usually after 28 weeks AOG
• Prior cesarean section and uterine surgery
• Multiparity
• Multiple gestation
Risk factors for placenta previa • Erythroblastosis
• Smoking
• History of placenta previa
• Increasing maternal age
Diagnosis ofvasa previa rupture at the • Apt test (examination for nucleated fetal
time of vaginal bleeding RBCs)
534
COMPLICATIONS OF LABOR AND DELIVERY
Principal goal oftocolysis • Delay delivery by at least 48 hrs
Prior to pharmacologic • Hydration ➔ decreases ADH (almost similar to
management, preterm
oxytocin) ➔ decreases binding to oxytocin receptors
contractions can be decreased
➔ reduced contractions
by
First-line treatment for
, Mgso.
eclampsia
• 6-10 mg/dL- decreased tendon reflexes
Magnesium toxicity
• >10 mg/dL- respiratory depression, cardiac arrest
Antidote for magnesium • 10 mL of 10% calcium gluconate or calcium chloride
toxicity for cardioprotection
Black box warning for
• Pulmonary edema, cardiac events
terbutaline use >24-48 hrs
Percentage of patients with
ruptured membranes going • 50% within 24 hrs, 75% within 48 hrs
into labor
Conjugatemeasurements • Obstetric conjugate= Diagonal conjugate - 1.5 to 2 cm
External version is • Before 36-37 weeks AOG;if not successful, repeat at
performed 39 weeks
Relative contraindications • Nulliparity
for trial of labor of breech • 1500 g < EFW < 3500 g
presentation • Incomplete breech
• Face - mentum
Non-vertex presentation
• Shoulder - acromion
landmarks
• Breech - sacrum
Most common position of the • Occiput transverse; persistence leading to arrest oflabor
fetus at labor onset is common with platypelloid pelvis
• Fetal macrosomia • Maternal obesity
Risk factors for shoulder
• Diabetes • Postterm deliveries
dystocia
• Previous dystocia • Prolongedstage 2 oflabor
• McRoberts maneuver - straightening of the sacrum
relative to the lumbar vertebrae, rotation of the
symphysis pubis toward the maternal head, and a
decrease in the angle of pelvic inclination
• Suprapubic pressure - oblique-angle pressure to
Maneuvers for shoulder dislodge anterior shoulder
dystocia • Rubin maneuver - pressure on accessible shoulder
toward the anterior chest wall to decrease the
bisacromial diameter
• Wood corkscrew maneuver - pressure behind the
posterior shoulder to rotate the infant and dislodge the
anterior shoulder under the symphysis pubis
During delivery, suspicion of
• "turtle sign" (incomplete delivery of head; chin tucked
macrosomia is increased if
against perineum)
you see
535
I
.
FETAL COMPLICATIONS OF PREGNANCY
Limits for fetal growth • >90th percentile: LGA, <10th percentile:SGA
Doppler investigation to
• Umbilical artery diastolic flow decreases or reverses
differentiate IUGRfetuses
Most classical risk factor for
• GDM
fetal macrosomia
• Rh positive fetuses with sensitized mothers ➔ maternal
antibodies cross the placenta ➔ hemolysis ➔ fetal anemia
Pathogenesis of Rh
➔ increased extramedullary hematopoiesis ➔ fetal hydrops
alloimmunization
• Hemolysis also causes bilirubin toxicity ➔ fetal neurologic
manifestations
536
Primarily disease related
• Chronic hypertension
• Chronic renal disease
• Antiphospholipid antibody syndrome (APAS)
• Collagen vascular disease (e.g., SLE)
• Pregestational diabetes
• African-American
• Maternal age (<20 or >35)
Risk factors for preeclampsia
Primarily immunogenic related
• Nulliparity
.
• Previous preeclampsia
Multiple gestation
• Abnormal placentation
• New paternity, co-habitation <1 y
Family history
• Female relatives of parturient
One of the most interesting protective
• Smoking
factors against preeclampsia
537
I
.
