TEXTBOOK OF

OBSTETRICS

including Perinatology and Contraception

OTHER BOOKS BY THE SAME AUTHOR

y Textbook of Gynecology

y A guide to Clinical Obstetrics and Gynecology y Bedside Clinics & V iva-voce in Obstetrics and Gynecology y Master Pass in

Obstetrics and Gynecology

y Emergencies in Manipulative and Operative Obstetrics

TEXTBOOK OF

OBSTETRICS

including

Perinatology and Contraception

Enlarged & Revised Reprint of Seventh Edition

DC DUTTA

MBBS, DGO, MO(CAL)

Professor and Head, Department of Obstetrics and Gynecology

Nilratan Sircar Medical College and Hospital, Kolkata, India

Edited by

HIRALAL KONAR

(HONS; GOLD MEDALLIST)

MBBS (CAL), MD (PGI), DNB (INDIA)

MNAMS, FACS (USA), FRCOG (LONDON)

Chairman, Indian College of Obstetricians and Gynecologists

Professor, Department of Obstetrics and Gynecology

Calcutta National Medical College and C.R. Hospital, Kolkata, India

One time Professor & Head, Dept. Obst. & Gyne.,

Midnapore Medical College & Hospital, West Bengal University of Health Sciences, Ko lkata, India; Rotation Registrar in Obstetrics,

Gynecology and Oncology

Northern and Yorkshire Region, Newcastle-upon-Tyne, UK

Examiner of MBBS, DGO, MD and PhD of different Indian Universities

and National Board of Examination, New Delhi, India

JAYPEE BROTHERS MEDICAL PUBLISHERS (P) LTD

New Delhi • London • Philadelphia • Panama

Jaypee Brothers Medical Publishers (P) Ltd

Headquarters

Jaypee Brothers Medical Publishers (P) Ltd

4838/24, Ansari Road, Daryaganj

New Delhi 110 002, India

Phone: +91-11-43574357

Fax: +91-11-43574314

Email: jaypee@jaypeebrothers.com

Overseas Offices

J.P. Medical Ltd

83 Victoria Street, London

SW1H 0HW (UK)

Phone: +44-2031708910

Fax: +02-03-0086180

Email: info@jpmedpub.com

Jaypee Medical Inc

The Bourse

111 South Independence Mall East

Suite 835, Philadelphia, PA 19106, USA

Phone: +1 267-519-9789

Email: joe.rusko@jaypeebrothers.com

Jaypee Brothers Medical Publishers (P) Ltd

Bhotahity, Kathmandu, Nepal

Phone: +977-9741283608

Email: kathmandu@jaypeebrothers.com

Website: www.jaypeebrothers.com

Website: www.jaypeedigital.com

Jaypee-Highlights Medical Publishers Inc City of Knowledge, Bld. 237, Clayton Panam a City, Panama

Phone: +1 507-301-0496

Fax: +1 507-301-0499

Email: cservice@jphmedical.com

Jaypee Brothers Medical Publishers (P) Ltd 17/1-B Babar Road, Block-B, Shaymali M ohammadpur, Dhaka-1207

Bangladesh

Mobile: +08801912003485

Email: jaypeedhaka@gmail.com

The views and opinions expressed in this book are solely those of the original contribut or(s)/author(s) and do not necessarily represent

those of editor(s) of the book.

mechanical, photocopying, recording or otherwise, without the prior permission in writ ing of the publishers. All brand names and

product names used in this book are trade names, service marks, trademarks or register ed trademarks of their respective owners.

Information contained in this book is uptodate, believed to be reliable when checked wi th the sources and is in accordance with the

accepted standard, at the time of publication. However, with ongoing research and pass age of time, new knowledge may modify some of

it. The reader should, therefore, approach the book with a realistic attitude (particularly the drugs and doses) and should carry the

professional responsibility. The readers are asked to verify the information contained h erein from other sources. Neither the publisher

nor the author(s)/editor(s) assume any liability for any injury and/or damage to persons or property arising from or related to use of

material in this book.

This book is sold on the understanding that the publisher is not engaged in providing pr ofessional medical services. If such advice or

services are required, the services of a competent medical professional should be sough t.

Every effort has been made where necessary to contact holders of copyright to obtain permission to reproduce copyright material. If any

have been inadvertently overlooked, the publisher will be pleased to make the necessar y arrangements at the first opportunity.

Inquiries for bulk sales may be solicited at: jaypee@jaypeebrothers.com

Textbook of Obstetrics

Enlarged & Revised Reprint of Seventh Edition: November 2013

ISBN 978-93-5152-067-2

Printed at

Dedicated to

The students of obstetrics past and present

Preface to the seventh edition

It is almost 28 years now since the publication of its first edition that Dutta’s Textbook of Obs tetrics continues to provide basic

knowledge to medical students, trainee residents, doctors and midwives for improved p atient care. It is a great pleasure to see this book

come out with international quality in its seventh edition as there was an overwhelm ing demand for the new thoroughly revised edition of

the book in many parts of the world. Dutta’s text is committed to be revised and up dated continually. Maximum attention has been paid

to update the “core curricula” that impart fundamental knowledge, learning and skill. In v iew of expanding knowledge of molecular

biology, genetics, imaging and other diagnostic modalities, major changes have been inc orporated in all the chapters of the current

edition. New management options are also discussed. Object of the text is to provide a cu rrent cutting edge information which is again

easy to read, understand, and above all will be based on evidence.

This seventh edition of DC Dutta’s widely acclaimed comprehensive textbook of ob stetrics has come up in a fully colored format. It

is profusely illustrated with 407 full colored line drawings, photographs and sketches. The spe cial attractions of this text like summary

boxes, tables, algorithms are for easy understanding and reproducibility. The key point s at the end of each chapter is for quick revision

without referring to the text. The uniqueness of this text lies in its presentation style w hich is simple, clear and concise. The language

throughout the text has been kept lucid and unambiguous. Medical advances upto the tim e of publication have been incorporated.

Recent research has necessitated major changes in all the chapters in the text. Few chapt ers have been exhaustively updated while some

have been completely rewritten. Operative obstetrics (chapter 36) has been thoroughly updated and amply illustrated for easy learning of

common obstetric operations and skills. The chapter on practical obstetrics (chapter 41) has been rewritten considering the importance of

practical obstetrics. This chapter has been enriched with numerous (51) high quality pho tographs covering instruments, specimens, drugs

and plates of imaging studies. There are several hundreds of model questions with answ ers and explanations. This chapter is to help the

students while preparing for the clinical and viva voce part of the examination. In fact the total in formation given in chapter 41, amounts

to a “mini textbook-cum-color atlas” on obstetrics.

The volume of the text has been kept concise, in spite of incorporation of huge amount of new information. Contents and index have

been expanded for easy text references. A list of up to date reviews with few websites are included for enthusiastic readers who wish to

know more and strive for excellence.

The job of editing such a comprehensive text is stupendous. I have consulted many of m y esteemed colleagues in profession in this

country and abroad, a multitude of eminent authors, many current evidence based studies, guid elines and recommendations. I do

gratefully acknowledge my legacy to all the teachers and the related authors and publish ers. The editor expresses his sincere thanks to

many of his esteemed colleagues for their valued suggestions, criticisms and contribution of photo graphs. The editor sincerely

acknowledges the support of all the students (undergraduates and postgraduat es) of different medical institutions for their opinions,

valued suggestions and new ideas. The editor always welcomes the views of students an d the teachers who often write to us on emails

(h.kon@vsnl.net/ncbapvtltd@eth.net).

The editor is specially grateful to Dr KM Gun, MD, FRCOG, FRCS, FACS, Professor (Rtd); Dr BN Chakravorty MD, FRCOG, DSc

(Rtd), Director, Institute of Reproductive Medicine, Calcutta; Dr B Hore, MD Professor (Rtd), Consultant Anesthetist and Dr Subir

Kumar Dutta, MD, Professor (Rtd), Consultant Pathologist for their contribution, contin ued guidance and valuable suggestions. The

manuscript concerning viii TEXTBOOK OF OBSTETRICS

the chapters on Perinatology has been thoroughly read and revised authoritatively by D r Shymal Banerjee, Professor, Department of

Pediatrics, NRS Medical College, Calcutta for which I express my sincere thanks. Mrs Madhusri Konar, MA, BEd, deserves full credit

for her. sincere and patient secretarial job as ever.

Lastly, I am grateful to all who have taught me, most of all, the patients and my beloved students. I do hope this comprehensive textbook

will continue to be of immense value to the students as ever. According to the author’s d esire, the book is dedicated to the students of

Obstetrics—past and present who

strive continuously to improve the maternal and newborn health wherever they work.

Preface to the Enlarged and Revised Reprint of Seventh Edition Progress of science, technology and knowledge has n ecessitated

Dutta’s Textbook of Obstetrics to come up with an interim revision of the entire textb ook. Few chapters have been revised and updated as

to its need. New chapters have been incorporated. Contents and the index have b een expanded for easy text reference. The author, as in

the past always welcome the views of students and the teachers, who often write to us ( www. dcdutta.com). Information regarding

examination situation (theory questions, viva-voce, multiple choice questions and a nswers with explanatory notes, clinical examination

procedure, operation video-clips) have been provided through our electronic sourc es (www.dcdutta.com/www.hiralalkonar.com).

I gratefully acknowledge the help of Shri Jitendar P. Vij (Group Chairman), Mr Ankit Vij (Managing Director) and Dr Sakshi Arora

(Chief Development Editor) along with entire team of M/s Jaypee Brothers Medical Publishers (P) Ltd, New Delhi, for their professional

guidance, suggestion and support in bringing out the enlarged and revised reprint o f seventh edition.

I do hope this comprehensive textbook will continue to be of immense educational resou rce to the readers as ever.

P 13, New C.I.T Road HIRALAL KONAR Kolkata 700 01 4

Preface to the first edition

Over the years, there was an absolute dearth of a single comprehensive textbook of ob stetrics worth to prescribe to the students.

Moreover, of the textbooks currently available, most have been written with an orientat ion for the developed countries.

Being constantly insisted and hard pressed by my beloved students, I ultimately decided to write a compact, comprehensive and

practically oriented textbook of obstetrics. It is an attempt to encourage the students to lea rn obstetrics in a comparatively easy way. The

aim was to emphasize the simplicities rather than complexities of knowledge. The book is written in a clear and concise language and in

author’s own style which holds the reader’s interest. Controversies are avoided and the manage ment of the obstetrical problems being

highlighted with the facilities available to most of the Third World countries. Extensive illu strations and flow charts (schemes) have been

used as and where needed to add lucidity and clarity to the subject and to emphasize the practical nature of the book.

Although the book has been written primarily for the undergraduates, it should also pro ve to be useful to nurses (midwives), those

aspiring for diploma and postgraduate degrees in obstetrics and also to the practising ob stetricians. I, however, do not consider this book

to be an ideal one but a humble attempt has been made to remove the bottlenecks, a s far as possible, of the books available to the students

at present.

Acknowledgements: Very little of what is worthwhile in this book could have been brou ght to publication without the generous

cooperation, advice and assistance of many of my colleagues, seniors and juniors.

Dr BN Chakravarty, MBBS, DGO, MO (CaL), FRCOG (Eng.), Prof. Dept. of Obst. and Gyne., Nilratan Sircar Medical College,

Calcutta; Dr KM Gun, MBBS, DGO, MO (CaL), FRCOG (Eng.), FRCS (Edin.), FACS, Professor, Dept. of Obst. and Gyne., Medical

College, Calcutta; Dr Santosh Kr Paul, MBBS, DGO, MO (CaL), Reader, Dept. of Obst. and Gyne., Nilratan Sircar Medical College,

Calcutta; Dr B Hore, MBBS, DA, MS (CaL), Prof. and Head of the Dept. of A nesthesiology, North Bengal Medical College; Dr BC

Lahari, MBBS, DGO, MO (CaL), FRCS (Edin.), FRCOG (Eng.), FACS (USA) , FAMS (Ind.), Prof. Dept. of Obst. and Gyne., Medical

College, Calcutta; Dr P Raha, MBBS, DTM & H, PhD, FCAL, Prof. Dept. of Pathology and Bacteriology, RG Kar Medical College,

Calcutta; Dr J Mitra, MBBS, DGO, MO (CaL), FLCS, FIMS, FRCOG, Prof. Dept. o f Obst. and Gyne., Institute of Postgraduate Medical

Education and Research, Calcutta; Dr Aroti Roy, MBBS, FRCOG (Eng.), Prof. Dept. of O bst. and Gyne., RG Kar Medical College,

Calcutta, and Dr H Dattagupta, MBBS, DGO, FRCOG (Eng.), Asstt. Prof. Dept. of Obst. an d Gyne., Medical College, Calcutta; Dr NN

Roychowdhury, MBBS, DGO, MO (CaL), PhD, FRCS, FRCOG, FACS, FAMS, Prof . Dept. of Obst. and Gyne., Medical College,

Calcutta; Dr N Chowdhury, MBBS, DGO, MO (CaL), Prof., Dept. of Obst. an d Gyne., Institute of Postgraduate Medical Education and

Research, Calcutta.

Dr NG Das, BSc, MBBS, MS (CaL), Prof. and Head of the Dept. of Anatomy, Nilrata n Sircar Medical College, Calcutta; Dr PK

Talukdar, MBBS (CaL), DCH (Lond.), MRCP (Lond.), MRCP (Eng.), Lecturer, Pediatrics, NR S Medical College, Calcutta; Dr Subir

Kumar Dutta, MBBS, DCP, MD (Path. & Bact.), Lecturer, Dept. of Pathology and Bac teriology, University College of Medicine,

Calcutta; Dr Samar Rudra, MBBS, DGO, MRCOG. (Eng.), of Rama Krishna Mission Seva Pratisthan, Calcutta.

I have much pleasure in expressing my cordial appreciation to the House-Surgeons, In ternees and students of Nilratan Sircar Medical

College, Calcutta, for all the help they have rendered in preparation of the final drafts of th e manuscripts, checking the proofs and in

compiling the Index. Without their constant encouragement x TEXTBOOK OF OBSTETRICS

and active assistance, this book could never have been published. I express my sincere thanks to my publisher “Central Educational

Enterprises” for their sincere effort in publishing the book within the stipulated period in spite of the adverse circumstances.

In preparing a textbook like this, I have utilized the knowledge of a number of stalwart s in my profession and consulted many books and

publications. I wish to express my appreciation and gratitude to all of them including the rel ated authors and publishers.

As a teacher, I have learnt a lot from the students and more so while writing this book a nd as such I could not think to dedicate the book

of anyone else but the students of obstetrics for which I express my gratitude.

Mahalaya

8th September 1983 DC DUTTA P 13, New C.I.T Road

Kolkata 700 014

Contents

Preface vii-x

CHAPTER

1 ANATOMY OF FEMALE REPRODUCTIVE ORGANS 1

t External genitalia 1 t Internal genital organs 3 t Muscles and fas cia in relation to the pelvic organs 10 t Pelvic cellular tissue 13 t F emale

urethra 13 t The urinary bladder 14

t Pelvic ureter 14 t The breast 15

2 FUNDAMENTALS OF REPRODUCTION 17 t Gametogenesis 17 t Ovula tion 19 t Fertilization 21 t Morula 22 t Implantation 22 t

Trophoblast 24 t The decidua 24 t Chorion and Chorionic villi 25

t Development of inner cell mass 26

3 THE PLACENTA AND FETAL MEMBRANES 28 t Develop ment 28 t Structures 30 t Placenta circulation 31 t Placental ageing 34

t Placental function 35 t Amniotic cavity, Amnion and Amniotic fluid 37

t The umbilical cord 39

4 THE FETUS 41 t Fetal physiology 42 t The fetal circula tion 43 t Changes of fetal circulation at birth 44

5 PHYSIOLOGICAL CHANGES DURING PREGNANCY 46 t Genital o rgans 46 t Breasts 49 t Cutaneous changes 50 t Weig ht gain

t Body water metabolism 51 t Hematological changes 51 t Cardiovascular changes 52 t Metabolic changes 54 t Sy stemic changes 55

6 ENDOCRINOLOGY IN RELATION TO REPRODUCTION 57 t Placental end ocrinology 57 t Protein hormones 58 t Steroidal

hormones 60

t Changes of endocrine glands 61 t Maintenance of lactation 63

7 DIAGNOSIS OF PREGNANCY 64

t First trimester 64 t Second trimester 68 t Last trimester 70 t Dif ferential diagnosis of pregnancy 72 t Chronological appearance of

specific symptoms and signs of pregnancy 72

t Signs of previous child birth 73 t Estimation of gestational age and predic tion of expected date of delivery 73 t Estimation of fetal

weight 74

8 THE FETUS-IN-UTERO 75 t Methods of obstetrical examination 7 7

9 FETAL SKULL AND MATERNAL PELVIS 83 t Fetal skull 83 t Matern al pelvis 87 t Physiological enlargement of pelvis 93

xii TEXTBOOK OF OBSTETRICS

10 ANTENATAL CARE, PRE-CONCEPTIONAL COUNSELING AND CARE 94 t Procedure at the first visit 94 t Examination 96

t Procedure at the subsequent visits 98 t Antenatal advice 99 t Minor ailments in pregnancy 101 t Values of antenatal c are 102 t Pre-

conceptional counseling and care 102 t Summary 103

11 ANTENATAL ASSESSMENT OF FETAL WELL BEING 104 t Clinical evalu ation of fetal well being 104 t Special

investigations 105

t Early pregnancy assessment 105 t Assessment in late pregnancy 108

t Other investigations in late pregnancy 110 t Summary 111 t Key points 1 12

12 NORMAL LABOR 113 t Causes of onset of labor 113 t Contractile system of the myometrium 115

t True labor pains 116 t Stages of labor 116 t Physiology 117

t Events in labor: • First stage 118; • Second stage 121; • Th ird stage 122;

t Mechanism of normal labor 123 t Anatomy of normal labor 127

t Clinical course: • First stage 128; • Second stage 130; • Third stage 131

t Place of delivery 132

t Management of normal labor 132: • First stage 134; • Second stage 135;

• Immediate care of the newborn 137; • Third stage 139

t Scheme of management 141 t Key points 142

13 NORMAL PUERPERIUM 144 t Involution of the uterus 144 t Involution of other pelvic structures 145 t Lochia 146 t G eneral

physiological changes 146 t Menstruation and ovulation 147

t Lactation 148 t Management of normal puerperium 150 t Manag ement of ailments 151 t Postnatal care 153

14 VOMITING IN PREGNANCY 154 t Vomiting in pregnancy 154 t Hyper emesis gravidarum 154 t Summary 157

15 HEMORRHAGE IN EARLY PREGNANCY 158 t Spontaneous ab ortion (miscarriage) 158: • Threatened 160; • Inevitable 161; •

Complete 162

• Incomplete 163; • Missed 163; • Septic 164; • Recurrent 167

t Induction of abortion 172 t Medical Termination Of Pregnancy (MT P) 172:

• First trimester 174; • Midtrimester 175 t Complications of MTP 176

t Ectopic pregnancy 177: • Tubal 178; • Interstitial 183 ; • Unruptured tubal 185;

• Abdominal 188; • Ovarian 189; • Cornual 189; • Cervical 189

t Gestational Trophoblastic Diseases (GTD) 190: • Hydatidiform mole 190;

• Partial mole 198; • Placental Site Trophoblastic Tumor (PSTT) 198;

• Persistent gestational trophoblastic neoplasia 199

16 MULTIPLE PREGNANCY, HYDRAMNIOS AND ABNORMALITIES OF

PLACENTA AND CORD 200 t Twins 200 t Triplets, Quadru plets 210 t Polyhydramnios 211 t Oligohydramnios 215 t Abnormalities of

placenta and cord 216

CONTENTS xiii

17 HYPERTENSIVE DISORDERS IN PREGNANCY 219 t Pre-eclampsia 219: • Etiopathogenesis 220; • Pathophysiology 221; •

Clinical types 224

• Clinical features 224; • Complications 226; • Pr ediction and prevention 227; • Management 227

• Acute fulminant pre-eclampsia 230 t Eclampsia 230: • Manag ement 233

t Gestational 236 t Chronic 238 t Essential 238 t Chronic renal diseases 239 t Key points 240

18 ANTEPARTUM HEMORRHAGE 241 t Placenta previa 241 : • Clinical features 243; • Placentography 244; • Differentia l diagnosis

245

• Complications 246; • Management 248; • General remarks on cesarean s ection 250;

• Guide to lower segment approach 251 t Abruptio placentae 252: • C linical features 255;

• Complications 256; • Management 256 t Indeterminate bleeding 259 t Summary 259

19 MEDICAL AND SURGICAL ILLNESS COMPLICATING PREGNANCY 26 0 t Hematological disorders in pregnancy 260: •

Anemia 260; • Iron deficiency 262;

• Complications 264; • Treatment 264; • Megaloblastic 268; • Dimorphic 270; • Aplastic 270;

• Hemoglobinopathies 272; • Sickle cell hemoglobinopathies 272 ;

• Thalassemia syndromes 273; • Platelet disorders 274

t Heart disease in pregnancy 275; • Management 277;

• Specific heart disease and the management 279; • Rheumatic 279; • Congenital 279;

• Acyanotic 279; • Cyanotic 280; • Other congenital heart lesions 280 ; • Cardiomyopathies 280

t Diabetes Mellitus 281; • Gestational Diabetes Mellitus (GDM) 2 81; • Overt diabetes 282 t Thyroid dysfunction 287 t Jaundice 288 t

Cholestasis 289 t Viral hepatitis 289 t Epilepsy 291 t Asthma 291 t Systemic Lupus Erythematosus (SLE) 292

t Tuberculosis 293 t Syphilis 294 t Parasitic and Protozoal infecti ons 296

t Malaria 296 t Toxoplasmosis 297 t Listeriosis 297

t Intestinal worms 297 t Pyelonephritis 298 t Asymptomatic Bacteriuria ( ASB) 298 t Proteinuria 299 t Hematuria 299 t Retention of urine

299

t Viral infections 299: • Rubella 299; • Measles 300; • Influen za 300

• Chicken pox (varicella) 300; • Cytomegalovirus 300; • Parv o viruses 300;

• Mumps 300 • Herpes simplex virus 301; • HIV (AIDS) 301

t General surgery 303: • Acute appendicitis 304; • Trauma 304; • Acute pancreatitis 304;

• Symptomatic cholelithiasis 304; • Peptic ulcer 304 t Laparosc opy in pregnancy 304 t Acute pain abdomen 305

20 GYNECOLOGICAL DISORDERS IN PREGNANCY 306 t Abnorma l vaginal discharge 306 t Congenital malformations 306 t

Carcinoma cervix 307 t Abnormal cervical cytology 307 t Fibroid 309 t Ov arian tumor 310

t Retroverted gravid uterus 311 t Genital prolapse 312

21 PRETERM LABOR, PRETERM RUPTURE OF THE MEMBRANES,

POSTMATURITY, INTRAUTERINE DEATH OF THE FETUS 314 t Preterm labo r 314 t Prelabor Rupture Of The Membranes

(PROM) 317

t Post-term pregnancy 318 t Intrauterine Fetal Death (IUD) 322

22 SPECIAL CASES 327 t Pregnancy with prior cesarean delivery 327: • Scar integrity 328; • Scar dehiscence 328;

• Management 329; • Vaginal Birth After Previous Cesarean (VBAC ) 329

t Pregnancy in a Rh-negative woman 331: • Alloimmunization 33 2; • Fetal affection by the

Rh antibody 333; • Prevention of Rh-immunization 334; • Antenatal investigation protocol

of Rh-negative woman 335; • Plan of delivery 337; • Scheme of management of

Rh-negative women 338; • Intrauterine fetal transfusion 339; • Exchange transfusion in the

newborn 339; • Prognosis 341 t Elderly primigravida 341 t Grand multipara 342 t Bad obstetric history 342 t Obesity 343 t Key points

344

23 CONTRACTED PELVIS 345 t Variation of female pelvis 345 t Anatomical features of parent pelvic types 346 t Mechanism of

labor 348 t Diagnosis 349 t X-ray pelvimetry 351

t Disproportion 352: • Diagnosis 352; • Management 354

t Trial labor 355 t Midpelvic and outlet disproportion 356

24 ABNORMAL UTERINE ACTION 357 t Types 357 t Uterine in ertia 358 t Incoordinate uterine action 359

t Spastic lower segment 360 t Constriction ring 360 t Cer vical dystocia 360

t Generalized tonic contraction 361 t Precipitate labor 361

t Tonic uterine contraction and retraction 362 t Management of dysfun ctional labor 364 t Key points 364

25 MALPOSITION, MALPRESENTATION AND CORD PROLAPSE 365 t Occipito-posterior position 365 t Deep transve rse

arrest 372 t Breech presentation 374 t Antenatal Management 379 t Management of vaginal breech delivery 381

t Management of complicated breech delivery 385 t Face presentation 388

t Brow presentation 392 t Transverse lie 393 t Unstable lie 397

t Compound presentation 397 t Cord prolapse 398

26 PROLONGED LABOR, OBSTRUCTED LABOR, DYSTOCIA CAUSED

BY FETAL ANOMALIES 401

t Prolonged labor 401 t Obstructed labor 404

t Dystocia caused by fetal anomalies 405

t Shoulder dystocia 406: • Hydrocephalus 406; • Neural Tube Defects (NTD ) 408;

• Enlargement of fetal abdomen 409; • Monsters 409; • Conjoined twin s 409

t Key points 409

27 COMPLICATIONS OF THE THIRD STAGE OF LABOR 410 t Postpartum h emorrhage 410: • Management of third stage

bleeding 412;

• Manual removal of placenta 413; • Management of true postpartum hemo rrhage 414;

• Secondary postpartum hemorrhage 417

t Retained placenta 418 t Placenta accreta 419 t Inversion of the uterus 4 20

28 INJURIES TO THE BIRTH CANAL 422 t Vulva 422 t Perineum 422 t Vagina 423 t Cervix 423 t Pel vic hematoma 424 t Rupture

of the uterus 426 t Visceral injuries 431 t Key points 431

CONTENTS xv

29 ABNORMALITIES OF THE PUERPERIUM 432 t Puerperal pyrexia 432 t Puerperal sepsis 432 t Subinvolution 436

t Urinary complications 437 t Breast complications 437 t Puerp eral venous thrombosis 439 t Pulmonary embolism 441 t Obstetr ic palsies

442 t Puerperal emergencies 442 t Psychiatric disorders during puerperium 442

30 THE TERM NEWBORN INFANT 444 t Physical features 444 t Asses sment of gestational age 446

t Immediate care 447 t Daily observation and care 447 t In fant feeding 448

• Breast feeding 449; • Artificial feeding 453 t Childhood immunization program 455

31 LOW BIRTH WEIGHT BABY 456

t Preterm baby 456 t Intrauterine Growth Restriction (IUGR) 46 1 t Key points 467

32 DISEASES OF THE FETUS AND THE NEWBORN 468

t Asphyxia neonatorum 468 t Fetal respiration 468 t Perinatal as phyxia 469

t Resuscitation 472 t Respiratory distress 473

t Idiopathic respiratory distress syndrome 474 t Meconium Aspiration Syn drome (MAS) 476 t Jaundice 476 t Hemolytic disease 480 t

Hemorrhagic disease 480 t Anemia 481 t Seizures 48 1 t Birth injuries 483 t Perinatal infections 487 t Conjun ctivitis 489 t Congenital

malformations and prenatal diagnosis 491

t Prenatal dignosis and fetal therapy 492 t Down’s syndrome 494

t Surgical emergencies 495 t Non-immune fetal hydrops 497

33 PHARMACOTHERAPEUTICS IN OBSTETRICS 498 t Oxytocics 498: • Oxytocin 498; • Ergot derivatives 501; • Prostaglandins

503 t Antihypertensive therapy 505 t Diuretics 507 t Toc olytic agents 507

t Anticonvulsants 509 t Anticoagulants 510 t Maternal dru g intake and breast feeding 510; t Fetal hazards on maternal medicatio n 511; t

FDA risk categories 512;

t Maternal medication and fetal or neonatal affection 513

t Analgesia and anesthesia in obstetrics—(B Hore) 514: • Anatomy and physiology of

pain 514; • Analgesia for labor and delivery 515; • Sedatives and analgesics 5 16;

• Inhalation methods 516; • Regional anesthesia 517; • Infiltration ana lgesia 519;

• Psychoprophylaxis 519; • General anesthesia for cesarean section 520 t Key points 521

34 INDUCTION OF LABOR 522 t Indications and contraindications 522 t Parame ters to assess prior to induction 523 t Methods of

cervical ripening 523

t Methods of induction of labor 524: • Medical 524; • Surgical 52 5; • Combined 527 t Active management of labor 52 8 t Partograph 531 t

Key points 531

35 POPULATION DYNAMICS AND CONTROL OF CONCEPTION 532

t Population dynamics 532 t Control of conception 532 t Cont raception 533

t Methods 534: • Barrier methods 534; • Natural contraception 536;

• Intrauterine Contraceptive Devices (IUDs) 537; • Steroidal contraceptions 543 ;

• Combined oral contraceptives 543; • Injectable steroids 550;

• Emergency contraception 551; • Sterilization 552; • Vase ctomy 552;

• Female sterilization 554 t Contraceptive prescription 558

t Ongoing trials and selective availability 559: • Centchroman 559; • Combined injectable

contraceptives 560; • Biodegradable implants 560; • Newer I UDs 560; t Key points 561

36 OPERATIVE OBSTETRICS 563 t Dilatation and evacuation 563 t Manageme nt protocol of uterine perforation 565 t Suction

evacuation 566 t Menstrual regulation 566 t Manual vacuum aspiratio n 567 t Hysterotomy 567 t Episiotomy 568 t Operative vaginal

delivery 572 t Forceps 572 t Ventouse 580 t Version 583 t External cephalic version 583 t Internal version 585 t Bipolar version 585 t

Destructive operations 586 t Craniotomy 586 t Decapitation 587 t Evisc eration 588 t Cleidotomy 588 t Postoperative care 588 t Cesarean

section 588

• Lower segment 591; • Classical 595; • Complications 596;

• Measures to reduce cesarean births 598 t Symphysiotomy 598

37 SAFE MOTHERHOOD, EPIDEMIOLOGY OF OBSTETRICS 599 t Safe motherhood 599 t Obstetric care and the soc iety 600

t Reproductive and Child Health (RCH) care 600 t Epidemiolo gy of obstetrics 601 t Maternal mortality 602 t Maternal morbidity 605 t

Perinatal mortality 605

t Still births 607 t Neonatal deaths 608 t Key points 608

38 SPECIAL TOPICS IN OBSTETRICS 609 t Intrapartum fetal monitori ng 609: • Electronic Fetal Monitoring (EFM) 610

• Nonreassuring fetal status 613

t Shock in obstetrics (BN Chakraborty) 614: • Classification 618; • Hemorrhagic shock 6 18;

• Endotoxic shock 620 t Acute renal failure 621;

t Blood coagulation disorders in obstetrics 626 t High risk pregnancy (K M Gun) 630 t Immunology in obstetrics 634 t Critical care in

obstetrics 636; • ICU 638

39 CURRENT TOPICS IN OBSTETRICS 640 t Audit in obstetrics 6 40 t Medicolegal aspects of obstetric practice 641

t Day care obstetrics 641 t Antibiotic prophylaxis in cesarean section 642

t The pre-conception and prenatal diagnostic techniques and PNDT Act 642

t Umbilical cord blood banking 642 t Stem cells and therapies in obstetrics 643

40 IMAGING IN OBSTETRICS (USG, CT, MRI, RADIOLOGY),

AMNIOCENTESIS AND GUIDES TO CLINICAL TESTS 644 t Ultra sound in obstetrics 644: • 3-D scanning 644; • Indications 645;

• First trimester 646;

• Midtrimester 646; • Doppler 649; • Third trimester 649;

• Ultrasound markers of chromosomal abnormalities 650

t Magnetic resonance imaging 650 t Radiology in obstetrics 650 t Amniocentesis 651 t Guides to clinical tests 652: • Urine 652; • Tests

for blood coagulation disorders 653;

• Collection of blood sample 654; • Cervical and vaginal cytology 655

41 PRACTICAL OBSTETRICS 656 t Clinical thermometer 656 t Obstetric instru ments 656 t Specimens 667

t Imaging studies (USG plates) 668 t Processing of instruments 669

t Drugs 670 t Doppler fetal monitor 670

INDEX 671-692

Anatomy of Female Reproductive Organs

The reproductive organs in female are those which are concerned with copulation, fer tilization, growth and development of the fetus and

its subsequent exit to the outer world. The organs are broadly divided into:

• External genitalia • Internal genitalia • Accessory reproductive organs

EXTERNAL GENITALIA

(Synonyms: Vulva, Pudendum)

The vulva or pudendum includes all the visible external genital organs in the perineu m. Vulva consists of the following: The mons

pubis, labia majora, labia minora, hymen, clitoris, vestibule, urethra and Skene’s glands, Bartholin’s glands and vestibular bulbs (Fig.

1.1). It is therefore bounded anteriorly by mons pubis, posteriorly by the rectum, latera lly by the genitocrural fold. The vulvar area is

covered by keratinized stratified squamous epithelium.

MONS VENERIS (MONS PUBIS): It is the pad of subcutaneous adipose connective tis sue lying in front of the pubis and in the adult

female is covered by hair. The hair pattern (escutcheon) of most women is triangular with the base directed upwards.

LABIA MAJORA: The vulva is bounded on each side by the eleva tion of skin and subcutaneous tissue which form the labia majora.

They are continuous where they join medially to form the posterior commissure in f ront of the anus. The skin on the outer convex

surface is pigmented and covered with hair follicle. The thin skin on the inner surface h as sebaceous glands but no hair follicle. The labia

majora are covered with squamous epithelium and contain sweat glands. Beneath the sk in, there is dense connective tissue and adipose

tissue. The adipose tissue is richly supplied with venous plexus which may produce hemato ma, if injured during childbirth. The labia

majora are homologous to the scrotum in the male. The round ligament termin ates at its upper border.

LABIA MINORA: They are two thin folds of skin, devoid of fat, on eith er side just within the labia majora. Except in the parous

women, they are exposed only when the labia majora are separated. Anteriorly, they d ivide to enclose the clitoris and unite with each

other in front and behind the clitoris to form the prepuce and frenulum respectiv ely. The lower portion of the labia minora fuses across

the midline to form a fold of skin known as fourchette. It is usually lacerated dur ing childbirth. Between the fourchette and the vaginal

orifice is the fossa navicularis. The labia minora contain no hair follicle s or sweat glands. The folds contain connective tissues,

numerous sebaceous glands, erectile muscle fibers and numerous vessels and nerve en dings.Thelabia minora are homologous to the

penile urethra and part of the skin of penis in males.

CLITORIS: It is a small cylindrical erectile body, measuring about 1.5–2 cm situated in the most anterior part of the vulva. It consists

of a glans, a body and two crura. The clitoris consists of two cylindrical cor pora cavernosa (erectile tissue). The glans is covered by

squamous epithelium and is richly supplied with nerves. The vessels of the clitoris a re connected with the vestibular bulb and are liable

to be injured during childbirth. Clitoris is homologous to the penis in the male but it differs in being entirely separate from the urethra.

It is attached to the under surface of the symphysis pubis by the suspensory ligament.

VESTIBULE: It is a triangular space bounded anteriorly by the clitoris, posteriorly b y the fourchette and on either side by labia minora.

There are four openings into the vestibule.

(a) Urethral opening: The opening is situated in the midline just in front of the vaginal orifice about 1–1.5 cm below the pubic arch. The

paraurethral ducts open either on the posterior wall of the urethral orifice or directly in to the vestibule.

(b) Vaginal orifice and hymen: The vaginal orifice lies in the posterior end of the vestibule and is of varying size and shape. In virgins

and nulliparae, the opening is closed by the labia minora, but in parous, it may be exposed. It is in completely closed by a septum of

mucous membrane, called hymen. The membrane varies in shape but is usually circular or cresc entic in virgins. The hymen is usually

ruptured at the consummation of marriage. During childbirth, the hymen is extremely lacerated a nd is later represented by cicatrized

nodules of varying size, called the carunculae myrtiformes. On both sides it is line d by stratified squamous epithelium.

Fig. 1.1: The virginal vulva

(c) Opening of Bartholin’s ducts: There are two Bartholin glands (greater vestibular gland), one o n each side. They are situated in the

superficial perineal pouch, close to the posterior end of the vestibular bulb. The y are pea-sized and yellowish white in color. During

sexual excitement, it secretes abundant alkaline mucus which helps in lubrication. The glands are o f compound racemose variety and are

lined by cuboidal epithelium. Each gland has got a duct which measures about 2 cm and opens into the vestibule outside the hymen at

the junction of the anterior two-third and posterior one-third in the groove between the hymen and the labium minus. The duct is lined

by columnar epithelium but near its opening by stratified squamous epithelium. Bartho lin’s glands are homologous to the bulb of

the penis in male.

(d) Skene’s glands are the largest paraurethral glands. Skene’s glan ds are homologous to the prostate in the male. The two Skene’s

ducts may open in the vestibule on either side of the external urethral meatus.

VESTIBULAR BULB: These are bilateral elongated masses of erectile tissues situate d beneath the mucous membrane of the vestibule.

Each bulb lies on either side of the vaginal orifice in front of the Bartholin’s gland and is inc orporated with the bulbo-cavernosus muscle.

They are homologous to the bulb of the penis and corpus spongiosum in the male . They are likely to be injured during childbirth

with brisk hemorrhage (Fig.1.2).

PERINEUM: The details of its anatomy are described later in the chapter.

BLOOD SUPPLY: Arteries—(a) Branches of internal pudendal artery—the ch ief being labial, transverse

perineal, artery to the vestibular bulb and deep and dorsal arteries to the clitoris. (b) Bra nches of femoral artery—superficial and deep

external pudendal.

Veins —The veins form plexuses and drain into: (a) Internal pudendal vein (b) Vesical or vag inal venous plexus and (c) Long saphenous

vein. Varicosities during pregnancy are not uncommon and may rupture spontaneously causing visible bleeding or hematoma formation.

Fig. 1.2: Exposition of superficial perineal pouch with vestibular bulb and Bartholin’s gland

NERVE SUPPLY: The supply is through bilateral spinal somatic nerves— ( a) Anterosuperior part is supplied by the cutaneous

branches from the ilio-inguinal and genital branch of genito-femoral nerve (L

and L

) and the posterior-inferior part by the pudendal

branches from the posterior cutaneous nerve of thigh (S

1.2.3

). Between these two groups, the vulva is supplied by the labial and perineal

branches of the pudendal nerve (S

2.3.4

LYMPHATICS: Vulval lymphatics have bilateral drainage. Lymphatics drain into —(a) Superficial inguinal nodes, (b) Intermediate

groups of inguinal lymph nodes—gland of Cloquet and (c) External and internal iliac lymph nodes.

DEVELOPMENT: External genitalia is developed in the re gion of the cranial aspect of ectodermal cloacal fossa; clitoris from the

genital tubercle; labia minora from the genital folds; labia majora from the labio-scrotal swelling and the vestibule from the urogenital

sinus.

