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    Obgyn Pearls 2019 PDF

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    Wila Gatchalian

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    © All Rights Reserved
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    of 396
    ae PEARLS A QUICK REFERENCE ON COMMON CASES IN OBSTETRICS & GYNECOLOGY Daye CARE bree oar ted PANTS VIMO A sccolhotod Repropuctive ENDOCRINOLOGY Cae teee Latest DIAGNOSTICS & THERAPEUTICS bocce sett Trott) 9 CAGAYAN FACUN BRAVO CASTRO =SUPLIDO =TORRALBA re PO OOo aes Contributing ee than Cu, MD, DI coe M. Ortega, MD, DPOGS, FPSRM Elaine Johanna Limkin-El Jabbari, MD, DPBRO Karen Cybelle J. Sotalbo, MD, DPSP riston Van Manasan, MD Mary Rani M. Cadiz, MD Ana Rose Patupat, MD Maribel Co-van der Mee, up Ana Kristina M Hernande, 4p Amanda dela Cruz Dioman Katrina Aligamstia, MPM Mu Sigma Phi 2011200, 201620, Layout Editors: Martha Camille F,Dollete, MD Marian Clare U.Toledo, MD Samantha Beatrice A. de Guzman Illustrators: Faith Baccay Nonay Dela Calzada Til Wana Mica Gonzalez Kate Regala Hazel Lapitan Ina Aguirre Mikee Empleo Paula Maton Sam de Guzman Jitka Canlas Karin Bulong Claire Jacinto Sydney Madlangsakay fern taia Nicole Sacman Mary Elise Severino Glad Facun Mary Carabbacen Kyle Antonio Illustration, Book and Cover Design by Asia F. Chan Copyright © 2019 Mu Sigma Phi Sorority Inc. Published by: Mu Sigma Phi Sorority Inc UP College of Medicine Pedro Gil St, Malate Manila City Metro Manila 1004 Printed inthe Philippines ISBN: 978-621-96083-0-5 ALL RIGHTS RESERVED. Unless otherwise stated, all parts of this book are original and are protected by the Philippine Copyright Law enshrined in Republic Act No. 8293 or the Intellectual Property Code of the Philippines, No part of this book may be reproduced or transmitted in any form or by any means, including as photocopies or scanned-in or other electronic copies, or utilized by any information storage and retrieval system without written permission from the copyright owners, except for brief quotations embodied in critica articles and reviews. To request permission, please contact Mu Sigma Phi Sororily Inc. via email at obpearls@qmail, ice eo pearls@gmail.com or at our oficial Facebook page, https.//www facebook. nee additional copies of this book, please call (0956) 448-7035. You may also email usat opear's@amailcom or visit our official Facebook page at https: facebook con/OBpets0 Fe your orders, and to find out more information and updates, fi | Oscyn Pearis NOTICE The contents ofthis book have been appraised and cross-referenced with legitimate and up-to-date resources available to the authors and editors as of the time of writing. Similarly, the recommendations for management are in accordance to current clinical practice guidelines and are partially based on the knowledge and expertise of obstetrician-gynecologists practicing in the Philippines. It must be recognized, however, that the field of Ob-Gyn, as with the practice of medicine in general, is continuously evolving and that improvements and new recommendations may occasionally arise. While the author, editors, and publisher have utilized their best efforts in preparing this book and all its contents, they make no representations or warranties with respect to accuracy or completeness of all the information included therein and thus, do not guarantee any particular patient outcomes. Hence, the authors editors, and publisher duly express that they are not liable for any untoward incidences related to the direct application of information from the contents of this book, nor from its limitations in terms of coverage. The parties involved would thereby like to emphasize among its readers that confirmation with other sources and consultation with and affirmation from seniors or experts in the field are stil highly recommended when attempting to use the clinical approaches outlined within the bookii the actual management of their patients based on suitability and applicability. Notice | FOREWORD i tion of OB Pearlsis an exquisite manifestation of the passion and dedicat Hite from the UP College of Medicine who happen to be my sisses and bods ge Sigma Phi ed by my former student and resident, br. Stephanie Fay Samaden Cagayan Aproge of blood, sweat and tears in the tradition of Mu, this book offers a concise and comprehensive 6 av Enonedge and information geared towards medical student inthe field of Obstet se Gynecology asit offers an excellent source of reference and review for those who intend to utsue further training in Obstetrics and Gynecology. Practicing obstetrcian-gynecologists, and other es care providers, whose practices include women’s health, will definitely find this literature asa Useful reference inall aspects, covering the common ailments that women experience today, Source ‘The contents ofthis book encompass a wide range of topics, from the basics of health care for ‘wom. to complicated subspecialty problems such as malignancy and infertility. The last portion of the book deals with the most common laboratory stains in Gynecology, the tumor markers, hormone levels and surgical techniques which are of obvious importance to the patient and physician critical care, Every effort has been done to incorporate the new and exciting changes in Obstetrics and Gynecolog, Itsthe continued polcy ofthe authors to not only provide basic knowledge in Obsteticsand Gynecology, but, concepts that are novel to all practicing obstetrician-gynecologists. Indeed, this piece of literature, which possesses the enigma of being first, of being timeless, of being aa with glory, is never a destiny, but, an unwavering resolve, all for the glory of medicine and evan Po ARETAS P. SINGSON-ALDAY, M.D., FPOGS, FPCS Dean Emeritus(2016-present) Founding Dean (1996-2013) & (Ret. Professor Member, Board of Trustees (1997-present) University of Perpetual Help Rizal JONELTA Foundation School of Medicine Chairman Emeritus (2017-present) Department of Obstetrics & Gynecology Perpetual Help Medical Center-Las Pinas (Ret.) Professor of Obstetrics & Gynecology University ofthe Philippines College of Medicine and Philippine General Hosptl Mu Sigma Phi Sorority Batch 1961 iv | Oscyn Pears PREFACE COBGYN Pearlsis a concise but comprehensive reference book curated for medical students and residents alike ~ featuring basic Obstetrics and Gynecology information and clinical pearls deemed tobe helpful in practice. With contents based onthe latest clinical practice guidelines and the 25th edition of Willams Obstetrics and Gynecology books, the book covers P.E.A.R.L.S. - Perinatal Care, Essentials of Obstetrics, Abnormal Gynecology, Reproductive Endocrinology, Latest Diagnostic Trends in OB-GYN, and Surgical Procedures. The chapters are meant to supplement and teinforce the medical students’ and residents’ knowledge with must-knows necessary to their training in the field of OB-GYN. Summary drug tables and case studies are also conveniently included to facilitate reviews. Agood quick reference guide, the OBGYN PEARLS isan easy-to-tead book about basic to advanced principles of Obstetrics and Gynecology. Updated withthe latest CPGs, itis not only useful inthe proper care of pregnant patients but also those of women's health in general. Itaims to serve as a tool for aspiring health professionals for day to day rounds, conferences, and exams. This book was made possible through the combined efforts of distinguished experts from different medical