DIABETES DURING PREGNANCY
Anti-insulin hormones during • Human placental lactogen/human chorionic
pregnancy somatomammotropin
Racial predilection for diabetes in
• Hispanics, Asian/Pacific Islanders, Native Americans
pregnancy
Screening for low-risk
• Between 24-28 weeks AOG
populations
Screening for high-risk • At first prenatal visit, then if negative, retest between
populations 24-28 weeks AOG
Initial treatment for GDMpatients • Lifestyle modification
ADA diet plan calorie requirement • 2,200 calories per day, 200-220 g of carbohydrates per
for GDMpatients day
Gold standard for diagnosing UTI • Positive urine culture 2:100,000 CFU/mL
538
GBS culture is done during • 35-37 weeks AOG
Risk based criteria for GBS • Labor before 37 weeks of gestation
treatment for women with • ROMgreater than 18 hours
unknown GBSstatus • Temperature >100.4°F
• Fever 2:39°Cor 102.2°F based on oral maternal
temperature with another clinical sign, including
Diagnosis of chorioamnionitis 0 elevated maternal WBC count (>15,000/mL)
(Triple I) 0 purulent fluid from cervical os
0 fetal tachycardia (>160 beats per minute), or
539
I
.
OTHER MEDICAL COMPLICATIONS OF PREGNANCY
Hyperemesis gravidarum (HG) • Persistent vomiting, weight loss >5% of prepregnancy
symptoms weight, ketonuria
First-line antiemetics for HG • Promethazine
Best predictor of seizure
• Number of seizure episodes in prepregnancy year
frequency
• Increased P450 function
Increased seizure frequency in • Increased volume of distribution (Vd)
pregnant women is due to • Hypervolemia
• Sleep deprivation and stress
Most common congenital
abnormalities in infants born to • Cleft lip and palate (4x), cardiac anomalies (3x)
epileptic mothers
Lowest neurodevelopmental
outcomes in epileptic mothers • Lamotrigine
maintained on
• Folate deficiency
Mechanisms of teratogenicity
• Epoxide generation
• Switch to single AED
Changes in anti-epileptic
• 3x-4x/day dosing instead of standard 2x/day dosing
drug (AED) administration in
• Folate supplementation
pregnancy
• Monthly serum AEDlevels
Prevention of increased risk of
hemorrhage in newborns from • Aggressive vitamin K supplementation towards the end
epileptic mothers maintained on of pregnancy
AEDs
Surgical repair of cardiac lesions
• At least a year before pregnancy
must be done
Most common right-to-left shunts
• PDA,VSD
among pregnant mothers
For women with moderate to • Surgical treatment prior to becoming pregnant (but
severe valvular disease, the ideal pulmonary stenosis can be managed with valvuloplasty
management would be during the pregnancy)
Management for pregnant women
• Sedentary lifestyle and beta blockers
with Marfan syndrome
Criteria for peripartum • Heart failure symptoms during pregnancy
cardiomyopathy diagnosis • Dilated heart with EF at 20-40%
• Hypercoagulability
Virchow triad • Endothelial damage
• Venous stasis
Classical sign of superficial vein • Palpable, usually visible, venous cord that is tender,
thrombosis erythematous, and edematous
Majority of deep vein thrombosis
(DVT) patients will have • Left leg (90%)
unilateral symptoms at the
• Initial test - Doppler ultrasound
Diagnostics for DVT
• Gold standard - venography
• LMWH(enoxaparin)- preferred
Treatment for DVT • Unfractionated heparin (IV heparin) - transitioned to
subcutaneous heparin afterwards
Warfarin embryopathy • Nasal hypoplasia, skeletal abnormalities, optic atrophy
540
Symptoms of pulmonary em bolus • Acute dyspnea with pleuritic chest pain, hemoptysis/
(PE) tachycardia, and/or concomitant signs of DVT
Gold standard for PE diagnosis • Pulmonary angiography
• LMWH (enoxaparin) - first choice
• Unfractionated heparin (IV heparin) - ifhypotensive
Treatment for PE
or unstable
• Streptokinase - if massive PE
Most common cause of
• Graves disease
hyperthyroidism in pregnancy
Most common cause of
• Hashimoto thyroiditis
hypothyroidism in pregnancy
Systemic lupus erythematosus
• 1/3 resolves, 1/3 progresses, 1/3 unchanged
(SLE) prognosis in pregnancy
Two distinct manifestations of • Lupus syndrome
neonatal lupus • Irreversible congenital heart block
Most commonly abused
• Alcohol and cigarette
substances in pregnancy
Most commonly abused illicit drug
• Marijuana
in pregnancy
• Growth retardation
Fetal alcohol syndrome • Abnormal facies
• CNSeffects (mental retardation)
Primary treatment for smoking • Smoking cessation programs
Most common narcotics used in
• Oxycodone, heroin, methadone
pregnancy
541
I
.