INTERNAL GENITAL ORGANS

The internal genital organs in female include vagina, uterus, Fallopian tubes and the ovaries. Thes e organs are placed internally and

require special instruments for inspection.

VAGINA

The vagina is a fibromusculomembranous sheath communicating the uterine cavity with the exterior at the vulva. It constitutes the

excretory channel for the uterine secretion and menstrual blood. It is the organ of copu lation and forms the birth canal of parturition. The

canal is directed upwards and backwards forming an angle of 45° with the horizontal in erect po sture. The long axis of the vagina almost

lies parallel to the plane of the pelvic inlet and at right angles to that of the uterus. The diameter of the canal is about 2.5 cm, being

widest in the upper part and narrowest at its introitus. It has got enough power of distensi bility as evident during childbirth.

Fig. 1.3: Mid-sagittal section of the female pelvis showing relative position of the pelvic organs

WALLS: Vagina has got an anterior, a posterior and two lateral walls. The anterior and p osterior walls are apposed together but the

lateral walls are comparatively stiffer specially at its middle, as such, it looks ‘H’ shaped on transverse section. The length of the anterior

wall is about 7 cm and that of the posterior wall is about 9 cm.

FORNICES: The fornices are the clefts formed at the top of vagina (vault) due to the projection of the uterine cervix through the

anterior vaginal wall where it is blended inseparably with its wall. There are four fornic es— one anterior, one posterior and two lateral;

the posterior one being deeper and the anterior, most shallow one.

RELATIONS:

Anterior —The upper one-third is related with base of the bladder and the lower two-thirds are with the urethra, the lower half of

which is firmly embedded with its wall.

Posterior—The upper one-third is related with the pouch of Douglas, the middle-third with the anterior rectal wall separated by

rectovaginal septum and the lower-third is separated from the anal canal by the p erineal body (Fig. 1.3).

Lateral walls—The upper one-third is related with the pelvic cellular tis sue at the base of broad ligament in which the ureter and the

uterine artery lie approximately 2 cm from the lateral fornices. The middle thir d is blended with the levator ani and the lower-third is

related with the bulbocavernosus muscles, vestibular bulbs and Bartholin’s glands (Fig. 1.11).

STRUCTURES: Layers from within outwards are—(1) mucous coat which is lined by stratified squamous epithelium without any

secreting glands (2) submucous layer of loose areolar vascular tissues (3) muscular laye r consisting of indistinct inner circular and

outer longitudinal muscles and (4) fibrous coat derived from the endopelv ic fascia and is highly vascular.

VAGINAL SECRETION: The vaginal pH, from puberty to meno pause, is acidic because of the presence of Doderlein’s bacilli which

produce lactic acid from the glycogen present in the exfoliated cells. The pH varies with th e estrogenic activity and ranges between

4–5.

BLOOD SUPPLY:The arteries involved are—(1) Cervicovaginal bran ch of the uterine artery (2) Vaginal artery—a branch of anterior

division of internal iliac or in common origin with the uterine (3) Middle rectal and (4) I nternal pudendal. These anastomose with one

another and form two azygos arteries— anterior and posterior.

Veins drain into internal iliac veins and internal pudendal veins.

LYMPHATICS: On each side, the lymphatics drain into—(1) Upper one-third— internal iliac group, (2) Middle one-third up to hymen

—internal iliac group (3) Below the hymen—superficial inguinal group.

NERVE SUPPLY: The vagina is supplied by sympathetic and parasympath etic from the pelvic plexus. The lower part is supplied by

the pudendal nerve.

DEVELOPMENT:The vagina is developed from the following sources: (a) U pper 4/5th, above the hymen— the mucous membrane

is derived from endoderm of the canalized sino-vaginal bulbs. The musculature is deve loped from the mesoderm of two fused Müllerian

ducts. (b) Lower 1/5th, below the hymen is developed from the endoderm of the urogenital sinus. (c) External vaginal orifice is formed

from the genital fold ectoderm after rupture of the urogenital membrane.

THE UTERUS The uterus is a hollow pyriform muscular organ situated in the p elvis between the bladder in front and the rectum

behind.

POSITION: Its normal position is one of the anteversion and anteflexion. Th e uterus usually inclines to the right (dextrorotation) so that

the cervix is directed to the left (levorotation) and comes in close relation with the left ur eter.

MEASUREMENTS AND PARTS: The uterus measures about 8 cm long, 5 cm wide at the fundus and its walls are about 1.25 cm

thick. Its weight varies from 50–80 gm. It has got the following parts:

• Body or corpus • Isthmus • Cervix

(1) Body or corpus: The body is further divided into fundus—the part which lies abo ve the openings of the uterine tubes. The body

proper is triangular and lies between the openings of the tubes and the isthmus. The superola teral angles of the body of the uterus project

outwards from the junction of the fundus and body and is called the cornua of the uterus. The ute rine tube,round ligament and

ligament of the ovary are attached to it. (2) Isthmus is a constricted part measurin g about 0.5 cm, situated between the body and the

cervix. It is limited above by the anatomical internal os and below by the histological internal os (Ascho ff). Some consider isthmus as a

part of the lower portion of the body of the uterus. (3) Cervix is cylindrical in shape and measu res about 2.5 cm. It extends from the

isthmus and ends at the external os which opens into the vagina after perforatin g its anterior wall. The part lying above the vagina is

called supravaginal and that which lies within the vagina is called the vaginal part (Fig. 1.4).

CAVITY: The cavity of the uterine body is triangular on coronal section with the base above a nd the apex below. It measures about 3.5

cm. There is no cavity in the fundus. The cervical canal is fusiform and measures abo ut 2.5 cm. Thus, the normal length of the uterine

cavity is usually 6.5–7 cm.

Fig. 1.4: Coronal section showing different parts of uterus

RELATIONS

Anteriorly —Above the internal os, the body forms the posterior wall of the u terovesical pouch. Below the internal os, it is separated

from the base of the bladder by loose areolar tissue.

Posteriorly —It is covered with peritoneum and forms the anterior wall of the pouch o f Douglas containing coils of intestine.

Laterally —The double fold of peritoneum of the broad ligament are attached between which the uterine artery ascends up. Attachment

of the Mackenrodt’s ligament extends from the internal os down to the supravaginal ce rvix and lateral vaginal wall. About 1.5 cm away

at the level of internal os, a little nearer on the left side is the crossing of the uterine arter y and the ureter. The uterine artery crosses from

above and in front of the ureter, soon before the ureter enters the ureteric tunnel (Fig. 1.5).

STRUCTURES

Body — The wall consists of 3 layers from outside inwards:

Fig. 1.5: The relation of the ureter to the uterine artery

— Parametrium: It is the serous coat which invests the entire organ except on the lateral bord ers. The peritoneum is intimately adherent

to the underlying muscles.

— Myometrium:It consists of thick bundles of smooth muscle fibers held by connective tissues and a re arranged in various directions.

During pregnancy, however, three distinct layers can be identified—outer longitudinal, middle interlacing and the inner circular.

— Endometrium: The mucous lining of the cavity is called endometrium. As there is no submucous layer, the endometrium is

directly apposed to the muscle coat. It consists of lamina propria and surface epithelium. The surface epithelium is a single layer of

ciliated columnar epithelium. The lamina propria contains stromal cells, endometrial gland s, vessels and nerves. The glands are simple

tubular and lined by mucus secreting non-ciliated columnar epithelium which penetrate t he stroma and sometimes even enter the muscle

coat. The endometrium is changed to decidua during pregnancy.

Cervix —The cervix is composed mainly of fibrous connective tissues. The smooth muscle fibers average 10–15%. Only the posterior

surface has got peritoneal coat. Mucous coat lining the endocervix is simple columnar w ith basal nuclei and that lining the gland is non-

ciliated secretory columnar cells. The vaginal part of the cervix is lined by stratified squa mous epithelium. The squamo-columnar

junction is situated at the external os.

SECRETION: The endometrial secretion is scanty and watery. Secretion of t he cervical glands is alkaline and thick, rich in

mucoprotein, fructose and sodium chloride.

PERITONEUM IN RELATION TO THE UTERUS: Traced anteriorly—The peritoneum c overing the superior surface of the bladder

reflects over the anterior surface of the uterus at the level of the internal os. The pouch , so formed, is called uterovesical pouch.The

peritoneum thereafter, is firmly attached to the anterior and posterior walls of the uterus and u pper one-third of the posterior vaginal wall

where from it is reflected over the rectum. The pouch, so formed, is called Pouch of Dou glas (Fig. 1.3).

Traced laterally —The adherent peritoneum of the anterior and posterior walls of the uterus is continuous laterally forming the broad

ligament. Laterally, it extends to the lateral pelvic walls where the layers reflec t to cover the anterior and posterior aspect of the pelvic

cavity. On its superior free border, lies the Fallopian tube and on the posterior layer, the ovary is attached by mesovarium. The lateral

one fourth of the free border is called Infundibulopelvic ligament.

BLOOD SUPPLY: Arterial supply — The blood supply is from the uterine artery one on each side. The artery arises directly from the

anterior division of the internal iliac or in common with superior vesical artery. The other sources are ovarian and vaginal arteries with

which the uterine arteries anastomose. The internal supply of the uterus is shown in the Figure 1.6.

Veins: The venous channels correspond to the arterial course and drain into inte rnal iliac veins. LYMPHATICS: Body— (1) From the

fundus and upper part of the body of the uterus, the lymphatics drain into pre-aortic and late ral aortic groups of glands. (2) Cornu drains

to superficial inguinal gland along the round ligament. (3) Lower part of the body dr ains into external iliac groups.

A B

Figs 1.6A and B: (A) Showing pattern of basal and spiral arteries in the endometr ium; (B) Internal blood supply of uterus

Cervix — On each side, the lymphatics drain into: (1) external iliac, obturator lymph nodes either directly or through para-cervical

lymph nodes, (2) internal iliac groups and (3) sacral groups.

NERVES: The nerve supply of the uterus is derived principally from the sympathetic syste m and partly from the parasympathetic

system. Sympathetic components are from T

and T

(motor) and T

to L

spinal segments (sensory). The somatic distribution of

uterine pain is that area of the abdomen supplied by T

to L

. The parasympathetic system is represented on either side by the pelvic

nerve which consists of both motor and sensory fibers from S

, S

and ends in the ganglia of Frankenhauser. The details are

described in Ch. 33.

The cervix is insensitive to touch, heat and also when it is grasped by any instrument. The uterus, too, is insensiti ve to handling and

even to incision over its wall.

DEVELOPMENT: The uterus is developed from the fused vertical part of the two Mullerian ducts.

FALLOPIAN TUBE

Synonyms: Uterine tube, oviduct

The uterine tubes are paired structures, measuring about 10 cm and are situated in the m edial three-fourth of the upper free margin of the

broad ligament. Each tube has got two openings, one communicating with the lateral angle of t he uterine cavity called uterine opening

and measures 1 mm in diameter, the other is on the lateral end of the tube, called pelv ic opening or abdominal ostium and measures

about 2 mm in diameter.

PARTS: There are four parts. From medial to lateral are—(1) intramural or interstitial lying in the uterine wall and measures 1. 25

cm in length and 1 mm in diameter, (2) isthmus—almost straight and measures about 3–4 cm in length and 2 mm in diameter, (3)

ampulla—tortuous part and measures about 5 cm in length which ends in, (4) wide infundibulum measuring about 1.25 cm long with a

maximum diameter of 6 mm. The abdominal ostium is surrounded by a number of rad iating fimbriae (20–25), one of these is longer than

the rest and is attached to the outer pole of the ovary called ovarian fimbria (Fig. 1.7).

STRUCTURES: It consists of 3 layers—(1) Serous: consists of peritoneum on all si des except along the line of attachment of

mesosalpinx, (2) Muscular: arranged in two layers outer longitudinal and inner circular, (3) Mucous membrane has three different cell

types and is thrown into longitudinal folds. The epithelium rests on a delicate vascular reticulum of connective tissue. Mucous

membrane is lined by:

(i) Columnar ciliated epithelial cells that are most predominant near the ovarian end of the tub e. These cells compose 25% of the

mucosal cells, (ii) Secretory columnar cells are present at the isthmic segment and compose 60% of epithelial cells, (iii) Peg cells are

found in between the above two cells. They are the variant of secretory cells.

FUNCTIONS: The important functions of the tubes are—(1) Transport of the gametes, (2) To fac ilitate fertilization and survival of

zygote through its secretion.

BLOOD SUPPLY:Arterial supply is from the uterine and ovarian. Veno us drainage is through the pampiniform plexus into the

ovarian veins.

Fig. 1.7: Half of uterine cavity and fallopian tube of one side are cut open to show different parts of t he tube. The vestigial structures in

the broad ligament are shown

LYMPHATICS: The lymphatics run along the ovarian vessels to para-aortic nod es.

NERVE SUPPLY: The nerve supply is derived from the uterine and ovaria n nerves. The tube is very much sensitive to handling.

DEVELOPMENT: The tube is developed from the upper vertical part of the c orresponding Mullerian duct at about 6–10th week .

THE OVARY

The ovaries are paired sex glands or gonads in female which are concerned for (i) germ cell maturation, storage and its release and (ii)

steroidogenesis. Each gland is oval in shape and pinkish gray in color and the surface i s scarred during reproductive period. It measures

about 3 cm in length, 2 cm in breadth and 1 cm in thickness. Each ovary presents two e nds-tubal and uterine, two borders-mesovarium

and free posterior and two surfaces —medial and lateral.

The ovaries are intraperitoneal structures. In nullipara, the ovary lies in the ovarian foss a on the lateral pelvic wall. The ovary is

attached to the posterior layer of the broad ligament by the mesovarium, to the lateral pelvic wall by the infundibulopelvic ligament and

to the uterus by the ovarian ligament.

RELATIONS: Mesovarium or anterior border—A fold of peritoneu m from the posterior leaf of the broad ligament is attached to the

anterior border through which the ovarian vessels and nerves enter the hilum of the gland.

Posterior border is free and is related to the tubal ampulla. It is separated by the periton eum from the ureter and the internal iliac artery.

Medial surface is related to fimbrial part of the tube.

Lateral surface is in contact with the ovarian fossa on the lateral pelvic wa ll.

The fossa isrelatedsuperiorly to the external iliac vein, poster iorly to the ureter and internal iliac vessels and laterally to the peritoneum

separating the obturator vessels and nerves (Fig. 1.8).

STRUCTURES: The ovary is covered by a single layer of cubical cell kn own as germinal epithelium. The substance of the gland

consists of outer cortex and inner medulla.

Cortex—It consists of stromal cells which are thickened beneath the germinal epithelium to form tunica albuginea. During reproductive

period (i.e. from puberty to menopause) the cortex is studded with numerous follicular structures, called the functional units of the ovary,

in various phases of their development. These are related to sex hormone production a nd ovulation. The structures include—primordial

follicles, maturing follicles, Graafian follicles and corpus luteum. Atresia of the structure s results in formation of atretic follicles or

corpus albicans (Fig. 1.9).

Fig. 1.8: The ovarian fossa with the structures in the lateral pelvic wall

Fig. 1.9: Histological

structure of the ovary

Medulla —It consists of loose connective tissues, few unstriped muscles, blood vessels an d nerves. There is a small collection of cells

called “hilus cells” which are homologous to the interstitial cells of the testes.

BLOOD SUPPLY: Arterial supply is from the ovarian artery, a branch of the abdominal aorta. Venous drainage is through

pampiniform plexus, to form the ovarian veins which drain into inferior vena cava on the ri ght side andleft renal veinonthe left

side. Part of the venous blood from the placental site drains into the ovarian vein s and thus may become the site of thrombophlebitis in

puerperium.

LYMPHATICS: Through the ovarian vessels drain to the para-aortic lymph nod es.

NERVE SUPPLY: Sympathetic supply comes down along the ovarian arter y from T

segment. Ovaries are sensitive to manual

squeezing.

DEVELOPMENT: The ovary is developed from the cortex of the undifferen tiated genital ridges by about 9th week; the primary germ

cells reaching the site migrating from the dorsal end of yolk sac.

MUSCLES AND FASCIA IN RELATION TO THE PELVIC ORGANS

The most important muscle supporting the pelvic organs is the levator ani which forms th e pelvic floor. The small muscles of the

perineum also have got some contribution.

PELVIC FLOOR

(Synomym: Pelvic diaphragm)

Pelvic floor is a muscular partition which separates the pelvic cavity from the anat omical perineum . It consists of three sets of

muscles on either side—pubococcygeus, iliococcygeus and ischiococcygeus and these are collectively called levator ani. Its upper

surface is concave and slopes downwards, backwards and medially and is covered by parietal layer of pelvic fascia. The inferior surface

is convex and is covered by anal fascia. The muscle with the covering fascia is called th e pelvic diaphragm.

ORIGIN: Each levator ani arises from the back of the pubic rami, from the cond ensed fascia covering the obturator internus (white line)

and from the inner surface of the ischial spine.

INSERTION: From this extensive origin,the fiberspass,backwardsandmedially to be inserted in the midline fro m before backwards to

the vagina (lateral and posterior walls), perineal body and anococcygeal raphe, lateral b orders of the coccyx and lower part of the sacrum

(Fig. 1.10).

Fig. 1.10: Levator ani muscles viewed from above

GAPS: There are two gaps in the midline—(1) The anterior one is called hiatusurogenitalis which is bridged by the muscles and fascia

of urogenital triangle and pierced by the urethra and vagina. (2) The posterior one is call ed hiatus rectalis, transmitting the rectum.

STRUCTURES IN RELATION TO PELVIC FLOOR

The superior surface is related with the following:

(1) Pelvic organs from anterior to posterior are bladder, vagina, uterus and rect um. (2) Pelvic cellular tissues between the pelvic

peritoneum and upper surface of the levator ani which fill all the available spaces. (3) Ureter lies on the floor in relation to the lateral

vaginal fornix. The uterine artery lies above and the vaginal artery lies below it. (4 ) Pelvic nerves.

The inferior surface is related to the anatomical perineum.

NERVE SUPPLY: It is supplied by the 4th sacral nerve, inferior rectal nerv e and a perineal branch of pudendal nerve S

2,3,4

FUNCTIONS: (1) To support the pelvic organs—The pubovaginalis which forms a ‘U’ shaped sling, supports the vagina which in turn

supports the other pelvic organs— bladder and uterus. Weakness or tear of this sling d uring parturition is responsible for prolapse of the

organs concerned. (2) To maintain intra-abdominal pressure by reflexly responding to its changes. (3) Facilitates anterior internal

rotation of the presenting part when it presses on the pelvic floor. (4) Puborectalis plays an ancillary role to the action of the external

anal sphincter. (5) Ischiococcygeus helps to stabilize the sacroiliac and sacrococcygeal j oints. (6) To steady the perineal body.

PELVIC FLOOR DURING PREGNANCY AND PARTURITION: During pregn ancy levator muscles undergo hypertrophy,

become less rigid and more distensible. Due to water retention, it swells up and sags dow n. In the second stage, the pubovaginalis and

puborectalis relax and the levator ani is drawn up over the advancing presenting part in the second stage. Failure of the levator ani to

relax at the crucial moment may lead to extensive damage of the pelvic structures. The e ffect of such a displacement is to elongate the

birth canal which is composed solely of soft parts below the bony outlet. The soft canal has got deep lateral and posterior walls and its

axis is in continuation with the axis of the bony pelvis.

PERINEUM

ANATOMICAL PERINEUM: Anatomically,the perineum is bounded above by the inferior surface of the pelvic floor, below by the

skin between the buttocks and thighs. Laterally, it is bounded by the ischiopubic ram i, ischial tuberosities and sacrotuberous ligaments

and posteriorly, by the coccyx. The diamond shaped space of the bony pelvi c outlet is divided into two triangular spaces with the

common base formed by the free border of the urogenital diaphragm. The anterior tria ngle is called the urogenital triangle which fills

up the gap of the hiatus urogenitalis and is important from the obstetric point of view. The posterio r one is called the anal triangle.

Urogenital triangle: It is pierced by the terminal part of the vagina and the urethra. Th e small perineal muscles are situated in two

compartments formed by the ill-defined fascia. The compartments are superficial and deep perineal pouch. The superficial pouch is

formed by the deep layer of the superficial perineal fascia (Colles fascia) and inferior layer of the urogenital diaphragm (perineal

membrane). The contents are (Fig.1.2) superficial transverse perinei (paire d), bulbospongiosus covering the bulb of the vestibule,

ischiocavernosus (paired) covering the crura of the clitoris and the Bartholin’s gland (paired ). The deep perineal pouch is formed by

the inferior and superior layer of the urogenital diaphragm—together called urogenital diaphragm or triangular ligament. Between the

layers there is a potential space of about 1.25 cm. The contents are the following muscles—deep transverse perinei (paired) and

sphincter urethrae membranaceae. Both the pouches contain vessels and nerves (Fig. 1 .11).

Anal triangle: It has got no obstetric importance. It contains the terminal part of the a nal canal with sphincter ani externus, anococcygeal

body, ischiorectal fossa, blood vessels, nerves and lymphatics.

OBSTETRICAL PERINEUM: (Synonyms: Perineal body, central point of the perin eum). The pyramidal shaped tissue where the

pelvic floor and the perineal muscles and fascia meet in between the vagina and the ana l canal is called the obstetrical perineum. It

measures about 4 cm × 4 cm with the base covered by the perineal skin and the apex is pointed an d is continuous with the rectovaginal

septum.

The musculofascial structures involved are :

• Fasciae—(1) Two layers of superficial perineal fascia-superficial fatty lay er and deeper layer called Colles fascia. (2) Inferior and

superior layer of urogenital diaphragm, together called triangular ligament.

• Muscles—(1) Superficial and deep transverse perinei (paired). (2) B ulbospongiosus. (3) Levator anipubococcygeus part (paired),

situated at the junction of the upper two-third and lower one-third of

the vagina. (4) Sphincter ani externus (few fibers).

Importance: (1) It helps to support the levator ani which is placed above it. (2) B y supporting the posterior vaginal wall, it indirectly

supports the anterior vaginal wall, bladder and the uterus. (3) It is vulnerable to injury d uring childbirth. (4) Deliberate cutting of the

structures during delivery is called episiotomy.

PELVIC FASCIA For descriptive purpose, the pelvic fascia is grouped under the he ading that covers the pelvic wall, the pelvic floor

and the pelvic viscera.

Fascia on the pelvic wall: It is very tough and membranous. It covers the obturator internus and pyrifo rmis and gets attached to the

margins of the bone. The pelvic nerves lie external to the fascia but the vessels lie internal to it.

Fascia on the pelvic floor: It is not tough but loose. The superior and the inferior surfaces are covered by th e parietal layer of the pelvic

fascia which runs down from the white line to merge with the visceral layer of the pe lvic fascia covering the anal canal (Fig. 1.11).

Fascia covering the pelvic viscera: The fascia is not condensed and often contains loose areolar tissue to allow disten sion of the organs.

Fig. 1.11: Schematic diagram showing the pelvic muscles, fascia and cellular tissue as seen from th e front

PELVIC CELLULAR TISSUE

It lies between the pelvic peritoneum and the pelvic floor and fills up all the available em pty spaces. It contains fatty and connective

tissues and unstriated muscle fibers. Its distribution around the vaginal vault, supra vagin al part of the cervix and into the layers of the

broad ligament is called parametrium. Condensation occurs especially near the cervico-vaginal junc tion to form ligaments which extend

from the viscera to the pelvic walls on either side. These are Mackenrodt’s ligaments, ut erosacral ligaments and vesicocervical ligaments

(fascia). All these constitute important supports of the uterus to keep it in position (Fig. 1.12).

Fig. 1.12: The main supporting ligaments of the uterus viewed from above

Importance: (1) To support the pelvic organs. (2) To form protective sheath for the blood vessels and the terminal part of the ureter. (3)

Infection spreads along the track, so formed, outside the pelvis to the perinephric regio n along the ureter, to the buttock along the gluteal

vessels, to the thigh along the external iliac vessels and to the groin along the round ligam ent. (4) Marked hypertrophy occurs during

pregnancy to widen up the spaces.

FEMALE URETHRA

The female urethra extends from the neck of the bladder to the external urethral meatu s which opens into the vestibule about 2.5 cm

below the clitoris. It measures about 4 cm and has a diameter of 6 mm. Its upper half is separated from the anterior vaginal wall by

loose areolar tissue and the lower half is firmly embedded in its wall. Numerous tubular glands called paraurethral glands open into the

lumen through ducts. Of these, two are larger called Skene’s ducts which open either o n the posterior wall just inside the external meatus

or into the vestibule. These glands are the sites for harboring infection and occasional d evelopment of benign adenoma or malignant

changes. While piercing the deep perineal pouch it is surrounded by sphincter urethrae membranaceae which acts as an external

sphincter.

STRUCTURES: Mucous membrane in the distal one- third is lined by stratified s quamous epithelium but in the proximal two-third it

becomes stratified transitional epithelium. Submucous coat is vascular. Muscle coat is arranged as inne r longitudinal and outer circular.

BLOOD SUPPLY: Arterial supply—Proximal parts ar e supplied by the inferior vesical branch and the distal part by a branch of

internal pudendal artery. The veins drain into vesical plexus and into int ernal pudendal veins. LYMPHATICS: Ear the meatus, t he

lymphatics drain into superficial inguinal glands and the rest drain into internal and exte rnal iliac group of glands.

NERVE SUPPLY: It is supplied by the pudendal nerve.

DEVELOPMENT: The urethra is developed from the vesico-urethral portion of the cloaca.

THE URINARY BLADDER

The bladder is a hollow muscular organ with considerable power of distension. Its capa city is about 450 mL (15 oz) but can retain as

much as 3–4 liters of urine. When distended it is ovoid in shape. It has got— (1) an ap ex (2) superior surface (3) base (4) two infero-

lateral surfaces and (5) neck, which is continuous with the urethra. The base and the neck rem ain fixed even when the bladder is

distended.

RELATIONS: The superior surface is related with the pe ritoneum of the uterovesical pouch. The base is related with the supravagin al

cervix and the anterior fornix. The ureters, after crossing the pelvic floor at the sides o f the cervix, enter the bladder on its lateral angles.

In the interior of bladder, the triangular area marked by three openings — two ureteric and one urethral, is called the trigone. The

inferolateral surfaces are related with the space of Retzius. The neck rests on the superior layer of the urogenital diaphragm.

STRUCTURES: From outside inwards—(1) Outer-visceral layer of the pelvic fascia. (2) M uscle layer composed of muscles running

in various directions. Near the internal urethral opening the circular muscle fibers provi de involuntary sphincter. (3) Mucous coat is

lined by transitional epithelium with no gland. There is no submucous coat.

BLOOD SUPPLY: The blood supply is through superior and inferi or vesical arteries. The veins drain into vesical and vaginal plexus

and thence to internal iliac veins.

LYMPHATICS: Lymphatics drain into external and internal iliac lymph nodes.

NERVE SUPPLY: The sympathetic supply is from the pelvic plexus and the parasympathetic via the pelvic plexus from the nervi

erigentes (S

2,3,4

). The parasympathetic produces contraction of the detrusor muscles and relaxation of the internal sphincter (nerve of

evacuation). Sympathetic conveys afferent painful stimuli of overdistension.

DEVELOPMENT: The urinary bladder is developed from the upper part of the urogenital sinus.

PELVIC URETER

It extends from the crossing of the ureter over the pelvic brim up to its opening into the bladder. It measures about 13 cm in length and

has a diameter of 5 mm. Ureter is retroperitoneal in course.

COURSE AND RELATIONS: The ureter enters the pelvis in front of the bifurcation of the common iliac artery over the sacroiliac

joint behind the root of the mesentery on the right side and the apex of the mesosigmoid on the left side. As it courses downwards in

contact with the peritoneum, it lies anterior to the internal iliac artery and behind the ovar y and forms the posterior boundary of ovarian

fossa (Fig. 1.8). On reaching the ischial spine, it lies over the pelvic floor and as it cours es forwards and medially on the base of the

broad ligament, it is crossed by the uterine artery anteriorly (Fig. 1.5). S oon, it enters into the ureteric tunnel and lies close to the

supravaginal part of the cervix,about 1.5 cm lateral to it. After traversing a short distance on th e anterior fornix of the vagina, it

courses into the wall of the bladder obliquely for about 2 cm by piercing the lateral ang le before it opens into the base of the trigone. In

the pelvic portion, the ureter is comparatively constricted (a) where it crosse s the pelvic brim (b) where crossed by the uterine artery

and (c) in the intravesical part.

STRUCTURES: From outside inwards—(1) Fibers derived from the visceral layer of the pelvic fascia (2) Muscle coat consisting of

three layers—outer and inner longitudinal and intermediate circular. (3) Mucous layer lined by transitional epithelium.

BLOOD SUPPLY: It has got segmental supply from nearly all the visce ral branches of the anterior division of the internal iliac

(uterine, vaginal, vesical, middle rectal) and superior gluteal arteries. The venous draina ge corresponds to the arteries.

LYMPHATICS: The lymphatics from the lower part drain into the external and internal iliac lymph nodes and the upper part into the

lumbar lymph nodes.

NERVE SUPPLY: Sympathetic supply is from the hypogastric and pelvic p lexus; parasympathetic from the sacral plexus.

DEVELOPMENT: It is developed as an ureteric bud from the caudal end of the mesonephric duct.

THE BREAST

The breasts are large, modified sebaceous glands. The breasts are bilateral and in femal e constitute accessory reproductive organs as the

glands are concerned with lactation following childbirth.

The shape of the breast varies in women and also in different periods of life. But the size of the base of the breast is fairly con stant. It

usually extends from the second to sixth rib in the midclavicular line. It lies in the subcuta neous tissue over the fascia covering the

pectoralis major or even beyond that to lie over the serratus anterior and external obliqu e. A lateral projection of the breast towards the

axilla is known as axillary tail of Spence. It lies in the axillary fossa, sometimes deep to the deep fascia. The breast weighs 200–300 gm

during the childbearing age.

A B

Figs 1.13A and B: (A) Structure of the basic unit of the mammary gland;. (B) Str ucture of adult female breast

STRUCTURES (Non-lactating breasts):The areola is placed about the center of the breast and is pigmented. It is about 2.5 cm in

diameter. Montgomery glands are accessory glands located around the periphery of the areola. They can secrete milk. The nipple is a

muscular projection covered by pigmented skin. It is vascular and surrounded by unstr iated muscles which make it erectile. It

accommodates about 15–20 lactiferous ducts and their openings. The whole breast i s embedded in the subcutaneous fat. The fat

is,however,absent beneath the nipple and areola.

The mature breast consists of about 20% glandular tissue and 80% fat and the rest conn ective tissue (Fig. 1.13). The breast is composed

of 12–20 lobes. Each lobe has one excretory duct (lactiferous duct) that opens at the nipple. E ach lobe has about 10 to 100 lobules.

Cooper’s ligaments are the fibrous septa, that extend from the skin to the underlyi ng pectoral fascia. These ligaments provide support to

the breast. One lactiferous duct drains a lobe. The lining epithelium of the duct is cubical, becom es stratified squamous near the

openings. Each alveolus is lined by columnar epithelium where milk secretion occurs. A network of branching longitudinal striated cells

calledmyoepithelial cells surround the alveoli and the smaller ducts. There is a dense network of capillari es surrounding the alveoli.

These are situated between the basement membrane and epithelial lining. Contraction o f these cells squeezes the alveoli and ejects the

milk into the larger duct. Behind the nipple, the main duct (lactiferous) dilates to for m ampulla where the milk is stored.

Breast tissue is sensitive to the cyclic changes of hormones estrogen and progesterone. Women often feel breast tenderness and fullness

during the luteal phase of the cycle. During the follicular phase, there is proliferation of the d uctal system whereas during the luteal

phase there is dilatation of the ductal system and differentiation of the alveolar cells in to secretory cells. In postmenopausal women, the

breast lobules and ducts atrophy. Accessory breasts or nipples can occur along the breast o r milk line which extends from the axilla to

the groin. Asymmetry of breasts is a normal variation.Massive hypertrophy of the breasts is a rare problem .

BLOOD SUPPLY: Arterial supply: (1) Lateral thoracic — branches of the axillar y artery, (2) Internal mammary, (3) Inter costal

arteries. Veins—The veins follow the courses of the arteries.

LYMPHATICS: (1) Lateral hemisphere—anterior axillary node s (75%). (2) Upper convexity—infra- clavicular group. (3) Medial

convexity—internal mammary chain of nodes (cross connection between the two b reasts). There is no contralateral drainage of lymph,

until and unless there is ipsilateral obstruction. (4)Inferior convexity — mediast inal glands.

NERVE SUPPLY: The nerve supply is from fourth, fifth and sixth intercos tal nerves.

DEVELOPMENT:The parenchyma of the breasts is developed from the ec toderm. The connective tissue stroma is from the

mesoderm.

Fundamentals of Reproduction

GAMETOGENESIS

The process involved in the maturation of the two highly specialized cells, spermatozo on in male and ovum in female before they

unite to form zygote, is called gametogenesis.

Oogenesis

The process involved in the development of a mature ovum is called oogenesis . The primitive germ cells take their origin from the

yolk sac at about the end of 3rd week and their migration to the developing gonadal ridge is completed round about the end of 4th week.

In the female gonads, the germ cells undergo a number of rapid mitotic divisions and d ifferentiate into oogonia. The number of oogonia

reaches its maximum at 20th week, numbering about 7 million. While the majo rity of the oogonia continue to divide, some enter into

the prophase of the first meiotic division and are called primary oocytes. These are sur rounded by flat cells and are called primordial

follicles and are present in the cortex of the ovary. At birth, ther e is no more mitotic division and all the oogonia are repla ced by

primary oocytes which have finished the prophase of the first meiotic division and rema in in resting phase (dictyotene stage) between

prophase and metaphase. Total number of primary oocytes at birth is estimated to be about 2 million. The primary oocytes do not

finish the first meiotic division until puberty is reached. At puberty, some 400 ,000 primary oocytes are left behind, the rest being

atretic. Out of these, some 400 are likely to ovulate during the entire reproductive per iod.

Maturation of the oocytes : The essence of maturation is reduction of the number of chromosom es to half. Before the onset of first

meiotic division, the primary oocytes double its DNA by replication, so they contain d ouble the amount of normal protein content. There

are 22 pairs of autosomes which determine the body characteristics and 1 pair of sex c hromosomes, named “XX”. The first stage of

maturation occurs with full maturation of the ovarian follicle just prior to ovulatio n but the final maturation occurs only after

fertilization.

The primary oocyte undergoes first meiotic division giving rise to secondary oocyte and one polar body. The two are of unequal size, the

secondary oocyte contains haploid number of chromosomes (23, X), but nearly all the cytoplasm and the small polar body also contains

half of the chromosomes (23, X) but with scanty cytoplasm. Ovulation occurs soon after the formation of the secondary oocyte.

The secondary oocyte completes the second meiotic division (homotypical) only aft er fertilization by the sperm in the Fallopian

tube and results in the formation of two unequal daughter cells, each possessing 23 ch romosomes (23, X), the larger one is called the

mature ovum and the smaller one is the second polar body containing the same number of chromosomes. The first polar body may also

undergo the second meiotic division. In the absence of fertilization, the secondary oocyte doe s not complete the second meiotic division

and degenerates as such.

Chromosome nomenclature: The number designates the total number of chromosom es (in numerals) followed by the sex chromosome

constitution after the comma.

Structure of a mature ovum: A fully mature ovum is the largest cell in the body and is about 130 microns in diameter. It consists of

cytoplasm and a nucleus with its nucleolus which is eccentric in position and contains 23 chromosomes (23, X). During fertilization, the

nucleus is converted into a female pronucleus. The ovum is surrounded by a cell membra ne called vitelline membrane.

There is an outer transparent mucoprotein envelope, the zona pellucida. The zona pellucida is penetrated b y tiny channels which are

thought to be important for the transport of the materials from the granulosa cells to the oocyte. In between the vitelline membrane and

the zona pellucida, there is a narrow space called perivitelline space which accommod ates the polar bodies. The human oocyte, after

its escape from the follicle, retains a covering of granulosa cells known as the corona radiata derived from the cumulus oophorus (Fig.

2.1).

A B C

D E

Figs 2.1A to E: Schematic diagram showing: (A) Mature Graafian follicle on the verge of ov ulation (B) Ovulation with discharge of

secondary oocyte surrounded by cumulus oophorus (C) Formation of corpus luteum (D) Secondary oocyte aftrer first maturation

division with formation of first polar body and (E) Microscopic structure of corpus lute um.

Spermatogenesis

The process involved in the development of spermatids from the primordial male g erm cells and their differentiation into

spermatozoa is called spermatogenesis. Shortly before puberty, the primord ial germ cells develop into spermatogonia and remain in

the wall of seminiferous tubules. The spermatogonia, in turn, differentiate into primary spermat ocytes which remain in the stage of

prophase of the first meiotic division for a long time (about 16 days). Each spermatocyte contains 22 pairs of autosomes and 1 pair of sex

chromosomes, named “XY”. With the completion of the first meiotic division, two se condary spermatocytes are formed having equal

share of cytoplasm and haploid number of chromosomes either 23, X or 23, Y. Imme diately follows the second meiotic division

(homotypical) with the formation of four spermatids, each containing haploid number o f chromosomes, two with 23, X and two with 23,

Y. Immediately after their formation, extensive morphological differentiation of the sper matids occurs without further cell division to

convert them into spermatozoa. The process is called spermiogenesis. In man, the time r equired for a spermatogonium to develop

into a mature spermatozoon is about 61 days.

Sperm capacitation and acrosome reaction: Capacitation is the ph ysiochemical change in the sperm by which it becomes hypermotile

and is able to bind and fertilize a secondary oocyte. Capacitation takes place in the genita l tract and takes about 2–6 hours. The changes

involve cyclic AMP dependent phosphorylation with increase in intracellular pH (influx of Ca

and efflux of H

). Activation of

acrosomal membranes causes release of hyaluronidase, hydrolytic enzymes, proacrosin , acrosin, that help the sperm to digest the zona

pellucida and to enter into the oocyte. During acrosomal reaction the sperm plasma membrane fu ses with the outer acrosomal

membrane (Fig. 2.2). The sperm with acrosomal membrane bind the Zona Protein (ZP

), after passing between the corona radiata cells

(Fig. 2.3). After acrosome reaction, the sperm binds

to Zona Protein ZP

. Then there is zona reaction to prevent polyspermy. Acrosome sperm penetrate the zo na pellucida → reaches the

perivitelline space → fuses with the oocyte plasma membrane. The sperm head swells an d the fused membrane vesiculates. The whole

sperm head, mid piece and tail are drawn into the cytoplasm. Gamete fusion is an integr in mediated process. About 3–6 hours after

insemination, two pronuclear and one polar bodies are visible and they migrate to the ce ntre of the oocyte (Fig. 2.3).

Fertilization in vitro: Capacitation and acrosome reaction occur within few hours in simple media. Wash ed and motile sperm (2 ×

/mL) are added to the oocyte. In ICSI, micro injection of a single sperm into the oocyte is done.

Structure of a mature spermatozoon: It has got two parts, a head and a tail. The head consists pri ncipally of the condensed nucleus and

acrosomal cap (Fig. 2.2). Acrosome is rich in enzymes. The tail is divided into four zones — the neck, the middle piece, the principal

piece and the end piece.