institutions together with the members of the Mu Sigma Phi Sorority alumnae and undergraduates. MARIA STEPHANIE FAY S. CAGAYAN, MD GLADDY MAURA G. FACUN, MD. SYBIL LIZANNE R. BRAVO, MD CAROLYN R. ZALAMEDA-CASTRO, MD SHERRI ANN L. SUPLIDO, MD MARIA GERALDINE N. CASTILLO-TORRALBA, MD Prerace | Vv PREFACE COBGYN Peatlsisa concise but comprehensive reference book curated for medical students and residents alike ~ featuring basic Obstetrics and Gynecology information and clinical pearls deemed tobe helpful in practice. With contents based onthe latest clinical practice guidelines and the 25th exition of Willams Obstetrics and Gynecology books, the book covers PE.A.R.LLS. - Perinatal Care, Essentials of Obstetrics, Abnormal Gynecology, Reproductive Endocrinology, Latest Diagnostic Trends in OB-GYN, and Surgical Procedures. The chapters are meant to supplement and reinforce the medical students and residents’ knowledge with must-knows necessary to their training in the field of OB-GYN. Summary drug tables and case studies are also conveniently included to facilitate reviews. ‘Agood quick reference guide, the OBGYN PEARLS is an easy-to-read book about basic to advanced principles of Obstetrics and Gynecology. Updated with the latest CPGs, itis not only useful inthe proper cate of pregnant patients but also those of women's health in general. Itaims to serve as a tool for aspiring health professionals for day to day rounds, conferences, and exams. This book was made possible through the combined efforts of distinguished experts from different medical institutions together with the members of the Mu Sigma Phi Sorority alumnae and undergraduates. MARIA STEPHANIE FAY S. CAGAYAN, MD GLADDY MAURA G. FACUN, MD SYBIL LIZANNE R. BRAVO, MD CAROLYN R. ZALAMEDA-CASTRO, MD ‘SHERRI ANN L. SUPLIDO, MD MARIA GERALDINE N. CASTILLO-TORRALBA, MD PREFACE v AUTHORS MARIA STEPHANIE FAY S. CAGAYAN, MD, PhDHS (cand), FPOGS, FPSSTD, Fpsecp Professor 7 Department of Pharmacology and Toxicology Consultant Department of Obstetrics and Gynecology UP-PGH Medical Center, Manila Doctors Hospital : Philippine Representative, International Society for the Study of Trophoblastic Diseases (2001-2019) Past President, Philippine Society of Experimental and Clinical Toxicology (2015-2017) Ector in Chief, Philippine Journal of Experimental and Clinical Pharmacology (2014-2019) Editor in Chief, Journal of Perinatal Association of the Philippines (2015-2019) Honorary Editorial Advisory Board Asia- MIMS Obstetrics and Gynecology Disease Management Guidelines (2005-2019) MARIA GERALDINE N. CASTILLO-TORRALBA, MD, FPOGS, FPSMFM, FPSUOG Associate Professor Ill at the UP College of Medicine Consultan at he Department of Obstetrics and Gynecology, UP-PGH Medical Center Practicing Maternal and Fetal Medicine Specialist and OB Sonologist at the UP-PGH and Manila Doctors Hospital Board Member, Philippine Society of Maternal and Fetal Medicine ‘CAROLYN R. ZALAMEDA-CASTRO, MD, FPOGS, FSGOP Clinical Associate Professor Department of Obstetrics and Gynecology UP College of Medicine Practicing Obstetrcian-Gynecologist, Gynecologic Oncologist, Colposcopist UP. Philippine General Hospital, ManilaMed (Medical Center Manila), Manila Doctors’ Hospital and National Kidney and Transplant Institute Board Secretary, Philippine Board of Obstetrics and Gynecology 2019 Board Member, Society of Gynecologic Oncologists of the Philippines, 2019-2020 Board Secretary, Philippine Society for Cervical Pathology and Colposcopy, 2019-2020 PRO, Asia-Oceania Research Organization on) Genital Infections and Neoplasia Pilippines SYBIL LIZANNE R. BRAVO, RPH, MD, MSC, FPOGS, FPIDSOG Clinical Associate Professor Department of Obstetrics and Gynecology UP College of Medicine Practicing OB GYN and Reproductive Infectious Diseases Specialist, UP-PGH, Manila Doctors Hospital Medical Center Manila ce President Philippine Infectious Diseases Society for Obstetics and Gynecology (P10S06) vi | Oacyn Pearts SHERRI ANN L. SUPLIDO, MD, FPOGS, FPSMFM, FPSUOG Clinical Associate Professor Department Sa and Gynecology f Medicine Tree psttidan Gmecaogs, Maternal- Fetal Medicine Specialist, Obstetric and Gynecologic upPuinie General Hospital, ManilaMed (Medical Center Manila), Manila Doctors’ Hospital Head, Maternal-Fetal Medicine Unit, Center for Women’s Health, ManilaMed ao Board Member, 2017-2019, Public Relations Officer, 2017-2018, Assistant Treasurer, 2019, Philippine Society of Maternal-Fetal Medicine Board Member, Public Relations Officer, 2019, Bayside Council of Obstetrics and Gynecology Member, Panel 4, University of the Philippines Manila, Research Ethics Board, 2017-2019 GLADDY MAURA G. FACUN, MD Assistant Chief Resident (2015) Fellow, Section of Gynecologic Oncology Department of Obstetrics and Gynecology UP-PGH Medical Center Reviewers FILOMENA SANTIAGO- SAN JUAN, MD, PhD, FPOGS, FSGOP, FPSUOG, FPSO, FPSSTD Professor 6 Department of Obstetrics and Gynecology University ofthe Philippines College of Medicine Chair Department of Obstetrics and Gynecology Manila Medical Center(1992-1995), Quezon City Medical Center (1995), Manila Doctors Hospital (20142016) Editor in Chief Philippine Journal of Obstetrics and Gyencology (2011-2013) Editorin-Chief, Philippine Journal of Gynecologic Oncology, 2017 Founding Member( 1994), President (2002) Philippine Society of Ultrasound in Obstetrics and Gynecology Founding Incorporator and President, Philippine Society of Therapeutic High Intensity Focus Ultrasound in Obstetrics and Gynecology, 2018 President Philippine Society forthe Study of Trophoblastic Diseases 2013-2014 President, Philippine Society forthe Study of Cervical Pathology and Colposcopy 2017-2018 Member, Journal Committee, DOST-PCHRD Associate Member, National Research Council of the Philippines (Obstetrics and Gynecology, Gynecologic Oncology, Trophoblastic Disease) Founding Incorporator, Philippine Association of Medical Journal Editors (PAMJE) MARCELA DIANALYN SAZON-CARLOS, MD, FPOGS, FPSRM, FPSUOG, FPSGE, FIFEPAG Active Consultant and Past Chair, Angeles University Foundation Medical Center Board Member, Philippine Society of Reproductive Medicine 2018 - present MARIA ANGELA SIAN RODRIGUEZ-BANDOLA, MD, FPOGS, FPIDSOG Clinical Associate Professor, UPCM Department of OBGYN, Section of Infectious Diseases Section Chief OB-IDS St. Luke's Medical Center Global City Former Section Chief, OB-IDS UP-PGH Former President, Philippine Infectious Diseases Society for Obstetrics and Gynecology Autors | vii TABLE OF CONTENTS Foreword iv Preface v Authors vi A. PERINATALCARE 1 ees ow sa eenousn 16. 17. 18, 19. 20. 21, 22. 23. 24, Perinatal Counseling 2 Physiological Changes in Pregnancy Family Planning 17 Essentials of obstetrics 21 Placental Abnormalities 22 Abortion 26 Ectopic Pregnancy 34 Recurrent Pregnancy Loss 40 Gestational Trophoblastic Disease 46 Physiology of Normal Labor 55 Dysfunctional Labor 63 Essential Newborn Care (ENC) and Breastfeeding 67 1a. Breastfeeding 68 Puerperium 74 The Newborn 74 Fetal Growth Disorders 80 ‘14a. Intrauterine Growth Restriction (IUGR) 81 14b, Macrosomia 85 Disorders of Amniotic Fluid Volume 97 15a. Oligohydramnios 88 15b. Polyhydramnios 89 Preterm Labor 94 Postterm Pregnancy 101 Induction of Labor 104 Breech Delivery 109 Vaginal Birth After Cesarean Section 113 Intrauterine Fetal Demise 148 Obstetric Hemorrhage 122 Multiple Gestation 128 Hypertension in Pregnancy 134 2da. HELLP Syndrome 146 24b, Eclampsia 147 vili | Opeyn Pearts 25. 26. 27. 28. 29. 30. 31, 32. 33. 