• Atelectasis (wind) • Day0
• UTl (water] • Day 1-2
• Endometritis (womb) • Day 2-3
Postpartum fever differentials
• Wound infection (wound) • Day 4-5
• Septic pelvic thrombophlebitis (walk) • Day 5-6
• Mastitis • Day 7-21
Hematoma is suspected if • There is a larger than expected drop in hematocrit
Management for retroperitoneal
• Embolization
hematoma
Leading cause of postpartum
• Uterine atony
hemorrhage
• IV oxytocin + uterine massage ➔
Management of uterine a tony methylergonovine (contraindicated in asthma) ➔
542
SECTION TWO
GYNECOLOGY
543
I
'
BENIGN DISORDERS OF THE UPPER GENITAL TRACT
Notable association ofuterine septums • First-trimester spontaneous abortion
• Ectopicendometriumtravelsvia lymphatics(Halban)
Theories on the pathogenesis of
• Metaplastic transformation (Meyer)
endometriosis
• Retrograde menstruation (Sampson)
Hallmark sign of endometriosis • Cyclic pelvic pain before menses
Definitive diagnosis of endometriosis • Direct visualization
Best management option for endometriosis • Surgical management
• Induction of pseudopregnancy ➔ induction of
Medical management of endometriosis
pseudomenopause
Definitive management for • Total hysterectomy and bilateral salphingo-
endometriosis oophorectomy
• Direct endometrial invasion through the
Theories on the pathogenesis of
myometrium
adenomyosis
• Metaplastic transformation of Mullerian rest cells
Most common sign of adenomyosis • Prolonged or heavy menstrual bleed
• MRI (most accurate)
Diagnostics for adenomyosis
• Pelvic ultrasound (most common)
Most effective temporizing treatment for
• Levonorgestrel-containing IUD
adenomyosis prior to hysterectomy
544
Definitive managem_enf for adenomyosis • Hysterectomy
Most common functional ovarian cysts • Follicular cysts
Ovarian cysts resulting from elevated
• Theca lutein cysts
13-hCG
• Chocolate cysts, from thick brown old blood
Endometriomas are also called
collected inside
• Acutely symptomatic with pain, hemorrhage, or
Indications for surgical management in
infection
ovarian cysts
• Growth observed
I
Treatment of pediculosis
butoxide
545 '
Treatment of scabies • Permethrin or ivermectin
Gold standard for diagnosis of bacterial • Gram stain and demonstration of bacterial
vaginosis presence
Primary complaint in bacterial vaginosis • Malodorous discharge
Treatment of bacterial vaginosis • Metronidazole or clindamycin
• Pruritus (only 20% experience the white curd-
Primary complaint in candidiasis
like discharge)
• Fluconazole
Treatment of candidiasis
• Non-albicans: boric acid
Considered the most common ST! • Trichomoniasis vs chlamydia
• Profuse frothy discharge (only 10% experience
Primary complaint in trichomoniasis
the "strawberry cervix")
Diagnostics for trichomoniasis • Wet prep (most common), culture (gold standard)
546
PELVIC ORGAN PROLAPSE (POP)
• Level 1 - cardinal and uterosacral ligaments
(compromise: apical prolapse)
De Lancey levels of vaginal support
• Level2 - levator ani (compromise: cystocele, rectocele)
• Level 3 - perinea! body (perinoecele, urethrocele)
URINARY INCONTINENCE
• Stress incontinence (involuntary urine
Most common type of incontinence
loss on physical exertion)
• Overflow incontinence (detrusor
More common type of incontinence in men
underactivity or bladder outlet obstruction)
547
I
.
PUBERTY, THE MENSTRUAL CYCLE, AND MENOPAUSE
• Thelarche, pubarche, accelerated growth,
Pubertal sequence
menarche
Average years after menarche for ovulation
• 2years
regularization
Delayed menarche is common in these • Athletic women, or women with lesser body
populations fat
548
Only indication for MHT as PREVENTION • Osteoporosis
549
I
.