OVULATION

Ovulation is a process whereby a secondary oocyte is released from the ovary follo wing rupture of a mature Graafian follicle and

becomes available for conception. Only one secondary oocyte is likely to rupture in each ovarian cycle which starts at puberty and ends

in menopause. In relation to the menstrual period, the event occurs about 14 days prio r to the expected period. However, menstruation

can occur without ovulation and ovulation remains suspended during pregnancy and l actation.

MECHANISM: The process of ovulation is a complex one. Preovulatory changes occur both in the follicle and the oocyte.

Figs 2.2A and B: Structure of a mature spermatozoon: (A) PM = Plasma membra ne; A = Acrosome; OAM = Outer acrosomal

membrane; IAM = Inner acrosomal membrane; N = Nucleus; AC = Acrosomal cap; ES = Equatorial segment; PA = Post acrosomal

region. (B) The sperm tail with the axonemal complex which is essential for sperm motil ity. Cross sectional view shows 9 pairs of

peripheral doublets, joined each other by nexin links via two dynein protein arms. Ener gy for sperm motility is derived from

mitochondria in the mid piece.

Changes in the follicle: There is preovulatory enlargement of the Graafian follicle due to a ccumulation of follicular fluid and measures

about 20 mm in diameter. The cumulus oophorus separates from the rest of the granulosa cells and floats freely in the antrum. The inner

layer of the cells surrounding the oocyte is arranged radially and is termed corona radiata (Fig. 2.1). The follicular wall near the ovarian

surface becomes thinner. The stigma develops as a conical projection which penetrates the outer surface layer of the ovary and persists

for a while (

– 2 minutes) as a thin membrane. The cumulus escapes out of the follicle as a slow oozing process, t aking about 1–2

minutes along with varying amount of follicular fluid (Fig. 2.1). The stigma is soon clo sed by a plug of plasma.

Changes in the oocyte: Significant changes in the oocyte occur just prior to ovulation (fe w hours). Cytoplasmic volume is increased

along with changes in the number and distribution of mitochondria and in the Golgi app aratus. Completion of the arrested first meiotic

division occurs with extrusion of first polar body, each containing haploid numbe r of chromosomes (23, X).

CAUSES: The following are the possible explanations which may operate singly or in combinat ion : — Endocrinal • LH surge:

Sustained peak level of estrogen for 24–36 hours in the late follicular phase →LH surg e occurs from the anterior pituitary. Ovulation

approximately occurs 16–24 hours after the LH surge. LH peak persists for about 24 hours. The LH surge stimulates completion of

reduction division of the oocyte and initiates leutinization of the granulosa cells, synthesis of progesterone and prostaglandins.

• FSH rise:Preovulatory rise of progesterone facilitates the positive feedback action o f estrogen to induce

FSH surge → increase in plasminogen activator → plasminogen → plasmin → helps ly sis of the wall of the follicle.

Thus, the combined LH/FSH midcycle surge is responsible for the final stage of matura tion, rupture of

the follicle and expulsion of the oocyte.

— Stretching factor: It is more a passive stretching than rise in intrafollicular pressur e which remains

static at about 15 mm Hg.

— Contraction of the micromuscles in the theca externa and ovarian stroma due to increased p rostaglandin

secretion.

EFFECT OF OVULATION: Following ovulation, the follicle is changed into corpus luteum (Fig. 2.1).

The ovum is picked up into the Fallopian tube and undergoes either degeneration or fu rther maturation, if fertilization is to occur.

Menstruation is unrelated with ovulation and anovular menstruation is quite comm on during adolescence, following childbirth and in

women approaching menopause.

FERTILIZATION

Fertilization is the process of fusion of the spermatozoon with the mature ovum . It begins with sperm eg g collision and ends with

production of a mononucleated single cell called the zygote. Its objectives are : (1) To in itiate the embryonic development of the egg and

(2) To restore the chromosome number of the species. Almost always, fertilization occurs in the ampullary part of the uterine tube.

APPROXIMATION OF THE GAMETES: The ovum, immediately following ovulation is picked u p by the tubal fimbriae which

partly envelope the ovary, specially at the time of ovulation. The pick up action might b e muscular or by a kind of suction or by ciliary

action or by a positive chemotaxis exerted by the tubal secretion. The ovum is rapidly transp orted to the ampullary part. Fertilizable life

span of oocyte ranges from 12 to 24 hours whereas that of sperm is 48 to 72 hours .

Out of hundreds of millions of sperms deposited in the vagina at single ejaculation, only thousands capacitated spermatozoa enter the

uterine tube while only 300–500 reach the ovum. The tubal transport is facilitated by mu scular contraction and aspiration action of the

uterine tube. It takes only few minutes for the sperm to reach the fallopian tube.

CONTACT AND FUSION OF THE GAMETES (Fig. 2.3): Comp lete dissolution of the cells of the corona radiata occurs by the

chemical action of the hyaluronidase liberated from the acrosomal cap of the hundreds of sperm present at the site (see p. 18).

A B

Figs 2.3A and B: Schematic diagram showing sequence of changes during fertiliz ation : (A) Sperm (acrosome intact) in between the

corona radiata cells →attachment with zona →acrosome reacted sperm penetrating the zona → acrosomereacted sperm in

theperivitellinespace→incorporated sperm with vesiculatinghead. (B) Formation of male and female pronuclei with completion of second

polar body.

— Penetration of the zona pellucida is facilitated by the release of hyaluronidase from th e acrosomal cap.

More than one sperm may penetrate the zona pellucida.

— Out of the many sperms, one touches the oolema. Soon after the sperm fusion, pene tration of other sperm

is prevented by zona reaction (hardening) and oolema block. This is due to release of cortical granules by

exocytosis from the oocyte.

— Completion of the second meiotic division of the oocyte immediately follows, each containing haploid numb er of chromosomes

(23, X). The bigger one is called the female pronucleus and the smaller one is called second polar body which is pushed to the

perivitelline space.

— In the human, both the head and tail of the spermatozoon enter the cytoplasm of the oocyte but the plasma membrane is left behind on

the oocyte surface. Head and the neck of the spermatozoon become male pronucleus c ontaining haploid number of chromosomes (23, X)

or (23, Y).

— The male and the female pronuclei unite at the center with restoration of the diploid n umber of chromosomes (46) which is constant

for the species. The zygote, thus formed, contains both the paternal and m aternal genetic materials. In some instances, an antigen called

fertilizin present on the cortex and its coat of the ovum, reacts with the antibody calle d antifertilizin liberated at the plasma membrane of

the sperm head. Thus the union between the two gametes may be an immunologica l reaction (chemotaxis).

— Sex of the child is determined by the pattern of the sex chromosome supplied by the spermatozoon. If the spermatozoon

contains ‘X’ chromosome, a female embryo (46, XX) is formed; if it contains a ‘Y’ ch romosome, a male embryo (46, XY) is formed.

MORULA

After the zygote formation, typical mitotic division of the nucleus occurs producing two blastomeres.

The two cell stage is reached approximately 30 hours after fertilization . Each contains equal cytoplasmic volume and chromosome

numbers. The blastomeres continue to divide by binary division through 4,8,16 cell stag e until a cluster of cells is formed and is called

morula, resembling a mulberry. As the total volume of the cell mass is not increased and the zona pellucida remains intact, the morula

after spending about 3 days in the uterine tube enters the uterine cavity throu gh the narrow uterine ostium (1 mm) on the 4th

day in the 16-64 cell stage. The transport is a slow process and is controlled b y muscular contraction and movement of the cilia. The

central cell of the morula is known as inner cell mass which forms the embryo proper a nd the peripheral cells are called outer cell mass

which will form protective and nutritive membranes of the embryo.

BLASTOCYST

While the morula remains free in the uterine cavity on the 4th and 5th day it is covered b y a film of mucus. The fluid passes through

the canaliculi of the zona pellucida which separates the cells of the morula and is now termed blastocyst (Fig. 2.4). Zona hatching is the

next step so that trophectoderm cells interact with endometrial cells and implantation occurs.

A B C D

Figs 2.4A to D: Schematic representation of the mitotic division of the zygote resulting in fo rmation of: (A) Two cell stage; (B) Four cell

stage; (C) Morula and (D) Blastocyst (see p. 24)

Due to blastocyst enlargement the zona pellucida becomes stretched, thinned and gradu ally disappears. Lysis of zona and escape of

embryo is called zona hatching. The cells on the outer side of the morula (po lar) become trophectoderm and the inner cells (apolar)

become inner cell mass by the mediation of epithelial cadherin (E-cadherin) (protein). Trophectoderm diff erentiates into chorion

(placenta) and the inner cell mass into the embryo. Completely undifferentiated cells are called the pleuripotent embryonic stem (ES)

cells. ES cells are able to produce mature somatic cells of any germ layers (ecto derm, mesoderm and endoderm).

IMPLANTATION (SYN: NIDATION)

Implantation occurs in the endometrium of the anterior or posterior wall of the body nea r the fundus on the 6th day which

corresponds to the 20th day of a regular menstrual cycle. Implantation occurs throug h four stages e.g. apposition, adhesion,

penetration and invasion.

CHANGES IN THE BLASTOCYST: The polar trophoblast cells adjacent to the inner cell mass are primarily involved in adhesion to

the endometrial cells. The factors responsible for blastocyst attachment are: P. selectin, heparin sulphate, proteoglycan, EGF,

integrins, trophinin, tasin and others. The signals for trophoblast multiplication arise from the in ner cell mass.

ENDOMETRIUM AT THE IMPLANTATION SITE : (1) The endometrium is in the secretory pha se corresponding to 20–21 days of

cycle. (2) The microvilli on the surface of the trophectoderm interdigitate with the decid ual cells to form the junctional complexes.

Endometrial receptivity and molecular signalling during implantation is induced by prog esterone, LIF (Ieukemia inhibitory factor),

prostaglandins and COX-2.

Fig. 2.5:Schematic representation showing interstitial implantation of the blastocyst in stratum compa ctum of the decidua

APPOSITION: Occurs through pinopod formation. Pinopods are long fing er like projections (microvilli) from the endometrial cell

surface. These pinopods absorb the endometrial fluid which is secreted by the endomet rial gland cells. This fluid, rich in glycogen and

mucin provides nutrition to the blastocyst initially. Unless this fluid is absorbed, adhesion phase cannot occur. Adhesion of blastocyst

to the endometrium occurs through the adhesion molecules like integrin, selectin an d cadherin (glycoproteins).

PENETRATION: Actual penetration and invasion occur through the stromal c ells in between the glands and is facilitated by the

histolytic action of the blastocyst. With increasing lysis of the stromal cells, the blastocyst is burro wed more and more inside the

stratum compactum of the decidua. Vacuoles appear in the advancing syncytium whi ch fuse to form large lacunae. These are more

evident at the embryonic pole. Concurrently, the syncytial cells penetrate deeper into the stroma and erode the endothelium of the

maternal capillaries. The syncytium by penetrating the vessels, not only becomes continu ous with the endothelial lining but permits the

maternal blood to enter into the lacunar system. Ultimately erosion of few maternal arter ies with formation of blood space (lacunae)

occurs. Nutrition is now obtained by aerobic metabolic pathway from the maternal bloo d. Further penetration is stopped probably by

the maternal immunological factor and the original point of entry is sealed b y fibrin clot and later by epithelium. The process is

completed by 10th or 11th day which corresponds to D 24-25 from LMP (Fig. 2.5).

This type of deeper penetration of the human blastocyst is called interstitial implant ation and the blastocyst is covered on all sides

by the endometrium (decidua). Occasionally, there may be increased blood flow into th e lacunar spaces at the abembryonic pole. This

results in disruption of the lacunae and extravasation of blood into the endometrial cavity . This corresponds approximately to 13th day

after fertilization (at about the expected day of the following period). This m ay produce confusion in determination of the expected

date of delivery. The process of implantation is controlled by the immunomodulatory role of var ious cytokines (interleukins 3, 4, 5, 6, 10,

13), many local peptides like epidermal growth factor (EGF), insulin like growth factor ( IGF) and prostaglandins. Both the decidua and

the embryo synthesize these molecules.

Fig. 2.6 : Diagrammatic representation of the events — ovulation, fertilization and implantation : (1 ) Secondary oocyte extruded at

ovulation (day 14 from LMP) (2) Secondary oocyte in tube (3) Fertilization with extru sion of second polar body (day 14–16) (4)

Formation of zygote (5) Two cell stage (6) Four-cell stage (7) Early morula (day 17) (8) Late morula (day 18) (9) Early blastocyst stage

with disappearance of zona pellucida (day 19–20) (10) Early phase of implantation (d ay 20–21).

TROPHOBLAST

As previously mentioned, the cells of the blastocyst differentiate into an outer trophectoderm and an inner cell mass. Jus t before

implantation, the trophectoderm is further differentiated into an inner mononuclear cellu lar layer called cytotrophoblast or Langhans’

layer and an outer layer of multinucleated syncytium called syncytiotrophoblast. T he cytotrophoblasts that line the villous stems are

the villous cytotrophoblasts (see Fig. 3.5). The cytotrophoblast cells that invade the decidua are known as ‘interstitial extravillous

cytotrophoblast’ (Fig. 3.5) and those that invade the lumens of the maternal spiral a rteries (see Fig. 3.7) are known as ‘intravascular

extravillous cytotrophoblast’. Throughout pregnancy, syncytiotrophoblast is derived from the cytotro phoblast. Placenta and the fetal

membranes are developed from the trophoblast. It is involved in most of the functions ascribed to the placenta as a whole. Thus, it

serves at least 3 important functions — invasion, nutrition and production of hormones for the maintenance of pregnancy. Local

cytokines regulate the invasion of the cytotrophoblasts in the decidua.

THE DECIDUA

The decidua is the endometrium of the pregnant uterus. It is so named because much of it is shed following delivery.

Decidual reaction : The increased structural and secretory activity of the e ndometrium that is brought about in response to

progesterone following implantation is known as decidual reaction.

Changes occur in all the components of the endometrium but most marked at the implan tation site and first commence around maternal

blood vessels. The fibrous connective tissues of the stroma become changed into epitheloid cells called decidual cells. The glands show

marked dilatation and increased tortuosity with its lining epithelium showing ev idences of active cell proliferation with increased

secretory activity. There are areas of small interstitial hemorrhage and leucocytic infiltration spe cially at the implantation site.

The well developed decidua differentiates into three layers (Fig. 2.7) : (1) Superficial compact layer consists of compact mass of

decidual cells, gland ducts and dilated capillaries. The greater part of the surface epithelium is e ither thinned out or lost. (2)

Intermediate spongy layer (cavernous layer) contains dilated uterine glan ds, decidual cells and blood vessels. It is through this layer

that the cleavage of placental separation occurs. (3) Thin basal layer containing the basal portion of the glands and is apposed to the

uterine muscle. Regeneration of the mucous coat occurs from this layer follo wing parturition.

After the interstitial implantation of the blastocyst into the compact laye r of the decidua, the different portions of the decidua are

renamed as — (1) Decidua basalis or serotina — the portion of the decidua in contact with th e base of the blastocyst (2) Decidua

capsularis or reflexa — the thin superficial compact layer covering the blastocyst and (3) Decidua vera or parietalis — the rest of the

decidua lining the uterine cavity outside the site of implantation. Its thickness progressive ly increases to maximum of 5–10 mm at the

end of the second month and thereafter regression occurs with advancing pre gnancy so that beyond 20th week, it measures not more than

1 mm.

As the growing ovum bulges towards the uterine cavity, the space between the decidua capsularis and the decidua vera, called the

decidual space is gradually narrowed down and by 4th month, it is completely o bliterated by the fusion of the decidua capsularis with the

decidua vera. At term, they become atrophied due to pressure and the two cannot be d efined as a double layer. The decidua basalis,

however, retains its characteristic appearance till term and becomes the mate rnal portion of the placenta (see Fig. 3.1).

Functions : (1) It provides a good nidus for the implantation of the blastocyst. (2) It supplies nutrition to the early stage of the growing

ovum by its rich sources of glycogen and fat. (3) Deeper penetration of the trophoblas t is controlled by local peptides, cytokines and

integrins. (4) Decidua basalis takes part in the formation of basal plate of the placenta.

Fig. 2.7: Structure of decidua

CHORION AND CHORIONIC VILLI

The chorion is the outermost layer of the two fetal membranes (chorion and amn ion) . It consists of two embryonic layers — outer

trophoblast and inner primitive mesenchyme which appears on 9th day. At the beginnin g of the 3rd week, the syncytiotrophoblast

produces irregular finger like projections which are lined internally by the cyt otrophoblast. These finger like buds are called primary

stem villi — surrounded by lacunar spaces which will later form into intervillous spa ces.

After the appearance of the primitive mesenchyme and the development of the chorion , the primary stem villi are named chorionic villi.

With the insinuation of the primary mesoderm into the central core of the villi stru ctures, secondary villi are formed on 16th day. Later

on mesodermal cells in the villi begin to differentiate into blood cells and blood vessels, th us forming villous capillary system. These

vascularized villi are called tertiary villi which are completed on 21st day. Later on, this extra embryonic circulatory system

establishes connection with the intraembryonic circulatory system through the body stalk (see Fig. 3.6).

Meanwhile, the cytotrophoblastic cells beyond the tips of the villus system penetrate into the overlying syncytium adjacent to the

decidua. The cells become continuous with those of the neighboring villus system travers ing through the syncytium. Thus, a thin outer

cytotrophoblastic shell is formed which surrounds the entire blastocyst. The zone o f the decidua immediately adjacent to the

trophoblastic shell is called trophosphere which comprises of the compact layer of the d ecidua. Fibrinoid deposit appears on the

syncytiotrophoblast outside the trophoblastic shell and is called Nitabuch’s membrane. Maternal blood v essels pass through all the

layers to reach the intervillous space (see Fig. 3.5).

The villi overlying the decidua basalis continue to grow and expand and are call ed chorion frondosum which subsequently forms the

discoid placenta. The chorionic villi on the decidua capsularis gradually undergo atroph y from pressure and become converted into

chorion laeve by the 3rd month and lies intervening between the amnion and decidua on its outer su rface. Remnant of decidual cells

and of the trophoblast can however be distinguished microscopically (see Fig. 3.4).

DEVELOPMENT OF INNER CELL MASS

Along with the changes in the trophoblast, on the 8th day, the embryoblast diffe rentiates into bilaminar germ disc which consists of

dorsal ectodermal layer of tall columnar cells and ventral endodermal layer of flattened polyhedral cells. The bilaminar germ disc is

connected with the trophoblast by mesenchymal condensation, called connecting sta lk or body stalk which later on forms the

umbilical cord (Fig. 2.9).

Two cavities appear one on each side of the germ disc. (1) On 12th post ovulatory day, a fluid filled space appears between the

ectodermal layer and the cytotrophoblast which is called amniotic cavity. Its floor is formed by the ectoderm and the rest of its wall by

primitive mesenchyme. (2) The yolk sac appear on the ventral aspect of the bilaminar disc and is lined externally by the primitive

mesenchyme and internally by the migrating endodermal cells from the endo dermal layer of the germ disc (Fig. 2.9A).

Formation of trilaminar embryonic disc: Fourteen days after fertilization, proliferatio n of ectodermal cells in the midline, leads to

formation of primitive streak (Fig. 2.8). Cells within the streak spread laterally between the ectoderm and endoderm as intraembryonic

mesoderm. This intraembryonic mesoderm becomes continuous with the extraembryon ic mesoderm at the lateral border of the

embryonic disc.

Extraembryonic coelom (Fig. 2.9): Extraembryonic mesenchyme , derived from the trophoblast appears to separate the yolk sac from

the blastocyst wall and also the amniotic cavity from the trophoblast of the chorion. Sma ll cystic spaces (lacuna) now appear within the

extraembryonic mesenchyme. These spaces gradually enlarge and fuse to form extraembryon ic coelom. Progressive enlargement of the

extraembryonic coelom,

Fig. 2.8: Transversesection through theprimitivestreakregion,showing invagin ation and lateral migration of the mesodermal cells,

converting the bilaminar disc into a trilaminar one.

separates the amnion from the inner aspect of the chorion except at the caudal end of th e embryo. There, the mesenchymal attachment

persists to form body stalk (Fig. 2.9A). Umbilical cord develops from thi s body stalk.

Subsequently the amniotic cavity enlarges at the expense of the ext raembryonic coelom. The developing embryo bulges into the

enlarged amniotic cavity. The yolk sac becomes partly incorporated into the embryo to form the gu t. The part that remains outside is

incorporated into the body stalk (Fig. 2.9B, C). Gradually the extraembryonic coelom i s totally obliterated. The extraembryonic

mesenchyme covering the amnion now fuses with the lining of the chorion. The single layer of fused amniochorion is now formed (Fig.

2.9C).

During the embryonic stage which extends from the fourth to eighth week, individual d ifferentiation of the germ layers and formation of

the folds of the embryo occur. Most of the tissues and organs are developed during th is period, the details of which are beyond the

description of this book. However, the major structures which are developed from the three germinal layers are mentioned below. The

embryo can be differentiated as human at 8th week.

ECTODERMAL LAYER: Central and peripheral nervous system, epidermis of skin with its append ages, pituitary gland, chromaffin

organs, salivary glands; mucous lining of the nasal cavity, paranasal sinus, roof of the m outh etc.

MESODERMAL LAYER: Bones, cartilage, muscles, cardiovascular system, kidney, gonads, s uprarenals, spleen, most of the genital

tract; mesothelial lining of pericardial, pleural and peritoneal cavity etc.

ENDODERMAL LAYER: Epithelial lining of the gastrointestinal tract, liver, gallbladder, pancreas ; epithelial lining of respiratory tract

and most of the mucous membrane of urinary bladder and urethra; bulbo-urethral and greater vestibular glands etc.

Figs 2.9A to C: Schematic representation of formation of amniotic cavity, secondary yolk sac, extraembryonic coelom and body stalk:

(A) Enlargement of extraembryonic coelomic cavity (B) The amniotic sac enlarges and begins to occupy the extraembryonic coelom (C)

The amniotic sac has surrounded the embryo with almost completely obliterating the extr aembryonic coelom; formation of body stalk

completed.

Table 2.1: Important events followIng fertIlIzatIon

‘0’ hour — Fertilization (day-15 from LMP) 9–10th day — Lacunar network forms

30 hours — 2 cell stage (blastomeres) 10–11th day — • Trophoblasts invade endometr ial

40-50 hours — 4 cell stage

72 hours — 12 cell stage

96 hours — 16 cell stage. Morula enters the uterine cavity

5th day — Blastocyst 13th day

4–5th day — Zona pellucida disappears 16th day

5–6th day — Blastocyst attachment to endometrial 21st day surface 21st–22nd day — Fetal heart. Fetoplacental circulation

6–7th day — Differentiation of cyto and

syncytiotrophoblastic layers

10th day — Synthesis of hCG by syncytiotrophoblast

sinusoids establishing uteroplacental circulation

• Interstitial implantation completed with entire decidual coverage — Primary villi

— Secondary villi

— Tertiary villi

The Placenta and Fetal Membranes

THE PLACENTA

Only eutherian mammals possess placenta. The human placenta is discoid, because o f its shape; hemochorial, because of direct

contact of the chorion with the maternal blood and decidua, because some maternal tissue is shed at parturition. The placenta is attached

to the uterine wall and establishes connection between the mother and fetus through the umbilical cord. The fact that maternal and fetal

tissues come in direct contact without rejection suggest immunological acceptance of the fetal graft by the mother.

DEVELOPMENT

The placenta is developed from two sources. The principal component is fetal which de velops from the chorion frondosum and the

maternal component consists of decidua basalis.

When the interstitial implantation is completed on 11th day, the blastocyst i s surrounded on all sides by lacunar spaces around cords

of syncytial cells, called trabeculae. From the trabeculae develops the stem villi on 13th day wh ich connect the chorionic plate with the

basal plate. Primary, secondary and tertiary villi are successively developed from th e stem villi. Arterio-capillary-venous system in the

mesenchymal core of each villus is completed on 21st day. This ultimately ma kes connection with the intraembryonic vascular system

through the body stalk (Fig. 2.9).

Simultaneously, lacunar spaces become confluent with one another and by 3rd and 4th week, form a multilocular receptacle lined by

syncytium and filled with maternal blood. This space becomes the future intervillous spa ce. As the growth of the embryo proceeds,

decidua capsularis becomes thinner beginning at 6th week and both the villi and the lacu nar spaces in the abembryonic area get

obliterated, converting the chorion into chorion laeve. This is, however, compensated b y (a) exuberant growth and proliferation of the

decidua basalis and (b) enormous and exuberant division and sub-division of the chori onic villi in the embryonic pole (chorion

A B C Figs 3.1A to C: Relation of the amniotic cavity, chorionic cavity and uterine cavity of successive stages —

(A) end of the 8th week, (B) ten weeks after the last period and (C) end of the 12th w eek

frondosum). These two, i.e. chorion frondosum and the decidua basalis form the dis crete placenta. It begins at 6th week and is

completed by 12th week (Fig. 3.1).

Until the end of the 16th week, the placenta grows both in thickness and circumference due to growth of the chorionic villi with

accompanying expansion of the intervillous space. Subsequently, there is little increase in thickness but it increases circumferentially till

term.

The human hemochorial placenta derived its name from hemo (blood) that is in co ntact with the syncytiotrophoblasts of

chorionic tissue (Fig. 3.4).

THE PLACENTA AT TERM

GROSS ANATOMY: The placenta, at term, is almost a circular disc with a diameter o f 15–20 cm and thickness of about 3 cm at its

center. It thins off toward the edge. It feels spongy and weighs about 500 gm, the proportion to the weight of the baby being roughly 1 : 6

at term and occupies about 30% of the uterine wall. It presents two surfaces, fetal and maternal, and a peripheral margin.

Fetal surface: The fetal surface is covered by the smooth and glistening amnion wi th the umbilical cord attached at or near its center.

Branches of the umbilical vessels are visible beneath the amnion as they radiate fr om the insertion of the cord (Fig. 3.2). The amnion can

be peeled off from the underlying chorion except at the insertion of the cord . At term, about four-fifths of the placenta is of fetal

origin.

Fig. 3.2:Fetalsurface of the placenta showing attachment of the umbilical cord with ramification of the umbilical vessels Fig. 3.3:

Maternal surface of the placenta showing shaggy look with cotyledons limited by fissures

Maternal surface: The maternal surface is rough and spongy (Fig. 3.3). Maternal blood gives it a dull red color. A thin greyish,

somewhat shaggy layer which is the remnant of the decidua basalis (compact and spongy la yer) and has come away with the

placenta, may be visible. The maternal surface is mapped out into 15–20 somewhat con vex polygonal areas known as lobes or

cotyledons which are limited by fissures. Each fissure is occupied by the decidual septum which is derived from the basal plate .

Numerous small greyish spots are visible. These are due to deposition of calcium in the degenerated areas and are of no clinical

significance. The maternal portion of the placenta amounts to less than one fifth of the to tal placenta. Only the decidua basalis and the

blood in the intervillous space are of maternal origin.

Margin: Peripheral margin of the placenta is limited bythe fused basal and chorionic plate s and is continuous with the chorion laeve and

amnion. Essentially, the chorion and the placenta are one structure but the placenta is a specializ ed part of the chorion.

Attachment: The placenta is usually attached to the upper part of the body of the uter us encroaching to the fundus adjacent to the

anterior or posterior wall with equal frequency. The attachment to the uterine wall is eff ective due to anchoring villi connecting the

chorionic plate with the basal plate and also by the fused decidua capsularis and vera with the c horion laeve at the margin.

Separation: Placenta separates after the birth of the baby and the line of separation is throug h the decidua spongiosum.

STRUCTURES

The placenta consists of two plates . The chorionic plate lies internally. It is lined by the amniotic membrane. The umbilical cord is

attached to this plate. The basal plate lies to the maternal aspect . Between the two plates lies the intervillous space containing the stem

villi with their branches, the space being filled with maternal blood (Fig. 3.4).

AMNIOTIC MEMBRANE: It consists of single layer of cubical epithelium loosely attached to t he adjacent chorionic plate. It takes no

part in formation of the placenta.

CHORIONIC PLATE: From within outwards, it consists of (i) primitive mesen chymal tissue containing branches of umbilical

vessels (ii) a layer of cytotrophoblast and (iii) syncytiotrophoblast. The stem villi arise from the plate. It forms the inner boundary of

the choriodecidual space.

BASAL PLATE: It consists of the following structures from outside inwards. (1) Part of the co mpact and spongy layer of the

decidua basalis. (2) Nitabuch’s layer of fibrinoid degeneration of the outer syncytiotro phoblast at the junction of the cytotrophoblastic

shell and decidua. (3) Cytotrophoblastic shell. (4) Syncytiotrophoblast (Figs 3.4 and 3.5 ).

Fig. 3.4: Schematic view of (A) Structure of placenta at term, (B) Structure of the membranes in r elation to decidua.

The basal plate is perforated by the spiral branches of the uterine vessels through which the maternal blood flows into the intervillous

space. At places, placental or decidual septa project from the basal plate into the intervillo us space but fail to reach the chorionic plate.

The septum consists of decidual elements covered by trophoblastic cells. The ar eas between the septa are known as cotyledons (lobes),

which are observed from the maternal surface, numbering 15–20.

Fig. 3.5: Schematic diagram of Stem villi, showing connection of the chorionic plate with the basal pla te

Figs 3.6A to C:Schematicdiagramto showthedevelopment of the villus (A) Primary (B) Se condary (C) Tertiary

INTERVILLOUS SPACE: It is bounded on the inner side by the chorio nic plate and the outer side by the basal plate, limited on the

periphery by the fusion of the two plates. It is lined internally on all sides by the sync ytiotrophoblast and is filled with slow flowing

maternal blood. Numerous branching villi which arise from the stem villi project into the space and constitute chief content of the

intervillous space (Figs 3.4A and 3.5).

STEM VILLI: These arise from the chorionic plate and extends to the basal plate. With th e progressive development — primary,

secondary and tertiary villi are formed (Fig. 3.6). Functional unit of the placenta is called a fetal cotyledon or placentome, which is

derived from a major primary stem villus. These major stem villi pass down thro ugh the intervillous space to anchor onto the basal

plate (see Fig. 3.5). Functional subunit is called a lobule which is derived from a t ertiary stem villi. About 60 stem villi persist in human

placenta. Thus, each cotyledon (totalling 15–29) contains 3–4 major stem villi . The villi are the functional unit of the placenta. The

total villi surface, for exchange, approximately varies between 10–14 square meters. Th e fetal capillary system within the villi is almost

50 km long. Thus, while some of the villi are anchoring the placenta to the decidua, the majority are free within the intervillous space

and are called nutritive villi. Blood vessels within the branching villi do not anastomose with the neighboring one.

STRUCTURE OF A TERMINAL VILLUS: In the early placenta , each terminal villus has got the following structures from outside

inward: (1) Outer syncytiotrophoblast (2) Cytotrophoblast (3) Basement membrane (4 ) Central stroma containing fetal capillaries,

primitive mesenchymal cells, connective tissue and a few phagocytic (Hofbauer) cells.

In placenta at term , syncytiotrophoblast becomes relatively thin at places overlying the fetal capillaries and thicker at other areas

containing extensive endoplasmic reticulum. The former is probably the site for transfer and the latter, the site for synthesis. The

cytotrophoblast is relatively sparse. Basement membrane becomes thicker. Stroma con tains dilated vessels along with all the constituents

and few Hofbauer cells (Fig. 3.11). Hofbauer cells are round cells (see Fig. 3.11) that are capable of phagocytosis and can trap maternal

antibodies crossing through the placenta (immune suppressive). These cells can express class II MHC molecules.

PLACENTAL CIRCULATION

Placental circulation consists of independent circulation of blood in two systems:

• Uteroplacental circulation • Fetoplacental circulation

UTEROPLACENTAL CIRCULATION: (Maternal circulation) : It is concern ed with the circulation of the maternal blood

through the intervillous space. A mature placenta has a volume of about 500 mL of b lood; 350 mL being occupied in the villi system

and 150 mL lying in the intervillous space. As the intervillous blood flow at term is estimated to be 500–600 mL per minute, the blood

in the intervillous space is completely replaced about 3–4 times per minute. The villi depend on the maternal blood for their

nutrition, thus it is possible for the chorionic villi to survive for a varying period even af ter the fetus is dead. The pressure within the

intervillous space is about 10–15 mm Hg during uterine relaxation and 30–50 mm H g during uterine contraction. In contrast, the fetal

capillary pressure in the villi is 20–40 mm Hg.

Arterial circulation: About 120–200 spiral arteries open into the intervillous space b y piercing the basal plate randomly at numerous

sites. Normally, there is cytotrophoblastic invasion into the spiral arteries initially upto the intra-dec idual portion within 12 weeks of

pregnancy. Not only the endothelial lining is replaced but also the musculoelastic media is d estroyed and replaced by fibrinoid material.

There is a secondary invasion of trophoblast between 12–16 weeks extending up to rad ial arteries within the myometrium. Thus, spiral

arteries are converted to large bore uteroplacental arteries. The net effect is funnelling of the arteries which reduces the pressure of the

blood to 70–80 mm Hg before it reaches the intervillous space. It thus increases the blood flow .

Fig. 3.7: Spiral arterioles at the placental site in normal and pre-eclamptic pregnancies

Trophoblast cells that do not take part in villous structure are known as extravillou s trophoblast (EVT). EVT are of two types : (i)

endovascular that migrates down the lumen of the spiral arteries and replaces th e endothelium (Fig. 3.7). (ii) Interstitial that invades as

far as the inner third of the myometrium. Further invasion is limited by the NK cells to p revent morbid adhesion of placenta (placenta

accreta). Defects in trophoblast invasion and failure to establish maternal circulation correctly leads to complications of pregnancy (PIH,

IUGR).

Venous drainage: The venous blood of the intervillous space drains through the u terine veins which pierce the basal plate randomly like

the arteries.This concept of uteroplacental circulation is based on the studies Table 3.1: Summar y of intervillous hemodynamics

Volume of blood in mature placenta —500 mL Volume of blood in intervillous space — 150 mL Blood flow in intervillous space —500–

600 mL/min Pressure in intervillous space :

During uterine contraction —30–50 mm Hg During uterine relaxation —10–15 mm H g Pressure in the supplying uterine artery —70–80

mm Hg Pressure in the draining uterine vein —8 mm Hg

of Ramsey and co-workers (1963, 1966). Intervillous hemodynamics is mentioned in Table 3.1.

Circulation in the intervillous space: The arterial blood enters the space under pressur e (Fig. 3.8). Lateral dispersion occurs, after it

reaches the chorionic plate. Villi help in mixing and slowing of the blood flow . Mild stirring effect by the villi pulsation aided by uterine

contraction help migration of the blood toward the basal plate and thence to the uterine v eins. Sometimes syncytial sprouts are set free in

the

Fig. 3.8: Diagram of an intervillous space showing intervillous circulation

intravillous circulation and are carried through the maternal circulation to the lungs whe re they disappear by lysis. About 100,000

syncytial sprouts circulate in maternal blood in 24 hours.

Short circuit of the arterial blood into the neighboring venous channels is prevented by the increased pressure of the endometrial arteries

driving the blood in jets towards the chorionic plate. During uterine contraction, the vein s are occluded but the arterial blood is forced

into the intervillous space; while uterine relaxation facilitates venous drainage. This is bro ught about by the fact that the spiral arteries

are perpendicular and the veins are parallel to the uterine wall. Thus during contraction, la rger volume of blood is available for

exchange even though the rate of flow is decreased. The blood in the intervillou s space is protected from clotting by some fibrinolytic

enzyme activity of the trophoblast.

FETOPLACENTAL CIRCULATION: The two umbilical arteries carry the impur e blood from the fetus. They enter the chorionic

plate underneath the amnion, each supplying one half of the placenta. The arteries brea k up into small branches which enter the stems of

the chorionic villi. Each in turn divides into primary, secondary and tertiary vessels of the corre sponding villi. The blood flows into the

corresponding venous channels either through the terminal capillary networks or through the shunts (Fig. 3.9). Maternal and fetal blood

streams flow side by side, but in opposite direction. This counter current flow facilita tes material exchange between the mother and fetus.

The villous capillary pressure varies from 20–40 mm Hg. The fetal blood flow through the placenta is about 400 mL/min. This is

mainly facilitated by the pumping action of the fetal heart.

PLACENTAL BARRIER (Placental membrane): It is a partition between fetal and ma ternal circulation. However, this barrier is not

a perfect barrier as fetal blood cells are found in maternal circulation so also the maternal blood cells are found in fetal circulation. The

Table 3.2: Summary of fetal hemodynamics Fetal blood flow — through the placen ta

Pressure in the — umbilical artery

Pressure in the — umbilical vein

Fetal capillary — pressure in villi

400 mL/min

60 mm Hg

10 mm Hg

20–40 mm Hg

Umbilical artery

saturation

50–60% PO

20–25 mm Hg Umbilical vein

70–80%

30–40 mm Hg

Fig. 3.9: Schematic diagram showing terminal capillary networks in the villi

Fig. 3.10: Schematic diagram showing layers of placental barrier

above two are separated by tissues called placental membrane or barrier, consisting of t he following. In early pregnancy, it consists of

(1) syncytiotrophoblast (2) cytotrophoblast (3) basement membrane (4) stromal tissue, and (5) endothelium of the fetal capillary wall

with its basement membrane. It is about 0.025 mm thick (Fig. 3.10) .

Near term, there is attenuation of the syncytial layer. Sparse cytotrophoblast and distended fetal capillaries almost fill the villus. The

specialized zones of the villi where the syncytiotrophoblast is thin and anuclear is known as Vasculosyncytial membrane (Fig. 3.11).

These thin zones (0.002 mm) of terminal villi alpha zones are for gas exchange. The thick ‘beta zones’ of the terminal villi w ith the

layers remaining thick in patches are for hormone synthesis. An increase in thickness of the vil lous membrane is seen in cases with

IUGR and cigarette smokers.

PLACENTAL AGEING

As the placenta has got a limited life span, it is likely to undergo degenerative changes as a mark of senescence. The ageing process

varies in degree and should be differentiated from the morbid process likely to affect th e organ in some pathological states. The ageing

process involves both the fetal and maternal components.

VILLI CHANGES: The following changes are observed as pregnancy advances toward term (Fig. 3 .11). (1) Decreasing thickness of

the syncytium and appearances of syncytial knots (aggregation of the syncytium in small areas on the sides of the villus). (2) Partial

disappearance of trophoblast cells. (3) Decrease in the stromal tissue including Hofbaue r cells (fetal macrophages). (4) Obliteration of

some vessels and marked dilatation of the capillaries. (5) Thickening of the basement layer of the fetal endothelium and the

cytotrophoblast. (6) Deposition of fibrin on the surface of the villi.

A B

Figs 3.11A and B: Schematic diagram showing transverse section of a villus in (A ) Early month and (B) Near term

DECIDUAL CHANGES : There is an area of fibrinoid degeneration where trophoblast cells (cove red with syncytium) meet the

decidua. This zone is known as Nitabuch layer. This layer limits further invasion o f the decidua by the trophoblast. The membrane is

absent in placenta accreta.