34, 35. Cardiovascular Disorders 149 Thromboembolic Diseases 154 Diabetes Mellitus 159 Thyroid Disorders. 165 28a. Hyperthyroidism 165 28b. Hypothyroidism — 166 Pulmonary Disorders 170 29a, Bronchial Asthma 170 29b. Pneumonia 175 29c. PulmonaryTuberculosis 180 Anemiain Pregnancy 184 Urinary Tract Infections 189 HiVin Pregnancy 192 Seizure Disorder 194 Adnexal Massesin Pregnancy 197 Cervical Cancerin Pregnancy 200 Cc. Abnormal Gynecology 202 36, 37. 38. 39. 40. a1. 42, 43. 44. 45. 46. 47. 48, 49. 50. 51. Reproductive Anatomy 203 Pediatric Gynecology 244 Cervicovaginitis 213 Genital Ulcers 216 Bartholin’s Gland Cyst/Abscess 220 Upper Genital Tract Infections 223 41a. Pelvicinflammatory Disease 223 4b, Tubo-Ovarian Abscess 225 41c. Abdominal Koch's Infection 226 Pelvic Organ Prolapse 229 Colposcopy 233 Endometrial Hyperplasia 236 Cervical Cancer 239 Endometrial Cancer 248 Ovarian Cancer 256 Vulvar Cancer 263 Vaginal Cancer 268 Diseases of the Breast. 271 Scales Used in Oncology 276 Taste oF Contents | ix D. REPRODUCTIVE endocrinology & infertility an 52. Menstrual Cycle 278 53, Amenorthea 283 54. Abnormal Uterine Bleeding 287 55. Menopause 293 56. Polycystic Ovary Syndrome (PCOS) 296 57. Endometriosis 304 57a. Adenomyosis 309 58. Infertility 370 E. Latest Diagnostics & Therapeutics 315 9. Establishing Age of Gestation 316 60. Fetal Surveillance 320 61. Immunohistochemistry Staining for Gynecologic Neoplasms 330 62. TumorMarkers 337 63. Overview Of Laboratory Tests In Ob-Gyn 334 64. Ultrasound for Ovarian Masses 337 65. Fluid And Electrolytes 340 66. Chemotherapeutic Drugs 342 67. Radiation Therapy 344 F. Surgicaltechniques 347 68. Endoscopy 348 69, Laparoscopy 350 70. Endometrial Biopsy 352 71. Peripartum Hysterectomy 353 72. Operative Vaginal Delivery 354 72a. Forceps Delivery 354 72b. The ABCD Of Operative Vaginal Delivery 356 73. Abdominal incisions 359 74. Anesthesia For Obstetric Procedures 364 Appendix xij Case Studies xiif Approach toCases xiii Case 1 xiii Case2 xy Abbreviations xvii References xa Index soeviz x | OBoyn Pearis PERINATAL CARE 2 PERINATAL COUNSELING 1. DIAGNOSIS OF PREGNANCY [—progasteevpence = «Enlargement of abdomen > Starts at 6 wks - > At12wks-fundus felt on bimanual exam, uterine body is almost, 8 emaverage diameter : Changes in uterine size, shape, and consistency ; © HEGAR'S SIGN ~ 6-8 wks: softening of uterine isthmus Changes in cervix ; > GOODELL'S SIGN - 6-8 wks: softening, change in position * BRAXTON-HICKS CONTRACTIONS <> 28wks: painless, perceptible, not regular Ballotment Physical outlining of fetus Detection of B-HCG 6 days after fertilization, 8-9 days post-implantation Urine Pregnancy Test - (+) at 25 mlU (very sensitive) lobular and ity POSITIVE SIGNS Unquestionable proof | Fetal heart tone © Normal rate: 120-160 bpm © Auscultation: 17 wks (19 wks in 95%) © Doppler: 10 weeks | © Transvaginal-Ultrasound: 6 weeks Perception of fetal movement by examiner (20 weeks AOG) Sonographic recognition of pregnancy © Early UTZ~done before 12 wks AOG (most accurate in establishing age of gestation) * Gestational sac- first sonographic evidence of pregnancy; seen at 45 weeks AOG by Ws PRESUMPTIVE Gives grounds for reasonable opinion or belief ‘Symptoms Nausea and vomiting (morning sickness) | © 6-18 wks (peak of HCG 8-10 wks) * Disturbances in urination (T frequency) * 1and 3¢trimester * Fatigue . Perception of fetal movement (quickening) * 16-18 weeks - multigravid * 18-20 weeks - primigravid PERINATAL CARE Ey Cessation of menses more than 10 days from expected menses © Changes in cervical mucus © Starts at 6 wks AOG * Elevated progesterone during pregnancy lowers NaCl concentration inthe cervical mucus that prohibits ferning Changes in the breast © Engorgement starts at 6-8 wks Discoloration of vaginal mucosa © Atoweeks * Chadwick’ sign - dark-bluish or purplish-red and congested vaginal mucosa Thermal signs * At6 weeks: T Temp = T Progesterone ‘© Skin pigmentation * Striae = T melanocyte stimulating hormone (MSH) * Chloasma / Melasma - mask of pregnancy * Linea nigra - darkening of linea alba * Siriae Gravidarum = collagen breakdown * Spider Telangiectasia = T estrogen Il, COMPONENTS OF A ROUTINE PRENATAL CARE TABLE-1.1. Schedule of Components of a Routine Prenatal Care FIRSTVISIT 15. History Complete © Updated Physical examination Complete Blood pressure Maternal weight Internal exam Fundal height Fetal heart rate/position Laboratory test Hematocit or hemoglobin Blood type and Rh factor Antibody screen ©/O/E/@/e/@ © © © @/e|e/e@ PAP smear screening Glucose tolerance test Fetal aneuploidy screening Bt andlor Neural tube defect screening Urine protein assessment Urine culture e|® 1. Perinatat Counseuins | 3 FIRST VISIT 244 Rubella serology Syphilis serology Gonococeal culture Chlamydia culture Hep B serology Hiv serology Group B streptococcus culture 2/©|@\c|@\eo + wimester aneuploidy may be offered between 11-14 weeks A-testat 28 weeks if indicated B-test should be offered f high risk women should be e-tested at the start of 3 trimester D high sk women shoud be screened atthe fist vist and retested at the start of 3 trimester E-rectovaginal culture should be done between 35-37 weeks lil, HIGH RISK PREGNANCIES Maternal age <17 Primigravides >35 Poor OB history ‘© 2 consecutive spontaneous abortions ‘© 3 ormore repeated spontaneous abortions * Premature delivery * Fetal death-in-utero © Neonatal death Previousbirth with congenital anomalies Problems in fetal aging, structure, and size © Beyond 41 weeks © Growth restriction (IUGR) © Macrosomia © Unsure of LMP ‘Fetal congenital anomalies . © Multiple gestation Placenta previa / abruptio placenta Medical conditions Reproductive tract disorders Malignancy Psychiatric conditions / mental retardation Trophoblastic disease Oligohydramnios / polyhydramnios 10 DANGER SIGNS OF PREGNANCY . : tate _ © Decrease in fetal movement 5 Blutng of vision © Uterine contractions fioonged vomiting © Dysuria © Fever i Fever : * Vaginal bleeding/discharge EpigastridRUQ pain © Edema (face, fingers) PERINATAL CARE IV, RECOMMENDATIONS FOR TOTAL AND RATE OF WEIGHT GAIN DURING PREGNANCY TABLE-1.2. Recommendations for total and rate of weight gain during pregnancy (taneous Cinna ‘Mass k Ib (Ibs/week) aa inex : oa Underweight <185 125.18 28-40 143 Normal weight 18,5-24.9 11.5-16 25-35 08-1 Overweight 2529.9 715 1525 05.07 Obese 230 59 11-20 04.0.6 “Empirical ecommendations for weight gain in win pregnancies include: normal BMI, 37-54 Ib; overweight women, 31-50 Ib; and obese women, 25-42 Ib, BMI = (weightin kilogram (height in meter) V. RECOMMENDED DAILY DIETARY ALLOWANCE FOR PREGNANT AND LACTATING ADOLESCENT AND ADULT TABLE-1.3. Recommended daily dietary allowance for pregnant Eo LACTATING Fatsoluble vitamins Vitamin A 770 ug 1300 ug Vitamin Da Sug 154g Vitamin E 15mg 19 ug Vitamin Ka 90 ug ug Water-soluble vitamins Vitamin € 85mg 120mg Thiamin 14mg 14mg Riboflavin 14mg 16mg Niacin 18mg 17mg Vitamin B6 1.9mg 2mg Folate 600 ug 500 ug Vitamin B12 2.6ug 289 Minerals Gliuma 1000 mg 1000 mg Sodium a 159 159 Potassium a 479 51g tron 27mg 91mg Tine img 12mg lodine 220 ug 290 ug Selenium 601g 70u9 Protein Tig 79 Carbohydrates 175q 210g Fibera 28g 299 Recommendations measured as adequate intake. 