AMENORRHEA
• Absence of menarche by 15 years old
Primary amenorrhea • Absence of secondary sexual characteristic development
by 13 years old
• Absence of menses for 3 months if with regular cycles
Secondary amenorrhea
• Absence of menses for 6 months if with irregular cycles
• Hypergonadotropic hypogonadism
Breasts absent, uterus present • Defects in steroid pathways
• Hypogonadotropic hypogonadism
Most common enzyme defect in • 21-alpha-hydroxylase
congenital adrenal hyperplasia • (Others: 11-beta-hydroxylase, 3-beta-hydroxysteroid
(CAH) dehydrogenase)
Confirmatory test for CAH • ACTHstimulation test
Kallmann syndrome • Hypogonadotropic hypogonadism and anosmia
Most common cause of secondary
• Pregnancy
amenorrhea
Asherman syndrome • Intrauterine adhesions
Rotterdam criteria (2/3)
Diagnostic criteria for polycystic • Oligo/anovulation
ovary syndrome (PCOS) • Hyperandrogenism
• Polycystic ovaries
• Oral progesterone for 7-10 days
• If(-) withdrawal bleeding ➔ estrogen and progesterone
challenge
Progesterone challenge test
• If still(-) withdrawal bleeding ➔ outflow tract disorder.
procedure
• If (+)withdrawal bleed after estrogen and progesterone
challenge ➔ hypothalamic-pituitary disorder vs ovarian
failure
550
• Menometrorrhagia (excessive bleeding at irregular
Formerterm for heavy irregular bleeding
intervals)
Former term for infrequent
• Oligomenorrhea (irregular cycles> 35 days apart)
menstrual cycles
Etiologies of abnormal uterine • Structural: PALM
bleeding (AUB) • Non-structural: COEIN
Best treatment of acute hemorrhage
• IV conjugated estrogen
fromAUB
Most common cause of
• Endometrial and/or vaginal atrophy
postmenopausal bleeding
Expected EMstripe thickness for
• s4mm
postmenopausal women
551
I
..
• Suppression of LH
Contraceptive effects of
• Induces a thin, decidualized EM unreceptive to implantation
progestins
• Thickens sperm mucus
Contraceptive effects of
• Suppression of FSH
estrogens
Low-dose COCcontain • ,;35 mcg of ethinyl estradiol (EE]
High-dose COCcontain • 50 mcg of EE
Complications associated with • Thrombotic events, stroke, MI, benign hepatic tumors,
coc gallbladder disease
Transdermal contraceptive
• Higher by 60% estrogen exposure
patch
Vaginal ring • Lower hormone exposure
• Effectiveness: 92%
Progestin-only contraceptive
• Taken every day of the cycle at the same time
pills {POPs)
(3 hrs delay= missed pill)
• Does not interfere with breastfeeding
Advantages of POPs
• Given for those with contraindications to estrogen
• Effectiveness: 97%
Injectable progestin
• Given every 3 months
{Depo-Provera)
• Most common cause of discontinuation: irregular bleeding
• Effectiveness: 99.5%
Implantable progestin • Provides 3 years of uninterrupted protection
{Nexplanon) • Most highly effective reversible contraception
• Most common cause of discontinuation: irregular bleeding
• Morning-after pill
Emergency contraception
• ParaGard
options
• Ulipristal acetate
• 1.5 mg LNGsingle dose OR
Plan B for emergency
• 0.75 mg LNGq12 for two doses
contraception
• Taken within 72 hrs of intercourse
ParaGard for emergency
• Inserted within 120 hrs of intercourse
contraception
Ulipristal acetate for emergency
• 30 mg single dose within 120 hrs after intercourse
contraception
Most common technique of tubal
• Modified Pomeroy technique
sterilization
Window period until vasectomy
• 3 months and/or 20 ejaculations
becomes fully effective
'Effectiveness ranges for cited contraceptive techniques are obtained from Blueprints Obstetrics and
Gynecology, 7th edition.