INTERVILLOUS SPACE: The syncytium covering the villi and extendin g into the decidua of intervillous space undergoes fibrinoid

degeneration and form a mass entangling variable number of villi. These are called whi te infarcts which vary in size from few

millimetres to a centimetre or more. Calcification or even cyst formation may occur on it . Such type of degeneration is usually near the

placental margin. There may be inconsistent deposition of fibrin called Rohr ’s stria at the bottom of the intervillous space and

surrounding the fastening villi.

PLACENTAL FUNCTION

The main functions of the placenta are:

1. Transfer of nutrients and waste products between the mother and fetus. In this respe ct it attributes to the following functions: •

Respiratory • Excretory • Nutritive

2. Endocrine function: Placenta is an endocrine gland. It produces both steroid and peptide hormones to maintain pregnancy (p. 58).

3. Barrier function.

4. Immunological function.

FACTORS FOR PLACENTAL TRANSFER FROM MOTHER TO FETUS A. Substance properties

Molecular weight: Lower the molecular weight more is the transfer

t Lipid solubility: Lipophilic substances diffuse readily t Ionisation: Nonionised form crosses lipid membr ane freely

pH of blood: Lower pH favours ionisation of many drugs

t Protein binding

t Spatial configuration

B. Maternal properties

Drug concentration in the maternal blood

t Uterine blood flow

t Concentration gradient on either side of placental

membranes

C. Placental properties

Lipid membrane of placenta enhances transfer t Total surface area of placental memb rane

t Functional integrity and thickness of placental barrier

(p. 33)

Mechanisms involved in the transfer of substances across the placenta are:

(1) Simple diffusion. (2) Facilitated diffusion (transporter mediated) using transporter p roteins in syncytiotrophoblast. (3) Active

transfer (against concentration gradient, energy ATPase, mediated). (4) Endocytosis: Invagination of the cell membrane to form an

intracellular vesicle which contains the extracellular molecules. (5) Exocytosis: Release of the molecule within vesicle to the

extracellular space. Immunoglobulin IgG is taken up by endocytosis from maternal circ ulation and is transferred to the fetus via

exocytosis. (6) Leakage (break in the placental membranes).

Respiratory function: Although the fetal respiratory movements are observed as early as 11 weeks, th ere is no gaseous exchange. Intake

of oxygen and output of carbon dioxide take place by simple diffusion across the fetal membr ane. Partial pressure gradient is the driving

force for exchange between the maternal and fetal circulations. The oxygen sup ply to the fetus is at the rate of 8 mL/Kg/min and this

is achieved with cord blood flow of 165–330 mL/min.

Excretory function: Waste products from the fetus such as urea, uric acid, and creatinine are excreted to the maternal blood by simple

diffusion.

Nutritive function: The fetus obtains its nutrients from the maternal blood and when th e diet is inadequate, then only, depletion of

maternal tissue storage occurs.

• Glucose which is the principal source of energy is transferred to the fetus by facilitated diffus ion. There are transporter proteins

(GLUT I) for facilitated diffusion. Glucose transfer from mother to fetus is not linear. T ransfer rates decrease as maternal glucose

concentration increases. Fetal glucose level is lower than that of the mother indicating rapid rate of fetal utilization of glucose.

• Lipids for fetal growth and development are transferred across the fetal membrane or synthesized in the fetus. Triglycerides and fatty

acids are directly transported from the mother to the fetus in early pregnancy bu t probably are synthesized in the fetus later in pregnancy.

Essential fatty acids are transferredmorethan the non-essential fatty acids. Cholesterol is cap able of direct transfer. Thus, fetal fat has

got a dual origin.

• Amino acids are transferred by active transport (energy requiring transp ort) through enzymatic mechanism (ATPase). Amino acid

concentration is higher in the fetal blood than in the maternal blood. Some proteins (IgG), cross by the proces s of endocytosis. Fetal

proteins are synthesized from the transferred amino acids and the level is lower th an in mother.

• Water and electrolytes such as sodium, potassium and chloride cr oss through the fetal membrane by simple diffusion, whereas

calcium, phosphorus and iron cross by active transport (active transporter proteins) against a concentration gradient, since their levels

are higher in fetal than in maternal blood. Water soluble vitamins are transferred by active transport but the fat soluble vitamins are

transferred slowly so that the latter remains at a low level in fetal blood.

• Hormones— insulin, steroids from the adrenals, thyroid, chorionic gonadotro phin or placental lactogen cross the placenta at a very

slow rate, so that their concentration in fetal plasma are appreciably lower than in maternal pla sma. Neither parathormone nor

calcitonin crosses the placenta.

ENZYMATIC FUNCTION: Numerous enzymes are elaborated in the placenta, mentioning only few of them are: (1) diamine oxidase

which inactivates the circulatory pressure (or pressor) amines, (2) oxytocinase which ne utralises the oxytocin, (3) phospholipase A

which synthesizes arachidonic acid, etc. Placental endocrinology is discussed in the chapter 6 (p. 57).

BARRIER FUNCTION: Fetal membrane has long been considered as a protective barrier to the fetus against noxious agents circulating

in the maternal blood. In general, substances of high molecular weight of more than 50 0 daltons are held up but there are exceptions.

Antibody and antigens in immunological quantities can traverse across the placental barrier in bo th directions. The transfer of the larger

molecule is probably facilitated by pinocytosis. The race of drug transfer is increased in late pregnancy.

Maternal infection during pregnancy by virus(rubella, chickenpox, measles, mumps, p oliomyelitis), bacteria (Treponema pallidum,

Tubercle bacillus) or protozoa (Toxoplasma gondii, malaria parasites) may be transmitted to the fetus across the so called placental

barrier and affect the fetus in utero. Similarly, almost any drug used in pregnancy can cross the placental barrier and may have

deleterious effect on the fetus.

IMMUNOLOGICAL FUNCTION (for details see p. 167, 634): The fetus and th e placenta contain paternally determined antigens,

which are foreign to the mother. In spite of this, there is no evidence of graft rejection. Placenta probably offers immunological

protection against rejection. The exact mechanism is yet speculative but the interest ha s centred on the following:

— Placental hormones, proteins (SP1), Early Pregnancy Factor (EPF), PAPP-A, steroid s and chorionic gonadotropin, have got some

immunosuppressive effect.

— Villous trophoblasts (Fig. 3.5) do not express HLAClass I or Class II molecules. E xtravillous trophoblast (Fig. 3.7) only express

HLA Class I molecules and no HLA Class II molecules (see p. 24).

— Though anti-HLA antibodies and sensitized T cells against paternal antigens have bee n detected in the maternal serum, they have no

significant effects on pregnancy.

— There is a shift of maternal response from cell mediated (T helper I) to humoral ( T helper 2) immunity, which may be

beneficial to pregnancy (see p. 635).

— Decidual natural killer (NK) cells and trophoblast (extravillous) HLA Class I molecules interact. The cytokines thus derived, will

regulate the invasion of extravillous trophoblast cells into the spiral arteries. The spiral ar teries are thus converted to low resistance, high

conductance, uteroplacental arteries (Fig. 3.7).

— The decidual NK cells and the extravillous interstitial trophoblast cells interact at the tro phoblast myometrial junction. Excessive

myometrial invasion of trophoblast cells is thus prevented.

— The immunological response of implantation and that of organ transplantation are dif ferent and not comparable.

— Syncytiotrophoblast has got trophoblast lymphocyte cross reactive antigen (TLX). C onsequently there is production of antibodies

(blocking antibodies)by the mother in response to this TLX (due to maternal-paternal immunoinco mpatibility). These blocking

antibodies protect the fetus from rejection (see p. 167).

THE FETAL MEMBRANES

It consists of two layers — outer chorion and the inner amnion.

CHORION: It represents the remnant of chorion laeve and ends at the marg in of the placenta. It is thicker than amnion, friable and

shaggy on both the sides. Internally, it is attached to the amnion by loose areolar tissue and re mnant of primitive mesenchyme.

Externally, it is covered by vestiges of trophoblastic layer and the decidual cells of the fus ed decidua capsularis and parietalis which can

be distinguished microscopically (Fig. 3.4B). Therefore human placenta is a discoid , deciduate, larynthine and haemochorial type

(p. 29).

AMNION: It is the inner layer of the fetal membranes. Its internal surface is smo oth and shiny and is in contact with liquor amnii. The

lining epithelium is described later in the chapter. The outer surface consists of a laye r of connective tissue and is apposed to the similar

tissue on the inner aspect of the chorion from which it can be peeled off. The amnion can also be peeled off from the fetal surface of

the placenta except at the insertion of the umbilical cord.

Functions: (1) Contribute to the formation of liquor amnii (2) Intact membranes pre vent ascending uterine infection (3) Facilitate

dilatation of the cervix during labor (4) Has got enzymatic activities for steroid hormon al metabolism (5) Rich source of

glycerophospholipids containing arachidonic acid — precursor of prostaglandin E

and F

2α

AMNIOTIC CAVITY, AMNION AND AMNIOTIC FLUID

DEVELOPMENT: The formation of the amniotic cavity and its lining membra ne amnion has already been described with the

development of the inner cell mass. Fluid accumulates slowly, at first, but ultimately the fl uid filled cavity becomes large enough to

obliterate the chorionic cavity; the amnion and the chorion come in loose contact by thei r mesenchymal layers.

Initially, the cavity is located on the dorsal surface of the embryonic disc. With the form ation of the head, tail and lateral folds, it comes

to surround the fetus in a manner as described in the Fig. 2.9 and Fig. 2.10. Its two gro wing margins finally merge into the body stalk.

Thus, the liquor amnii surrounds the fetus everywhere except at its attachment wit h the body stalk. The amnion is firmly attached

to the umbilical cord up to its point of insertion to the placenta but everywhere, it can be separated from the underlying chorion.

PRODUCTION

Transudation of maternal serum across the placental membranes

t Transudation from fetal circulation across the umbilical cord or placental membranes

t Secretion from amniotic epithelium

t Transudation of fetal plasma through the highly permeable fetal skin before it is keratinized at 2 0th week

t Fetal urine — daily output at term is about

REMOVAL

n Fetus swallows about 400–700 mL of liquor every day every day.

n Intramembranous absorption of water and solutes (200–500 mL/day) f rom the amniotic compartment to fetal circulation through the

fetal surface of the placenta.

400–1200 mL

Fetal lung that enters the amniotic cavity to add to its

volume.

STRUCTURE OF AMNION : Fully formed amnion is 0.02-0.5 mm in thickness and from within outwards the layers are — (1)

single layer of cuboidal epithelium, (2) basement membranes, (3) compact layer of retic ular structure, (4) fibroblastic layer and (5)

spongy layer. The amnion has got neither blood nor nerve supply nor any lymphatic system .

AMNIOTIC FLUID

ORIGIN OF AMNIOTIC FLUID: The precise origin of the liquor amnii still not well understood. It is pro bably of mixed maternal and

fetal origin.

CIRCULATION: The water in the amniotic fluid is completely changed and replaced in every 3 hours as shown by the clearance of

radioactive sodium injected directly into the amniotic cavity. The presence of lanugo and epithelial scales in the meconium shows that

the fluid is swallowed by the fetus and some of it passes from the gut into the fetal plasm a (vide scheme).

VOLUME: Amniotic fluid, volume is related to gestational age. It measures about 50 mL at 12 weeks, 400 mL at 20 weeks and reaches

its peak of 1 liter at 36–38 weeks. Thereafter the amount diminishes, till at term it measu res about 600–800 mL. As the pregnancy

continues post term, further reduction occurs to the extent of about 200 mL at 43 wee ks.

PHYSICAL FEATURES: The fluid is faintly alkaline with low specific gravity of 1.010. It becomes highly hypotonic to maternal

serum at term pregnancy. An osmolarity of 250 mOsmol/L is suggestive o f fetal maturity. The amniotic fluid’s osmolality falls with

advancing gestation.

Color: In early pregnancy, it is colorless but near term it becomes pale straw col ored due to the presence of exfoliated lanugo and

epidermal cells from the fetal skin. It may look turbid due to the presence of vernix cas eosa. Abnormal color: Deviation of the normal

color of the liquor has got clinical significance.

— Meconium stained (green) is suggestive of fetal distress in presentations o ther than the breech or transverse. Depending upon the

degree and duration of the distress, it may be thin or thick or pea souped (thick with fla kes). Thick with presence of flakes suggests

chronic fetal distress.

— Golden color in Rh incompatibility is due to excessive hemolysis of the f etal RBC and production of excess bilirubin. — Greenish

yellow (saffron) in post maturity.

— Dark colored in concealed accidental hemorrhage is due to contam ination of blood.

— Dark brown (tobacco juice)amniotic fluid is found in IUD. The dark color is du e to frequent presence of old HbA.

COMPOSITION: In the first half of pregnancy, the composition of the fluid i s almost identical to a transudate of plasma. But in late

pregnancy, the composition is very much altered mainly due to contamination of fetal urinary me tabolites. The composition includes—

(1) water 98–99% and (2) solid (1–2%). The following are the solid constituents:

(a) Organic:

Protein–0.3 mg% NPN–30 mg% Total lipids–50 mg% Glucose–20 mg% Uric acid–4 m g% Hormones (Prolactin, insulin andrenin)

Urea–30 mg% Creatinine–2 mg%

(b) Inorganic — The concentration of the sodium, chloride and potassium is alm ost the same as that found in maternal blood. As

pregnancy advances, there may be slight fall in the sodium and chloride concentration prob ably due to dilution by hypotonic fetal urine,

whereas the potassium concentration remains unaltered.

(c) Suspended particles include—Lanugo, exfoliated squamous epithelial cells fr om the fetal skin, vernix caseosa, cast off amniotic cells

and cells from the respiratory tract, urinary bladder and vagina of the fetus.

FUNCTION: Its main function is to protect the fetus. Durin g pregnancy: (1) It acts as a shock absorber, protecting the fetus from

possible extraneous injury. (2) Maintains an even temperature. (3) The fluid distends th e amniotic sac and thereby allows for growth and

free movement of the fetus and prevents adhesion between the fetal parts and amniotic sac. (4) Its nutritive value is negligible because of

small amount of protein and salt content, however, water supply to the fetus is quite adequate.

During labor: (1) The amnion and chorion are combined to form a hydrostatic wedge wh ich helps in dilatation of the cervix. (2) During

uterine contraction, it prevents marked interference with the placental circulation so long as the membranes remain intact. (3) It flushes

the birth canal at the end of first stage of labor and by its aseptic and bacterici dal action protects the fetus and prevents ascending

infection to the uterine cavity.

Fig. 3.12 : Amniotic fluid volume is measured to determine AFI

CLINICAL IMPORTANCE: (1) Study of the amniotic fluid provides useful information ab out the well being and also maturity of the

fetus. (2) Intra-amniotic instillation of chemicals is used as method of induction of abortion . (3) Excess or less volume of liquor amnii is

assessed by amniotic fluid index (AFI) p. 214, 464. Maternal abdomen is divided into qua drants taking the umbilicus, symphysis pubis

and the fundus as the reference points. With ultrasound, the largest vertical pocket in ea ch quadrant is measured. The sum of the four

measurements (cm) is the AFI. It is measured to diagnose the clinical conditio n of polyhydramnios or oligohydramnios

respectively. (4) Rupture of the membranes with drainage of liquor is a helpful m ethod in induction of labor (p. 525).

THE UMBILICAL CORD

The umbilical cord or funis forms the connecting link between the fetus and the placenta through which the fetal blood flows to and from

the placenta. It extends from the fetal umbilicus to the fetal surface of the placenta. DEVE LOPMENT: The umbilical cord is developed

from the connective stalk or body stalk, which is a band of mesoblastic tissue stretching betwe en the embryonic disc and the chorion.

Initially, it is attached to the caudal end of the embryonic disc but as a result of cephaloc audal folding of the embryo and simultaneous

enlargement of the amniotic cavity, the amnioectodermal junction converges on the vent ral aspect of the fetus. As the amniotic cavity

enlarges out of proportion to the embryo and becomes distended with fluid, the embryo is carried more and more into the amniotic cavity

with simultaneous elongation of the connective stalk, the future umbilical cord.

A A Figs 3.13A and B: Schematic drawing of the primitive um bilical cord of — (A) Ten week embryo and (B) Cross section of a term

umbilical cord

STRUCTURES: The constituents of the umbilical cord when fully formed are as follow s (Fig. 3.13).

1. Covering epithelium: It is lined by a single layer of amniotic epithelium but shows stratification like that of fetal epidermis at term.

2. Wharton’s jelly: It consists of elongated cells in a gelatinous fluid formed by mucoid d egeneration of the extraembryonic mesodermal

cells. It is rich in mucopolysaccharides and has got protective function to the umbilical v essels.

3. Blood vessels: Initially, there are four vessels — two arteries and two veins. The arteries are derived from the internal iliac arteries of

the fetus and carry the venous blood from the fetus to the placenta. Of the two umbilica l veins, the right one disappears by the 4th

month, leaving behind one vein which carries oxygenated blood from the placenta to the fetus. Pr esence of a single umbilical artery

is often associated with fetal congenital abnormalities (see p. 218).

4. Remnant of the umbilical vesicle (yolk sac) and its vitelline duct: Remnant of the yolk sac may be found as a small yellow b ody near

the attachment of the cord to the placenta or on rare occasion, the proximal part of the duct per sists as Meckel’s diverticulum.

5. Allantois: A blind tubular structure may be occasionally present near the fetal end which is continuous inside the fetus with its

urachus and bladder.

6. Obliterated extraembryonic coelom: In the early period, intraembryonic coelom is cont inuous with extraembryonic coelom along with

herniation of coils of intestine (midgut). The condition may persist as congenital umbilical hernia or exomphalos.

CHARACTERISTICS: It is about 40 cm in length with an usual variation of 30–1 00 cm. Its diameter is of average 1.5 cm with

variation of 1–2.5 cm. Its thickness is not uniform but presents nodes or swelling at plac es. These swellings (false knots) may be due to

kinking of the umbilical vessels or local collection of Wharton’s jelly. True knots (1%) a re rare. Long cord may form loop around the

neck (20–30%). It shows a spiral twist from the left to right from as early as 12th week due to spiral turn taken by the vessels—vein

around the arteries. The umbilical arteries do not possess an internal elastic la mina but have got well developed muscular coat.

These help in effective closure of the arteries due to reflex spasm soon after the birth o f the baby. Both the arteries and the vein do not

possess vasa vasorum.

ATTACHMENT: In the early period, the cord is attached to the ventral surface of the embryo close to the caudal extremity but as the

coelom closes and the yolk sac atrophies, the point of attachment is moved permanently to the center of the abdomen at fourth month.

Unlike the fetal attachment, the placental attachment is inconsistent. It usually attaches to th e fetal surface of the placenta somewhere

between the center and the edge of the placenta—called eccentric insertion. The attachment may be central, m arginal or even on the

chorion laeve at a varying distance away from the margin of the placenta, called velamentous insertion. The anomalies and various

abnormalities of the umbilical cord are discussed in chapter 16 (p. 216).

The Fetus

Three periods are distinguished in the prenatal development of the fetus. (1) Ovula r period or germinal period—which lasts for first 2

weeks following ovulation. In spite of the fact that the ovum is fertilized, it is still d esignated as ovum. (2) Embryonic period—begins

at 3rd week following ovulation and extends upto 10 weeks of gestation (8 w eeks post conception). The crown-rump Length (CRL) of

the embryo is 4 mm. (3) Fetal period begins after 8th week following concepti on and ends in delivery. The chronology in the fetal

period is henceforth expressed in terms of menstrual age and not in embryonic age.

LENGTH OF THE FETUS: To determine the length of the fetus, the measurement is commo nly taken from the vertex to the coccyx

(crown-rump length) in earlier weeks. While, from the end of 20th week onwards, the measurement is taken from the vertex to the heel

(crown-heel length).

Calculation of the length: The crown heel (CH) measurement of the first 5 months is calculated by squaring the number of the lunar

months to which the pregnancy belongs. In the second half, the same is calculated by multiplying the lunar months by 5. The length is

expressed in centimeters.

AGE OF THE FETUS: Gestational age is the duration of pregnancy calculated from the first day of last menstrual period (LMP ). It is

greater than the post conception (fertilization) age by 2 weeks. The length is more reliab le criterion than the weight to calculate the age

of the fetus. In the first trimester, CRL (mm) + 6.5 = gestational age in weeks. Assessme nt of gestational age by sonography have been

discussed in p. 647.

TABLE 4.1: PRINCIPAL EVENTS OF EMBRYONIC AND FETAL DEVELOP MENT Days 14–21 post conception

Days 21–28 post conception

Weeks 4–6 post conception (4–15 mm embryo)

Weeks 6–8 post conception (15–30 mm embryo)

Weeks 8–12 post conception ((30–60 mm embryo)

Weeks—20

Weeks—28

Weeks—36

Weeks—40

— Notocord develops.

Ectoderm thickens to form neural plate and neural folds. — Neural folds fuse to form n eural tube, four primitive cardiac chambers, first

heart beats on D-21

— Optic vesicles appear, complete neural tube closure (D-30) Limb buds ap pear. Formation of face

— All major structures form, complete ventricular septum (D-46), recognisably human

— External genitalia develop

— Skin is covered with lanugo. Vernix caseosa is present

— Testes descend to the internal inguinal ring. Baby is viable

— One testicle usually descends into the scrotum. Lanugo tends to disappear

— Both the testicles descend into the scrotum. Nails project beyond the finger tips. Posterior fontanelle is closed

GROWTH OF THE FETUS: Normal fetal growth is characterized by cellular hy perplasia followed by hyperplasia and hypertrophy

and lastly by hypertrophy alone. The fetal growth increases linearly until 37th week. It is con trolled by genetic factor in the first half and

by environmental factors in the second half of pregnancy. The important physiologica l factors are: Race (European babies are heavier

than Indians); Sex (male baby weighs > female); Parental height and weight (tall and he avier mother have heavier babies); Birth order

(weight rises from first to second pregnancy) and Socioeconomic factors (heavier bab ies in social class I and II). Fetal growth is

predominantly controlled by IGF-1, insulin and other growth factors. Growth hormon e is essential for postnatal growth. At term, the

average fetal weight in India varies from 2.5–3.5 kg. Pathological factors affect it a dversely (p. 463).

FETAL PHYSIOLOGY

NUTRITION: There are three stages of fetal nutrition following fertilization:

(1) Absorption: In the early post fertilization period, the nutrition is stored in the deut oplasm within the

cytoplasm and the very little extra nutrition needed is supplied from the tubal and uterine secretion. (2) Histotrophic transfer: Following

nidation and before the establishment of the utero-placental circulation,

the nutrition is derived from the eroded decidua by diffusion and later on from the stag nant maternal blood

in the trophoblastic lacunae.

(3) Hematotrophic: With the establishment of the fetal circulation, nutrition is obtained by active an d passive

transfer from the 3rd week onwards.

The fetus is a separated physiological entity and it takes what it needs from the mother ev en at the cost of

reducing her resources. While all the nutrients are reaching the fetus throughout the int rauterine period, the

demand is not squarely distributed. Two-thirds of the total calcium, three-fifths of the tot al proteins and

four-fifths of the total iron are drained from the mother during the last 3 months . Thus, in preterm births,

the store of the essential nutrients to the fetus is much low. The excess iron reserve is to compensate for the

low supply of iron in breast milk which is the source of nutrients following birth.

FETAL BLOOD: Hematopoiesis is demonstrated in the embryonic phase first in the yolk sac by 14th

day. By 10th week, the liver becomes the major site. The great enlargement of the early fetal liver is due to its

erythropoietic function. Gradually, the red cell production sites extend to the spleen and bone marrow and

near term, the bone marrow becomes the major site of red cell production.

In the early period, the erythropoiesis is megaloblastic but near term it becomes normob lastic. The fetal blood

picture at term shows RBC 5–6 million per cu mm; Hb = 16.5–18.5 gm%, reticulocytes –5% and erythroblast

–10%. During the first half, the hemoglobin is of fetal type (α-2, γ-2) but from 24 wee ks onwards, adult type

of hemoglobin (α-2, β-2) appears and at term about 75–80% of the total hemoglobin is of fetal type HbF.

Between 5–8 weeks, the embryo manufactures some additional hemoglobin: Hb Gowe r 1 (ξ- and ε-chains),

Hb Gower 2 (α- and ε-chains) and Hb Portland (ξ- and γ-chains). Between 6–12 mon ths after birth, the fetal

hemoglobin is completely replaced by adult hemoglobin. The fetal hemoglobin has got a greater affinity to

oxygen due to lower binding of 2, 3-diphosphoglycerate compared to adult hemoglobi n. It is also resistant

to alkali in the formation of alkaline hematin. Total fetoplacental blood volume at term is estimated to be 125

mL/kg body weight of the fetus. The red cells develop their group antigen quite early a nd the presence of Rh

factor has been demonstrated in the fetal blood from as early as 38 days after concept ion. The life span of the

fetal RBC is about two-thirds of the adult RBC, i.e. about 80 days. The activities of all glycolytic enzymes in

fetal erythrocytes except phosphofructokinase and 6-phosphogluconate dehydrogenas e are higher than those

of adults or term or premature infants.

Cord blood level of iron, ferritin, vitamin B

, folic acid are consistently higher than maternal blood. LEUKOCYTES AND

FETAL DEFENCE: Leukocytes appear after 2 months of gestation. The white cell count

rises to about 15–20 thousand per cu mm at term. Thymus and spleen soon develop an d produce lymphocytes,

a major source of antibody formation. The fetus, however, rarely forms antibody beca use of relatively sterile

environment. Maternal immunoglobulin G(IgG) crosses the placenta from 12th week onwards to give the

fetus a passive immunity which increases with the increase in gestation period. At term f etal IgG level is 10%

higher than the mother.

IgM is predominantly of fetal origin and its detection by cordocentesis may be helpful in diagnosis of

intrauterine infection. IgA is produced only after birth in response to antigens of enteric infection. URINARY SYSTEM: By the end of

the first trimester, the nephrons become active and secrete urine. Near term,

the urine production rises to 650 mL/day. However, kidneys are not essential for survival of the fetus in utero

but are important in regulation of the composition and volume of the liquor amnii. Oligo hydramnios may be

associated with renal hypoplasia or obstructive uropathy.

SKIN: At 16th week, lanugo (downy thin colorless hairs) appears but near term almost complet ely disappears.

Sebaceous glands appear at 20th week and the sweat glands somewhat later. Vernix c aseosa — the secretion

of the sebaceous glands mixed with the exfoliated epidermal cells is abundantly present smearing the skin. The

horny layer of the epidermis is absent before 20th week which favors transudation fr om the fetal capillaries

into the liquor amnii.

GASTROINTESTINAL TRACT: As early as 10–12 week, the fetus swallows amniotic fluid. The meconium

appears from 20th week and at term, it is distributed uniformly throughout the gu t upto the rectum indicating

the presence of intestinal peristalsis. In intrauterine hypoxia (vagal stimulation), the anal s phincter is relaxed

and the meconium may be voided into the liquor amnii.

Composition of the meconium: It is chiefly composed of the waste products of the hepatic secretion. It

contains lanugo, hairs and epithelial cells from the fetal skin which are swallowed with th e liquor amnii. Mucus,

exfoliated intestinal epithelium and intestinal juices are added to the content. The greenish black color is due

to the bile pigments, specially biliverdin.

RESPIRATORY SYSTEM: In the early months, the lungs are solid. At 28th week, alveoli expa nd and are lined

by cuboidal epithelium. There is intimate contact with the endothelium of the capillaries. A t 24th week, lung

surfactant related to phospholipids—phosphatidylcholine (lecithin) and phosphatidylg lycerol appear.

Surfactant is secreted by type-II alveolar cells. These substances lower the surface tension of the lung fluid

so that the alveoli can be opened up easily when breathing starts following delivery. A lecithin : sphingomyelin

(L:S) ratio of 2:1 in the liquor amnii signifies full maturity of the fetal lung. Fetal c ortisol is the natural

trigger for augmented surfactant synthesis. Fetal growth restriction and prolonged rupture of membranes

also accentuates surfactant synthesis.

Breathing movements are identified by 11 weeks but are irregular until 20th week. Their freq uency varies

from 30–70 per minute and is dependant on the maternal blood sugar concentration. H ypoxia and maternal

cigarette smoking reduces FBM while hyperglycemia increases it. The tracheobronchial tree is filled up with

liquor amnii.

FETAL ENDOCRINOLOGY: Growth hormone, ACTH, prolactin, TSH and gonadotrop hic hormones are

produced by the fetal pituitary as early as the 10th week. Vasopressor and oxytoc ic activity of the posterior

pituitary have also been demonstrated as early as 12 weeks. Fetal adrenals show hy pertrophy of the reticular

zone (fetal zone) which is the site of synthesis of estriol precursor, cortisol and dehydr oepiandrosterone. This

fetal zone is absent in anencephaly. The adrenal medulla produces small amount of cate cholamines. Fetal thyroid

starts synthesising small amount of thyroxine by 11th week. While the fetal ovaries remain inactive, the fetal

testicles mediate the development of the male reproductive structures. Fetal pancreas secrete s insulin as

early as 12th week and glucagon by 8 weeks.

THE FETAL CIRCULATION

The umbilical vein carrying the oxygenated blood (80% saturated) from the placen ta , enters the fetus at the umbilicus and runs

along the free margin of the falciform ligament of the liver. In the liver, it gives off bra nches to the left lobe of the liver and receives the

deoxygenated blood from the portal vein. The greater portion of the oxygenated blood , mixed with some portal venous blood, short

circuits the liver through the ductus venosus to enter the inferior vena cava and thence to right atrium of the heart. The O

content of this

mixed blood is thus reduced. Although both the ductus venosus and hepatic portal/fetal tr unk bloods enter the right atrium through the

IVC, there is little mixing. The terminal part of the IVC receives blood from the right he patic vein.

In the right atrium, most of the well oxygenated (75%) ductus venosus blood is prefere ntially directed into the foramen ovale by the

valve of the inferior vena cava and crista dividens and passes into the left atrium. Here it is mixed with small amount of venous blood

returning from the lungs through the pulmonary veins. This left atrial blood is passed on thro ugh the mitral opening into the left

ventricle.

Fig. 4.1: Fetal circulation. Number inside the circle indicates the percentage saturation of O

Remaining lesser amount of blood (25%), after reaching the right atrium via the superi or and inferior vena cava (carrying the venous

blood from the cephalic and caudal parts of the fetus respectively) passes through the tricuspid opening into the right ventricle.

During ventricular systole, the left ventricular blood is pumped into the ascending and a rch of aorta and distributed by their branches to

the heart, head, neck, brain and arms. The right ventricular blood with low oxygen con tent is discharged into the pulmonary trunk. Since

the resistance in the pulmonary arteries during fetal life is very high, the main p ortion of the blood passes directly through the ductus

arteriosus into the descending aorta bypassing the lungs where it mixes with the blood from the proximal aorta. 70% of the cardiac

output (60% from right and 10% from left ventricle) is carried by the ductus arteriosus to the descending aorta. About 40% of the

combined output goes to the placenta through the umbilical arteries. The deoxygenated bl ood leaves the body by way of two umbilical

arteries to reach the placenta where it is oxygenated and gets ready for recirculation. The mean cardiac output is comparatively

high in fetus and is estimated to be 350 mL/kg/min.

CHANGES OF THE FETAL CIRCULATION AT BIRTH

The hemodynamics of the fetal circulation undergoes profound changes soon after bir th due to— (1) cessation of the placental blood

flow and (2) initiation of respiration. The following changes occur in the vascular system :

1. Closure of the umbilical arteries: Functional closure is almost instantaneous preventing even sligh t amount of the fetal blood to drain

out. Actual obliteration takes about 2–3 months. The distal parts form the lateral umbilical ligaments and the proximal parts

remain open as superior vesical arteries.

2. Closure of the umbilical vein: The obliteration occurs a little later than the arteries, allowing few extra v olume of blood (80–100

mL) to be received by the fetus from the placenta. The ductus venosus collapses and th e venous pressure of the inferior vena cava falls

and so also the right atrial pressure. After obliteration, the umbilical vein forms the ligamentum teres and the ductus venosus

becomes ligamentum venosum (Fig. 4.2).

3. Closure of the ductus arteriosus: Within few hours of respiration, the muscle wall o f the ductus arteriosus contracts probably in

response to rising oxygen tension of the blood flowing through the duct. The effects o f the variation of the O

tension on the ductus

arteriosus are thought to be mediated through the action of prostaglandins. Prostaglandi n antagonists given to the mother may lead to the

premature closure of the ductus arteriosus. Whereas functional closure of the du ctus may occur soon after the establishment of

pulmonary circulation, the anatomical obliteration takes about 1–3 months and be comes ligamentum arteriosum.

4. Closure of the foramen ovale: This is caused by an increased pressure of the left atrium combined with a decreased pressure on the

right atrium. Functional closure occurs soon after birth but anatomical closure occu rs in about 1 year time. During the first few

days, the closure may be reversible. This is evidenced clinically by the cyanotic look of the baby during crying when there is shunting of

the blood from right to left.

Within 1 or 2 hours following birth, the cardiac output is estimated to be about 500 mL/min and the heart rate varies from 120–140

per minute.

Fig. 4.2: Change in the fetal circulation after birth

Physiological Changes During Pregnancy

During pregnancy there is progressive anatomical, physiological and biochemical chang e not only confined to the genital organs but also

to all systems of the body. This is principally a phenomenon of maternal adaptation to the increasing demands of the growing fetus.

Unless well understood, this physiological adaptations of normal pregnancy can be misi nterpreted as pathological.

GENITAL ORGANS

VULVA: Vulva becomes edematous and more vascular; superficial varicosities may appea r specially in multiparae. Labia minora are

pigmented and hypertrophied.

VAGINA: Vaginal walls becomes hypertrophied, edematous and more vascular. Increase d blood supply of the venous plexus

surrounding the walls gives the bluish coloration of the mucosa (Jacquemier’s sign). The length of the anterior vaginal wall is

increased.

Secretion : The secretion becomes copious, thin and curdy white, due to marked exfoliated cells a nd bacteria. The pH becomes acidic

(3.5–6) due to more conversion of glycogen into lactic acid by the Lactobacillus ac idophilus consequent on high estrogen level. The

acidic pH prevents multiplication of pathogenic organisms.

Cytology: There is preponderance of navicular cells in cluster (small intermediate cells with elongated nuclei) and plenty of

lactobacillus.

UTERUS

There is enormous growth of the uterus during pregnancy. The uterus which in nonpr egnant state weighs about 60 gm, with a cavity of

5–10 mL and measures about 7.5 cm in length, at term, weighs 900–1000 g and measures 3 5 cm in length. The capacity is increased

by 500–1000 times. Changes occur in all the parts of the uterus—body, isthmus and cerv ix.

BODY OF THE UTERUS: There is increase in growth and enlargement of the body of the u terus. Enlargement: The enlargement of

the uterus is affected by the following factors:

• Changes in the muscles—(1) Hypertrophy and hyperplasia: Not only the indiv idual muscle fiber increases in length and breadth but

there is limited addition of new muscle fibers. These occur under the influence of the hor mones-estrogen and progesterone limited to the

first half of pregnancy but pronounced upto 12 weeks. (2) Stretching: The muscle fib ers further elongate beyond 20 weeks due to

distension by the growing fetus. The wall becomes thinner and at term, measures about 1.5 cm or less. The uterus feels soft and elastic in

contrast to firm feel of the nongravid uterus.

Arrangement of the muscle fibers: Three distinct layers of muscle fibers are evident: (1) Outer longitudinal— It follows a hood like

arrangement over the fundus; some fibers are continuous with the round ligamen ts. (2) Inner circular—It is scanty and have sphincter

like arrangement around the tubal orifices and internal os. (3) Intermediate —It is the thickest and strongest layer arranged in criss-cross

fashion through which the blood vessels run. Apposition of two double curve muscle fib ers give the figure of ‘8’ form. Thus, when the

muscles contract, they occlude the blood vessels running through the fibers and hence called living ligature (Figs 5.1 and 5.2).

• There is simultaneous increase in number and size of the sup porting fibrous and elastic tissues.

Fig. 5.1:Schematic presentation of the longitudinal, oblique and circular muscle fibers of the pregn ant uterus

Vascular system —Whereas in the nonpregnant state, the blood supply to the uterus is mainly th rough the uterine and least through the

ovarian but in the pregnant state, the latter carries as much the blood as the former. The re is marked spiralling of the arteries, reaching

the maximum at 20 weeks; thereafter, they straighten out. Doppler velocimetry has show n uterine artery diameter becomes double and

blood flow increases by eight fold at 20 weeks of pregnancy. This vasodilatation is mainly due to estradiol and progesterone. Veins

become dilated and are valveless. Numerous lymphatic channels open up. The vascular changes are most pronounced at the placental

site.

The uterine enlargement is not a symmetrical one. The fundus enlarges more than the body . It is evident by the low down attachment

of the round ligaments or insertion of the uterine end of the Fallopian tubes at term.

Weight : The increase in weight is due to the increased growth of the uterine muscles, connectiv e tissues and vascular channels.

Relation : Shape—Nonpregnant pyriform shape is maintained in early months. It becom es globular at 12 weeks. As the uterus enlarges,

the shape once more becomes pyriform or ovoid by 28 weeks and changes to spheric al beyond 36th week (see Fig. 7.5).

Position: Normal anteverted position is exaggerated upto 8 weeks. Thus, the enlarged uterus ma y lie on the bladder rendering it

incapable of filling, clinically evident by frequency of micturition. Afterwards, it becom es erect, the long axis of the uterus conforms

more or less to the axis of the inlet. As the term approaches, specially in multiparae with lax abdominal wall, there is a tendency of

anteversion. But in primigravidae with good tone of the abdominal muscles, it is held fir mly against the maternal spine.

Lateral obliquity: As the uterus enlarges to occupy the abdominal cavit y, it usually rotates on its long axis to the right (dextrorotation).

This is due to the occupation of the rectosigmoid in the left posterior quadrant of the pel vis. This makes the anterior surface of the uterus

to turn to the right and brings the left cornu closer to the abdominal wall. The cervix , as a result, is deviated to the left side

(levorotation) bringing it closer to the ureter.

Uterine peritoneum: The peritoneum maintains the relation proportionately with the growing uterus. The uterosacral ligaments and the

bases of the broad ligament rise upto the level of the pelvic brim. This results in deepe ning of the pouch of Douglas. Large areas of the

lower lateral walls of the uterus remains uncovered by peritoneum. These places are fill ed up by loose and vascular connective tissues.

Contractions (Braxton-Hicks) : Uterine contraction in pregnancy has been named after Braxton-Hicks who first described its entity

during pregnancy. From the very early weeks of pregnancy, the uterus undergoes sp ontaneous contraction. This can be felt during

bimanual palpation in early weeks or during abdominal palpation when the u terus feels firmer at one moment and soft at another.