1, PERINATAL COUNSELING | 5 vi. EXERCISEIN PREGNANCY BLE-1.4, Contraindications to aerobic exercises during pregnancy TABLE-1.4. RELATIVE CONTRAIND) Severe anemia Unevaluated maternal aria Chronic bronchits Pootly controlled type 1 DM Extiere morbid obesity Extreme underweight (BMI <12) History of extremely sedentary lifestyle Fetal growth restriction in current pregnan Poorly contrlled hypertension a] Orthopedic limitations Poorly controlled seizure disorder Poorly controlled hyperthyroidism Heavy smoker [ABSOLUTE CONTRAINDICATIONS icant heart disease iy Hemodynamicaly signifi Rese lung dese, Incompetent cervndcercage Nolftl gestation at ikfor peter ber Paste second nh inet bleeding Placenta preva after 26 weeks Preterm labor during the current pregnancy Ruptured membranes Preedampsia camhythmia Trivia: Sayuntis: Sayaw ng mga Buntis is an exercise program pioneered by Dra. Ma, Stephanie Fay Samadan Cagayan which aims to promote health behaviors for pregnant women by focusing con proper nutrition, and appropriate exercise. VII. IMMUNIZATION DURING PREGNANCY TABLE-1.5. Summary Table of Vaccines and Dosing Schedule for Pregnant Women VACCINE Do Eee Ca Tetanus-iphtheia | Toxoid 05m 1#-single tetanus | Updating immune {Td)fetanus- toxoid given any status should be part dightheraacellular timeafter 4th | of antepartum are pertussis (dap) week AOG | 21 dose- given as | tetanus-diphtheria- acellularpertussis | (1DaP) vaccine preferably at around 28th weeks AOG 3 doseat6 months after the fist dose Booster every 10 years MMR Liveattenusted | O.5miSC Single dose, Containdcated | postpartum for in pregnancy ; susceptible women Varicella Uveattenuated —[ O.5miSC Two doses, 2* dose | Contraindisted should be 4-8 weeks | in pregnancy ; after 1¥dose Hepatitis A Inactivated 518,yo: 0.5mlIM | Two doses, 6 and postexposuie 219yo:1.0mlIM _ | months apart ifatrsk Hepatitis Inactivated <<19y0:0.5mlIM | Three dose seiesat | and postegosue# = 220yo: 1.0mlIM | 0,1,and6 months _| atrisko infection PERINATAL cane “CINE TYPE Css sila Mae = Inactivated O.Sml IM One dose every year | pregnant women, Vofluence regardless of trimester during fluseason Inactivated 0.5ml IM (if One dose, Mestancea polysaccharide) 0.5. | revaccination mIM(ifconjugate) | every 35 years May be given during pregnancy if needed Pneumococcal | Inactivated O.5SmiiM One dose, revaccnation after 6 yeas, May be given during pregnancy if needed Human Inactivated OSmiIM Three dose series at_| Not recommended papillomavius 0,1,and 6 months _| in pregnant women VIII. OTHER FAQ DURING PREGNANCY Travel Automobile * Lap belt snugly positioned under ab * Shoulder belt between breasts Air * Can safely fy ifless than 36 weeks domen and on top of upper thighs Coitus Caffeine intake * Is not harmful to pregnancy But should be avoided if there is iskof abortion o preterm pregnancy * Limited to ess than 300mg/day or 35 cupts of coffee Alcohol * Causes fetal alcohol syndrome: growth restriction, facial abnormalities and CNS dysfunction * Avoid or stop alcohol intake Cigarette | smoking * Causes preterm pregnancy, growth restriction, sudden infant death syndrome (SIDS), abortion fetal death, fetal digital anomalies ‘Smoking cessation * Nicotine medications may be recommended if non-pharmacologic intervention failed 1, PERINATAL COUNSELING | 7 PHYSIOLOGICAL CHANG, PREGNANCY N ‘A. ANATOMIC CHANGES UTERUS rn 7 ‘© Enlarges with an average volume of 5 liters, average weigt tof 1100 gram: Enlargement due to stretching and matted hypertrophy of myocytes . Uterine hypertrophy in early pregnancy due to estrogen and perhaps, pr spherical by “12 weeks AOG and now outside the pelvis Progesterone Dextrorotation - caused by rectosigmoid on the left Braxton-Hicks contractions - irregular uterine contractions more pronou ed dingy end regnan | theropicental blood flow: 450-600 ml/minute near term CERVIX Softening and cyanosis. Vasculaity and edema ‘© Eversion of the columnar epithelium ‘© Beading - crystallization of cervical mucus under the microscope due to progesterone ‘* Ferning - arborization pattern under the microscope indicative of amniotic fluid leakage OVARIES + Owlation ceases * CORPUS LUTEUM --maximum function 67 weeks of pregnancy or 4-5 weeks post oan produces progesterone ‘ VAGINA AND PERINEUM * CHADWICK SIGN - violaceous color of the vagina secondary to increased vasculaity © Loosening of connective tissue Increase mucosal thickness Fine, hob nailed appearance of the vaginal epithelium SKIN Abdominal wall STRIAE GRAVIDARUM - stretch marks DIASTASIS RECTI - separation of rectus muscles at the midline Hyperpigmentation LINEA NIGRA - hyperpigmentation of midline abdominal skin MELASMA GRAVIDARUM OR CHLOASMA - “mask of pregnancy” brownish patches on fxt and neck Vascular changes Vascular spiders Palmar erythema BREASTS * Breast tenderness and paresthesia Increase in size 8 | Periatat care Nipples darken and enlarge : © Glands of Montgomery - hypertrophic sebaceous glands Increased by additional 10% in twin gestation METABOLIC CHANGES: ‘Average weight gain = 12.5 kilos or 27.5 Ibs Increased water retention BMR by the 3° trimester is 10-20% higher Increased by additional 10% in twin gestation Protein Metabolism Products of conception, uterus, fetus are all protein rich * More eficient use of protein during pregnancy Carbohydrate Metabolism Mild fasting hyperglycemia Postprandial hyperglycemia Hyperinsulinemia Pregnancy induced peripheral insulin resistance (to sustain a postprandial supply of glucose to the fetus) HEMATOLOGIC CHANGES ‘Hemoglobin and hematocrit decrease © Blood viscosity decreases © "Hypervolemia of pregnancy" + Averages 40-45% above the non-pregnant volume after 32-34 weeks ‘* Tomeetthe demands of the enlarging uterus and hypertrophied vascular system Provide nutrients for fetus and placenta £ Protect against impaired venous return inthe supine and erect position * Safeguard against the effects of blood loss CARDIOVASCULAR SYSTEM * Changes occur as early as 8th week AOG * Increased cardiac output + Reduced systemic vascular resistance Increased heart rate - resting pulse rate increase of 10 bpm Displaced tothe left and upward-arge cardiac silhouette on xay, ficult to detect cardiomegaly Altered cardiac sounds Exaggerated splitting of the 1% heart sound No definite aortic or pulmonary elements of the 2" heart sound * Loud, easily audible 3¢ heart sound Heart * Systolic murmur in 90% of cases, intensified during inspiration * Increased production of prostaglandin E2 and prostacyclin (PGI2). during the latter part of pregnancy to help regulate blood pressure and platelet function * Supine hypotension occurs in about 10% of women secondary to compression of the great vessels by the uterus Cardiac output * MAP and vascular resistance decrease - decreased blood pressure * Basal metabolic rate and blood volume increase * Cardiac output, stroke volume and heart rate increase 2. PHYSIOLOGICAL CHANGES IN PREGNANCY | 9 RESPIRATORY SYSTEM © Diaphragm rises Respiratory rate, Me minute ventilation increases Tidal volume and resting n Functional residual capacity and residual volume decrease because of the el Maternal arteriovenous oxygen Is decreased , aed tial olume -» Increased oxygen delivered > Increased total hemoglp Increased oxygen capacity and increased CO 44cm during pregnancy [ung compliance, max breathing capacity, forced time vital @paciy ed daphao, in mas, URINARY SYSTEM Kidney size increases slightly ‘ / Glomerular filtration rate and renal plasma flow increase (urinary frequency is commor Serum creatinine decreases; creatinine clearance increases n) Glucosuriaon UAmay be normal to an extent because ofthe increased GFR and decea tubular reabsorption of glucose sed Proteinuria normally not evident except in small amounts or after vigorous exercise © Hematuria