552
INFERTILITY
• Failure of a couple to conceive after 12 months of
Infertility
unprotected intercourse
Fecund~bility • Ability to achieve pregnancy in one menstrual cycle
• 20% - within 1 month
Average conception rates for • 60% - within 6 months
couples • 75% - within 9 months
• 80% - within 12 months
• 10% - unexplained
-
Contribution of factors to • 10-20% - combination of male and female factors
infertility • 35% - male factor only
• 45-55% - female factor only
Most common cause of oligo/
• PCOS
anovulation
Most common cause of tubal
• PID
infertility
Most common aneuploidy
• 45XO (Turner syndrome)
associated with female infertility
• Clomiphene citrate on Day 5-9, and measurement of FSH
on Day 3 and 10
• Day 3 FSH (<10 mlU/mL is adequate, >20 mIU/mL is poor)
• Day 3 estradiol (<80 pg/mL is adequate, >80 pg/mL is poor)
Assessment of ovarian reserve
• Day 2-4 antral follicle count (4-10 antral follicles is
~, adequate, <4 is poor)
• AMHmeasurements (>0.5 ng/mL is adequate, <0.15 ng/mL
is poor) ~
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I
'
VULVAR AND VAGINAL NEOPLASIA
• HPV 16 and 18 infection, cigarette smoking,
Risk factors for VIN
immunodeficiency
Characteristic iesions of extramammary • Longstanding pruritus with beefy red lesions,
Paget disease of the vulva eventually becoming eczematous white plaques
CERVICAL NEOPLASIA
Top cancer killer of women in the
• Cervicalcancer
developing world
Highest oncogenic potential among
• HPV 16, 18
HPVserotypes
• Cervarix (16, 18)
Types ofHPVvaccines • Gardasil (6, 11, 16, 18)
• Gardasil-9 (6, 11, 16, 18, 31, 33, 45, 52, 58)
• Persistent high risk HPV type ( necessary cause of
cervical cancer)
• Parity of 7 or more
• OCP use >5 years with HPV
• Current smokers & younger age at smoking
• Co-infected with Chlamydia or HSV-2
Risk factors for cervical cancer • HIV
• Early age at sex <14 years old
• Sex partners >6
• Pregnancy <17 years old
• No cervical cancer screening
• Low socio-economic status
• Poor access to healthcare services, poor nutrition, etc.
Initiation of cervical cancer
screening • Age 25
554
• Age 65: if with no history ofCIN 11/111/CIS/cervical
cancer, and with prior negative results (Two negative
Cessation of screening
primary HPVtests, two negative co-tests, or three
negative Pap smears within the last 10 years)
cancer,may
• Ifwith no historyofCIN 11/111/CIS/ceIVical
Screening after total hysterectomy
stop screening after total hysterectomy
• Continue screening for a total of 20 years after
Screening after history of CIN 11/111 spontaneous regression or treatment of lesions, even
beyond 65 years old
• If 21-24 years old: Repeat Pap smear in 12 months
(preferred), OR reflex HPV testing:
• If negative, return to routine screening
• If positive, repeat cytology in 12 mo
Management of ASC-US • If;eZS years old: Repeat Pap smear in 1 year
(acceptable) OR HPV testing (preferred):
• lfHPV negative test: Repeat co-testing in 3 years.
• If HPV positive test: Colposcopy and cervical
biopsy if needed
Management of ASC-H • Colposcopy with cervical biopsies if indicated
• If 21-24 years old: Manage as ASC-USexcept reflex
HPV testing
• If ;e25 years old:
Management of LSIL • If HPV unknown: Repeat Pap smear in 1 year
(acceptable) OR HPV testing (preferred):
• If HPV negative: Repeat co-testing in 3 years
• If HPV positive: Colposcopy and cervical biopsy
if needed
• Colposcopy with cervical biopsies if indicated;
Management of HSIL
immediate LEEP acceptable if ;e25 years old
• If 21-24 years old: Colposcopy with cervical biopsies
if indicated
• If 25 years old: Colposcopy, HPV screen, cervical
Management of AGC biopsies, endocervical sampling
• Endometrial,:jopsy in women ;,35 years old
and in women with risk factors for endometrial
hyperplasia, EIN, and endometrial cancer
Most common route of spread • Direct extension
555
I
.