Although spontaneous, the contractions may be excited by rubbing the uterus. The contractio ns are irregular, infrequent, spasmodic

and painless without any effect on dilatation of the cervix. The patient is no t conscious about the contractions. Intrauterine pressure

remains below 8 mm Hg. Near term, the contractions become frequent with increase i n intensity so as to produce some discomfort to the

patient. Ultimately, it merges with the painful uterine contractions of labor. In abdomi nal pregnancy, Braxton-Hicks contraction is

not felt.

A B

Figs 5.2A and B: (A) Marked elongation of themusclefibers duringpregnancy,(B ) Blood vessels in between interlacing muscle fibers

During contraction there is complete closure of the uterine veins with partial occlusion o f the arteries in relation to intervillous space

resulting in stagnation of blood in the space. This diminishes the placental perfusion, causing t ransient fetal hypoxia which leads to fetal

bradycardia coinciding with the contraction.

Endometrium : The changes of the endometrium of the nonpregnant uterus into dec idua of pregnancy has already been described (p. 24).

ISTHMUS

There are important structural and functional changes in the isthmus during pregna ncy.

During the first trimester, isthmus hypertrophies and elongates to about 3 times its origina l length. It becomes softer. With advancing

pregnancy beyond 12 weeks, it progressively unfolds from above, downwards until it is incorporated into the uterine cavity. The

circularly arranged muscle fibers in the region function as a sphincter in early pregnanc y and thus help to retain the fetus within the

uterus. Incompetency of the sphincteric action leads to mid-trimester abortion and the encirclage operation done to rectify the defect is

based on the principle of restoration of the retentive function of the isthmus (Fig. 5 .3).

A B C

Figs 5.3A to C: Elongation and formation of the lower uterine segment: (A) At 8 weeks (B) At 12 weeks (C) At 16 weeks

CERVIX

Stroma : There is hypertrophy and hyperplasia of the elastic and connective tissu es. Fluids accumulate inside and in between the

fibers. Vascularity is increased specially beneath the squamous epithelium of the portio vaginalis which is responsible for its bluish

coloration. There is marked hypertrophy and hyperplasia of the glands which oc cupy about half the bulk of the cervix. All these lead to

marked softening of the cervix (Goodell’s sign) which is evident as early as 6 week s. It begins at the margin of the external os and then

spreads upwards. It not only provides diagnostic aid in pregnancy but the changes in th e cervix facilitate its dilatation during labor.

Epithelium: There is marked proliferation of the endocervical mucosa with downward ex tension beyond the squamocolumnar junction

(Fig. 5.4).

This gives rise to clinical appearance of ectopy (erosion) cervix. Sometimes, the squa mous cells also become hyperactive and the

mucosal changes simulate basal cell hyperplasia or cervical intraepithelial neoplasia (CIN). These changes are hormone induced

(estrogen) and regress spontaneously after delivery.

Secretion : The secretion is copious and tenacious-physiological leucorrhea of pregnancy. This is due to the effect of progesterone. This

mucous is rich in immunoglobulins and cytokines. The mucus not only fills up the glands but forms a thick plug effectively sealing the

cervical canal. Microscopic examination shows fragmentation or crystallization (beading) du e to progesterone effect.

Fig. 5.4: Changes of the cervix during advanced pregnancy

Anatomical : The length of the cervix remains unaltered but becomes bulky. The cervix is directed posterior ly but after the engagement

of the head, directed in line of vagina. There is no alteration in the relation of the cer vix. There is unfolding of the isthmus; beginning 12

weeks onwards and takes part in the formation of the lower uterine segment. Variable amount of effacement is noticed near term in

primigravidae. In multiparae, the canal is slighly dilated.

FALLOPIAN TUBE: As the uterine end rises up and the fimbrial end is held up by the infundibulo-pelvic ligament, it is placed almost

vertical by the side of the uterus. At term, its attachment to the uterus is placed at the lowe r end of the upper one-third, because of

marked growth of the fundus. The total length

is somewhat increased. The tube becomes congested. Muscles undergo hypertrophy. E pithelium becomes flattened and patches of

decidual reaction are observed.

OVARY: The growth and function of the corpus luteum reaches its maximum at 8th w eek when it measures about 2.5 cm and becomes

cystic. It looks bright orange, later on becomes yellow and finally pale. Regression occu rs following decline in the secretion of human

chorionic gonadotropin (hCG) from the placenta. Colloid degeneration occurs at 12th week which later becomes calcified at term.

Hormones-estrogen and progesterone secreted by the corpus luteum maintain the environm ent for the growing ovum before the action is

taken over by the placenta. These hormones not only control the formation and mainten ance of decidua of pregnancy, but also inhibit

ripening of the follicles. Thus both the ovarian and uterine cycles of the norm al menstruation remain suspended. Luteoma of

pregnancy results from exaggerated, luteinization reaction of the ovary.

Decidual reaction : There may be patchy sheet of decidual cells on the outer surface of the ovary. These are metaplastic changes due

to high hormonal stimulation. The same stimulus may also produce luteinization of atreti c or partially developed follicles.

BREASTS

The changes in the breasts are best evident in a primigravida. In multipara who has once lactated, the changes are not clearly

defined.

SIZE: Increased size of the breasts becomes evident even in early weeks. This is d ue to marked hypertrophy and proliferation of the

ducts (estrogen) and the alveoli (estrogen and progesterone) which are marked in the peripheral lobules. There is also hypertrophy of the

connective tissue stroma. Myoepithelial cells become prominent. Vascularity is increas ed which results in appearance of bluish veins

running under the skin. Quite often, the “axillary tail” (prolongation of the breast tissue under cover of the pectoralis major) becomes

enlarged and painful. There may be evidence of striation due to stretching of the cutis.

NIPPLES AND AREOLA: The nipples become larger, erectile and deeply pigmented. Variable number of sebaceous glands (5–15)

which remain invisible in the nonpregnant state in the areola, become hypertrophied and ar e called Montgomery’s tubercles. Those are

placed surrounding the nipples. Their secretion keeps the nipple and the areola moist an d healthy. An outer zone of less marked and

irregular pigmented area appears in second trimester and is called secondary a reola.

SECRETION: Secretion (colostrum) can be squeezed out of the breast at ab out 12th week which at first becomes sticky. Later on, by

16th week, it becomes thick and yellowish. The demonstration of secretion from the brea st of a woman who has never lactated is

an important sign of pregnancy. In latter months, colostrum may be expressed fro m the nipples. For normal changes and lactation see

page 63 and 499.

CUTANEOUS CHANGES

PIGMENTATION: The distribution of pigmentary changes is selective.

1. Face (chloasma gravidarum or pregnancy mask): It is an extreme form of pigme ntation around the cheek, forehead and around the

eyes. It may be patchy or diffuse; disappears spontaneously after delivery.

2. Breast: The changes are already described (vide supra).

3. Abdomen:

• Linea nigra: It is a brownish black pigmented area in the midline stretching from the xiphisternum to the symphysis pubis (Fig. 7.7B).

The pigmentary changes are probably due to melanocyte stimulating hormone from the anterior pituitary . However, estrogen and

progesterone may be related to it as similar changes are observed in women taking oral contraceptives. The pigmentation disappears after

delivery.

• Striae gravidarum: These are slightly depressed linear marks with varying length and breadth found in pregnancy. They are

predominantly found in the abdominal wall below the umbilicus, sometimes over the thighs and breasts. These stretch marks represent

the scar tissues in the deeper layer of the cutis. Initially, these are pinkish but after the de livery, the scar tissues contract and obliterate

the capillaries and they become glistening white in appearance and are called striae albicans. Apart from the mechanical stretching of

the skin, increase in aldosterone production during pregnancy are the responsible facto rs. Controlled weight gain during pregnancy and

massaging the abdominal wall by lubricants like olive oil may be helpful in reducing their formation. Apart from pregnancy, it may

form in cases of generalized edema, marked obesity or in Cushing’s syndrome (see Fig . 8.5).

OTHER CUTANEOUS CHANGES: These include vascular spider and palmar erythem a which are due to high estrogen level. Mild

degrees of hirsutism may be observed and in puerperium the excess hair is lost.

WEIGHT GAIN

WEIGHT GAIN: In normal pregnancy, variable amount of weight gain is a constant phenomeno n. In early weeks, the patient may lose

weight because of nausea or vomiting. During subsequent months, the weight gain is progressive until the last 1 or 2 weeks, when the

weight remains static. The total weight gain during the course of a singleton pregn ancy for a healthy woman averages 11 kg (24

lb). This has been distributed to 1 kg in first trimester and 5 kg each in seco nd and third trimester. The total weight gain at term is

distributed approximately as follows:

I. Reproductive weight gain: 6 kg – Fetus—3.3 kg, placenta—0.6 kg and liquor—0.8 kg – Uterus—0.9 kg and breasts—0.4 kg

II. Net maternal weight gain: 6 kg – Increase in blood volume—1.3 k g – Increase in extracellular fluid—1.2 kg

– Accumulation of fat (mainly) and protein—3.5 kg

During pregnancy, there is variable amount of retention of electrolytes—sodium (1000 mEq), potassium (10 g) and chlorides. The

sodium is osmotically active and partially controls the distribution of water in various com partments of the body. Causes of increased

sodium retention during pregnancy are: (1) increased estrogen and progeste rone (2) increased aldosterone consequent on the

activation of the renin-angiotensin system and possibly (3) due to increased antidiuretic hormon e. The amount of water retained

during pregnancy at term is estimated to be 6.5 liters.

The increased accumulation of fluid in the tissue spaces mainly below the uterus is du e to —(1) diminished colloid osmotic tension

due to hemodilution driving the fluid out of the vessels and (2) increased venous pressu re of the inferior extremities. Thus, slight edema

of the legs is not uncommon, in otherwise normal pregnancy.

Importance of weight checking: Single weight checking is of little value except to identify th e overweight or underweight patient.

Periodic and regular weight checking is of importance to detect abnormality.

• Rapid gain in weight of more than 0.5 kg (1 lb) a week or more than 2 kg (5 lb) a month i n later months of pregnancy may be the early

manifestation of pre-eclampsia and need for careful supervision.

• Stationary or falling weight may suggest intrauterine growth retardation o r intrauterine death of fetus.

Ideally weight gain should depend on pre-pregnancy body mass index (BMI) level (s ee p. 344). Weight gain for a woman with

normal BMI (20–26) is 11–16 kg. An obese woman (BMI > 29) should not gain mor e than 7 kg. whereas an under weight woman (BMI

< 19) may be allowed to gain upto 18 kg.

Maternal nutrition and weight gain during pregnancy is directly related to the newborn weight. However, it may not be a specific

indicator as there are other factors for low birth weight infant.

BODY WATER METABOLISM

During pregnancy, the amount of water retained at term is about 6.5 liters . The water content of the fetus, placenta and amniotic fluid

is about 3.5 liters. Pregnancy is a state of hypervolemia. There is active retention of sod ium (900 mEq), potassium (300 mEq) and

water. The important causes of sodium retention and volume overload ar e:(i) changes in osmoregulation, (ii) increased estrogen and

progesterone, (iii) increase in reninangiotensin activity, (iv) increased aldosterone, deox ycorticosterone, (v) control by arginine

vasopressin (AVP) from posterior pituitary and (vi) atrial natriuretic peptide. Serum sod ium level and plasma osmolality decreases.

There is resetting of the osmotic thresholds for thirst and AVP (ADH) secretion. Plasma levels of AVP (ADH) remains un changed,

in spite of increased production. This is due to increased metabolic clearance of AVP by the enzyme vasopressinase from the placenta.

Increase in water intake due to lowered osmotic threshold for thirst causes pol yuria in early pregnancy. The threshold for AVP

secretion has been reset after 8 weeks for a new steady state of osmolality.

Atrial and brain natriuretic peptide, secreted by atrial myocytes and by the brain ventricles act as diuretic, a natriuretic and

vasorelaxant. Both the peptides are antagonist to the renin angiotensin system.

HEMATOLOGICAL CHANGES

BLOOD VOLUME: During pregnancy there is increased vascularity of the enlarging u terus with the interposition of uteroplacental

circulation. The activities of all the systems are increased. Blood volume is markedly raised during pregnancy. The rise is progressive

and inconsistent. All the constituents of blood are affected with increased blood volume . The blood volume starts to increase from about

6th week, expands rapidly thereafter to maximum 40–50% above the nonp regnant level at 30–32 weeks. The level remains almost

static till term (Table 5.1).

PLASMA VOLUME: It starts to increase by 6 weeks and it plateaus at 30 weeks o f gestation. The rate of increase almost parallels to

that of blood volume but the maximum is reached to the extent of 50%. Total plasma volume increases to th e extent of 1.25 liters.

The increase is greater in multigravida, in multiple pregnancy and with large baby .

RBC AND HEMOGLOBIN: The RBC mass is increased to the exten t of 20–30%. The total increase in volume is about 350 mL.

This increase is regulated by the increased demand of oxygen transport during pregna ncy. RBC mass begins to increase at about 10

weeks and continue till term without plateauing. Iron supplementation increases the RBC mass by 30%. Reticulocyte count increases by

2%. Erythropoietin level is raised.

Blood volume (mL)

Plasma volume (mL) Red Cell volume (mL) Total Hb (g)

Hematocrit (whole body)

Table 5.1: Principal blood changes during pregnancy

Nonpregnant Pregnancy near term Total increment Change 4000 5500 1500 + 30–40 % 2500 3750 1250 + 40–50% 1400 1750 350 + 20–

30% 475 560 85 + 18–20%

38%

32% Diminished

Table 5.2: Plasma protein changes during pregnancy Parameters

Total protein (g)

Plasma protein concentration

(g/100 mL)

Albumin

(g/100 mL)

Globulin

(g/100 mL)

Albumin: Globulin Nonpregnant Pregnancy near term

180 230

7 6

Change

Increased Decreased

4.3 3

2.7 3

(30%)

Slight increase 1.7 : 1 1 : 1 Decreased Decreased

Table 5.3: Changes in blood coagulation factors Parameters

Platelets (cu mm) Nonpregnant Pregnancy near term 1,60,000– Conflicting 2,00,000 observation

Fibrinogen (mg%)

Fibrinolytic activity

Clotting

time

ESR

200–400 300–600 Change

Static or 15% reduction of the count

+ 50%

— Depressed —

— Unaffected —

10 mm/h 40 mm/h Marked increase (4 times)

The disproportionate increase in plasma and RBC volume produces a state of hem odilution (fall in hematocrit) during

pregnancy. Thus, even though the total hemoglobin mass increases during pregnancy to the extent of 18–20%, there is apparent fall in

hemoglobin concentration. At term, the fall is about 2 g% from the nonpregnant value. There is simultaneous fall in number of red cells

by 15–20% and the hematocrit level. The excess of circulating hemoglobin left behind after delivery yields iron for storage.

The advantages of relative hemodilution are: (1) Diminished blood viscosity ensures optimum gaseous exchange between the

maternal and fetal circulation. This is facilitated by lowered oxygen affinity of maternal red cells observed in later half of pregnancy. (2)

It protects the woman against the adverse effects of supine and erect posture. (3) Prote ction of the mother against the adverse effects of

blood loss during delivery.

LEUKOCYTES and IMMUNE SYSTEM: Neutrophilic leucocytosis occurs to the extent of 80 00/mm

and even to 20,000/cu.mm in

labor. The increase may be due to rise in the levels of estrogen and cortisol. The major c hange in the immune system is the modulation

away from cell-mediated cytotoxic immune response toward increased humoral and innate imm une responses.

TOTAL PROTEIN: Total plasma protein increases from the normal 180 g (nonpregnant) t o 230 g at term. However, due to

hemodilution, the plasma protein concentration falls from 7 g% to 6 g%. This results in diminished viscosity of the blood and reduced

colloid osmotic tension. Because of marked fall in albumin level from 4.3 g% to 3 g%— a fall of about 30% and only slight rise of

globulin (mainly a globulin), the normal albumin: globulin ratio of 1.7:1 is dimin ished to 1:1 (Table 5.2).

BLOOD COAGULATION FACTORS: Pregnancy is a hypercoagulable sta te. Fibrinogen level is raised by 50% from 200–400

mg/dL in nonpregnant to 300–600 mg/dL in pregnancy. As a result of rise in fibrinogen and g lobulin level and diminished blood

viscosity, erythrocyte sedimentation rate (ESR) gives a much higher value (four fold increase) during pregnancy. As such, ESR has

got little diagnostic value in pregnancy. Platelets count, however, gives a conflicting picture. R ecent studies

show a static or even a fall to the extent of 15% of pre-pregnant level. Gestational thrombocytopenia may be due to increased platelet

consumption (p. 274). Fibrinolytic activity is depressed till 15 minutes after delivery. There is increase in activities of clotting factors

like X, IX, VIII, VII and I. The levels of II, V and XII are either unchanged or mildly increas ed. The level of factors XI and XIII are

slightly decreased. The clotting time does not show any significant change. These are all effective to control blood loss and hemostasis

after the separation of placenta (Table 5.3). Levels of coagulation factors normalize 2 w eeks postpartum. Leukocyte levels return to

normal within 1–12 weeks of delivery.

CARDIOVASCULAR SYSTEM

ANATOMICAL CHANGES: Due to elevation of the diaphragm consequent to the enlarge d uterus, the heart is pushed upwards and

outwards with slight rotation to left (Table 5.4).

Abnormal clinical findings: The displacement, may at times, be responsible for palpitation. Th e apex beat is shifted to the 4th

intercostal space about 2.5 cm outside the midclavicular line. Pulse rate is slightly raised, oft en with extrasystoles. A systolic murmur

may be audible in the apical or pulmonary area. This is due to decreased blood v iscosity and torsion of the great vessels. A continuous

hissing murmur may be audible over the tricuspid area in the left second and third intercostal spaces called the “mammary murmur”.

It is due to increased blood flow through the internal mammary vessels. Doppler echocardiog raphy shows an increase in the left

ventricular end diastolic diameters. The left and right atrial diameters also increase. A thir d heart sound (S3) due to rapid diastolic filling

and rarely a fourth heart sound may be auscultated. ECG reveals normal pattern except e vidences of left axis deviation. The physician

should be familiar with these physiological findings and should execute a cautious appr oach in diagnosis of heart disease during

pregnancy (see p. 276).

CARDIAC OUTPUT: The cardiac output (CO) starts to increase from 5th week of pregnancy, reaches its peak 40–50% at about 30–34

weeks. Thereafter the CO remains static till term when the observation is made at lateral r ecumbent position. CO is lowest in the sitting

or supine position and highest in the right or left lateral or knee chest position. Cardiac outp ut increases further during labor

(+50%) and immediately following delivery (+70%) over the pre-labor values. MAP also rises. There is squeezing out of blood from the

uterus into the maternal circulation (auto transfusion) during lab or and in the immediate postpartum. CO returns to pre-labor values

by one hour following delivery and to the pre-pregnant level by another 4 weeks tim e.

The increase in CO is caused by: (1) Increased blood volume (2) To meet the additio nal O

required Table 5.4: Hemodynamic

changes during pregnancy due to increased metabolic activity during pregnancy. No npregnant Pregnancy Change

near term

6.26 + 40%

The increase in CO is chiefly affected by increase in stroke volume and increase in pulse rate to ab out 15

Cardiac output

(L/min)

Stroke volume

(mL)

Heart rate

(per minute)

Blood pressure

4.5

per minute. A normal heart has got enough reserve power to cope with the increased lo ad but a damaged

+ 27%

heart fails to do so.

BLOOD PRESSURE: Systemic vascular resistance 70

+ 17%

(SVR) decreases (–21%) due to the smooth muscle relaxing effect of progesterone, N O, prostaglandins or ANP. Inspite of the large

increase in cardiac output,

Unaffected or mid-pregnancy drop of

diastolic pressure by 5–10 mm Hg

10 cm 20–25 cm + 100%

(femoral) water

20 18 – 14%

the maternal BP (BP = CO × SVR) is decreased due to decrease in SVR. There is overall decrease in diastolic

Venous

pressure

Colloid oncotic

pressure

(mm Hg)

Systemic

vascular

resistance

blood pressure (BP) and mean arterial pressure (MAP) by 5–10 mm Hg (see chapter 17). The decrease in maternal blood pressure

parallels that of SVR.

VENOUS PRESSURE: Antecubital venous pressure remains unaffected. F emoral venous pressure is – 21%

markedly raised specially in the later months. It is due to pressure exerted by the g ravid uterus on the common iliac veins, more on

the right side (SVR)

– 34%

vascular

reistance (PVR)

due to dextrorotation of the uterus. The femoral

Pulmonary

venous pressure is raised from 8–10 cm of water in nonpregnant state to about 25 cm of water during pregnancy in lying down position

and to about 80–100 cm of water in standing position. This explains the fact t hat the physiological edema of pregnancy

subsides by rest alone. Distensibility of the veins and stagnation of blood in the venou s system explain the development of edema,

varicose veins, piles and deep vein thrombosis.

CENTRAL HEMODYNAMICS: In pregnancy there is no significant change in CVP, MAP and PCWP though there is increase in

blood volume, cardiac output and heart rate. The reasons are: there is significant fall in SVR, pulmonary vascular resistance (PVR) and

colloidal osmotic pressure.

SUPINE HYPOTENSION SYNDROME (POSTURAL HYPOTENSION): During late pre gnancy, the gravid uterus produces a

compression effect on the inferior vena cava when the patient is in supine position. This , however, results in opening up of the collateral

circulation by means of paravertebral and azygos veins. In some cases (10%), when th e collateral circulation fails to open up, the venous

return of the heart may be seriously curtailed. This results in production of hypotension , tachycardia and syncope. The normal blood

pressure is quickly restored by turning the patient to lateral position. The augmentation o f the venous return during uterine

contraction prevents the manifestation from developing during labor.

REGIONAL DISTRIBUTION OF BLOOD FLOW: Uterine blood flow is increased from 50 mL/min in non-pregnant state to

about 750 mL near term. The increase is due to the combined effect of uteroplacenta l and fetoplacental vasodilatation (see p. 32). The

vasodilatation is due to the smooth muscle relaxing effects of progesterone, estrogen, nitric oxide (endothelium derived factor),

prostaglandins and atrial natriuretic peptide (ANP). In a normal pregnancy, vascular sy stem becomes refractory to angiotensin II,

endothelin I and other pressure agents (see p. 221). Pulmonary blood flow (normal 6000 mL/min) is incr eased by 2500 mL/min. Renal

blood flow (normal 800 mL) increases by 400 mL/min at 16th week and rem ains at this level till term. The blood flow through the skin

and mucous membranes reaches a maximum of 500 mL/min by 36th week. Heat sens ation, sweating or stuffy nose complained by

the pregnant women can be explained by the increased blood flow.

METABOLIC CHANGES

GENERAL METABOLIC CHANGES: Total metabolism is increased due to the need s of the growing fetus and the uterus. Basal

metabolic rate is increased to the extent of 30% higher than that of the average for the n onpregnant women.

PROTEIN METABOLISM: There is a positive nitrogenous balance throughout pregn ancy. At term, the fetus and the placenta

contain about 500 gm of protein and the maternal gain is also about 500 gm chiefly dist ributed in the uterus, breasts and the maternal

blood. As the breakdown of amino acid to urea is suppressed, the blood urea level falls to 15–20 m g%. Blood uric acid and

creatinine level, however either remain unchanged or fall slightly. Amino acids are actively transported across the placenta to the fetus.

Pregnancy is an anabolic state.

CARBOHYDRATE METABOLISM: Transfer of increased amount of glucose from mother to the fetus is needed throughout

pregnancy. Insulin secretion is increased in response to glucose and amin o acids. There is hyperplasia and hypertrophy of beta cells of

pancreas. Sensitivity of insulin receptors is decreased (44%) specially during later months of preg nancy. Plasma insulin level is

increased due to a number of contrainsulin factors. These are: estrogen, progesterone, h uman placental lactogen (hPL), cortisol,

prolactin, free fatty acids and increased tissue resistance to insulin. This mechani sm ensures continuous supply of glucose to the fetus.

Increased insulin level favors lipogenesis (fat storage). During maternal fa sting, there is hypoglycemia, hypoinsulinemia,

hyperlipidemia and hyperketonemia. Lipolysis generates fatty acids for gluconeogenesi s and fuel supply. Plasma glucagon level

remains unchanged.

Overall effect is maternal fasting hypoglycemia (due to fetal consumption) and post prandial hyperglycemia and

hyperinsulinemia(due to anti-insulin factors). Oral glucose tolerance test may show an abnorma l pattern. This helps to maintain a

continuous supply of glucose to the fetus. As maternal utilization of glucose is r educed, there is gluconeogenesis and glycogenolysis.

Glomerular filtration of glucose is increased to exceed the tubular absorption threshold (normal 180 mg%). So glycosuria is detected in

50% of normal pregnant women.

FAT METABOLISM: An average of 3–4 kg of fat is stored during pregnancy mostly in th e abdominal wall, breasts, hips and thighs.

Plasma lipids and lipoproteins increase appreciably during the later half of pregnancy d ue to increased estrogen, progesterone, hPL and

leptin levels.

LIPID METABOLISM: HDL level increases by 15%. LDL is utilized for placental steroid synthesis. This hyperlipidemia of normal

pregnancy is not atherogenic. The activity of lipoprotein lipase is increased. Changes in the lipid components are tabulated in Table 5.5.

Leptin, a peptide hormone, is secreted by the adipose tissue and the placenta. I t regulates the body fat metabolism.

IRON METABOLISM: Iron is absorbed in ferrous form duodenum and jejunum and is released into the circulation as transferrin.

About 10% of ingested iron is absorbed. Iron freed from transferrin is incorporated into hemoglobin (75%) and myoglobin or stored as

ferritin or hemosiderin. Iron is transported actively across the placenta to the fetus. Iron requirement during pregnancy is considerable

and is mostly limited

Table 5.5: Changes in lipid metabolism NonPregnancy Change pregnant near term

650 1000 + 50%

180 260 + 40% Total lipid

(mg/100 mL)

LDL and

Cholesterol

(mg/100 mL)

HDL (mg/100 mL) Triglycerides

(mg/100 mL)

60 70 + 15%

80 160 + 50% to the second half of the pregnancy specially to the last 12 weeks. Tota l iron requirement during pregnancy is

estimated approximately 1000 mg. This is distributed in fetus and placenta 3 00 mg and expanded red cell mass 400 mg. (Total increase

in red cell volume—350 mL and 1 mL contains 1.1 mg of iron). There is obligatory los s of about 200 mg through normal routes. The iron

in the fetus and placenta is permanently lost and a variable amount of iron in the expanded RBC volume is also lost due to blood loss

during delivery (45 mg/100 mL) and the rest is returned to the store. However, there is saving of about 300 mg of iron due to amenorrhea

for 10 months. (Iron loss in menstrual bleeding per cycle is 30 mg). This iron nee d is not squarely distributed throughout the

pregnancy but mostly limited to the third trimester. (Daily iron requiremen t in non-menstruating women to compensate the average

daily loss is 1 mg). Thus, in the second half, the daily requirement, actually beco mes very much increased to the extent of about

6–7 mg.

The amount of the iron absorbed from the diet and that mobilized from the store are ina dequate to meet the demand. This, is inspite of

the fact that absorption through the gut is enhanced during pregnancy. Serum ferritin lev el actually reflects the body iron stores. In the

absence of iron supplementation, there is drop in hemoglobin, serum iron and serum f erritin concentration at term pregnancy

(p. 261, Table 19.1). Thus pregnancy is an inevitable iron deficiency state. However, pl acenta transfers adequate iron to the fetus,

despite severe maternal iron deficiency. Thus, there is no correlation between hemoglob in concentrations of the mother and the fetus.

SYSTEMIC CHANGES

RESPIRATORY SYSTEM: With the enlargement of the uterus, specially in the later months, the re is elevation of the diaphragm by 4

cm. Total lung capacity is reduced by 5% due to this elevation. However, diaphragmati c excursion is increased by 1–2 cm and breathing

becomes diaphragmatic. Total pulmonary resistance is reduced due to progesterone eff ect. The subcostal angle increases from 68° to

103°, the transverse diameter of the chest expands by 2 cm and the chest circumference increases by 5–7 cm. The mucosa of the

nasopharynx becomes hyperemic and edematous. This may cause nasal stuffine ss and rarely epistaxis. A state of hyperventilation

occurs during pregnancy leading to increase in tidal volume and therefore respiratory minute volume by 40% (see Table 5.6). It is

probably due to progesterone acting on the respiratory center and also to increase in s ensitivity of the center to carbon dioxide. The

woman feels shortness of breath.

Acid base balance —The hyperventilation causes changes in the acid base balance. The arterial PaCO

falls from 38–32 mm Hg and

PaO

rises from 95–105 mm Hg. These facilitate transfer of CO

from the fetus to the mother and O

from the mother to the fetus (see

Table 5.7).

The pH rises in order of 0.02 unit and there is a base excess of 2 mEq/L. Thus, pregnan cy is in a state of respiratory alkalosis. Partial

renal compensation occurs through increased excretion of bicarbonate. Maternal O

consumption is increased by 20–40% due to

increased demand of the fetus, placenta and maternal tissues.

URINARY SYSTEM: Kidney—There is dilatation of the ureter, renal pelvis and the calyces. The kidneys enlarge in length by 1 cm.

Renal plasma flow is increased by 50–75%, maximum by the 16 weeks and is maintained until 34 weeks. Thereafter it falls by 25%.

Glomerular filtration rate (GFR) is increased by 50% all throughout pregn ancy. Increased GFR causes reduction in maternal plasma

levels of creatinine, blood urea nitrogen (BUN) and uric acid. Renal tubules fail to reab sorb glucose, uric acid, amino acids, water soluble

vitamins and other substances completely.

Ureter: Ureters become atonic due to high progesterone level. Dilatation of the ureter above the pe lvic brim with stasis is marked on

the right side specially in primigravidae. It is due to dextrorotation of the uterus pressing the right ureter against the pelvic brim and also

due to pressure by the right ovarian vein which crosses the right ureter at right angle. The stasis is marked between 20–24 weeks. There

is marked hypertrophy of the muscle and the sheath of the ureter specially the pelvic pa rt probably due to estrogen. There is elongation,

kinking and outward displacement of the ureters.

Bladder: There is marked congestion with hyper-trophy of the muscles and elastic tissues of the wall. In late pregnancy, the bladder

mucosa becomes edematous due to venous and lymphatic obstruction especially in prim igravidae following early engagement. Increased

frequency of micturition is noticed at 6–8 weeks of pregnancy which subsides after 12 weeks. It may be due to resetting of

osmoregulation causing increased water intake and polyuria. In late pregnancy, frequen cy of micturition once more reappears

due to pressure on the bladder as the presenting part descends down the pelvis. Stress incontinence may be observed in late pregnancy

due to urethral sphincter weakness.

ALIMENTARY SYSTEM: The gums become conge-sted and spongy and may bleed to touch. Muscle tone and motility of the entire

gastrointestinal tract are diminished due to high progesterone level. Cardiac sphincter is relaxed and r egurgitation of acid gastric

content into the esophagus may produce chemical esophagitis and heart burn. There is diminished gastric secretion and delayed

emptying time of the stomach. Risk of peptic ulcer disease is reduced. Aton icity of the gut leads to constipation, while diminished

peristalsis facilitates more absorption of food materials. LIVER AND GALLBL ADDER: Although there is no histological change in

the liver cells, but the functions are depressed. With the exception of alkaline phosphatas e, other liver function tests (serum levels of

bilirubin, AST, ALT, CPK, LDH) are unchanged. There is mild cholestasis ( estrogen effect). There is marked atonicity of the

gallbladder (progesterone effect). This, together with high blood cholesterol level durin g pregnancy, favor stone formation.

NERVOUS SYSTEM: Some sorts of temperamental changes are found during pregnancy and in the puerperium. Nausea, vomiting,

mental irritability and sleeplessness are probably due to some psychological background . Postpartum blues, depression or psychosis

may develop in a susceptible individual (p. 442).

Compression of the median nerve underneath the flexor retinaculum over the wrist joint leading to pain and paresthesia in the hands and

arm (Carpal tunnel syndrome) may appear in the later months of pregnancy . Similarly paresthesia and sensory loss over the

anterolateral aspect of the thigh may occur. It is due to compression of the lat eral cutaneous nerve of the thigh.

CALCIUM METABOLISM AND LOCOMOTOR SYSTEM: During pregnancy ther e is increase in the demand of calcium by the

growing fetus to the extent of 28 g, 80% of which is required in the last trimester. Daily require ment of calcium during pregnancy and

lactation averages 1–1.5 g. Maternal total calcium levels fall but serum ionized calc ium level is unchanged. 50% of serum calcium

is ionized which is important for physiological function. Calcium absorption from intestine and kidneys are doubled due to rise in the

level of 1, 25 dihydroxy vitamin D

. Pregnancy does not cause hyperparathyroidism. Calcitonin levels increase by 20%. C alcitonin

protects the maternal skeleton from osteoporosis. Maternal serum phosphate level is unchange d.

There is increased mobility of the pelvic joints due to softening of the ligaments caused m ainly by hormone. This along with increased

lumbar lordosis during later months of pregnancy due to enlarged uterus produces backache and waddling gait.

ENDOCRINE SYSTEM: The endocrinology in relation to pregnancy is discussed in the chapter 6.

•

Table 5.6: Changes in respiratory system

Respiration rate/min

Vital capacity (ml)

Tidal volume (ml)

Residual

volume (ml) Total lung

capacity

NonPregnancy pregnant near term 15 15

Change

Unaffected

3200 3300

475 675 Almost

unaltered

+ 40%

965 765 – 20%

5000 4750

Table 5.7: Acid base changes NonPregnancy pregnant near term

95 mm Hg 106 mm Hg

38 mm Hg 32 mm Hg

7.40 7.42

Arterial PO

Arterial PCO

Plasma HCO

– 3

26 m mol/L 22 mmol/L –5%

Change

Increased Diminished

Slight

increase

Decreased

Endocrinology in Relation to Reproduction

The endocrine glands play very important role in the physiology of reproduction. Endocrinology in relation to reproduction includes

the knowledge of:

— Hormones essential for the maturation of the Graafian follicles, ovulation and mainte nance of corpus luteum after fertilization.

— Following conception, transfer of function of pituitary—ovarian axis to placenta, wh ich acts temporarily as a new powerhouse or

endocrine organ.

— During pregnancy, physiological alteration of various endocrine glands namely, the pituitary, thyroid, parathyroid, adrenals and

pancreas.

— Endocrine control of labor. This is discussed in Ch.12.

— Hormonal influence during puerperium necessary for maintenance of lactation.

MATURATION OF GRAAFIAN FOLLICLES AND OVULATION

Follicular maturation takes place during the first half of the cycle. The hormones essential for follicular maturation are mainly FSH

and a small proportion of LH. For continued FSH activity, estrogen is necessary.

OVULATION: Under the influence of FSH, about 20 Graafian follicles develop syn chronously and only one of them will be able to

ovulate. The rest become atretic, mix up with interstitial tissue and acquire the potentiality to produce hormones. For details see author’s

Text Book of Gynecology — chapter 7.

CAUSES OF OVULATION: The possible factors involved in ovulation have been describe d in p. 19. CHANGES WITHIN THE

FOLLICLE AFTER OVULATION: The avascular Graafian follicle becomes vas cularized and the granulosa cells become luteinized.

The morphologically altered Graafian follicle is now changed into corpus luteu m. The corpus luteum secretes progesterone, 17 a

hydroxy progesterone (luteinized granulosa cells) and estradiol, androstenedione (th eca cells).

MAINTENANCE OF CORPUS LUTEUM AFTER FERTILIZATION

Function of corpus luteum is essential to maintain the early pregnancy. Corpus luteum se cretes about 40 mg of progesterone a day. After

implantation, human chorionic gonadotropin (hCG) and possibly placental lactogen (hPL), sec reted by the syncytiotrophoblast cells

maintain the growth and function of the corpus luteum.

PLACENTAL ENDOCRINOLOGY

At 6–8 weeks, there is transfer of functions of corpus luteum to the placenta — which acts temporarily as a new endocrine organ or

powerhouse of hormone production.

HORMONES OF PLACENTA

Placenta produces a variety of hormones of which protein and steroid hormones are signif icantly important. Syncytiotrophoblasts

contain abundant rough endoplasmic reticulum, golgi bodies and mitochondria. Syncytio trophoblasts are the principal site of protein

and steroid hormones in pregnancy.

HORMONES OF PLACENTA AND THEIR CYTOCHEMICAL ORIGIN

Hypothalamic-like (releasing) Cytochemical origin hormones

• Corticotropin releasing (CRH) Cytotrophoblast and

syncytiotrophoblast

• Gonadotropin releasing + (GnRH)

• Thyrotropin releasing (TRH) +

• Growth hormone releasing + (GHRH)

Pituitary-like hormones Cytochemical origin

• Adrenocorticotropic hormone Syncytiotrophoblast (ACTH)

• Human chorionic + gonadotropin (hCG)

• Human chorionic thyrotropin + (hCT)

• Human placental lactogen

+ (hPL)

Other pregnancy proteins

• PSβG, PAPP – A

• Relaxin

• Prolactin

• Atrial natriuretic peptide (ANP)

• Early pregnancy factor (EPF)

Cytochemical origin

Syncytiotrophoblast Corpus luteum,

Decidua, Placenta Decidua

Atrial myocyte

(see p. 51)

Activated platelets ovaries

Growth factors

• Inhibin, activin, transforming growth factor b (TGF – b)

IGF–1 and 2, Epidermal growth factor (EGF)

Cytochemical origin

Syncytiotrophoblast

Steroid hormones

• Estrogens (estriol)

• Progesterone

• Cortisol

Cytochemical origin

Fetoplacental unit

Before 6 weeks — corpus luteum thereafter placenta

Decidua, adrenal

PROTEIN HORMONES

Protein hormones are similar but not necessarily identical with those produced by the pit uitary. For example, placental lactogen is

chemically similar to both pituitary growth hormone and prolactin, but biological activity of placental lactogen is much inferior than

prolactin or growth hormone produced by pituitary.

HUMAN CHORIONIC GONADOTROPIN (hCG): hCG is a glycoprotein. Its molecu lar weight is 36000–40000 daltons. It consists

of a hormone non-specific a (92 amino acids) and a hormone specific b (145 amino a cids) subunit. hCG is chemically and functionally

similar to pituitary luteinizing hormone. The a subunit is biochemically similar to LH, FSH and TSH whereas the b subunit is relatively

unique to hCG. Placental GnRH may have a control on hCG formation.

Functions:

(1) It acts as a stimulus for the secretion of progesterone by the corpus luteum of pregn ancy. The rescue and maintenance of co rpus

luteum till 6 weeks of pregnancy is the major biological function of hCG. (2) hCG stimulates Leydig cells of the male fetus to produce

testosterone in conjunction with fetal pituitary gonadotropins. It is thus indirectly involved in the development of male external genitalia.

(3) It has got immunosuppressive activity which may inhibit the maternal proces ses of immunorejection of the fetus as a homograft.

(4) Stimulates both adrenal and placental steroidogenesis.

(5) Stimulates maternal thyroid because of its thyrotropic activity.

(6) Promotes secretion of relaxin from the corpus luteum.

Level of hCG at different periods of pregnancy: hCG is produced by the syncytiotrophoblast of the

placenta and secreted into the blood of both mother and fetus. The plasma half life of hCG is about 36 hours.