usually because of contamination; if not, may signify urinary tract disease Ureters «© Laterally displaced and compressed atthe pelvic brim © Useteral dilatation takes place (R>L) © Unequal dilatation # Dueto cushioning effect on the left by the sigmoid © Greater compression on the right because of dextrorotation © Right ovarian complex is dilated and lies obliquely over the right ureter © Ureteral elongation accompanies distention Bladder © After 12 weeks, the bladder trigone elevates Near term, with an engaged fetus, there is impaired blood and lymph drainage from the bladder base a edematous, easily traumatized, prone to infection GASTROINTESTINAL TRACT Stomach and intestines are displaced by the uterus; PE findings may be greatly altered Appendix displaced upward and laterally Gastric emptying time unchanged during pregnancy but prolonged during labor (danger of aspiration during general anesthesia) Pyrosis (heartburn) caused by acid reflux * Altered position of the stomach ‘* Decreased tone of the lower esophageal sphincter Hepatic blood flow increases Portal vein diameter increases Gall bladder contractility is reduced (cholestasis of pregnancy) increased risk of gallstones 10 | PeRaraL care B. ORGAN SYSTEM PHYSIOLOGIC CHANGES CARDIOVASCULAR SYSTEM TABLE-2.1. Cardiovascular Changes in Pregnancy ei ualais ea eS Ey | Heartsize Increases Increased diastolic filling and muscle hypertrophy [Murmurs ~~ | Physiological systolic Ejection murmurs attributable to increased stroke and diastolic volume usually occur in early or mid-systolic and - __| are best heard along the left sternal edge fece Hearts pushed upward and forward, deviating tesultin changes that _| electrical axis tothe left by 15-20 degrees, | resemble ischemia | causing flattened or inverted in lead th | Cardiac output Increases 1.5Umin Greatest increase occurs immediately after delivery _ with redistribution of blood flow from uterus ‘Rhythm Increase in atrial and ‘Supraventricular tachycardia not infrequent ventricular extra systole Heart Rate Increases from 70 10 | 85 beats per minute | Stoke Volume Increases from 63 0 70 ml Systolicand Decreases soon after ‘Supine hypotension - decreased venous return Diastolic BP beginning of pegnancy | due to compression from the gravid uterus and mid-pregnancy Increased blood flow through alternative pathways | (100-110160:70 mean _| suchas paravertebral azygous veins levels); then returns to pre-pregnant values by third timesterand term Pulse Pressure Increases | Venous Pressure | Increases in femoral system Unchanged in arms Peripheral resistance _| Decreases Pulmonary BP Unchanged Blood flow to uterus | Increases by500 ml/min _| No autoregulation Blood flow to kidneys _| Increases by 400 ml/min - Blood low toskin | Increases by 300 400 ml/min Blood flow to breasts | Increases by 200 mlimin | 2. PHYSIOLOGICAL CHANGES IN PREGNANCY | 11 RESPIRATORY SYSTEM TABLE-2.2. Respiratory Changes in Pregnancy Valais Dasa eu ld Sy Anatomy increases of subcostal angle from | Increased upper espiata, 480t0 1030» 3cmincrease | capillary engorgement crc in wansthoracc diameter increased congestion eps, and intubation trauma Tidal volume increases by 300 ml or 40% Expratory reserve volume Decreases by 200 ml Cephalad displacement | of diaphragm Residual volume | Decreases by 300 ml or 20% [inspiratory capacity T increases by 300 ml Functional residual volume Decreases by 500 mi Minute volume Increases by 40% or 3Umin Increased rate of induction ah and beginning in fist trimester emergency from inhaled anes. Maximum breathing capacity __| Unchanged Forced expiratory volume Unchanged Peakerpiratory ow ate Unchanged Closing volume May increase Pulmonary dfusing capacity | Decreases by 4 mllminimmig Oxygen requirement increases by 30-40milimin Carbon dioxide output Increases; expressed as respiratory quotient Carbon doxide pressure Decreases from 35-40 mmmig to 28:30 mmHg Oxygen pressure Increases pH Mild increase (7-40-7.44 is normal) | Compensated respiratory alls p02 Mild increase (100-104is normal) p02 Decreases (30-31 mig is normal) RENAL SYSTEM AND HOMEOSTASIS Renal System and Homeostasis Changes in Pregnancy TABLE: eas eee eels re EY Glomerular filtration rate Increases from 97 ml/min to 128 milmin by 10 weeks Glucose excretion Increases Random glycosuria Protein excretion Increases less than 300 mg/24 hours is normal Renin, Angiotensin | and i Increases Diminished vascular response causes less pressor effect from angiotensin Anatomic changes Dilation of renal calyces and ureters | Increased risk of pyelonephritis to pelvic brim; ‘physiological’ screen for asymptomatic bacteria"? hydronephrosis, right >left Potassium Increased retention 12 | PeRIvaTat cane aig EXPECTED CHANGE ae Sodium Increased retention Urine output No significant change Vitamin excretion Increased loss of folate vitamin 812, and ascorbic acid | Osmolality Decreases 10 mOsmikg in first trimester, then stable ‘Sodium Decreases 3 mEqiLin fist trimester, then stable hs Potassium Decreases 0.5 mEq/L Calcium Decreases (total and ionized) Increased intestinal absorption of calcium and increased bone turnover Magnesium Decreases 10-20% in fist half of pregnancy Tine Decreases Copper Increases from 1.14 mall 02,03 mg/L.by term Chloride Unchanged Bicarbonate Decreases markedly(18- Compensates for decrease in pCO2 22 mE qlLis normal) Total protein Decreases from 72 gl. t0 62 g/L ‘Albumin Decreases from 47 g/L.to 36 gi. Urea, creatinine, and uric acd Decrease fist trimester, stabilize second trimester increase toward term Vitamin B6 Decreases Blood glucose Fasting levels decrease in first trimester, then unchanged Postprandial levels remain elevated longer, prolonging return to fasting state Increased glucose levels allow passive difusion weightthan adult male | across placenta to fetus Folate Decreases 50% toward term Vitamin B12 Decreases 50% or more Vitamin B12 levels in folate- deficient women will increase with folate supplementation alone ENDOCRINE SYSTEM ‘TaBLE-2.4. Endocrine Changes in Pregnancy alas rata ed Ey Pituitary gland Increases to 50% greater Attributable to increase of prolactin secreting cells in anterior lobe Increases from 300 to 5000 miU/L Prolactin FSHI/LH Decrease to nearly undetectable ACH Increases Human growth hormone Decreases 2. PHYSIOLOGICAL CHANGES IN PREGNANCY | 13 as Gia kad COMMENTS Melanocyte-stimulating hormone | Increases May be responsible fortnes niga chloasma, and inceseg ateolae pigmentation Vasopressin Unchanged Stimulation of nerve ending in breast causes ree incesse in oxytocin and vasopressin Oxytocin Unchanged Thyroid anatomy Unchanged TSH Unchanged May be suppressed dur toes tineer de HCG-metiated incase in thnig hormone production -subletug may be exacerbated by concn, that increase HCG levels, suche hyperemesis, molar pregnancies, and multiple pregnancy Thytoid binding globulin Increases - doubles by end of first trimester; triples by term Due to estrogen effect on ver Thyroxine (T4) Increased total circulating Fetal thyroid hormone production level; unchanged free T4 commences at about 18 weeks Tiodothyronine (13) Increased total circulating level, unchanged free fraction Reverse T3 Unchanged in maternal circulation; | increased in cord blood | ‘Adrenal anatomy Unchanged | CBG Increases - doubles by | second trimester | Cortisol Increases to 3 times Episodic patter of release onpregnant values is maintained Aldosterone _| Increases 2-fold by term | Deoxycorticosterone Increases by 20-100 times Testosterone