ENDOMETRIAL NEOPLASIA
Most common exogenous source of • Estrogen hormone replacement without
estrogen leading to EIN progesterone
Classical symptom ofEIN and
• Postmenopausal bleeding or AUB
endometrial cancer
• Woman >45 years old with abnormal uterine
bleeding
Criteria for endometrial biopsy
• Postmenopausal women with abnormal uterine
bleeding, or EM stripe ~4 mm
• Oral medroxyprogesterone acetate or megestrol
Initial treatment for EIN
acetate
Definitive management for EIN • Hysterectomy
• Occurs in women with history of chronic
unopposed estrogen exposure
Type I endometrial cancer • Start as atypical endometrial hyperplasia or EIN
• Endometrioid
• More favorable prognosis
• Non-estrogen dependent
• Start in atrophic endometrium
Type II endometrial cancer • Serous or clear cell histology
• Associated with p53 mutations
• Less favorable prognosis
556
OVARIAN CANCER
Most common cause of gynecologic
• Ovarian cancer
cancer death
Reasons for high mortality among • Lack of effective screening tools
ovarian cancer patients • Presentation at late stages of the disease
Most common route of spread • Peritoneal
Most common lymph node site • Retroperitoneal pelvicand para-aortic lymph nodes
Main etiology of ovarian cancer • STIC,incessant ovulation
• Age
• Diet
• Family history
• Industrialized country
Risk factors for ovarian cancer
• Infertility
• Nulliparity
• Ovulation and ovulatory drugs
• Talc (controversial)
Eponym for ovarian malignant
• Sister Mary Joseph nodule
metastases to the umbilicus
• Peritoneal fluid cytology, total
abdominal hysterectomy with bilateral
Primary staging for epithelial ovarian
salpingooophorectomy (TAHBSO),
cancer
omentectomy, peritoneal biopsy, and pelvic and
para-aortic lymph node dissection
Serum marker for epithelial ovarian
• CA-125
cancer monitoring
Treatment of epithelial ovarian cancer • Surgery ± chemotherapy
Most common ovarian malignancy in
• Germ cell tumors
women <20 years old
Most common germ cell tumor • Benign cystic mature teratoma (dermoid cyst)
Most common malignant germ cell tumor • Dysgerminoma
• LDH - dysgerminoma
• AFP - endodermal sinus (yolk sac) tumor,
Serum markers for germ cell tumors
immature teratoma
• hCG - choriocarcinoma
• Unilateral salpingooophorectomy with complete
surgical staging± multiagent chemotherapy
Treatment of germ cell tumors
(surgery only for Stage IA dysgerminoma and
immature teratoma, grade 1)
Functional ovarian tumors • Granulosa cell tumor, Sertoli-Leydig cell tumor
Pathognomonic sign for granulosa cell • Call-Exner bodies (coffee bean nuclei, with cells
tumors arranged in small clusters around a central cavity)
Meigs syndrome • Fibroma, ascites, pleural effusion
• Granulosa-theca - estradiol and inhibin
Hormones produced by sex-cord stromal
• Sertoli-Leydig - androgens
tumors
• Fibroma - none
• Unilateral salpingooophorectomy with complete
surgical staging ± multiagent chemotherapy if
desirous of future pregnancy
Treatment of sex cord stromal tumors • Primary staging (same as that for epithelial
ovarian cancer) if completed family size or
557
postmenopausal
I
.
GESTATIONAL TROPHOBLASTIC DISEASE (GTD)
• Molar pregnancy (most common)
• Persistent GTD and invasive moles
Four classifications of GTDs
• Gestational choriocarcinoma
• Placental site trophoblastic tumors (PSTI) (rare)
• Extremesin age,prior historyof GTD(most common)
• Nulliparity
• Paternal age > 45 years
Risk factors for molar pregnancy • Diet low in beta-carotene, folic acid, animal fat
• Smoking
• Infertility
• Spontaneous abortion, previousmolarpregnancy
Most common symptom of molar pregnancy • Vaginal bleeding
Racial predilection for GTD • Southeast Asians, particulary Japanese
Pathogenesis ofcomplete molar pregnancy • Fertilization of empty egg
Most common karyotype of complete moles • 46XX
Effects of extreme levels of beta hCGin • Theca lutein cysts, hyperthyroidism,
complete moles hyperemesis gravidarum, preeclampsia
• Snowstorm pattern secondary to widespread
Ultrasound pattern for complete moles
chorionic villi swelling
Pathogenesis of partial molar pregnancy • Fertilization of normal ovum with two sperms
Most common karyotype of partial moles • 69XXY
Partial moles are often misdiagnosed as • Spontaneous or missed abortions
Ultrasound pattern for partial molar • Swiss-cheese appearance secondary to focal
pregnancy hydropic villi
Treatment for molar pregnancy • Suction curettage
• 48 hrs after evacuation, then every 1-2 weeks
Monitoring hCGlevels post-molar
until negative for 3 consecutive weeks, then
pregnancy
monthly for 6 months
• 14 weeks for complete mole
Average hCGnormalization time
• 8 weeks for partial mole
• 1-2% after one molar pregnancy
Risk of recurrent GTD
• 16-32% after two molar pregnancy
Low-risk GTNtreatment • Single-agent chemotherapy
High-risk GTNtreatment • Combination chemotherapy
• hCG >100,000 mlU/mL
Risk factors for persistent postmolar • Uterine size >14-16 weeks
GTDand invasive moles • Theca lutein cysts >6 cm
• Coexistent fetus
REFERENCES
I.Callahan T.Caughey A. Blueprints: Obstetrics and Gynecology, 7th Edition. 2018
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