Fig. 6.1: Mean serum levels of placental hormones during pregnancy as measured by rad ioimmunoassay

By radioimmunoassay, it can be detected in the maternal serum or urine as early a s 8-9 days postfertilization. In the early

pregnancy, the doubling time of hCG concentrations in plasma is 1.4–2 days. The blood and urine values reach maximum levels

ranging 100 IU and 200 IU/mL between 60–70 days of pregnancy. The concentration falls s lowly reaching a low level of 10–20 IU/

mL between 100–130 days. Thereafter, the levels remain const-ant throughout pregnancy , with a slight secondary peak at 32 weeks.

High levels of hCG could be detected in—(a) multiple pregnancy (b) hydati-difor m mole or choriocarcinoma and relatively high in—(c)

pregnancy with a 21-trisomy fetus (Down’s syndrome). Plasma lower levels are found in ectopic pregna ncies and in spontaneous

abortion. hCG disappears from the circulation within 2 weeks following delivery (Fig . 6.1).

HUMAN PLACENTAL LACTOGEN (hPL): This is also known as hu man chorionic somatomammotropin (hCS).

The hormone is synthesized by the syncytiotrophoblast of the placenta. The hormone is chemically and immunologically similar to

pituitary growth hormone and prolactin. hPL in maternal serum is first detected during th e 3rd week. The level rises progressively from 5

to 25 μg/mL until about 36 weeks. The plasma concentration of hPL is proportional to placent al mass.

Functions: hPL antagonises insulin action. High level of maternal insulin helps protein synthesis. hPL causes maternal lipolysis and

promotes transfer of glucose and amino acids to the fetus. As a potent angiogenic hormone, it he lps to develop fetal vasculature. It

promotes growth of breasts for lactation.

PREGNANCY SPECIFIC b-1 GLYCOPROTEIN (PS b-1 G): It is produced by th e trophoblast cells. It can be detected in the

maternal serum 18–20 days after ovulation. PS b-1 G is a potent immunosupp ressor of lymphocyte proliferation and prevents

rejection of the conceptus.

Early pregnancy factor (EPF) is a protein, produced by the activated platelets and other maternal tissues. It is detectable in the

circulation 6 to 24 hours after conception. EPF is immunosuppressant and prevents reje ction of the conceptus.

Growth factors: Inhibin, activin, insulin like growth factor (IGF-1 and 2), transforming growth fac tor b (TGFb) and epidermal growth

factor (EGF) are produced by the syncytiotrophoblast cells. They have varied functions inclu ding immunosuppressive, paracrine and

steroidogenic.

Pregnancy associated plasma protein—A (PAPP-A) is s ecreted by the syncytiotrophoblast. It acts as an immunosuppressant in

pregnancy.

STEROIDAL HORMONES

ESTROGEN: In late pregnancy, qualitatively, estriol is the most important amongst the three major estrogens. The site of its

production is in the syncytiotrophoblast.

Fetoplacental unit and biosynthesis of estriol:

The placenta is an incomplete endocrine organ as it has no capability of independent ste roidogenesis like that of ovary. For

steroidogenesis, it depends much on the precursors derived mainly from the fetal and p artly from the maternal sources. Fetal adrenal

gland and the placenta contain the complementary enzyme system. This is the key of Dic zfalusy’s concept of fetoplacental or better still

maternal-fetoplacental unit. The biosynthesis pathway in the f inal formation of estriol is shown diagrammatically in the scheme above.

Estriol is first detectable at 9 weeks (0.05 ng/mL) and increases gradually to about 30 ng/m L at term. Fetal death, fetal anomalies

(adrenal atrophy, anencephaly, Down’s syndrome), hydatidiform moles, placental sulfatase or aromatase deficiency are associated with

low estriol.

PROGESTERONE: Before 6 weeks of pregnancy, the corpus luteum secrete s 17-hydroxyprogesterone. Following the development of

trophoblast, progesterone is synthesized and secreted in increasing amount from the placenta. Precursors from fetal origin are not

necessary as in estrogen production. The placenta can utilize cholesterol as a precursor derived from t he mother for the production of

pregnenolone. Pregnenolone is converted to progesterone in the endoplasmic reticulum by 3 b-hydroxy steroid dehydrogenase. The daily

production rate of progesterone in late normal pregnancy is about 250 mg. Low progester one levels are observed in ectopic pregnancy

and in abortion. High values are observed in hydatidiform mole, Rh-isoimmunization. After delivery, the plasma progeste rone

decreases rapidly and is not detectable after 24 hours.

Functions of the steroid hormones (estrogen and progesterone):

It is indeed difficult to single out the function of one from the other.

— Together they play an important role in the maintenance of pregnancy. Estrogen causes hypertrophy and hyperplasia of the uterine

myometrium, thereby increasing the accommodation capacity and blood flow of the uterus. Progesterone in conjunction with estrogen

stimulates growth of the uterus, causes decidual changes of the endometrium required fo r implantation and it inhibits myometrial

contraction.

— Development and hypertrophy of the breasts during pregnancy are achieved by a numb er of hormones. Hypertrophy and

proliferation of the ducts are due to estrogen, while those of lobulo-alve olar system are due to combined action of estrogen and

progesterone (details — below).

— Both the steroids are required for the adaptation of the maternal organs to the constantly incr easing demands of the growing fetus.

— Progesteronemaintains uterine quiescence, by stabilizing lysosomal membrane s and inhibiting prostaglandin synthesis. Progesterone

and estrogens are antagonistic in the process of labor (see ch. 12).

— Estrogens sensitizes the myometrum to oxytocin and prostaglandins. Estro gens ripen the cervix.

— Progesterone along with hCG and decidual cortisol inhibits T-lymphocyte mediated tissue rejection and protects the conceptus.

— Together they cause inhibition of cyclic fluctuating activity of gonadotropin–gonadal ax is thereby preserving gonadal function.

DIAGNOSTIC VALUE OF PLACENTAL HORMONES

(a) Diagnosis of pregnancy—Presence of hCG in the plasma can be detected by radioimm unoassay and in urine by either biological or

immunological tests.

Radioimmunoassay can detect minute quantity of plasma hCG b subunit soon after the im plantation of blastocyst but biological and

immunological tests do not become positive at least 44 days after the last menstru al period.

(b) Follow-up cases who had trophoblastic tumors—Rad ioimmunoassay for the detection of hCG b subunit is more sensitive in the

follow up study of hydatidiform mole or choriocarcinoma.

(c) Detection of function of fetoplacental unit—The placental hormones commonly studied for evaluating placental insufficiency and

status of the fetus-in-utero are hPL and estriol. These biochemical changes have been largely replaced by biophysical profiles (see

ch.11).

RELAXIN: It is a peptide hormone structurally related to insulin. The main source of pr oduction is the corpus luteum of the ovary but

part of it may be also produced by the placenta and decidua. It has been claimed that re laxin relaxes myometrium, the symphysis and

sacroiliac joints during pregnancy and also helps in cervical ripening by its biochem ical effect.

CHANGES OF ENDOCRINE GLANDS DURING PREGNANCY

Pituitary, thyroid, adrenal cortex, parathyroid and pancreas show distinct physiological changes during pregnancy leading to increase in

output of respective hormones. The basic purpose of these changes is to adjust the inter nal environment of the mother to meet the

additional requirements imposed by metabolic changes during pregnancy as well as to mee t the extra demands by the growing fetus.

The specific anatomical and physiological changes in the individual endocrine glands ar e described in the next page.

PITUITARY GLAND

MORPHOLOGICAL CHANGES IN NORMAL PREGNANCY: During normal pregnancy , the pituitary increases in weight by 30–

50% and is enlarged to about twice its normal size. This is principally due to hyperplasia of acidophilic prolactin secreting cells.

Sometimes, the pituitary enlargement may impinge on the optic chiasma causing bitemporal h emianopia. Maternal pituitary gland is not

necessary for the maintenance of pregnancy.

PHYSIOLOGICAL CHANGES: Pituitary gonadotropin levels are low due to increased lev el of estrogens and progesterone. Growth

hormone level is elevated due to growth hormone variant made by syncytiotrophoblast of the placenta and this explains partly the weight

gain observed during normal pregnancy. Serum prolactin level increases by 10 times. TSH secretion is same as in nonpregnant state.

ACTH and corticotropin releasing hormone (CRH) levels increase. ACTHdoes not cross the placenta while TR H does. Plasma

vasopressin (ADH) level remains unchanged during pregnancy. All the pregnanc y induced changes in the pituitary revert to normal

within few months after delivery.

THE THYROID

MORPHOLOGICAL CHANGES DURING PREGNANCY: Hyperplasia of the thyroid gland oc curs during normal pregnancy and

causes slight generalized enlargement of the gland. However, pregnant women remain euthyroid.

PHYSIOLOGICAL CHANGES: Renal clearance of iodine is increased due to increased g lomerular filtration. Maternal serum iodine

levels fall due to increased renal loss and also due to transplacental shift to the fetus.There is also s timulatory effect of hCG (chorionic

thyrotropin). These cause hyperplasia of the gland. Iodine intake during pregnancy sho uld be increased from 100–150 μg/day to 200

μg/day as recommended by WHO. There is rise in the basal metabolic rate , which begins at about the third month, reaches a value of

+25% during the last trimester. The increase in BMR is probably due to increase in net oxygen consumption of mother and fetus.

The serum protein bound iodine is increased in pregnancy , the range being 6.2 – 11.2 μg% instead of the usual 4–8 μg %. Thyroxin

binding globulin (TBG) increases and reaches a plateau by 20 weeks. It remains unchanged at that level until delivery. The increase in

TBG is due to estrogen stimulation. Iodine and drugs used to treat hyperthyroidism cross the placenta freely whereas thyroid hormones

) and TSH cross very minimally. Total T

and T

are increased but free T

and T

levels are unchanged. TSH remains normal.

Level of calcitonin — a thyroid hormone secreted by the parafollicular cells, increases by 20%. Since the incr ease in TBG is dependent

on estrogens, a failure of the PBI to rise may also indicate fetal compromise.

THE ADRENAL CORTEX MORPHOLOGICAL CHANGES DURING PREGNANCY : There is slight enlargement of the adrenal

cortex, particularly the thickness of the zona fasciculata is increased.

PHYSIOLOGICAL CHANGES: There is significant increase in the serum levels of aldo sterone, deoxycorticosterone (DOC),

corticosteroid binding globulin (CBG), cortisol and free cortisol .The increase of CBG (double) is due to high estrogen level. The

level of fetal cortisol rise is nearly 3 times the nonpregnant values (10.5 μg/dL to 30.1 μg/dL). The levels of total cortisol

(metabolically active) nearly doubles. The level of corticotropin releasing hormone (C RH) increases markedly.

Dehydroepiandrosterone sulfate (DHEAS) levels are decreased. Testosterone and an drostenedione levels are slightly raised. The

physiological correlation of CRH, ACTH and cortisol concentrations are maintained. A bsence of features of Cushing’s syndrome with

such a high level of cortisol might indicate that tissue target sites are less sensitive to cortis ol. Cortisol does cross the placenta but not

ACTH.

The explanations of hypercortisolism in pregnancy are: Increased plasma c ortisol half life, delayed plasma clearance by the kidneys

and resetting of hypothalamo-pituitary and adrenal feedback mechanism.

THE PARATHYROID GLAND

MORPHOLOGICAL CHANGES IN NORMAL PREGNANCY: Maternal parathyroid hyp erplasia occurs during pregnancy.

PHYSIOLOGICAL CHANGES: The concentration of parathyroid hormone (PTH) is nor mal during pregnancy. The main functions of

PTH are to regulate the renal synthesis of 1, 25 dihydroxy vitamin D

and mobilization of calcium from bone. 1, 25 dihydroxy vitamin

enhances calcium reabsorption from the kidneys and small intestines. Calcitonin opposes the action of PTH and vitamin D. PTH

does not cross the placenta but the calcium ions do cross against a concentration gr adient. The marked demand of calcium (25–30

g) by the fetus during the second half of pregnancy is achieved by an increase in ma ternal 1, 25 dihydroxy vitamin D levels. The

absorption and turnover of calcium occur well in advance of fetal skeletal mineralization .

THE PANCREAS

PHYSIOLOGICAL CHANGES IN PREGNANCY: In pregnancy, there is hyperinsulin ism particularly during third trimester which

coincides with the peak concentration of placental hormones. However, despite the incr ease in postprandial insulin level, the fasting

insulin concentration is reduced. Several anti-insulin factors and tissue insulin r esistance modify the action of insulin during

pregnancy (see p. 54).

HORMONAL INFLUENCES NECESSARY FOR MAINTENANCE OF LACTA TION

The breast is a modified sweat gland. It consists of ducts, alveoli and fibrofatty connecti ve tissue. During puberty, there is proliferation

of fibrofatty tissue, without any change in the alveoli-ductal system. The endocr ine control of lactation can be divided into following

stages:

(a) Preparation of breast (mammogenesis) (b) Synthesis and secretion of mi lk by breast alveoli (lactogenesis) (c) Ejection of milk

(galactokinesis) (d) Maintenance of lactation (galactopoiesis).

The preparation of breast development has been described in p. 49. Secretion and ejec tion of milk and maintenance of lactation are

discussed in p. 148. The hormones responsible are schematically represented in Fig. 6.2 .

Fig. 6.2:Endocrine glands in relation to lactation

Diagnosis of Pregnancy

The reproductive period of a woman begins at menarche and ends in menopause. It us ually extends from 13–45 years. While biological

variations may occur in different geographical areas, pregnancy is rare below 12 year s and beyond 50 years. Lina Medina in Lima, Peru

was the youngest one, delivered by cesarean section when she was only 5 year s 7 months old and the oldest one at 57 years and 120

days old.

DURATION OF PREGNANCY: The duration of pregnancy has traditionally been calculated by the clinicians in terms of 10 lunar

months or 9 calendar months and 7 days or 280 days or 40 weeks, calculated from t he first day of the last menstrual period. This is

called menstrual or gestational age.

But, fertilization usually occurs 14 days prior to the expected missed period and in a pre viously normal cycle of 28 days duration, it is

about 14 days after the first day of the period. Thus, the true gestation period is to b e calculated by subtracting 14 days from 280 days,

i.e. 266 days. This is called fertilization or ovulatory age and is widely used by the embryol ogist.

FIRST TRIMESTER (FIRST 12 WEEKS)

SUBJECTIVE SYMPTOMS

The following are the presumptive symptoms of early months of pregnancy:

Amenorrhea during the reproductive period in an otherwise healthy individu al having previous normal periods, is likely due to

pregnancy unless proved otherwise. However, cyclic bleeding may occur upto 12 wee ks of pregnancy, until the decidual space is

obliterated by the fusion of decidua vera with decidua capsularis. Such bleeding is usua lly scanty, lasting for a shorter duration than her

usual and roughly corresponds with the date of the expected period. This is termed as placental sign. This type of bleeding should not

be confused with the commonly met pathological bleeding, i.e. threatened abortion. Pregnanc y, however, may occur in women who are

previously amenorrheic — during lactation and puberty.

Morning sickness is inconsistently present in about 50% cases, more often in the firs t pregnancy than in the subsequent one. It usually

appears soon following the missed period and rarely lasts beyond the first trimester. Its intens ity varies from nausea on rising from

the bed to loss of appetite or even vomiting. But it usually does not affect the health status o f the mother.

Frequency of micturition is quite troublesome symptom during 8–12th week of pregnanc y. It is due to (1) resting of the bulky uterus on

the fundus of the bladder because of exaggerated anteverted position of the uterus, (2) congestion of the bladder mucosa and (3) change

in maternal osmoregulation causing increased thirst and polyuria (p. 51). As the uterus straighte ns up after 12th week, the symptom

disappears.

Breast discomfort in the form of feeling of fullness and ‘pricking sensation’ is evid ent as early as 6–8th week specially in primigravidae.

Fatigue is a frequent symptom which may occur early in pregnancy.

OBJECTIVE SIGNS:t Breast changes are valuable only in primigravidae, as in multiparae , the breasts are enlarged and often contain

milk for years. The breast changes are evident between 6–8 weeks. There is enlargem ent with vascular engorgement evidenced by the

delicate veins visible under the skin (Fig. 7.1).

The nipple and the areola (primary) become more pigmented specially in dark women. Montgomery’s tubercles are prominent. Thick

yellowish secretion (colostrum) can be expressed as early as 12th week.

A B

Figs 7.1A and B: Breast changes during pregnancy; (A) Pronounced pigmentatio n of the primary areola and nipple; (B) Appearance of

secondary areola, development of Montgomery tubercles and increased vascularity.

t Per abdomen — Uterus remains a pelvic organ until 12th week, it m ay be just felt per abdomen as a suprapubic bulge.

t Pelvic changes — The pelvic changes are diverse and appear at different period s. Collectively, these may be informative in arriving at

a diagnosis of pregnancy.

• Jacquemier’s or Chadwick’s sign: It is the dusky hue of the vestibule and anterior vaginal wall visible at about 8th week of

pregnancy. The discoloration is due to local vascular congestion.

• Vaginal sign: (a) Apart from the bluish discoloration of the anterior vaginal wall (b) The walls become softened and (c) Copious non-

irritating mucoid discharge appears at 6th week (d) There is increased pulsation, felt through the lateral fornices at 8th week called

Osiander’s sign.

• Cervical signs:(a) Cervix becomessoft as early as6th week (Goodell’s sign), a little earlier in multiparae. The pregnant cervix feels like

the lips of the mouth, while in the non-pregnant state, like that of tip of the nos e. (b) On speculum examination, the bluish discoloration

of the cervix is visible. It is due to increased vascularity.

t Uterine signs: (a) Size, shape and consistency — The uterus is enlarged to the size of hen’s egg at 6th week, size of a cricket ball at 8th

week and size of a fetal head by 12th week. The pyriform shape of the non-pregnant uterus becomes globular by 12 weeks. There may be

asymmetrical enlargement of the uterus if there is lateral implantation. This is called Piskacek’s signwhere o ne half is more firm than

the other half. As pregnancy advances, symmetry is restored. The pregnant uterus feels soft and elastic.

(b) Hegar’s sign:It ispresent in two-thirdsof cases. It can be demonstrated betwee n 6–10 weeks,a little earlier in multiparae. This sign

is based on the fact that : (1) upper part of the body of the uterus is enlarged by the gr owing fetus (2) lower part of the body is empty

and extremely soft and (3) the cervix is comparatively firm. Because of variation in consiste ncy, on bimanual examination (two fingers

in the anterior fornix and the abdominal fingers behind the uterus), the abdominal and vaginal fi ngers seem to appose below the body of

the uterus (Fig. 7.2). Examination must be gentle to avoid the risk of abortion.

(c) Palmer’s sign: Regular and rhythmic uterine contraction can be elicite d during bimanual examination as early as 4–8 weeks. Palmer

in 1949, first described it and it is a valuable sign when elicited.

To elicit the test , the uterus is cupped between the internal fingers and the extern al fingers for about 2–3 minutes. During contraction,

the uterus becomes firm and well defined but during relaxation, becomes soft an d ill defined. While the contraction phase lasts for about

30 seconds, with increasing duration of pregnancy,

Fig. 7.2: Demonstration of Hegar’s sign

A B

Fig. 7.3: Graphic representation of Palmer’s sign — (A) at 4–8th week, (B) at 10th week.

the relaxation phase increases (Fig. 7.3). After 10th week, the relaxation phas e is so much increased that the test is difficult to

perform.

IMMUNOLOGICAL TESTS FOR DIAGNOSIS OF PREGNANCY

Principle: Pregnancy tests depend on detection of the antigen (hCG) present in the maternal urine or serum with antibody either

polyclonal or monoclonal available commercially.

Tests used: A. Immunoassays without radioisotopes

• Agglutination inhibition tests — Using latex (LAI). The materials for these te sts are supplied in kits containing all the reagents

needed to do a test.

Principle of agglutination inhibition tests: One drop of urine is mixed with one drop of a so lution that contains hCG antibody. If hCG is

not present in the urine sample (e.g. the woman is not pregnant), the antibody remains f ree. Now one drop of another solution that

contains latex particles coated with hCG is added. Agglutination of the latex particles can be observed easily this time. Therefore, the

pregnancy test is negative if there is agglutination. On the other hand, if hCG were p resent in the urine sample (e.g. woman was

pregnant), it would bind the available antibody. There would be no further agglutinatio n when the solution containing hCG coated latex

particles was added. Therefore, pregnancy test is positive if there is no agglutination (schematic presentation above).

• Direct agglutination test (hCG direct test)— Latex particles coated with anti-hCG monoclonal antibodies are mixed with urine. An

agglutination reaction indicates a positive result when the urine sample contains hCG. Ab sence of agglutination (urine without hCG)

indicates a negative one. The sensitivity is 0.2 IU hCG/mL.

• Enzyme-linked immunosorbent assay (EL-ISA) — It is based on one m onoclonal antibody that binds the hCG in urine and serum. A

second antibody that is linked with enzyme alkaline phosphatase is used to ‘sandwich’ th e bound hCG. It is detected by color change

after binding. This is more sensitive and specific. ELISA can detect hCG in serum upto 1– 2 mIU/mL and as early as 5 days before the

first missed period.

• Fluoroimmunoassay (FIA) — It is a highly precise sandwich assay. I t uses a second antibody tagged with a fluorescent label. The

fluorescence emitted is proportional to the amount of hCG. It can detect hCG as low as 1 mIU/mL. FIA takes 2–3 hours. It is used to

detect hCG and for follow up hCG concentrations.

B. Immunoassays with radioisotopes

• Radioimmunoassay (RIA) — It using I

125

ido hCG antibodies. It is more sensitive and can detect β subunit of hCG upto 0.002 IU /mL

in the serum. It can detect pregnancy as early as 8–9 days after ovulation (day of blastoc yst implantation). Radio receptor assay gives

highest sensitivity of 0.001 IU/mL in the serum. RIAs are quantitative, so can be used for determining the doubling time of hCG (ectopic

pregnancy monitoring). RIAs require 3–4 hours to perform.

• Immunoradiometric assay (IRMA) — It uses sandwich principle to detect whole hCG molecu le. IRMAs use

125

I labelled hCG and

require only 30 minutes. It can detect hCG as low as 0.05 mIU/mL. Selection of time: Diagno sis of pregnancy by detecting hCG in

maternal serum or urine can be made by 8 to 11 days after conception. The test is not reli able after 12 weeks.

SUMMARY OF PREGNANCY TESTS (BETA hCG) Test Test sensitivity Time taken Immunological tests (Urine)

Inference Positive on

Agglutination

inhibition test (Latex test)

Direct latex

agglutination test

Two-site sandwich immunoassay

(membrane ELISA/ card tests)

0.5–1 (IU/mL) 2 minutes (Urine)

Absence of agglutination 2 days after missed period

0.2 (IU/mL) 2 minutes (Urine)

30–50 mIU/mL 4–5 minutes (Urine)

Presence of agglutination 2–3 days after missed period

On the first day of the missed period (28th day of cycle)

Color bands in the control as well as in test window

Various kits in card forms are available + Pregnant

(Card test) – Not pregnant (Card test)

S C T

Enzyme-linked 1–2 mIU/mL 2–4 hours Immunosorbent Assay (Serum)

5 days before the first missed period

(ELISA)

Radioimmunoassay

(β subunit) 0.002 IU/mL 3–4 hours

25th day of cycle Immuno-radiometric 0.05 mIU/mL 30 minutes 8 days after con ception assay (IRMA) (Serum)

Collection of urine: The patient is advised to collect the first voided urine in the morning in a clean container (not to wash with soap).

Kits to perform the test at home are also available.

Other uses of pregnancy tests: Apart from diagnosis of uterine pregnancy, the tests are employed in the diagnosis of ectopic pregnancy

(see p. 185), to monitor pregnancy following in vitro fertilization and embryo transfer and to follow up cases of hydatidiform

mole and choriocarcinoma. Test accuracy ranges from 98.6 – 99%. Non-pregnant lev el is below 1 mIU/mL.

Limitations: Test accuracy is affected due to presence of (i) hemoglobin (ii) albumin (iii) LH and (iv) immunological diseases.

Advantages: They are advantageous over the biological methods because of their speed, simplicity, accuracy and less cost. Biological

tests were based on the classic discovery of Aschheim and Zondek in 1927. All these tests are of historical interest.

Fig. 7.4 : Gestational ring at 5th week

ULTRASONOGRAPHY: Intradecidual gestational sac (GS) is identified as early as 29 to 35 days of gestation. Fetal viability and

gestational age is determined by detecting the following structures by transvaginal ultrasonography. Gestational sac and yolk sac by

5 menstrual weeks; Fetal pole and cardiac activity — 6 weeks; Embryonic movements by 7 weeks. Fetal gestational age is best

determined by measuring the CRL between 7 and 12 weeks (variation ± 5 days). Dopp ler effect of ultrasound can pick up the fetal

heart rate reliably by 10th week. The instrument is small, handy and cheap (see Fig. 41 .40). The gestational sac (true) must be

differentiated from pseudogestational sac (see p. 646).

SECOND TRIMESTER (13–28 WEEKS)

SYMPTOMS: The subjective symptoms — such as nausea, vomiting and freque ncy of micturition usually subside, while amenorrhea

continues. The new features that appear are:

— “Quickening” (feeling of life) denotes the perception of active fetal movements by the wo men. It is usually felt about the 18th

week, about 2 weeks earlier in multiparae. Its appearance is an useful guide to calculate t he expected date of delivery with reasonable

accuracy (see later in the chapter).

— Progressive enlargement of the lower abdomen by the growing uterus.

GENERAL EXAMINATION

— Chloasma: Pigmentation over the forehead and cheek may appear at about 24th we ek. — Breast changes: (a) Breasts are m ore

enlarged with prominent veins under the skin (b) Secondary areola

specially demarcated in primigravidae, usually appears at about 20th week (c) Montgom ery’s tubercles are prominent and extend to the

secondary areola (d) Colostrum becomes thick and yellowish by 16th week (e) Variable degree of striae may be visible with advancing

weeks.

ABDOMINAL EXAMINATION

Inspection: (1) Linear pigmented zone (linea nigra) exten ding from the symphysis pubis to ensiform cartilage may be visible as early as

20th week (2) Striae (both pink and white) of varying degree are visible in the lower abdomen, more towards the flanks (see Fig. 8.5).

Palpation: Fundal height is increased with progressive enlargement of the uterus. A pproximate duration of pregnancy can be

ascertained by noting the height of the uterus in relation to different levels in the abdom en. The following formula is an useful guide

for the purpose (Fig. 7.5).

The height of the uterus is midway between the symphysis pubis and umbilicus at 16th week; at the level of umbilicus at 24th week and

at the junction of the lower third and upper two-third of the distance between the umbili cus and ensiform cartilage at 28th week.

— The uterus feels soft and elastic and becomes ovoid in shape.

— Braxton-Hicks contractions are evident, the features of which have been mentioned in p. 47.

— Palpation of fetal parts can be felt distinctly by 20th week. The findings are of value not only to diagnose pregnancy but also to

identify the presentation and position of the fetus in later weeks.

— Active fetal movements can be felt at intervals by placing the hand over the uteru s as early as 20th week. It not only gives positive

evidence of pregnancy but of a live fetus. The intensity varies from a faint flutter in early months to stronger movements in later

months.

—External ballottement is usually elicited as early as 20th week when the fetus is relatively smaller than the volume of the amniotic

fluid (Fig. 7.6A). It is difficult to elicit in

Fig. 7.5: The level of fundus uteri at different weeks. Note the change of uterine shape

obese patients and in cases with scanty liquor amnii. It is best elicited in breech presentati on with the head at the fundus.

Auscultation

— Fetal heart sound (FHS) is the most conclusive clinical sign of pregnancy. With an ordin ary stethoscope, it can be detected

between 18–20 weeks. The sounds resemble the tick of a watch under a pillow. Its location varies with the position of the fetus. The rate

varies from 110–160 beats per minute. Two other sounds are confused with fetal he art sounds. Those are:

— Uterine souffleis a soft blowing and systolic murmur heard low down at the sides of the uterus, best on the left side. The sound is

synchronous with the maternal pulse and is due to increase in blood flow through th e dilated uterine vessels.It can be heard in big

uterine fibroid.

A C

Figs 7.6A to C: (A) External ballottement; (B and C) Steps showing how to elicit internal b allottement — Funic or fetal souffle is due

to rush of blood through the umbilical arteries. It is a soft, blowingmurmur synchronous with t he fetal heart sounds.

VAGINAL EXAMINATION

— The bluish discolorationof the vulva, vagina and cervix is much more evident, so also softening of the cervix.

—Internal ballottement can be elicited between 16–28th week (Figs 7.6B and C). The fetus is too small before 16th week and too large

to displace after 28th week. However, the test may not be elicited in cases with scanty liquo r amnii, or when the fetus is transversely

placed.

INVESTIGATIONS (Imaging Studies)

Sonography: Routine sonography at 18–20 weeks permits a detailed survey of fetal anatomy , placental localization and the integrity of

the cervical canal. Gestational age is determined by measuring the biparietal diameter (BPD ), head circumference (HC), abdominal

circumference (AC) and femur length (FL). It is most accurate when done between 12 and 20 weeks (variation ± 8 days). BPD is

measured at the level of the thalami and cavum septum pellucidum. BPD is measured from o uter edge of the skull to the inner edge of

the opposite side (see p. 645).

Fetal organ anatomy is surveyed to detect any malformation. Fetal viabilityis deter mined by real-time ultrasound. Absence of fetal

cardiac motion confirms fetal death.

Magnetic Resonance Imaging (MRI): MRI can be used for fetal anatomy survey, biometr y and evaluation of complex malformations (p.

650). Radiologic evidence of fetal skeletal shadow may be visible as early as 16th w eek (p. 651).

LAST TRIMESTER (29-40 WEEKS)

SYMPTOMS: (1) Amenorrhea persists (2) Enlargement of the abdomen is progressive which produces some mechanical discomfort

to the patient such as palpitation or dyspnea following exertion (3) Lightening — At abo ut 38th week, specially in primigravidae, a

sense of relief of the pressure symptoms is obtained due to engagement of the presentin g part (4) Frequency of micturition reappears

(5) Fetal movements are more pronounced.

SIGNS:

— Cutaneous changes are more prominent with increased pigmentation and striae. — U terine shape is changed from cylindrical to

spherical beyond 36th week.

— Fundal height: The distance between the umbilicus and the ensiform cartilage is d ivided into three equal

parts. The fundal height corresponds to the junction of the upper and middle third at 32 weeks, upto the level of ensiform cartilage at 36th

week and it comes down to 32 week level at 40th week because of engagemen t of the presenting part. To determine whether the height

of the uterus corresponds to 32 weeks or 40 weeks, engagement of the head sh ould be tested. If the head is floating, it is of 32 weeks

pregnancy and if the head is engaged, it is of 40 weeks pregnancy.

Fig. 7.7A: Position of the woman during obstetric examination

Fig. 7.7B: Symphysis fundal height (SFH)

Symphysis fundal height (SFH). The upper border of the fundus is located by th e ulnar border of the left hand and this point is marked.

The distance between the upper border of the symphysis pubis upto the marked point is measured by a tape in centimeter (Fig. 7.7B).

After 24 weeks, the SFH measured in cm corresponds to the number of weeks upto 36 weeks. A variation of ± 2 cm is accepted as

normal. Variation beyond the normal range needs further evaluation (see p. 78 and p. 464).

— Braxton-Hicks contractions are more evident.

— Fetal movements are easily felt.

— Palpation of the fetal partsand their identification become much easier. Lie, presentat ion and position of the fetus are determined.

— FHS is heard distinctly in areas corresponding to the presentation and position of the f etus. FHS may not be audible in cases of

maternal obesity, polyhydramnios, occipitoposterior position and certainly in IUD.

— Sonography — gestational age estimation by BPD, HC, AC and FL is less acc urate (variation ± 3 weeks). Fetal growth assessment

can be made provided accurate dating scan has been done in first or second trimester .

Fetal AC at the level of the umbilical vein is used to assess gestational age and feta l growth profile (IUGR or macrosomia) (see p. 464).

Fetal weight estimation can be done using tables (Hadlock – 1984, p. 74). Amniotic fluid vo lume assessment (see p. 39, 212, 464) is

done to detect oligohydramnios (AFI < 5) or polyhydramnios (AFI > 25).

Placental anatomy: Location (fundus or previa), thickness (placentomegaly in diabe tes) or other abnormalities (see p. 648) are noted.

Other information:Fetal life, number, presentation and organ anatomy as done in th e first and second trimester are surveyed again.

DIFFERENTIAL DIAGNOSIS OF PREGNANCY

While the clinical diagnosis of pregnancy at times becomes easy but there are occasions where the diagnosis poses a problem. The

enlargement of the uterus caused by pregnancy may have to be differentiated from ab dominopelvic swellings, such as uterine fibroid,

cystic ovarian tumor, encysted tubercular peritonitis, hematometra or even dis tended urinary bladder. The confusion is

accentuated by the presence of amenorrhea for some other reasons. Pregnancy may a lso coexist with the swellings.

Pseudocyesis (Syn : Phantom, spurious, false pregnancy): It is a psychological disorder where the woma n has the false but firm

belief that she is pregnant although no pregnancy exists. The woman often is infertile who has an intense desire to have a baby. The

conspicuous feature is cessation of menstruation. Other confusing manifestations are gr adual enlargement of the abdomen because of

deposition of fat, secretion from the breasts and intestinal movement, imagining it to be fetal move ment. In some cases, the condition

continues until eventually spurious labor sets in. Obstetric examination reveals absence of posi tive signs of pregnancy. Examination with

ultrasound and/or immunological tests for pregnancy may be required to negate the diagnosis.

Cystic ovarian tumor : The diagnostic points are: (1) The swelling is slow growing, usually t akes months to grow (2) Amenorrhea is

usually absent (3) It feels cystic or tense cystic (4) Absence of Braxton-Hicks contracti on (5) Absence of positive signs of pregnancy (6)

Ultrasonography shows absence of fetus.

Fibroid : (1) The tumor is slow growing, often takes years (2) Amenorrhea is abs ent (3) The feel is firm, more towards hard but may be

cystic in cystic degeneration (4) Positive signs of pregnancy are absent (5) Ultrasonogr aphy or immunological test for pregnancy gives

negative result.

Encysted peritonitis : (1) History of Koch’s infection (2) Amenorrhe a of longer duration may be present (3) Swelling is ill defined (4)

Absence of positive signs of pregnancy (5) Internal examination reveals normal uterus separated from the swelling (6) Ultrasonography

— absence of fetus.

Distended urinary bladder : In chronic retention of urine due to retrove rted gravid uterus, the distended bladder may be mistaken as

ovarian cyst or acute hydramnios. Catheterization of the bladder solves the problem.

SUMMARY OF DIAGNOSIS OF PREGNANCY

— Positive or absolute signs : (1) Palpation of fetal parts and perception of active fetal movements b y the examiner at about 20th week

(2) Auscultation of fetal heart sounds (3) Ultrasound evidence of embryo as early as 6 th week and later on the fetus (4) Radiological

demonstration of the fetal skeleton at 16th week and onwards.

— Presumptive symptoms and signs : It includes the features mainly app reciated by the women. (1) Amenorrhea (2) Frequency of

micturition (3) Morning sickness (4) Fatigue (5) Breast changes (6) Skin changes (7) Q uickening.

— Probable signs : (1) Abdominal enlargement (2) Braxton-Hicks cont ractions (3) External ballottement (4) Outlining the fetus (5)

Changes in the size, shape and consistency of the uterus (6) Jacquemier’s sign (7) Soft ening of the cervix (8) Osiander’s sign (9) Internal

ballottement (10) Immunological test.

CHRONOLOGICAL APPEARANCE OF SPECIFIC SYMPTOMS AND SIGNS O F PREGNANCY

AT 6–8 WEEKS: Symptoms — Amenorrhea, morning sickness, frequency of micturit ion, fatigue, breast discomfort.

Signs: Breast enlargement, engorged veins visible under the skin; nipples and areo la more pigmented. Internal examination reveals —

positive Jacquemier’s sign, softening of the cervix, bluish discoloration of the cervix an d Osiander’s sign; positive Hegar’s and Palmer’s

sign. Uterine enlargement varies from hen’s egg to medium size orange. Immunologica l tests will be positive. Sonographic evidence of

gestational ring.

AT 16TH WEEK: Symptoms — Except amenorrhea, all the previous symptoms disap pear.

A B

Nulliparous cervix Parous cervix Figs 7.8A and B: Appear ance of external os — (A) Nulliparous; (B) Parous

Signs: Breast changes — pigmentation of primary areola and prominence of Mon tgomery’s tubercles, colostrum. Uterusmidway

between pubis and umbilicus, Braxton-Hicks contractions, uterine souffle, internal ballo ttement. X-ray shows fetal shadow. Sonographic

diagnosis.

AT 20TH WEEK: Symptoms — Amenorrhea, quickening (18th week).

Signs: Appearance of secondary areola (20th week), linea nigra (20 weeks), uter us at the level of umbilicus at 24 weeks, Braxton-Hicks

contractions, external ballottement (20th week), fetal parts (20 weeks), fetal movements (20 weeks), FHS (20 weeks), internal

ballottement (16–28 weeks). X-ray shows fetal shadow. Sonographic diagnosis.

SIGNS OF PREVIOUS CHILD BIRTH

The following are the features which are to be considered in arriving at a diagnosis of having a previous birth. Breastsbecome more

flabby; nipples are prominent whoever breast-fed their infant; primary areolar

pigmentation still remains and so also the white striae.

Abdominal wall is more lax and loose. There may be presence of silvery white striae and linea a lba. Uterine wall is less rigid and the

contour of the uterus is broad and round, rather than ovoid. Perineum is lax and evidence of old scarring from previous perineal

laceration or episiotomy may be found. Introitus is gaping and there is presence of carunculae myrtifo rmes.

Vagina is more roomy.

Cervix: Nulliparous cervix is conical with a round external os. In parous w omen, it becomes cylindrical and the external os is a

transverse patulous slit and may admit the tip of the finger (Fig. 7.8). However, as a res ult of operative manipulation even a nulliparous

cervix may be torn and resembles a multiparous cervix.

ESTIMATION OF GESTATIONAL AGE AND PREDICTION OF EXPECTED D ATE OF DELIVERY

Estimation of gestational age and thereby forecasting the EDD is not only the concern o f the individual but it is invaluable in the

diagnosis of intrauterine growth retardation of the fetus or management of high risk pr egnancy.

Gestational age is about 280 days calculated from the first day of the last normal menstru al period (LMP). Accurate LMP is the most

reliable parameter for estimation of gestational age.

But in significant number of cases (20–30%), the patients either fail to remember the LM P or report inaccurately. The matter becomes

complicated when the conception occurs during lactation amenorrhea or soon followin g withdrawal of contraceptive pills (ovulation may

be delayed for 4–6 weeks) or in cases with bleeding in early part of pregnancy. The following parameters either singly or in

combination are useful in predicting the gestational age with fair degree of a ccuracy.