Increased total amount; Decreased free fraction ‘Androstenedione Increases by 50% TO-old increased rate of transformation to estradiol and estrone | DHEA Unchanged or small decrease | Catecholamines Unchanged Pancreas Hypertrophy of islets due | to hyperplasia of B cells, Insulin Increased fasting levels toward term | Proportionally les increase of Hyperplasia of pancreaticB cells | glucagon compared toisulin' ingulin: glucagon ratio is increased Glucagon Increased fasting levels Glucose Slight decrease Especially fasting levels Parathyroid hormone Increased during end of pregnancy | Maintains calcium levels in face of increased renal absorption and transfer to fetus 14 | Peninatat care Bunn Bick eo ‘COMMENTS 25-hydroxyitamin D Unchanged 1125 -Dihydroxyvitamin D Increases Calcitonin No change to slight increase Progesterone Increases from 0.2 giml to Production originates in corpus 139 g/ml (up to 1000-fold) luteum over frst 7-Bwe! then placenta takes over Estradiol Increases about 500-fold from 0.05 ug/l to 18 g/ml T7-Hydroxyprogesterone Increases to maximum level by week 8 Relaxin Increases Secreted by the corpus luteum as wells the decidua andthe placenta in apattem similar to that of hCG Estriol Increases Human Placental Lactogen (hPl) Increases about 5000 fold from 0.002 U/ml to 10 wim! HCG Plasma levels increases Peak 93 Ulml rapidly, doubling every 2 Term 14 Uiml daysin the first trimester GASTROINTESTINAL SYSTEM TABLE-2.5. Gastrointestinal Changes in Pregnancy ais sia lsd ee Appetite Increases Gastric reflux Increases Cardiac sphincter laxity and anatomic displacement “eated during labor and delivery! anesthetic procedures with non-particulate oral antacids Gastric secretion Decreased acidity; increased volume | ‘Fullstomach effect increases risk of aspiration Intubation requires cuffed endotracheal tube Gastic motlity Decreases Intestinal absorption Increases Intestinal transit time Delayed Large intestine Greater absorption; slower transit time liver Unchanged Gallbladder Larger due to passive dilation 2. PHYSIOLOGICAL CHANGES IN PREGNANCY | 15 HEMATOLOGIC SYSTEM TABLE-2.6, Hematologic Changes in Pregnancy acd FXPECTED CHANGES COMMENTS 40-60% increase from 12 to 36 wee Plasma volume 70-10% increase in multiple gestations ‘ Increases 15-30% Greater increase with iron Total erythrocyte volume Sipeneiees Henaioait Decreases 3 5th by 36 weeks Physiological anemia duet greater proportionate increase in plasma volume compared tp erythrocyte volume; ess change with iron supplementation Hemoglobin Decreases 210% by third trimester Jarvolume | Unchanged Good indicator aren status belied Slight increase with ron supplementation roe sedimentation ate | Signficamtly increased Provides litle dagnosticvalue, Eye combined with physiologic increase in WBCS can cause false suspicion for infection wats Increase 8% by term and may Predominantly due to increase futher postpartum increase in neutrophils Serum iron Decreases 35% by term Serum transferin Increases by 100% or more Total ron binding capacity | by second trimester markedly increased | Totaliron binding capacity —_ | Increases by 25-100% | Serum fertn Decreases markedly (even with Nadi 30% oles ofromalalis iron supplementation) Best test to assessiron deficiency anemia in pregnancy | Erythropoietin Increases 4fld | ‘Alpha ftopratein Increases Larger increase in neural tube defects, abdominal wall defects, and fetal death | Glutamate ovaloacetic Unchanged | transaminase and glutamatic- pyruvic transaminase Creatinine kinase Decreases fist half of pregnancy j Lipase Decreases | | Alkaline phosphatase Increases Heat stable fraction | formed by placenta Lipids Increase Triglycerides, cholesterol, phospholipids and reefaty acidsallincease progressively —_ Fibrinogen Increases 2g/L by term Overall increased tendency | towards thrombosis Factors Vi Vil and x increase FactorsXI and Xi Decrease by about 30% Antithrombin Decreases 16 | Perinatat care S 9 FAMILY PLANNING NATURAL METHOD These family planning methods predict the fertile days of each menstrual cycle and advise sexual abstinence during these days STANDARD DAYS METHOD The couple must avoid unprotected intercourse during cycle days 8 through 19 A prerequisite is a regular monthly cycle of 26 to 32 days; otherwise, it is not very successful They may use cycle-beads or may mark the calendar to identify the fertile days CALENDAR RHYTHM METHOD The woman must count the number of days in her shortest and longest menstrual cycle during a 6-to 12-month span Eleven days are subtracted from the longest cycle duration to identify the last fertile day. While, eighteen days are subtracted from the shortest cycle duration to calculate the first fertile day. During the interval of these fertile days, unprotected sexual intercourse must be avoided. TEMPERATURE RHYTHM METHOD This method predicts the day of ovulation by detecting a slight change in basal body temperature of around 0.4°F days before the ovulation Itis most effective when the couple abstains for unprotected sexual intercourse from the first day of menstruation until the 3° day of increased basal body temperature CERVICAL MUCUS METHOD |. BILLINGS METHOD: Abstinence is advised from the first of menstruation until 4 day of slippery mucus discharge. | TWO-DAY METHOD: The woman isnot fertile if she did not note mucus discharge on the day of intercourse orthe day prior - SYMPTOTHERMAL METHOD: This combines the cervical mucus method to identify start of fertile period and basal body temperature method to identily end of erie period. tentals more complex application but does not necessarily improves the failure rate. 3. Famiuy PLanninc | 17 TABLE-3.1. When to Start the Different Family Planning Methods ny Combination Oral Contraceptive Pills eau WOMEN d bcd LOTT Fist day of menstrvation * Quickstart: onthe day of prescription but with temas method forfirst 7 days * Sunday star frst Sunday ay onset of menstruation but neh, alternative method for fist, dag, Progestin Only ill not exclusively breasteeding, start 3 weeks postpartum. For mothers who are breastfe- eding exclusively ovulation during the fist 10 weeks after delivery is unlikely. Depot medroxyprogesterone acetate (DMPA) | The timing of initiation of DMPAis controversial in breastfeeding patients ‘The World Health Organization recommends tat injectable depot medroxyprogesterone acetate should not be used before 6 weeks postpartum. Within 5 days of menstruation Implant Before discharge Within 5 days of menstruation Intrauterine Device “I week postpartum or when uterine involution is completed at 3to 6 weeks postpartum “Anytime inthe cle Yurpe RegimenlEmergency Contraception Progesterone only regimen as soom as possible ater unprotected intercourse until 72 hours after * Combined regimen or progestin only as soanas possible ater unprotected intercourse until72 hours after 4 low dose pills within 72 hrs after unrpotected coitus followed by another 4 low dose pills afer 12 hs * OR: 2 high dos pls followed by another 2 pills aftr 12 rs Lactational Amenorrhea Immediately postpartum | Not applicable VI. COMBINATION ORAL CONTRACEPTIVE PILLS > Mechanism of Action Estrogen Progesterone Suppresses LH Thickens cervical mucus 18 | Periarat care Suppresses FSH thereby blocking ovulation Stabilizes endometrium which prevents breakthrough bleeding Renders endometrium unfavorable for implantation Pe ee rs) wee e ere ccc ne Ad Pillis taken daily, ideally at the same time each day. The hormone pills are taken fora specified time followed by placebo pills, where withdrawal bleeding is expected. The duration of time taking the hormone, or the placebo depends on the product regimen. istration . Contraindications Previous stroke Prior MI Hypertension Smokers Olderage>35 years old Diabetes Thrombophilia Migraine headaches with visual aura or other focal neurologic signs Active hepatitis Side Effects Altered drug efficacy Increase 1G, total cholesterol, HDL, VLDL, decrease LDL. Increase fibrinogen and clotting factors Increase angiotensinogen production Increase sex-hormone binding globulin levels Increase T4 and thyroid-binding proteins Increase risk of stroke, myocardial infarction, VTE, and pulmonary embolism in those with risk factors prior to pill use Cholestasis and cholestatic jaundice . Benefits Increased bone density Reduced menstrual blood loss and anemia Decreased risk of ectopic pregnancy Improved dysmenortheal from endometriosis Fewer premenstrual complaints Decreased risk of endometrial and ovarian cancer Reduction in various benign breast diseases Inhibition of hirsutism progression Improvement of acne Prevention of atherogenesis Decreased incidence and severity of acute salpingitis, Decreased activity of rheumatoid arthritis, 3. Fawity PLannins | 19 Vil. vil 20 | PROGRESTIN ONLY PILLS A. Mechanism of Action Cervical mucus thickening Endometrial atrophy 2 . Administration + The minipill should be taken each day, strongly advised to be taken at the same time each gy, If delayed for 4 hours, another contraception method should be done for the next 48 hours 9 Contraindications Pregnancy * Livertumors Breast cancer © SLE Componentallergy * APAs Severe, decompensated cirrhosis 2 Side effects Inegular menstrual bleeding Weight gain Loss of Bone mineral density Benefits Does not affect milk production in lactating mother Ill. LACTATIONAL AMENORRHEA ._ Physiologic Basis The prolactin hormone, responsible for milk production, also suppresses the FSH and LH thereby inhibiting the return of normal menstrual cycle including ovulation All conditions must be present to use lactational amenorrhea as contraceptive Menstruation has not yet returned Infant s less than 6 months old Infants fully breastfed most ofthe time .. Benefits No cost No side effects Promotes breastfeeding which is beneficial to both mother and child PERINATAL CARE EsseNrTIALS OF OBSTETRICS PLACENTAL ABNORMALITIEs 1. PLACENTA A. Typical Placenta Composed ofa placental disc, extraplacental membranes and three-vessl umbilical cag © Weighs 470 grams, round to oval wth a22-cm diameter, wth central thickness of2 Sov Sonographically, homogenous and 2 to 4 cm thick, ies against the myometrium ang indens into the amnionic sac | | ‘* Proportion of weight of baby is 1:6; occupies 30% of uterine wall B. Abnormal Placental Shapes ‘TABLE-4.1. Abnormal Placental Shapes Placenta bipartita or biloba * Multiple lacnis fh Single fetus F * Division incomplete, andthe vesels of eta orgin extend fy Ponaaeed lobes) one abet the cher before uniting to form the umber Placenta triplex {distinct lobes) * Small accessory lobes develop in the membranes ata distance from the periphery ofthe main placenta * The tissue ofthe ring has atrophied « Rare, occuring in 1 of 6000 deliveries « Higher risk of antepartum and postpartum bleeding and fetal growth restriction * Fetal membranes are covered by functioning vil, and the placenta develops asa thin membranous structure Membranous placentalplacenta diffusa | _ occupying the entire periphery of the chorion ‘ Placenta may not separate readily and may givers to beading which resembles that seen in central placenta previa ing central portion ofa discoidal placenta ‘Often mistaken asa placenta with retained cotyledons in the tens * The fetal side is smaller than the maternal side of the placenta + Etiology is unknown ‘© Acentral depression surrounded by a thickened, grayish-white ring, composed of a double fold of amnion and chorion with degenerated decidua and fibrin in between, is seen in the fetal surface * The chorion and amnion are raised at the margin by interposed decidua and fibrin, forming a rng atthe placental margin Succenturiate placenta Ring- shaped placenta Fenestrated placenta Extrachorial placenta Circumvallate placenta Circummarginate placenta C. Abnormal Placental Location Placenta previa * Describes a placenta that is implanted somewhere in the lower uterine segment, ether over! very near the internal cervical os * Clinically presents as painless bleeding during midpregnancy 22. | Essentials oF ossrerRics Risk Factors © Maternal age >35 years Multiparity =5 Prior cesarean delivery Cigarette smoking Elevated maternal serum alpha feto protein Diagnosis ‘© Transvaginal Ultrasound ~ frst line # TRANSABDOMINAL ULTRASOUND - has average accuracy of 96% but less superior to transvaginal ultrasound © Transperineal ultrasound MRI Digital examination done only when delivery is planned and with double-set up TABLE—4.2. New Classification of Placental Location based on Standardization of Contents of OB-GYN Ultrasound Reports 2017 CLASSIFICATION Pan NORMAL Inferior most placental edge is>2 cm from internal cevical os Low.lvING Inferior most placental edge is within 2 cm from te internal cervical os Placenta covers the cervical os (measure length of overiap) OR PREVIA Inferior most edge reaches the intemal cervical os Management © Ifthe mother is stable and there is no persistent active bleeding, and the fetus is preterm with good fetal heart tones —»> close observation at maternal unit « fthere isno bleeding and the fetus is near term — elective cesarean delivery at 36-37 weeks gestation « If there is active, profuse bleeding, the mother is unstable or if there are fetal heart rate decelerations —> emergency cesarean section regardless of age of gestation D. Abnormal Placental Size PLACENTOMEGALY - placentas that ae thicker than 40 mm that commonly results from villous enlargement; may be caused by maternal diabetes, severe maternal anemia, fetal hydrops or infection caused by syphilis, toxoplasmosis or cytomegalovirus E. Abnormal Placental Adherence © PLACENTA ACCRETA - villi attached to the myometrium © PLACENTA INCRETA - villi invade the myometrium © PLACENTA PERCRETA - villi penetrate the myometrium, may affect bladder or bowels FIGURE-<4.1. Different Placental Adherence 4, PLACENTAL ABNORMALITIES | 23 Pathology | ‘ Partial or total absence ofthe decidua basalis ‘Imperfect development of Nitabuch layer Risk Factors | ; © Placenta previa © Uterine anomalies © Prior cesarean delivery ° Mal levels >2.5 Mom, BHCG 325 * Prior uterine curettage jo © Prior uterine surgery Diagnosis ; © Usually presents asantepartal bleeding © Ultrasound shows lack of the normal hypoechoic retroplacental zone © poppLer STUDIES - distance between the uterine serosa-bladder wall interfa retroplacental vessels is <1 mm and with large intraplacental lacunae + MRishows uterine bulging, heterogeneous signal intensity within the placenta and da intraplacental bands on T2-weighted imaging 2 andthe Management * CSfollowed by hysterectomy at 36 weeks AOG + Preoperative arterial catheterization © If focal accreta and desirous of pregnancy, conservative management may be done by leaving the placenta in-situ then serial imaging to document resorption * These of methotrexate has been reported in some case studies, but this remains controvsl UMBILICAL CORD TABLE—4.3. Abnormal Umbilical Cord Tele eee) ty Length + worMat: 55 ~ 60cm (Benitschke and Kaufmann, 2000) (afeted by amniticuid | « stor