PATIENT’S STATEMENT

— Date of fruitful coitus: If the patient can remember the date of the single fruitful coitus with certainty, it is quite reliable to predict the

expected date of delivery with accuracy of 50% within 7 days on either side. As previo usly mentioned, 266 days are to be added to the

date of the single fruitful coitus to calculate the expected date. This is not much practicable except when the pregnancy occurs in

instances of sudden death or absence of the husband or rape.

— Naegele’s formula: Provided the periods are regular, it is very useful and commonly practice d means to calculate the expected date.

Its prediction range is about 50% with 7 days on either side of EDD. If the interval of cycles is longer, the extra days are to be added

and if the interval is shorter, the lesser days are to be subtracted to get th e EDD.

— Date of quickening: A rough idea about the probable date of delivery can be deduced by ad ding 22 weeks in primigravidae and 24

weeks in multiparae to the date of quickening.

PREVIOUS RECORDS: The required weeks are to be added to m ake it 40 weeks.

A. Clinical:

— Size of the uterus prior to 12 weeks more precisely corresponds with the pe riod of amenorrhea. — Palpation of fetal parts at the

earliest by 20th week.

— Auscultation of FHR at the earliest by 18–20 weeks using ordinary stethoscope and th at using Doppler principle

at 10th week.

B. Investigation records: Investigation records during first half of pregnancy are invalu able.

— Recording of positive pregnancy testusing immunological principle at first missed period by earlie st. — Ultrasonographicfindings

at the earliest are: (a) Gestation sac — at 5 weeks. (b) Measurement of crown rump len gth

(CRL) detected at 7 weeks, approximates 10 mm; at 10 weeks – 34 mm (CRL in cm + 6.5 = weeks of pregnancy). OBJECTIVE SIGNS

— Height of the uterus above the symphysis pubis in relation to the landmarks on the abdomi nal wall or SFH (see p. 71).

— Lightening: Following the appearance of the features suggestive of lightening (see p. 121), the labor is likely to commence within 3

weeks.

— Size of the fetus, change in the uterine shape, volume of liquor amnii, hardening of the skull and girth of the abdomen are of value in

assessing the maturity of the fetus specially if the examinations are done by the same per son at intervals.

— Vaginal examination:If the cervix becomes shorter and dilated, the labor is fairly no t far off. But labor may start even with long and

closed cervix.

INVESTIGATIONS: Sonography — The following parameters are of use.

• First trimester — See p. 71; Crown — Rump Length (CRL) is most acc urate. (Variation ± 5 days).

• Second trimester by BPD, HC, AC and FL measurement. Most accurate w hen done between 12 and 20 weeks (variation ± 8 days).

• Third trimester — Less reliable, variation ± 16 days.

Gestational age determined by sonographic measurement (in first or second trimester) s hould be compared with the menstrual age. In

clinical practice, when the difference between the two is less than 10 days, the EDD derived from the LMP is confirmed. When

the difference is more, the EDD should base on ultrasonographic fetal biometry .

X-ray — Appearance and density of ossification centers in the upper end of the tibia (38–40 weeks) and lower end of femur (36–37

weeks).

ESTIMATION OF FETAL WEIGHT

Approximate prediction of the fetal weight is more important than the mere estim ation of the uterine size . This is more important

prior to induction of labor or elective cesarean section. The following methods are usef ul when considered together to have a rough idea

about the size of the fetus:

A. Fetal growth velocity is maximum (26.9 g/day) over the 32–36 weeks of pregnancy. It declines gradually to 24 g/day over the 36–40

weeks of gestation. Individual fetal growth varies considerably. Conditional centiles dependin g on individual fetal growth velocity is

thought to be more important.

B. Johnson’s formula: Height of the uterus above the symphysis pubis in centimeters minus 12, if the vertex is at or above the level of

ischial spines or minus 11, if the vertex is below the level of ischial spines — multiplied b y 155 in either case gives the weight of the

fetus in grams. Example — Height of the uterus above the symphysis pubis = 32 cm and the st ation of the head is at — 2. The weight of

the fetus will be (32–12) × 155 = 3100 g. This is, however, applicable only in vertex presentati on. However, the approximate size of the

fetus is modified by the amount of liquor amnii and thickness of the abdominal wall.

C. Sonography: Fetal weight has been estimated by combining a number of biom etric data, e.g. BPD, HC, AC and FL. Tables

(Hadlock, Shepard) are currently in use (computer software). Estimated fetal w eight likely to be within 10 percent of actual weight.

— Shepard’s formula: Log 10 EFW (g) = 1.2508 + (0.166 × BPD) + 0.046 × AC) – (0.002646 × AC × BPD). — Hadlock’s formula:

Log 10 EFW (g) = 1.3596 – 0.00386 (AC × FL) + 0.0064 (HC) + 0.00061 (BPD × AC) + 0.0425

(AC) + 0.174 (FL).

The Fetus-in-Utero

The fetus lies inside the uterus in a closed sac filled with liquor amnii. It has enough free dom of movement until the later months of

pregnancy, when it becomes relatively fixed. Till then, periodic examination is essential t o note its lie, presentation, position and attitude.

Incidental idea can be gained about the size of the fetus or amount of liquor am nii.

LIE: The lie refers to the relationship of the long axis of the fetus to the long axis of the centralized uterus or maternal spine, the

commonest lie being longitudinal (99.5%). The lie may be transverse or oblique; sometimes the lie is unstable until labor sets in, when it

becomes either longitudinal or transverse (Fig. 8.1).

A B

Fig. 8.1: Fetal lie. (B), the fetus seems to lie in oblique position in relation to the maternal spine but rema ins in longitudinal lie in relation

to uterine axis. Correction of the uterine obliquity rectifies apparent oblique lie of the fetus (A)

PRESENTATION: The part of the fetus which occupies the lower pole of the uterus (pelvic brim) is called the presentation of the

fetus. Accordingly, the presentation may be cephalic (96.5%), podalic (3%) or should er and other (0.5%). When more than one part of

the fetus present, it is called compound presentation.

PRESENTING PART: The presenting part is defined as the part of the present ation which overlies the internal os and is felt by

the examining finger through the cervical opening. Thus, in cephalic presentatio n, the presenting part may be vertex (commonest), brow

or face, depending upon the degree of flexion of the head (Fig. 8.2).

Similarly, the fetal legs in a breech presentation may be flexed (complete breech), ext ended (frank breech) or a foot may be present

Table 8.1: Preponderance of lie, presentation and presenting part Lie

Longitudinal (99.5%)

Transverse }Breech (3%)

(0.5%) Shoulder (0.5%) }

Brow

}

(0.5%)

Oblique Face

Unstable

Presentation Presenting part of cephalic Cephalic (96.5%) Vertex – (96%)

(footling). However, the term presentation and presenting part are often used synonym ously and expressed more commonly in clinical

practice according to the latter definition.

ATTITUDE: The relation of the different parts of the fetus to one another is called attitude of the fetus. The universal attitude is that of

flexion. During the later months, the head, trunk and limbs of the fetus maintain the attitude of flexion on all joints and form an ovoid

mass that corresponds approximately to the shape of uterine ovoid. The characteristic flexed a ttitude may be modified by the amount of

liquor amnii. There may be exceptions to this universal attitude and extension of the head may oc cur (deflexed vertex, brow or face

presentation, according to the degree of extension), or the legs may become extended i n breech.The course of labor in such

circumstances may be modified accordingly.

A B C D

Figs 8.2A to D: Varieties of cephalic presentations in different attitude

DENOMINATOR: It is an arbitrary bony fixed point on the presenting pa rt which comes in relation with the various quadrants of

the maternal pelvis. The following are the denominators of the different prese ntations—occiput in vertex, mentum (chin) in face,

frontal eminence in brow, sacrum in breech and acromion in shoulder.

POSITION: It is the relation of the denominator to the different quadran ts of the pelvis. For descriptive purpose, the pelvis is

divided into equal segments of 45° to place the denominator in each segment. Thus, theoreti cally, there are 8 positions with each

presenting part (Fig. 8.3).

Anterior , posterior, right or left position is referred in relation to the maternal pelvis, with the mother in erect position. Howe ver,

some have retained the conventional description of four vertex positions. Vertex occupying the left anterior quadrant of the pelvis is

the commonest one and is called left occipitoanterior (LOA). This is the first vertex po sition. Similarly, right occipitoanterior (ROA) is

the second vertex; right occipitoposterior (ROP) third vertex and left occipitoposterior ( LOP) is the fourth vertex position.

Fig. 8.3: The position and relative frequency of the vertex at the onset of labor

Fig. 8.4: Diagrammatic representation of a fetus in flexed attitude

P–V—Vertico-podalic diameter;

A–A—Bisacromial diameter;

T–T—Bitrochanteric diameter

CAUSES OF PREPONDERANCE OF LONGITUDINAL LIE AND CEPHALIC PRESENTATION

The fetus in the attitude of flexion assumes a shape of an ovoid with its long vertico-pod alic axis measuring about 25 cm (10′′) at term

(Fig. 8.4).

The fetus accommodates comfortably along the long axis of the ovoid shape of the uter ine cavity at term. Hence, there is preponderance

of longitudinal lie.

The cephalic presentation, being the absolute majority amongst the longitudinal lie, can be explained by: (1) Gravitation—the

head being heavier comes down to the bottom. (2) Adaptation — the smallest circumfer ence of the flexed head is about 27.5 cm (11′′)

and the circumference of the breech with both thighs flexed is about 32.5 cm (13”). Th us the cephalic and the podalic poles can be

comfortably accommodated in the narrow lower pole and the wider fundal area of the uterus respectively.

METHODS OF OBSTETRICAL EXAMINATION

ABDOMINAL EXAMINATION: A thorough and systemic abdominal examination beyond 28 we eks of pregnancy can reasonably

diagnose the lie, presentation, position and the attitude of the fetus. It is not unlikely that t he lie and presentation of the fetus might

change, specially in association with excess liquor amnii and hence periodic check up is essential.

Preliminaries: Verbal consent for examination is taken. The patient is asked to evacuate the bladder. She is then made to lie in dorsal

position with the thighs slightly flexed (see Fig. 7.7A, p.70). Abdomen is fully exposed. The ex aminer stands on the right side of the

patient.

Inspection: To note (1) whether the uterine ovoid is longitudinal or transverse o r oblique (2) contour of the uterus—fundal notching,

convex or flattened anterior wall, cylindrical or spherical shape (3) undue enlargement of the uterus (4) skin condition of abdomen for

evidence of ringworm or scabies and (5) any incisional scar mark on the abdomen.

Palpation: Height of the uterus: The uterus is to be centralized if it is deviated. The ulnar border of t he left hand is placed on the upper

most level of the fundus and an approximate duration of pregnancy is ascertained in terms of we eks of gestation (Fig. 8.5). Alternatively,

the SFH can be measured with a tape (see Fig. 7.7).

Fig. 8.5: To note the height of the uterus. Linea nigra and striae gravidarum are also visible

There are conditions where the height of the uterus may not correspond with the perio d of amenorrhea. The conditions where the

height of the uterus is more than the period of amenorrhea are: (1) mistaken da te of the last menstrual period (2) twins (3)

polyhydramnios (4) big baby (5) pelvic tumors— ovarian or fibroid (6) hydatidiform mole and (7) concealed accidental hemorrhage.

The condition where the height of the uterus is less than the period of ameno rrhea are: (1) mistaken date of the last menstrual

period (2) scanty liquor amnii (3) fetal growth retardation and (4) intrauterine fetal d eath.

Obstetric grips (Leopold maneuvers) (Fig. 8.6): Palpation should be conducted with utmost ge ntleness. Clumsy and purposeless

palpation is not only uniformative but may cause undue uterine irritability. During Braxton-H icks contraction or uterine contraction

in labor, palpation should be suspended.

(i) Fundal grip: The palpation is done facing the patient’s face. The whole of the fundal area is palpated using both hands laid flat on it

to find out which pole of the fetus is lying in the fundus: (a) broad, soft and irregular mass suggestive of breech, or (b) smooth, hard and

globular mass suggestive of head. In transverse lie, neither of the fetal poles are palpated in the f undal area.

(ii) Lateral or umbilical grip: The palpation is done facing the pa tient’s face. The hands are to be placed flat on either side of the

umbilicus to palpate one after the other, the sides and front of the uterus to find out the po sition of the back, limbs and the anterior

shoulder. The back is suggested by smooth curved and resistant feel. The ‘lim b side’ is comparatively empty and there are small knob

like irregular parts. After the identification of the back, it is essential to note its position whether p laced anteriorly or towards the flank or

placed transversely. Similarly, the disposition of the small parts, whether placed to one si de or placed anteriorly occupying both the

sides, is to be noted. The position of the anterior shoulder is to be sought for. It forms a well ma rked prominence in the lower part of

the uterus above the head. It may be placed near the midline or well away from the midline.

(iii) Pawlik’s grip (Third Leopold): The examination is done facing towards the patient’s face. The overstre tched thumb and four

fingers of the right hand are placed over the lower pole of the uterus keeping

C D

Figs 8.6A to D: Obstetric grips (Leopold maneuvers): (A) Fundal grip (first Leopold); (B ) Lateral grip (second Leopold); (C) Pawlik’s

grip (third Leopold); (D) Pelvic grip (fourth Leopold)

the ulnar border of the palm on the upper border of the symphysis pubis. When the fin gers and the thumb are approximated, the

presenting part is grasped distinctly (if not engaged) and also the mobility from side to side is te sted. In transverse lie, Pawlik’s grip is

empty.

(iv) Pelvic grip (Fourth Leopold): The examination is done facing the patient’s feet. Four fingers of both the hands are placed on

either side of the midline in the lower pole of the uterus and parallel to the inguinal ligamen t. The fingers are pressed downwards and

backwards in a manner of approximation of finger tips to palpate the part oc cupying the lower pole of the uterus (presentation). If it is

head, the characteristics to note are: (1) precise presenting area (2) attitude and (3) engagem ent.

To ascertain the presenting part , the greater mass of the head (cephalic prominence) is caref ully palpated and its relation to the limbs

and back is noted. The attitude of the head is inferred by noting the relative position of the sinc ipital and occipital poles (Fig. 8.8). The

engagement is ascertained noting the presence or absence of the sincipital and occipit al poles or whether there is convergence or

divergence of the finger tips during palpation (Fig. 8.9). This pelvic grip using both the hands is f avored as it is most comfortable for

the woman and gives most information.

Auscultation: Auscultation of distinct fetal heart sounds (FHS) not only helps in the diagnosis of a live baby but its location of maximum

intensity can resolve doubt about the presentation of the fetus (Fig. 8.7A).

Fig. 8.7A: Auscultation of distinct fetal heart sounds (FHS)

The fetal heart sounds are best audible through the back (left scapular region) in vertex and breech presentation where the convex portion

of the back is in contact with the uterine wall. However, in face presentation, the heart s ounds are heard through the fetal chest.

As a rule, the maximum intensity of the FHS is below the umbilicus in cephalic presentati on and around the umbilicus in breech. In

different positions of the vertex, the location of the FHS depends on the position of the back and the degree of descent of the head. In

occipitoanterior position, the FHS is located in the middle of the spinoumbilical line o f the same side. In occipitolateral position, it is

heard more laterally and in occipitoposterior position, well back towards the mother’s flank on th e same side. In left occipitoposterior

position, it is most difficult to locate the FHS (Fig. 8.7B).

INTERNAL EXAMINATION: The diagnosis of the presentation and position of the fetus may not be accurate by internal examination

during pregnancy when the cervix remains closed. However, during labor, accurate informati on may be obtained by palpation of the

sagittal suture and fontanelles through the open cervix. Stress for strict aseptic precautio ns during vaginal examination needs no

emphasis.

ULTRASONOGRAPHY: The diagnosis of the lie, presentation and position may be difficult in the presence of marked obesity,

irritable uterus, excessive liquor amnii and deeply engaged head, specially in primigravi dae. Ultrasonography can locate the head and the

body (see p. 644). Alternatively, straight X-ray may be needed to arrive at a diagnosis in such cases.

INFERENCES: As the vertex is the commonest presentation, the relevant information in relation to the vertex are only mentioned.

Fig. 8.7B:Locationof the fetalheart sound in different presentation of position of the fetus

Lie: The longitudinal lie is evident from: (1) Longitudinal uterine ovoid on inspe ction (2) the poles of the fetal ovoid—cephalic and

podalic are placed, one at the lower and the other at the upper part of the uterine ca vity, as evident from the fundal and first pelvic grips.

Presentation: The cephalic presentation is evident from the first pelvic grip—smooth , hard and globular mass.

Attitude: From the first pelvic grip, the relative positions of the sincipital and occipita l poles are determined. In well flexed head, the

sincipital pole is placed at a higher level but in deflexed state, both the poles remain at a same level (Fig. 8.8).

Presenting part: Vertex is diagnosed from the first pelvic grip. The cephalic prominence , being the sinciput, is placed on the same

side towards which limbs lie.

Position: The occipitoanterior position is diagnosed by: (1) Inspection—conv exity of the uterine contour. (2) Lateral grip—(a) The back

is placed not far from the midline to the same side of the occiput (b) The anterior should er is near the midline (3) Auscultation—

maximum intensity of the FHS is close to the spino-umbilical line on the same side of the back.

Right or left position is to be determined by : (1) Position of the back (2) Position of the o cciput and (3) Location of the FHS.

ENGAGEMENT: When the greatest horizontal plane, the biparietal, has passe d the plane of the pelvic brim, the head is said to be

engaged.

Diagnosis: First pelvic grip: (1) Both the poles (sinciput and occiput) are not felt per abdo men. However, the sincipital pole can be felt

with difficulty even though the head is engaged (2) Divergence of the examining fin gers of both the hands while trying to push

downwards on the lower abdomen (Fig. 8.9).

Convergence of the fingers while palpating the lateral aspects of the fetal head indicates that the head is not yet engaged.

A B

Figs 8.8A and B:Relative position of the sincipital and the occipital pole as felt in fir st pelvic grip: (A) Well flexed (B) Deflexed

A B

Figs 8.9A and B: Abdominal palpation to determine engagement of the head: (A) Divergence of fingers— engaged head, (B)

Convergence fingers—not engaged

A B

Figs 8.10A and B: The relationship of the biparietal diameter to the pelvic brim and that of lower pole of the head to the ischial spines

in: (A) Non-engaged head; (B) Engaged head

Vaginal Examination: Lower pole of the unmoulded head is usually at or below the level of the ischial spines. The distance between

the pelvic inlet and ischial spines is about 5 cm. But the distance between the biparietal p lane of the unmoulded head to the vertex is

about 3 cm (Fig. 8.10).

Imaging: Lateral view sonography is confirmatory.

Significance: Engagement of the head always excludes disproportion at the brim, as th e head is the best pelvimeter.

The traditional concept that in primigravidae, the engagement occurs by 38 weeks is no t corroborative in clinical practice. In majority,

the engagement occurs between 38–42 weeks or even during first stage of labor. In m ultigravidae, however, the engagement occurs late

in first stage of labor after the rupture of the membranes. However, if the head fails to engage in primigravidae even at 38th week,

the causes are to be sought for. Common causes are: (1) Deflexed head placing the larger diameter to engage (2) Cephalopelvic

disproportion or big head or a combination of both (3) Polyhydramnios (4) Poor form ation or yielding of lower uterine segment—

preventing the head to sink into the pelvis, (5) Hydrocephalus (6) Placenta previa (7) P elvic tumors— ovarian or fibroid (8) High pelvic

inclination (9) Functional — when no cause can be detected (20%).

Fixed head: The word ‘fixed’ should not be used to designate an engaged head. Whereas, an en gaged head is fixed but conversely, the

fixed head is not necessarily engaged. When an egg is placed on the egg cup, it remain s fixed yet the maximum diameter does not pass

through the rim (Fig. 8.11).

Similarly the head may be fixed to the brim but that does not mean that the maximum dia meter of the head (biparietal) will pass through

the brim. As such, the use of the term ‘fixed’ should be abandoned. Similarly, the term ‘engaging’ should be withheld. A clear

statement is to be made as to whether the head is engaged or not.

Fig. 8.11: Diagrammatic representation showing the difference between an engaged and a f ixed head by use of egg cups and eggs

Fetal Skull and Maternal Pelvis

FETAL SKULL

Fetal skull is to some extent compressible and made mainly of thin pliable tabular (flat) bo nes forming the vault. This is anchored to the

rigid and incompressible bones at the base of the skull.

AREAS OF SKULL: The skull is arbitrarily divided into several zones of obstetrical im portance (Fig. 9.1). These are:

• Vertex : It is a quadrangular area bounded anteriorly by the bregma and coronal sutu res behind by the lambda and lambdoid sutures

and laterally by lines passing through the parietal eminences.

• Brow : It is an area bounded on one side by the anterior fontanelle and coronal sutures an d on the other side by the root of the nose and

supraorbital ridges of either side.

•Face : It is an area bounded on one side by root of the nose and supraorbital ridge s and on the other, by the junction of the floor of the

mouth with neck.

Sinciput is the area lying in front of the anterior fontanelle and corresponds to the ar ea of brow and the occiput is limited to the occipital

bone.

Flat bones of the vault are united together by non-ossified membranes attached to the m argins of the bones. These are called sutures and

fontanelles. Of the many sutures and fontanelles, the following are of obstetric significance.

Fig. 9.1: Fetal skull showing different regions and landmarks of obstetrical significance

SUTURES: (Figs 9.1 and 9.2)

• Thesagittalor longitudinal suture lies between tw o parietal bones.

• The coronal suturesrun between parietal and frontal bones on either side.

• The frontal suturelies between two frontal bones.

• The lambdoid sutures separate the occipital bone and the two parietal bones.

Importance: (1) It permits gliding movement of one bone over the other during m oulding of the head, a phenomenon of significance

while the head passes through the pelvis during labor. (2) Digital palpation of sagittal su ture during internal examination in labor gives

an idea of the manner of engagement of the head (asynclitism or synclitism), degree of internal rotation of the head and degree of

moulding of the head.

Fig. 9.2: Fetal skull showing important sutures, fontanelles and diameters of obstetric significance.

FONTANELLES:Wide gapinthesuturelineiscalledfontanelle.Ofthemany fontanelles(6innumber),two ar e of obstetric significance: (1)

Anterior fontanelle or bregma and (2) Posterior fontanelle or lambda.

Anterior fontanelle (Fig. 9.2): It is formed by joining of the fo ur sutures in the midplane. The sutures are anteriorly frontal, posteriorly

sagittal and on either side, coronal. The shape is like a diamond. Its anteroposterior and tr ansverse diameters measure approximately 3

cm each.The floor is formed by a membrane and it becomes ossified 18 months after birth. It becomes pathological, if it fails to ossify

even after 24 months.

Importance:

— Its palpation through internal examination denotes the degree of flexion of the head .

— It facilitates moulding of the head.

— As it remains membranous long after birth, it helps in accommodating the marked br ain growth; the brain becoming almost double its

size during the first year of life.

— Palpation of the floor reflects intracranial status—depressed in dehydration, elevated in raised intracranial tension.

— Collection of blood and exchange transfusion, on rare occasion, can be performed through it via the superior longitudinal sinus.

— Cerebrospinal fluid can be drawn, although rarely, through the lateral angle of the a nterior fontanelle from the lateral ventricle.

Posterior fontanelle:It is formed by junction of three suture lines — sagittal suture anteriorly and lambdoid suture on either side. It is

triangular in shape and measures about 1.2 × 1.2 cm (1/2′′ × 1/2′′). Its floor is membranous but becomes bony at term. Thus, truly its

nomenclature as fontanelle is misnomer. It denotes the position of the head in relation to maternal pelvis.

Sagittal fontanelle: It is inconsistent in its presence. When present, it is situated o n the sagittal suture at the junction of anterior two-third

and posterior one-third. It has got no clinical importance.

DIAMETERS OF SKULL (Fig. 9.3): The engaging diameter of the fetal s kull depends on the degree of flexion present. The

anteroposterior diameters of the head which may engage are:

Diameters

1. Suboccipito-bregmatic — extends from the nape of the neck to the center of the bregma

2. Suboccipito-frontal — extends from the nape of the neck to the anterior end of the a nterior fontanelle or center of the sinciput.

Measurement in cm (inches)

9.5 cm (3 ¾“)

10 cm (4”)

Attitude of the Presentation head

Complete Vertex flexion

Incomplete Vertex flexion

3. Occipito-frontal — extends from the occipital eminence to the root of the nose (Glabella).

4. Mento-vertical — extends from the mid point of the chin to the highest poin t on the sagittal suture.

5. Submento-vertical — extends from junction of floor of the mouth and neck to the highest point on the sagittal suture

6. Submento-bregmatic — extends from junction of floor of the mouth and neck to the centre of the bregma

11.5 cm (4 ½”)

14 cm (5 ½”)

11.5 cm (4 ½”)

9.5 cm (3 ¾”) Marked Vertex deflexion

Partial Brow extension

Incomplete Face extension

Complete Face extension

The transverse diameters which are concerned in the mechanism of labor are — (see Fig. 9.2).

— Biparietal diameter—9.5 cm (3 ¾′′): It extends between two parietal eminences. Whatever may be the position of the head, this

diameter nearly always engages.

— Super-subparietal—8.5 cm (3 ½′′): It extends from a point placed below one parietal eminenc e to a point placed above the other

parietal eminence of the opposite side.

— Bitemporal diameter—8 cm (3 ¼′′): It is the distance between the ante roinferior ends of the coronal suture.

— Bimastoid diameter — 7.5 cm (3′′): It is the distance between the tips of the mastoid processes. Th e diameter is incompressible and it

is impossible to reduce the length of the bimastoid diameter by obstetrical operatio n.

CIRCUMFERENCES: Circumference of the plane of the diameter of engagement diffe rs according to the attitude of the head.

Circumferences of the head in different attitudes:

Fig. 9.3: The important landmarks of fetal skull

Attitude of the head — Complete flexion

— Deflexed

— Incomplete extension — Complete extension

Plane of engagement Circumference Biparietal-suboccipito-bregmatic. Shape — almost ro und 27.5 cm (11”) Biparietal-occipito-frontal.

Shape — oval 34 cm (13 ½”) Biparietal-mento-vertical. Shape — bigger oval 37.5 cm (15”) Biparietal-submento-bregmatic. Shape —

almost round 27.5 cm (11”)

Conversion of the centimeters into inches is approximate

Fig. 9.4: Diagrammatic representation showing the principle of moulding of the head.

MOULDING: It is the alteration of the shape of the forecoming head while pas sing through the resistant birth passage during

labor. There is, however, very little alteration in size of the head, as volume of the content inside th e skull is incompressible although

small amount of cerebrospinal fluid and blood escape out in the process. During normal deli very, an alteration of 4 mm in skull diameter

commonly occurs.

Mechanism: There is compression of the engaging diameter of the head with c orresponding elongation of the diameter at right angle to

it (Fig. 9.4).

Thus, in well flexed head of the anterior vertex presentation, the engaging suboccipito- bregmatic diameter is compressed with elongation

of the head in mento-vertical diameter which is at right angle to suboccipito-bregm atic (Fig. 9.5).

During the process, the parietal bones tend to overlap the adjacent bones, viz. the occipi tal bone behind, the frontal bones in front and the

temporal bones at the sides. In first vertex position, the right parietal bone tends to override the left one and this becomes reverse in

second vertex position. Moulding disappears within few hours after birth .

A B C D

Figs 9.5A to D: Types of moulding in cephalic presentations (shown by dotted line: (A) V ertex presentation with well flexed head; (B)

Vertex presentation with deflexed head (sugar loaf head); (C) Face presentation; (D) B row presentation.

Grading : There are three gradings. Grade-1 — the bones touching but not overlapping, G rade-2 — overlapping but easily separated and

Grade-3 — fixed overlapping.

Importance:

— Slight moulding is inevitable and beneficial. It enables the head to pass more easily, th rough the birth canal.

— Extreme moulding as met in disproportion may produce severe intracranial disturban ce in the form of tearing of tentorium cerebelli or

subdural hemorrhage.

— Shape of the moulding can be an useful information about the position of the head occupied in the pelvis.

CAPUT SUCCEDANEUM:It is the formation of swelling due to stagnation of fluid in the lay ers of the scalp beneath the girdle of

contact. The girdle of contact is either bony or the dilating cervix or vulval ring. The swelling is diffuse, boggy and is not limited by the

suture line (Fig. 9.6). It may be confused with cephalhematoma (see ch. 32). It disappe ars spontaneously within 24 hours after birth.

Fig. 9.6: Formation of caput succedaneum

Mechanism of formation: While the head descends to press over the dilating cervix or vulval ring, the overlying scalp is free from

pressure, but the tissues in contact with the full circumference of the girdle of contact is compressed. This interferes with venous return

and lymphatic drainage from the unsupported area of scalp →stagnation of fluid and appearan ce of a swelling in the scalp (Fig. 9.6).

Caput usually occurs after rupture of the membranes.

Importance:

— It signifies static position of the head for a long period of time.

— Location of the caput gives an idea about the position of the head occupied in the pe lvis and the degree

of flexion achieved. In left position, the caput is placed on right parietal bone and in rig ht position, on left parietal bone. With increasing

flexion, the caput is placed more posteriorly.

PELVIS

From the obstetrical standpoint, it is useful to consider the bony pelvis as a whole rather than separately. For descriptive purpose, an

articulated pelvis is composed of four bones — two innominate bones, sacrum and co ccyx. These are unitedtogether by four joints—

twosacroiliacjoints, sacro-coccygeal joint andthe symphysis pubis.

The pelvis is anatomically divided into a false pelvis and a true pelvis, the boundary line being the brim of the pelvis. The bony

landmarks on the brim of the pelvis from anterior to posterior on each side are — upper b order of symphysis pubis, pubic crest,

pubic tubercle, pectineal line, iliopubic eminence, iliopectineal line, sacro-iliac articu lation, anterior border of the ala of sacrum and

sacral promontory (Fig. 9.7).

FALSE PELVIS

The false pelvis is formed by the iliac portions of the innominate bones and is limited above by the iliac crests. It has got little obstetric

significance except that its measurements can to a certain extent, predict the size and configur ation of the true pelvis. Its only obstetric

function is to support the enlarged uterus during pregnancy. Its boundaries are: po steriorly — lumbar vertebrae, laterally — iliac fossa

and anteriorly — anterior abdominal wall.

TRUE PELVIS

This part of the pelvis is chiefly of concern to the obstetricians, as it forms the canal through w hich the fetus has to pass. It is shallow in

front, formed by symphysis pubis and measures 4 cm (1 ½′′) and deep posteriorly, formed by the sacrum and coccyx and measures 11.5

cm (4 ½′′). For descriptive purpose, it is divided into inlet , cavity and outlet.

The pelvic measurements given in the text are average when measured radiologically an d vary within a limited degree in different

countries. The conversion of centimetres into inches is approximate.

Fig. 9.7: Bony landmarks on the brim of the pelvis separating the true from the false pelvis; 1-Sym physis pubis. 2-Pubic crest. 3-Pubic

tubercle. 4-Pectineal line. 5-Ilio-pubic eminence. 6-Iliopectineal line. 7-Sacroiliac articula tion. 8-Anterior border of the ala of sacrum and

9-Sacral promontory.

INLET As the inlet is the brim of the pelvis, the circumference of the inlet is forme d by the bony landmarks mentioned previously.

Shape:It is almost round (gynecoid) with the antero-posterior diameter being the shortest. Other different shapes of the inlet are

anthropoid, android and platypelloid (p. 345).

Plane: It is an imaginary flat surface bounded by the bony points mentioned as those of the brim. It is not strictly a mathematical plane

and is, therefore, often referred to as superior strait.

Inclination: Inthe erect posture,thepelvisistiltedforward. As such, the plane of the inlet ma kes an angle of about 55° with the horizontal

andiscalledangle of inclination. Another way of measuring the inclination radiographica lly is to take the angle between the plane of the

inlet and the front of the body of the fifth lumbar vertebra. The angle is normally abou t 135° (Fig. 9.8).

When the angle of inclination is increased due to sacralization of 5th lumbar vertebra, it is called high inclination. High inclination has

got obstetric significances: (1) There is delay in engagement because the uterine axis fails to coincide with that of inlet (2) It favors

occipito-posterior position (3) There is difficulty in descent of the head due to lo ng birth canal and flat sacrum interfering with internal

rotation.

The angle of inclination may be lessened in case of

Fig. 9.8: Diagrammatic representation showing plane of the inlet; inclination of the pelvis, sacral an gle and depth of the pelvis.

lumbarization of first piece of sacral vertebra and is calledlow inclination.It hasgotno obstetr icsignificance. It actually facilitates early

engagement.

Sacral angle: It is the angle formed by the true conjugate with the first two pieces of the sacrum (Fig. 9.8). Normally, it is greater than

90°. A sacral angle of lesser degree suggests funnelling of the pelvis.

Axis:It is a mid-perpendicular line drawn to the plane of the inlet (see Fig. 9.17) . Its direction is downwards andbackwards. When

extended, the line passes through the umbilicus to coccyx. It is important that the uterine axis should coincide with the axis of the inlet so

that the force of the uterine contractions will be spread in the right direction, to force the fetus to pass through the brim.

Diameters: The measurements of the diameters are all approximate and minor varia tion is the rule rather than the exception.

Anteroposterior (Syn : true conjugate, anatomical conjugate, conjugate vera): It is the distance b etween the midpoint of the sacral

promontory to the inner margin of the upper border of symphysis pubis (Fig. 9.9) It mea sures 11 cm (4 ¼′′). It is not the shortest

diameter of the inlet in the anteroposterior plane. In practice, the true conjugate cannot b e estimated directly. However, its measurement

is inferred by subtracting 1.2 cm (½′′) from the diagonal conjugate thus allowing fo r the inclination, thickness and height of the

symphysis pubis.

Obstetric conjugate: It is the distance between the midpoint of the sacral promontor y to prominent bony projection in the midline on

the inner surface of the symphysis pubis (Fig. 9.9).

The point is somewhat below its upper border. It is the shortest anteroposterio r diameter in the anteroposterior plane of the inlet. It

measures 10 cm (4′′). It cannot be clinically estimated but is to be inferred from the dia gonal conjugate — 1.5–2 cm (¾′′) to be deducted

or by lateral radio-pelvimetry.

Diagonal conjugate: It is the distance between the lower border of symphysis pubis to the m idpoint on the sacral promontory. It

measures 12 cm (4 ¾′′) (Fig. 9.9).

It is measured clinically during pelvic assessment in late pregnancy or in labor. Obstetric conjugate is c omputed

Fig. 9.9: Sagittal section of the pelvis showing antero-posterior diameters in different planes.

by subtracting 1.5–2 cm from the diagonal conjugate depending upon the height, thickn ess and inclination of the symphysis pubis.

How to measure ? The patient is placed in dorsal position. Two fingers are introduced into the vagina tak ing asepticprecautions.The

fingersare tofollow the anterior sacral curvature. In normal pelvis, it is difficult to feel th e sacral promontory or at best can be felt with

difficulty. However, in order to reach the promontory, the elbow and the wrist are to be depre ssed sufficiently while the fingers are

mobilized in upward direction. The point at which the bone recedes from the fingers is the sacral promontory. The fingers are then

mobilized under the symphysis pubis and a marking is placed over the gloved index f inger by the index finger of the left hand (Fig.

9.10).

The internal fingers are removed and the distance between the marking and the tip of th e middle finger gives the measurement of

diagonal conjugate. For practical purpose, if the middle finger fails to reach the promon toryortouches it with difficulty,it is likely

that the conjugate is adequate for an average size head to pass through.

Transverse diameter: It is the distance between the two farthest points on the pelvic b rim over the iliopectineal lines. It measures 13

cm (5 ¼′′) (Fig. 9.11).

The diameter usually lies slightly closer to sacral promontory and divides the brim into an terior and posterior segment. The head

negotiates the brim through a diameter, called available or obstetrical transverse. This is described as a diameter which bisects the

anteroposterior diameter in the midpoint. Thus the obstetrical transverse is eithe r equal or less than the anatomical transverse.

Oblique diameters:There are two oblique diameters — right and left. Each one exten ds from one sacroiliac joint to the opposite

iliopubic eminence and measures 12 cm (4 ¾′′).Right or left denotes the sacroiliac joint from which it starts ( Fig. 9.11).

Sacrocotyloid—9.5 cm (3 ¾′′):It is the distance between the mid point of the sacral promontory to il iopubic eminence (Fig. 9.11). It

represents the space occupied by the biparietal diameter of the head while negotiating the brim in flat pelvis.

Fig. 9.10: Measurement of diagonal conjugate

Fig. 9.11: Different diameters of the inlet of obstetrical significance. Bispinous diameter is also demon strated.

CAVITY

Cavity is the segment of the pelvis bounded above by the inlet and below by plane o f least pelvic dimensions . Shape : It is almost

round.

Plane : The plane extends from the midpoint of posterior

surface of symphysis pubis to the junction of second and third sacral vertebrae (see Fig. 9.17). It is called plane of greatest pelvic

dimensions. It is the most roomy plane of the pelvis and is almost round in shape.

Axis: It is the mid-perpendicular line drawn to the plane of the cavity. Its direc tion is almostdownwards (see Fig. 9.17).

Diameters : Anteroposterior (12 cm or 4 ¾′′): It measures from the mid-point on the posterior surface of the sym physis pubis to the

junction of 2nd and 3rd sacral vertebrae (Fig. 9.9).

Transverse (12 cm or 4 ¾ ′′): It cannot be precisely measured as the points lie over the soft tissues cove ring the sacrosciatic notches and

obturator foramina.

OUTLET

Obstetrical outlet: It is the segment of the pelvis bounded above by the plane of least pelvic dimensions and below by the

antomical outlet (Fig. 9.13).

Its anterior wall is deficient at the pubic arch; its lateral walls are formed by ischial bones and the posterior wall includes whole of the

coccyx.

Shape : It is anteroposteriorly oval.

Fig. 9.12:Composite measurements of thediameters of the inlet, cavity and outlet in centimeters

Fig. 9.13: Obstetrical outlet (shaded area)

Plane : The plane is otherwise known asplane of least pelvic dimensions or narrow pelvic plane. The plane extends from the lower

border of the symphysis pubis to the tip of ischial spines and posteriorly to meet the tip of the 5th sacral vertebra. It is the narrowest

plane in the pelvis and roughly corresponds to the origin of levator ani muscles. It is at thi s plane that the internal rotation occurs. It also

marks the beginning of the forward curve of the pelvic axis. It is a landmark used for pudenda l nerve block analgesia. It is irregularly

oval

and notched on each side by the ischial spine.

Diameters : Transverse — Syn :Bispinous (10.5 cm or 4

′′) : It is the distance between the tip of two ischial spines.

Anteroposterior (11 cm or 4 ¼ ′′) : It extends from the inferior border of the symphysis pubis to the tip of the sacrum ( Fig. 9.9).

Posterior sagittal (5 cm or 2′′): It is the distance between the tip of the sacrum and the mid point of b ispinous diameter.

Axis: It is represented by a line joining the center of the plane with the sacral promonto ry. Its direction is almost vertical.