coro: = 32cm from oligohydramnios or deceased fetal volume and feta movement) | movement; associated with growth esticion, congenital malfrmatons, intrapartum distress, fetal death, abruption placentae, and tein inversion * LONG CORD: = 70 cm frm cord stretching due to fetal movement; associated with entanglement or prolapse and with fetal anomalies, academia and demise * More frequently identified in fetuses who aborted spontaneously * ASSOCIATED WITH TRISOMY 1830% HAD ASSOCIATED r CONGENITAL ANOMALIES: renal aplasia, mb reduction Single Umbilical Artery | fects and ates of hollow organs (Pavlopoulos, 1998) * MATERWAL RISK FACTORS: diabetes epilepsy, antepartum hemartage, oligohydramnios, and hydramnios (Leung and Robson, 1989) * PERSISTENCE OF RIGHT UMBILICAL VEIN: associated with ongenitl anomalies suchas etopia cords, ata septal defec, symmetcal bid lve, cleft lip and palate arteriovenous fistulas of the placenta * PERSISTENCE OF SMALL VITELLINE ARTERIES: nO associated increase in congenital anomalies + NORMAL UMBILICAL COILING INDEX: 04 (antepartum ten Sonographical); 0.2 (actual measurement postpartum) Cord Clling * HvPOCOILING: linked with fetal demise * HYPERCOILING: associated with fetal growth esticion and fetal demise Signticant increase in meconium staining, preterm birt, and operative delivery for etal distress Four-vessel cord 24 | Essentials oF onsterics eed Cord Insertion ¢ NORMAL: at or near the center ofthe fetal surface ofthe placenta ‘* MARGINAL INSERTION/BATTLEDORE PLACENTA: at the placental margin; common in mulifetal pregnancy * CORD MAY BE PULLED OFF DURING DELIVERY OF THE PLACENTA * VELAMENTOUS: umbilical vessels separate in the membranes ata distance from the placental margin occurs more frequently with twins, and is almost the rule with triplets vulnerable to compression leading to academia and hypoperfusion * VASA Previa: fetal vessels in the membranes cross the region ofthe internal os and occupy a position ahead ofthe presenting part hence is vulnerable to compression and to avulsion delivery at 34 to 35 weeks by elective CS is indicated True knots TABLE-4.4. Abnormalities in the Cord that may impede Blood Flow CeO SR eR LUC aaa ee Result from active fetal movements False knots Result from kinking ofthe vessels to accommodate tothe length ofthe cord | Loops Those with nuchal cord had more moderate or severe fetal heart decelerations and a lower umbilical artery pH (Hankins, 1987) Torsion Cord normally becomes twisted asa result of fetal movement Stricture ‘Associated with focal deficiency in Wharton jelly majority of cases are seen in stillborns Rupture of a varix, usually of the umbilical vein Hematoma | Can be iatrogenic through ultra-sound directed umbilical vessel venipuncture True eysts __| From remnants ofthe umbilical vesicle or ofthe allantois _ False cysts __| Result fom liquefaction of Wharton jelly Edema Commonly seen in macerated fetuses Il MEMBRANES © consists of two layers: the outer chorion and the inner amnion # offers support to amniotic fluid and produces the fluid TABLE—4.5. Membranes of the Umbilical Cord Meconium staining Staining ofthe amnion can be obvious within 1 to3 hours Chorioamnionitis Fetal infection may be from hematogenous spread ifthe mother has bacteremia butis more likely from aspiration or direct contact with infected amniotic fluid Associated with ruptured membranes, preterm labor ‘Amnion nodosum Characterized by numerous small, light-tan nodules on the amnion Amnionic band sequence “Anatomic fetal disruption caused by bands of amnion that entrap| fetal structures and impair growth and development 4, Puacentat AsNormatiies | 25 ABORTION 1. DEFINITION <500 9 or terminated before 20 weeks AOG Spontaneous vs. induced termination of pregnancy EARLY: <12 weeks AOG; management is dilatation and curettage Late: >12 weeks but <20 weeks AOG; management to allow for spontaneous agin) delivery then completion curettage © PATHOLOGY: the presence of hemorrhage into the decidua basalis and ecrotic changes surrounding tissues causes detachment ofthe ovum stimulating uterine contactons tat in expulsion eit I. ETIOLOGY A. FETAL FACTORS: Chromosomal anomalies cause atleast half of cases of early abortion 1. ABNORMAL ZYGOTE DEVELOPMENT - most common morphological finding nearly spontaneous abortions 2. Aneuploid abortion a, AUTOSOMAL TRISOMY ~the most frequent identified chromosomal anomaly ih firsttrimester miscarriages b. monosomy x (45,x) - single most common specific chromosomal abnormaliy causes Turner Syndrome TRIPLOIDY - often associated with hydropic placental degeneration d. TETRAPLOIDY - often abort early in gestation and rarely born alive @. CHROMOSOMAL STRUCTURAL ABNORMALITIES - infrequently cause abortion 3, EUPLOIDY ABORTION - causes are poorly understood B. Maternal factors 4. INFECTIONS - systemic infections likely infect the fetoplacental unit by a blood-borne route 2. Endocrine abnormalities a. HYPOTHYROIDISM - severe iodine deficiency may be associated with miscarriages b. Diabetes mellitus and progesterone deficiency - increased risk of abortion 3. Drug use and environmental factors a. TOBACCO, ALCOHOL, AND CAFFEINE - increased risk of abortion b. RADIATION ~a recognized aborlfacient especially in therapeutic doses given to teat malignancy CONTRACEPTIVES - use of intrauterine device may increase the risk for septic abortion 4d. ENVIRONMENTAL TOXINS - arsenic, lead, formaldehyde, benzene, and ethylene oxide may cause abortion 4, Immunological factors 4, AUTOIMMUNE - antiphospholipid antibody predisposes to thrombosis by inhibiting endothelial cell from producing prostacyclin, by enhancing thromboxane release orb degrading some components of the clotting cascade; Miscarriages are more common a women with SLE b, ALLOIMMUNE - maternal immunity against the fetus . 5, INHERITED THROMBOPHILIA - positive association with spontaneous abortion AGING GAMETES - increased incidence of abortion, especially with maternal age 35yo 7. PHYSICAL TRAUMA ~ in general, contributes minimally to the incidence of abortion 26 | Essenviais oF osstetrics 8. Uterine defects a. ACQUIRED - uterine synechiae (Asherman syndrome) results in amenorrhea and recurrent abortion due to insufficient endometrium to support implantation b. DEVELOPMENTAL - due to abnormal Mullerian duct development or exposure to diethylstlbestrol in utero 9, INCOMPETENT CERVIX - painless cervical dilatation in the second trimester, with prolapse and ballooning of membranes into the vagina, followed by rupture of membranes and expulsion of an immature fetus * ETIOLOGY: obscure but previous trauma to the cervix such as dilatation and curettage, conization, cauterization or amputation appears to be implicated TREATMENT: surgical; reinforcement of the weak cervix PREOPERATIVE EVALUATION: UTZis done prior to the procedure; cerclage is delayed until after 14 weeks but not beyond 24-26 weeks ‘© CERCLAGE PROCEDURES: McDonald, Shirodkar, and Modified Shirodkar; there is less trauma and blood loss with McDonald and Modified Shirodkar © COMPLICATIONS: high incidence of membrane rupture, chorioamnionitis, and intrauterine infection when done after 20 weeks 10. PATERNAL FACTOR - chromosomal abnormalities in sperm can lead to abortion Ill, CATEGORIES AND TREATMENT OF SPONTANEOUS ABORTION TABLE-5.1. Categories and Treatment of Spontaneous Abortion Cc i Closed | (+) (+) | US=A06 | (+) (+) Bed rest with THREATENED | adequate | | analgesia Closed |) | 4 | US

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