Anatomical Outlet: It is otherwise known as bony outlet. It is bounded in front by the lower border of the symphysis pubis; laterally by

the ischiopubic rami, ischial tuberosity and sacrotuberous ligament and posteriorly by th e tip of coccyx (Fig. 9.14). Thus, it consists of

two triangular planes with a common base formed by a line joining the ischial tuberositie s. The apex of the anterior triangle is formed by

the inferior border of the pubic arch and that of the posterior triangle by the tip of the c occyx.

Shape : It is diamond shaped.

Plane: It is formed by a line joining the lower border of the symphysis pubis to the tip of the c occyx (see Fig. 9.17). It forms an

angulation of 10° with the horizontal.

Axis: It is a mid-perpendicular line drawn to the plane of the outlet. Its directio n is downwards and forwards (Fig. 9.17).

Diameters : Anteroposterior: It extends from the lower border of the symphysis pubis to the tip of the coccyx. It measures 13 cm or 5

¼′′with the coccyx pushed back by the head when passing through the introitus in the second stage of labor; with the coccyx in normal

position, the measurement will be 2.5 cm less (see Fig. 9.9).

Transverse — Syn :Intertuberous (11 cm or 4 ¼′′):It measures between inner borders of ischial tuberosities .

Posterior sagittal diameter (8.5 cm or 3 ½′′):It is the anteroposterior distance between the sacr ococcygeal joint and the mid point of

transverse diameter of outlet (TDO). It is clinically measured by the distance between th e sacrococcygeal joint and anterior margin of the

anus.

Subpubic angle:It is formed by the approximation of the two descending pubic rami. I n normal female pelvis, it measures 85°.

Pubic arch: Arch formed by the descending rami of both the sides is of obstetric importance. Normally, it measures 6 cm in between the

pubic rami at a level of 2 cm below the apex of the subpubic arch. Clinically, it is assessed by placing 3 fingers side by side.

The narrower the pubic arch, the more is the fetal head displaced backwards and the le ss the room available for it. Normally, the

subpubic arch is rounded and less space is wasted under the symphysis pubis. When a round d isc of 9.3 cm diameter (diameter of well

flexed fetal head) is placed under the arch, the distance between the symphysis pubis an d the circumference of the disc is measured. This

measurement is the waste space of Morris and should not exceed 1 cm in a normal pelvis.

Available anteroposterior diameter: When the waste space of Morris is more than 1 cm, the anterior point o f the anteroposterior

diameter of the outlet extends below the symphysis pubis on the pubic rami for a distanc e equivalent

tothewastespaceofMorris(Fig.9.15).The distancebetween the saidpoint andthetip ofthe sa crum is called available anteroposterior

diameter of the outlet. It is through this diameter that the head escapes out of the bony outlet.

Fig. 9.14: Boundary of the anatomical outlet with its measurements

B C

Figs 9.15A to C: Diagrammatic representation of — (A) Normal pubic arch; (B) Waste s pace of Morris; and (C) Available

anteroposterior diameter of the outlet.

MID PELVIS

Midpelvis is the segment of the pelvis bounded above by the plane of greatest pelvic dimensions and below by a plane known as

midpelvic plane.

Midpelvic plane: The midpelvic plane extends from the lower margin of the sy mphysis pubis through the level of ischial spines to meet

either the junction of S

and S

or tip of the sacrum depending upon the configuration of the sacrum. If the plane mee ts the tip of the 5th

sacrum, it coincides with the plane of least pelvic dimensions. If the plane meets the junc tion of S

and S

, the plane becomes a wedge

posteriorly (Fig. 9.16).

A B

Figs 9.16A and B: Diagrammatic representation of mid pelvis and mid pelvic plan e: (A) Zone of mid pelvis (shaded area) with the mid

pelvic plane becomes a wedge posteriorly; (B) Mid pelvic plane coincides with the plan e of least pelvic dimensions.

Diameters:Transverse diameter — Syn : bispinous (10.5 cm) : It measures between the two ischial sp ines. Anteroposterior diameter

(11.5 cm): It extends from the lower border of the symphysis pubis to the point on the sacrum at which the midpelvic plane meets.

Posterior sagittal diameter (4.5 cm): It extends from the midpoint of the bispinous diameter to the point on the sacrum at which the

midpelvic plane meets.

PELVIC AXIS: Anatomical (curve of Carus): Anatomical pelvic axis is formed by joini ng the axes of inlet, cavity and outlet. It is

uniformly curved with the convexity fitting with the concavity of the sacrum. The fetus does not, however, transverse the uniform curved

path (Fig. 9.17).

Obstetrical: It is through this axis that the fetus negotiates the pelvis. It is not uniformly curved . Its direction isfirst

downwardsandbackwardsuptothelevelofischialspinesandthendirectedabruptly forwards (Fig.9.17).

PELVIC JOINTS: Symphysis pubis: It is a secondary fibrocartilaginous joint. It has got no capsule a nd no synovial cavity. The

articular surfaces are covered with hyaline cartilage. Due to softening of the lig aments during pregnancy, there is considerable amount of

gliding movement.

Sacroiliac articulation:It is a synovial joint and is an articulation between the articular surface of the ilium and sacrum. The articulating

surfaces are not alike. It has got a capsule and a synovial cavity. Engagement to diagnose, it is b etter to palpate gently with two hands

facing down over the abdomen (Fig. 8.6) than to prod around with Pawlik’s grip, whi ch in non-experienced hands is painful.

Sacrococcygeal jointis a synovial hinge joint. It allows both flexion and extension. E xtension increases the anteroposterior diameter of

the outlet.

PHYSIOLOGICAL ENLARGEMENT OF PELVIS DURING PREGNANCY AN D LABOR

Imaging studies show an increase in width and mobility of the symphysis pubis during p regnancy which returns to normal following

delivery. The pubic bones may separate by 1 to 12 mm. Similar changes also occur in s acroiliac joints. There is gliding movement of the

symphysis pubis near term. Relaxation of the pelvic joints is due to progesterone and re laxin. There is increase of the anteroposterior

diameter of the inlet during labor by the rotatory movement of the sacroiliac joints. In d orsal lithotomy position, the anteroposterior

diameter of the outlet may be increased to 1.5–2 cm. Furthermore, the coccyx is pushed back while the head descends down to the

perineum.

A B

Figs 9.17A and B:Pelvic axis — (a) Axes of inlet, cavity and outlet are shown by arrows drawn perpendicular to the planes. The shaded

area over the axes is the anatomical pelvic axis (curve of Carus). (b) Obstetric pelvic axis — as shown by the shaded area is directed

downwards and backwards upto ischial spines and then directed forwards

Antenatal Care, Preconceptional Counseling and Care

Systematic supervision (examination and advice) of a woman during pregnancy is c alled antenatal (prenatal) care. The

supervision should be regular and periodic in nature according to the need of the indiv idual. Actually prenatal care is the care in

continuum that starts before pregnancy and ends at delivery and the postpartum period. Anten atal care comprises of:

• Careful history taking and examinations (general and obstetrical) • Ad vice given to the pregnant woman AIMS AND OBJECTIVE

The aims are: (1) To screen the ‘high risk’ cases (see p. 630). (2) T o prevent or to detect and treat at the earliest any complications. (3)

To ensure continued risk assessment and to provide ongoing primary preventive health care. (4) To educate the mother about the

physiology of pregnancy and labor by demonstrations, charts and diagrams (mother c raft classes), so that fear is removed and

psychology is improved. (5) To discuss with the couple about the place, time and mode of de livery, provisionally and care of the

newborn. (6) To motivate the couple about the need of family planning and also app ropriate advice to couple seeking medical

termination of pregnancy.

The objective is to ensure a normal pregnancy with delivery of a healthy bab y from a healthy mother. The criteria of a normal

pregnancy are—delivery of a single baby in good condition at term (between 38–42), with fetal weight of 2.5 kg or more and with no

maternal complication. As such, a normal pregnancy is a retrospective term.

PROCEDURE AT THE FIRST VISIT

The first visit should not be deferred beyond the second missed period. It may be earlie r if the patient desires to terminate the pregnancy.

OBJECTIVES: (1) To assess the health status of the mother and fetus. (2) To a ssess the fetal gestational age and to obtain baseline

investigations. (3) To organize continued obstetric care and risk assessment.

Components of routine prenatal care are recorded in a standardized proforma (antena tal record book).

History Taking

Vital statistics

Name: ........................................................

Date of first examination: .................................. Address: ................................................................... .

Age : A woman having her first pregnancy at the age of 30 or above (FIGO – 35 y ears) is called elderly primigravida. Extremes of age

(teenage and elderly) are obstetric risk factors (p. 342).

Gravida: Parity: Gravida denotes a pregnant state both present and past, irrespective of the period of gestatio n. Parity denotes a state of

previous pregnancy beyond the period of viability.

Gravida and para refer to pregnancies and not to babies. As such , a woman who delivers twins in first pregnancy is still a

gravida one and para one. A pregnant woman with a previous history of two abortions and one te rm delivery can be expressed as fourth

gravida but primipara. It is customary in clinical practice to summarize the past o bstetric history by two digits (the first one relates with

viable births and the second one relates with abortion) connected with a plus s ign affixing the letter ‘P’. Thus P

2+1

denotes the patient

had two viable births and one abortion. In some centers it is expressed by four digits co nnected by dashes. PA–B–C–D, wh ere A

denotes number of term (37 to 42 weeks) pregnancies, B – number of prete rm (28 to < 37 weeks) pregnancies, C – number of

miscarriages (< 28 weeks) and D – the number of children alive at present. A pregnan t woman with a previous history of four births or

more is called grand multipara.

Terminology:

A nullipara is one who has never completed a pregnancy to the stage of viabilit y. She may or may not have aborted previously.

A primipara is one who has delivered one viable child. Parity is not increased ev en if the fetuses are many (twins, triplets). A

multigravida is one who has previously been pregnant. She may have aborted or have d elivered a viable baby.

A parturient is a women in labor.

A nulligravida is one who is not now and never has been pregn ant.

A primigravida is one who is pregnant for the first time.

Multipara is one who has completed two or more pregnancies to the stage of viability or m ore.

A puerpera is a woman who has just given birth.

Duration of marriage : This is relevant to note the fertility or fecundity. A pregn ancy long after marriage without taking recourse to any

method of contraception is called low fecundity and soon after marriage is called high fecu ndity. A women with low fecundity is unlikely

to conceive frequently.

Religion: ...................................

Occupation: It is helpful in interpreting symptoms of fatigue due to excess phys ical work or stress or occupational hazards. Such women

should be informed to reduce such activities.

Occupation of the husband : A fair idea about the socioeconomic condition of the p atient can be assessed. This knowledge is of value:

(a) To anticipate the complications likely to be associated with low social status such as anemia, pre-eclampsia, prematurity, etc. (b) To

give reasonable and realistic antenatal advice during family planning guidance.

Period of gestation : The duration of pregnancy is to be expressed in terms of completed weeks. A fraction of a week of more than 3

days is to be considered as completed week. In calculating the weeks of gestation in ear ly part of pregnancy, counting is to be done from

the first day of last normal menstrual period (LNMP) and in later months of pregnancy, c ounting is to be done from expected date of

delivery (EDD).

Most reliable clinical parameter of gestational age assessment is an accurate LMP. In som e cases, LMP may be inaccurate, unknown or

following the use of oral contraceptives (OC). In the case of OC use, ovulation may no t have occurred 2 weeks after the LMP. In such a

situation, ultrasonography in first trimester of pregnancy is more reliable to estimate the g estational age.

Complaints: Categorically, the genesis of the complaints are to be noted. Even if ther e is no complaint, enquiry is to be made about the

sleep, appetite, bowel habit and urination.

History of present illness: Elaboration of the chief complaints as regard their onset, duration , severity, use of medications and progress is

to be made.

History of present pregnancy : The important complications in different trimesters of the present pregna ncy are to be noted carefully.

These are hyperemesis and threatened abortion in first trimester; features of pyelitis in se cond trimester and anemia, pre-eclampsia and

antepartum hemorrhage in the last trimester. Number of previous antenatal visits (bookin g status), immunization status, has to be noted.

Any medication or radiation exposure in early pregnancy, or medical-surgica l events during pregnancy should be enquired.

Obstetric history : This is only related with multigravidae. The previous obstetric events are to be recorded chro nologically as per the

proforma given in the next page. To be relevant, enquiry is to be made whether she had antenatal and intranatal care before.

No. Year and date

Pregnancy events

Labor events Methods of delivery

Puerperium

Baby

• Weight and Sex

• Condition at birth (Apgar score)

• Breast feeding

• Immunization

1. 2007 January 2. 2007 July

3. 2010

July Miscarriage at 8 weeks

Well covered antenatally. Uneventful

—do—

Uneventful Evacuation done

Spontaneous vaginal

Uneventful

—do— —do—

—do— Baby-boy, weight 2.6 kg

Cried at birth.

Breastfed (6 months), alive and well.

Girl weight 2.7 kg

Cried at birth.

Breastfed—6 months

Both the babies fully immunized, alive

and well.

The obstetric history is to be summed up as: Status of gravida, pari ty, number of delivery (term, preterm), miscarriage, pregnancy

termination (MTP) and living issue [e.g. Mrs. R.L, (P

2+0+1+2

) G4, P2, miscarriage 1, living 2, at 36 weeks of present pregnancy].

An undue long gap between the last and the present pregnancy requires careful super vision during pregnancy and labor. The minimum

spacing between one birth and subsequent pregnancy should be 2 years.

Menstrual history : Cycle, duration, amount of blood flow and first day of the last normal menstrual period (LNMP) are to be noted

(spontaneous). From the LNMP, the expected date of delivery (EDD) has to be calculated. T he first day of the menstruation being the

important event can be remembered precisely while the last day of the period is often tailed o ff and hence may be forgotten.

Calculation of the expected date of delivery (EDD) : This is done accordin g to Naegele’s formula (1812) by adding 9 calendar months

and 7 days to the first day of the last normal (28 day cycle) period. Alternatively, one can count back 3 cale ndar months from the first

day of the last period and then add 7 days to get the expected date of delivery; the former me thod is commonly employed.

Example: The patient had her first day of last menstrual period on 1st January. B y adding 9 calendar months it comes to 1st October and

then add 7 days, i.e. 8th October, which becomes the expected date of delivery. For IVF preg nancy date of LMP is 14 days prior to date

of embryo transfers (266 days).

Past medical history : Relevant history of past medical illnesses (urinary tract infections, tuberculosis ) is to be elicited.

Past surgical history: Previous surgery—general or gynecological, if any, is to be enquired.

Family history: Family history of hypertension, diabetes, tuberculosis, blood dyscrasia, known heredita ry disease, if any, or twinning is

to be enquired.

Personal history: Contraceptive practice prior to pregnancy, smoking or alcohol habits are to be enquired. LMP may be a withdrawal

bleed following pill usage. The first ovulation may be delayed for 4 to 6 weeks (see p. 95). Smoking or alcohol abuse has got some

relation with low birth weight of the baby. Previous history of blood transfusion, cortico steroid therapy, any drug allergy and

immunization against tetanus or prophylactic administration of anti-D immunoglobulin ar e to be enquired.

EXAMINATION

General Physical Examination

Build: Obese/Average/Thin. Nutrition: Good/Average/Poor. Height: Short stature is likely to be associated with a small pelvis.

Thus, in primigravidae, the height is to be measured to screen out the short stature. Whi le an arbitrary measurement of 5 ft. is considered

as short stature in western countries, it is 4'-7" in India, considering the low average height.

Weight : Weight should be taken in all cases in an accurate weighing machine. Repeated weigh t checking in subsequent visit should

preferably be done in the same weighing machine. The importance of weight checking has already been discussed (p. 50).

Pallor : The sites to be noted are lower palpebral conjunctiva, dorsum of the tongue and nail beds. Jaundice: The sites to be noted are

bulbar conjunctiva, under surface of the tongue, hard palate and skin.

Tongue, teeth, gums and tonsils : Evidences of malnutriton are evident from gl ossitis and stomatitis. Evidence of any source of infection

in the mouth is to be eradicated least there be a chance of autogenous infection in puer perium.

Neck: Neck veins, thyroid gland or lymph glands are looked for any abnormality. Slig ht physiological enlargement of the thyroid gland

occurs during pregnancy in 50% of cases.

Edema of legs : Both the legs are to be examined. The sites for evidence of edema are over the med ial malleolus and anterior surface of

the lower 1/3rd of the tibia. The area is to be pressed with the thumb for at least 5 secon ds. Varicosity in the legs, if any, is to be noted.

Causes of edema in pregnancy: (1) Physiological (2) Pre-eclampsia (3) Anemia and hypoproteinemia (4) Cardia c failure (5) Nephrotic

syndrome.

Physiological edema: The cause of physiological edema is due to increased venous pressure of the inferior extremities by the gravid

uterus pressing on the common iliac veins. The features of the physiological edema are: (1) Slight degree (ankle edema), usually

confined to one leg, more on the right (2) Unassociated with any other features of pre- eclampsia or proteinuria (3) Disappears on rest

alone (4) Other pathologies of cardiac, renal and hematological are absent.

Pulse:

Blood Pressure: Disappearance of sounds (Korotkoff 5) rather than muffling o f sounds (Korotkoff 4) is the best representation of

diastolic pressure during pregnancy.

Systemic examination :

Heart, Lungs, Liver and Spleen:

Breasts : Examination of the breasts helps to note the presence of pregnancy changes but also to note th e nipples (cracked or

depressed) and skin condition of the areola. The purpose is to correct the abnormality, if any, so that there will be no difficulty in

breastfeeding immediately following delivery.

Obstetrical examination (see details p. 77) : Abdominal: Tone of the abdominal mu scles, presence of any incisional scar or presence of

herniation and skin condition of the abdomen are to be looked for. Fundus of the uterus is just palpable above the symphysis pubis at 12

weeks.

Vaginal : Examination is done in the antenatal clinic when the patient attends the c linic for the first time before 12 weeks. It is done (1)

to diagnose the pregnancy (2) to corroborate the size of the uterus with the period of amenorrhea and (3) to exclude any pelvic

pathology. Internal examination is, however, omitted in cases with previous history o f abortion, occasional vaginal bleeding in present

pregnancy. Ultrasound examination has replaced routine internal examination. It is more informativ e and without any known adverse

effect.

Steps of vaginal examination: Vaginal examination is done in the antenatal clinic. T he patient must empty her bladder prior to

examination and is placed in the dorsal position with the thighs flexed along with the buttocks pl aced on the footend of the table. Hands

are washed with soap and a sterile glove is put on the examining hand (usually right).

Inspection: By separating the labia—using the left two fingers (thumb and index), the characte r of the vaginal discharge, if any, is

noted. Presence of cystocele or uterine prolapse or rectocele is to be elicited.

Speculum examination: This should be done prior to bimanual examin ation especially when the smear for exfoliative cytology or

vaginal swab is to be taken. A bivalve speculum is used. The cervix and the vault of the vagina are inspected with the help of good light

source placed behind. Cervical smear for exfoliative cytology or a vaginal swab from the upper vagina, in presence of discharge, may

be taken.

Bimanual: Two fingers (index and middle) of the right hand are introduced deep into the vagina while separating the labia by left hand.

The left hand is now placed suprapubically Gentle and systematic examination are to be don e to note: (1) Cervix: Consistency,

direction and any pathology. (2) Uterus: Size, shape, position and consistency. Ear ly pregnancy is the best time to correlate accurately

uterine size and duration of gestation. (3) Adnexae: Any mass felt through the forn ix. If the introitus is narrow, one finger may be

introduced for examination. No attempt should be made to assess the pelvis at this stage .

Routine investigations:

• Blood: Hemoglobin, hematocrit, ABO, Rh grouping, VDRL are done. Blood glucose and antibody screening are done in selected cases

(p. 282).

• Urine: Protein, sugar and pus cells. If significant proteinuria is found, “clean catch” s pecimen of midstream urine is collected for

culture and sensitivity test. To collect the midstream urine, the patient is advised to clean the vulva and to co llect the urine in a clean

container during the middle of the act of urination. Presence of nitrites and/or leu kocyte esterase by dipstick indicates urinary tract

infection.

• Cervical cytology study by Papanicolaou stain has become a routine in ma ny clinics.

Special investigations:

(a) Serological tests for rubella, hepatitis B virus and HIV—antibodies to dete ct rubella immunity and screening for hepatitis B virus

and HIV (with consent) (see Chapter 19).

(b) Genetic Screen: Maternal Serum Alpha Feto Protein (MSAFP), triple test at 15–18 wee ks for mother at risk of carrying a fetus

with neural tube defects, Down’s syndrome or other chromosomal anomaly (see p. 10 7).

(c) Ultrasound examination: First trimester scan either transabdominal (TAS) or transvaginal (TVS) helps to detect (i) early

pregnancy (ii) accurate dating (iii) number of fetuses (iv) gross fetal anomalies (v) any uterine or adnexal pathology (see p. 649). Use of

ultrasound should be selective rather than a routine.

Booking (18–20 weeks) scan has got advantages in addition to 1st trimester scan: (i) detailed fetal an atomy survey and to detect any

structural abnormality including cardiac (ii) Placental localization. Ultrasound examinatio n is also very reassuring to the couple (see p.

646).

Ultrasound examination is performed as a routine at 18–20 weeks though doubt remain s about its absolute benefit.

Repetition of the investigations: (1) Hemoglobin estimation is repeated at 28th and 36th wee k (2) Urine is tested (dipstick) for protein

and sugar at every antenatal visit.

PROCEDURE AT THE SUBSEQUENT VISITS

Generally check up is done at interval of 4 weeks up to 28 weeks ; at interval of 2 weeks up to 36 weeks and thereafter weekly till

delivery. Ideally this should be more flexible depending on the need and the convenienc e of patient. In the developing countries, as per

WHO recommendation, the visit may be curtailed to at least 4; first in second trimester around 16 w eeks, second between 24–28

weeks, the third visit at 32 weeks and the fourth visit at 36 weeks.

Objectives : (A) To assess—(1) Fetal well being, (2) Lie, presentation, position and number of fetus es, (3) Anemia, pre-eclampsia,

amniotic fluid volume and fetal growth, (4) To organize specialist antenatal clinics for pa tients with problems like cardiac disease and

diabetes. (B) To select, time for ultrasonography, amniocentesis or chorion villus biopsy w hen indicated (p. 107).

History : To note—(a) appearance of any new symptoms (headache, dysuria) (b) date of quickening. Examination:

General—In each visit the following are checked and recorded: (1) Weight (2) Pallor ( 3) Edema legs (4) Blood pressure.

Abdominal examination : Inspection—Abdominal enlargement, pregnancy marks—linae nigra, striae, surgical scars (midline or

suprapubic). Palpation—(a) To note the height of the fundus above the symp hysis pubis (p. 78). (b) In the second trimester, to identify

the fetus by external ballottement, fetal movements, palpation of fetal parts and auscultati on of fetal heart sounds. (c) In the third

trimester abdominal palpation will help to identify fetal lie, presentation, position, growth pattern, volume of liquor and also any

abnormality. Examination also helps to detect whether the presenting part is engaged or not. Girth of abdomen is measured at the level of

umbilicus. The girth increases by about 2.5 cm per week beyond 30 weeks and at term , measures about 95–100 cm. (d) Others—any

uterine mass (fibroid) or tenderness. Fetal activity (movements) is also recorded.

Vaginal examination : Vaginal examination in the later months of pregnancy (beyond 37 w eeks) with an idea to assess the pelvis is

not informative. Pelvic assessment is best done with the onset of labor or just before indu ction of labor. Methods of vaginal examination

for assessment of the pelvis and test for cephalopelvic disproportion are described in C hapter 23. Any history of vaginal bleeding

contraindicates vaginal examination.

ANTENATAL ADVICE

PRINCIPLES: (1) To counsel the women about the importance of reg ular check up. (2) To maintain or improve, the health status of

the woman to the optimum till delivery by judicious advice regarding diet, drugs and hy giene. (3) To improve the psychology and to

remove the fear of the unknown by counseling the woman.

DIET: The diet during pregnancy should be adequate to provide—(a) good maternal hea lth (b) optimum fetal growth (c) the strength

and vitality required during labor and (d) successful lactation. During pregnancy, there is increased calorie requirement due to increased

growth of the maternal tissues, fetus, placenta and increased basal metabolic r ate. The increased calorie requirement is to the extent of

300 over the nonpregnancy state during second half of pregnancy. Generally, the diet in pregnancy should be with woman’s choice

as regard the quantity and the type. Woman with normal BMI should eat adequately so as to gain the optimum weight (11 kg).

Overweight women with BMI between 26–29 should limit weight gain to 7 kg and obe se women (BMI > 29) should gain less weight.

Excessive weight gain increases antepartum and intrapartum complications including feta l macrosomia.

Table 10.1: Daily dietary allowances for a woman of reproductive age, pregnancy and lactatio n Nonpregnant Pregnancy second half

Lactation Sources

Energy (kcal) 2200 kcal 2500 kcal

Protein (gm) 50 gm 60 gm

Iron (mg) 18 mg 40 mg*

Calcium (mg) 500 mg 1000 mg

Zinc (mg) 12 mg 15 mg

Iodine (mg) 150 mg 175 mg

Vitamin A (IU) 5000 IU 6000 IU

Vitamin D (IU) 200 IU 400 IU

Thiamine (mg) 1.1 mg 1.5 mg

Riboflavin (mg) 1.1 mg 1.6 mg

Nicotinic acid (mg) 15 mg 17 mg

Ascorbic acid (mg) 60 mg 70 mg

Folic acid (mg) 200 mg 400 mg

Vitamin B

(mg) 2 mg 2.2 mg

2600 kcal Protein, fat, carbohydrate 65 gm Meat, fish, poultry, dairy product 30 mg* Meat, egg, grains [* to be supplemented] 1500 mg

Dairy products

19 mg Meat, egg, seafood

200 mg Iodized salt, seafood 8000 IU Vegetables, liver, fruits 400 IU Dairy products

Grains, cereals

ï Meat, liver, grains

ï Almost same Meat, nuts, cereals

as in pregnancy Citrus fruits, tomato

ï Leafy vegetables, liverï

ï Animal proteins

The pregnancy diet ideally should be light , nutritious, easily digestible and ric h in protein, minerals and vitamins. In terms of

figures, the daily requirement during pregnancy and lactation is given in Table 10.1. It is not an absolute recommendation but simply a

guide. The diet should consist in addition to the principal food at least half liter, if not, 1 lite r of milk (1 liter of milk contains about 1 gm

of calcium), plenty of green vegetables and fruits. The amount of salt should be of suffi cient amount to make the food tasty. At least, half

of the total protein should be first class containing all the amino acids and majority of the fat should be animal type which contains

vitamins A and D.

Dietetic advice should be given with due consideration to the socioeconomic conditio n , food habits and taste of the individual.

Woman with normal BMI (see p. 343) should eat as to maintain the schedule weight gain in pregnancy (see p. 50). The instruction

about diet should be reasonable and realistic to individual women.

Supplementary nutritional therapy : As previously mentioned, there is negative iron balance during p regnancy and the dietetic iron is

not enough to meet the daily requirement especially in the second half of the pregnancy . Thus, supplementary iron therapy is needed

for all pregnant mothers from 16 weeks onwards. Above 10 gm% of hemog lobin, 1 tablet of ferrous sulfate (Fersolate) containing 60

mg of elemental iron is enough. The dose should be proportionately increased with lo wer hemoglobin level to 2–3 tablets a day. 3 tablets

provide 45 mg of absorbable iron. As the essential vitamins are either lacking in the foo ds or are destroyed during cooking,

supplementary vitamins are to be given daily from 20th week onwards (Table 10.1).

ANTENATAL HYGIENE: In otherwise uncomplicated cases, the following advices are to be given.

Rest and sleep : The patient may continue her usual activities throughout pregnancy. However, e xcessive and strenuous work should be

avoided especially in the first trimester and the last 4 weeks. Recreational exercise (pren atal exercise class) are permitted as long as she

feels comfortable.

There is individual variation of the amount of sleep required. However, on an average , the patient should be in bed for about 10 hours (8

hours at night and 2 hours at noon) especially in the last 6 weeks. In late pregnancy lateral postur e is more comfortable.

Bowel : Constipation is common. It may cause backache and abdominal discomfort. Regula r bowel movement may be facilitated by

regulation of diet taking plenty of fluids, vegetables and milk or prescribing stool softne rs at bed time. There may be rectal bleeding,

painful fissures or hemorrhoids due to hard stool.

Bathing: The patient should take daily bath but be careful against slipping in the bathroom due to imba lance. Clothing, shoes and belt:

The patient should wear loose but comfortable garments. High heel shoes should bette r be avoided in advanced pregnancy when the

center of balance alters. Constricting belt should be avoided. Dental care: Good dental and oral hygiene should be maintained. The

dentist should be consulted, if necessary. This will facilitate extraction or filling of the car ies tooth, if required, comfortably in the 2nd

trimester. Care of the breasts: Breast engorgement may cause discomfort during late pregnancy. A well-fitting brassiere can give relief.

Coitus : Generally, coitus is not restricted during pregnancy. Release of prostaglandins and oxytocin with coitus may cause uterine

contractions. Women with increased risk of miscarriage or preterm labor should avoid coitus if they feel such increased uterine activity.

Travel : Travel by vehicles having jerks are better to be avoided especially in first trim ester and the last 6 weeks. The long journey is

preferably be limited to the second trimester. Rail route is preferable to bus route. Travel in pressurized aircraft is safe up to 36 weeks.

Air travel is contraindicated in cases with placenta previa, pre-eclampsia, severe anemia a nd sickle cell disease. Prolonged sitting in a

car or aeroplane should be avoided due to the risk of venous stasis and thromboembolism. Sea t belt should be under the abdomen.

Smoking and alcohol : In view of the fact that smoking is injurious to health, it is b etter to stop smoking not only during pregnancy but

even thereafter. Heavy smokers have smaller babies and there is also more chance o f abortion. Similarly, alcohol consumption is to be

drastically curtailed or avoided, so as to prevent fetal maldevelopment or growth restriction (see p. 465).

IMMUNIZATION: Fortunately, most of life-threatening epidemics are rare. In the devel oping countries immunization in pregnancy is

a routine for tetanus; others are given when epidemic occurs or traveling to an endemic zone or for traveling overseas.

Live virus vaccines (rubella, measles, mumps, yellow fever) are contraindicated. Ra bies, Hepatitis A and B vaccines, toxoids can

be given as in nonpregnant state.

Tetanus : Immunization against tetanus not only protects the mother but also the neonates . In unprotected women, 0.5 mL tetanus

toxoid is given intramuscularly at 6 weeks interval for 2 such, the first one to be given betw een 16–24 weeks. Women who are

immunized in the past, a booster dose of 0.5 mL IM is given in the last trimester .

Drugs : Almost all the drugs given to mother will cross the placenta to reach the fetus. Possib ility of pregnancy should be kept in mind

while prescribing drugs to any woman of reproductive age (see p. 511).

GENERAL ADVICE: The patient should be persuaded to attend for antenatal check up positive ly on the schedule date of visit. She

is instructed to report to the physician even at an early date if some untoward sympto ms arise such as intense headache, disturbed sleep

with restlessness, urinary troubles, epigastric pain, vomiting and scanty urination.

She is advised to come to hospital for consideration of admission in the fo llowing circumstances:

• Painful uterine contractions at interval of about 10 minutes or earlier and cont inued for at least an hour—suggestive of onset of labor.

• Sudden gush of watery fluid per vaginam—suggestive of premature rupture of the membranes.

• Active vaginal bleeding, however slight it may be.

MINOR AILMENTS IN PREGNANCY

Nausea and vomiting : Nausea and vomiting especially in the morning, soon after getting out of bed, are usually common in

primigravidae. They usually appear following the first or second missed period and sub side by the end of first trimester. 50% women

have both nausea and vomiting, 25% have nausea only and 25% are unaffected.

Three main measures can reduce the problem. Dietary changes: To take dry toast, biscuits and protein rich meals. Frequent small foods

are helpful. Fatty foods are avoided. Behavior modification: To avoid personal triggering factors. The woman can id entify herself, this

factor. Medications are discussed in p. 511.

Backache : It is a common problem (50%) in pregnancy. Physiological changes that contr ibute to backache are: joint ligament laxity

(relaxin, estrogen), weight gain, hyperlordosis and anterior tilt of the pelvis. Other factors may be faulty posture and high heel shoes,

muscular spasm, urinary infection or constipation. Excessive weight gain should be avo ided. Rest with elevation of the legs to flex the

hips may be helpful. Improvement of posture, well fitted pelvic girdle belt which corrects the lumbar lordosis during walking and rest in

hard bed often relieve the symptom. Massaging the back muscles, analgesics and rest relieve the pain due to muscle spasm.

Constipation : Constipation is a quite common ailment during pregnancy. Atonicity of the gut due to the effect of progesterone,

diminished physical activity and pressure of the gravid uterus on the pelvic colon are the p ossible explanations. Regular bowel habit may

be restored with advice mentioned earlier.

Leg cramps : It may be due to deficiency of diffusible serum calcium or elevation of serum phosphorus. Supplementary calcium therapy

in tablet or syrup after the principal meals may be effective. Massaging the leg, application of local heat and vitamin B

(30 mg) daily

may be effective.

Acidity and heartburn : Heartburn is common in pregnancy due to relaxation of the eso phageal sphincter. Patient is advised to avoid

over eating and not to go to bed immediately after the meal. Liquid antacids may be helpful. H iatus hernia which is common during the

pregnancy can also produce heart burn especially when the patient is in lying down po sition. Sleeping in semi-reclining position with

high pillows relieves the symptoms of hiatus hernia.

Varicose veins : Varicose veins in the legs and vulva (varicosities) or rectum (hemo rrhoids) may appear for the first time or aggravate

during pregnancy usually in the later months. It is due to obstruction in the venous return by the pregnant uterus. For leg varicosities,

elastic crepe bandage during movements and elevation of the limbs during rest can give sym ptomatic relief. Specific therapy is better

to be avoided. Varicosities usually disappear following delivery.

Hemorrhoids may cause annoying complications like bleeding or may get prolapsed. R egular use of laxative to keep the bowel soft, local

application of hydrocortisone ointment and replacement of the piles if prolapsed, are essential. Surgical treatment is better to be

withheld as the condition sharply improves following delivery.

Ankle edema : Excessive fluid retention as evidenced by marked gain in weight or evide nces of pre-eclampsia has to be excluded. No

treatment is required for physiological edema or orthostatic edema. Edema subsides on rest with slight elevation of the limbs. Diuretics

should not be prescribed.

Vaginal discharge : Assurance to the patient and advice for local cleanliness are all which are required . Presence of any infection

(Trichomonas, Candida, bacterial vaginosis) should be treated with vaginal application of metr onidazole or miconazole (see p. 306).

VALUES OF ANTENATAL CARE

The value of antenatal supervision is so much tested and recognized that it is needless to stress its importance. It should be borne in mind

that a successful obstetric outcome depends on continued careful supervision which star ts in pregnancy and ends in puerperal period.

Inadequacy of one cannot be compensated by the other. The chief values are:

• To screen the high risk cases. Medical disorders and obstetric complications are sorted out at the earliest (Ch. 19).

Risk assessment is a continued process and not once only.

• Detection of high risk factorsdeservesnocredit unlessproper stepsare taken to rectify it. Casesneedtobeadmitted,

investigated and treated.

• Pregnancy should be regularly supervised. Casual antenatal visit or inadequat e care is worse than no care at all.

Efficacy of prenatal care depends on the quality of care given to the woman.

• Antenatal care is said to be the strategy, the intranatal care is the t actics in obstetrics. One is indispensible

from the other to achieve a good result. Care should be thorough and based on individual woman’s

need.

• Acceptance of advice: During pregnancy, advice regarding diet, drugs, family pla nning guidance, immunization

schedule are better followed than in the nonpregnant state.

• It is an opportunity to make the patient realize that childbirth is a physiolog ical process and to boost up the

psychology so that the patient finds herself confident during the ordeal of labor.

• The net effect is marked reduction in maternal mortality(about 1/7th) and morbi dity. Similarly there is significant

reduction in perinatal mortality (about 1/5th) and morbidity.

DRAWBACKS: (1) Trifling abnormality may be exaggerated for which unnecessary medications or risky operative interference is

prescribed. (2) Quality is not always maintained specially in the developing countries wi th increasing population. (3) Faulty dietary

advice and prescription of harmful drugs produce injurious effects on the mother and/ or the baby.

LIMITATIONS: Even with thorough antenatal supervision, unexplained an d unpredicted complications may arise such as vaginal

bleeding in placenta previa, premature rupture of the membranes, unexplained intrauter ine deaths, cord prolapse, shoulder dystocia or

postpartum hemorrhage. These, at times depress the morale of the patient. Simultaneo us availability of Emergency Obstetric Care

(Em OC) should be present (p. 601).

PRECONCEPTIONAL COUNSELING AND CARE

When a couple is seen and counseled about pregnancy, its course and outcome well be fore the time of actual conception is called

preconceptional counseling. Objective is to ensure that a woman enters pregnancy with an optimal state of health which would

be safe both to herself and the fetus. Organogenesis is completed by the 1st trimester. By the tim e the woman is seen first in the

antenatal clinic, it is often too late to advice. Because all the adverse factors ha ve already begun to exert their effects.

Preconceptual phase is the time to identify any risk factor that could potentially affect the perinatal outcome adversely. The woman is

informed about the risk factor and at the same time care is provided to reduce or to elim inate the risk factor in an attempt to improve the

pregnancy outcome. Virtually preconceptional counseling is a part of prevent ive medicine.

PRECONCEPTIONAL VISIT, RISK ASSESSMENT AND EDUCATION:

– Identification of high risk factors by detailed evaluation of obstetric, medical, family and persona l history. Risk factors are assessed

by laboratory tests, if required.

– Base level health status including blood pressure is recorded.

– Rubella and hepatitis immunization in a nonimmune woman is offered (p. 290 , 300).

– Folic acid supplementation (4 mg a day) starting 4 weeks prior to conception up t o 12 weeks of pregnancy (see p. 409), is advised.

This can reduce the incidence of neural tube defects.

– Maternal health is optimized preconceptionally. Pr oblems of overweight, underweight, anemia, abnormal papanicolaou smears are

evaluated and treated appropriately.

– Fear of the incoming pregnancy is removed by preconceptional education.

– Patient with medical complicationsshould be educated about the effects of the disease on preg nancy and also the effects of

pregnancy on the disease. In extreme situation, the pregnancy is discouraged. Pre-existing c hronic diseases (hypertension, diabetes,

epilepsy) are stabilized in an optimal state by intervention.

– Drugs used before pregnancyare verified and changed if required so as to avoid any adverse effect on the fetus during the period of

organogenesis (see p. 511). For example, anticonvulsant drugs are checked (see p. 29 1), warfarin is replaced with heparin, oral

antidiabetic drugs are replaced with insulin.

– Woman should be urged to stop smoking, taking alcohol and abusing drugs. Addicted woman is given special ized care.

– Inheritable genetic diseases(sickle cell disease, cystic fibrosis) are screened before conception a nd risk of passing on the condition to

the offspring is discussed (p. 271).

– Importance of prenatal diagnosis for chromosomal or genetic diseases are discussed (p. 106, 493).

– Inheritable genetic diseases could be managed either by primary prevention (e liminating the causal factor) or by secondary

prevention (terminating the affected fetus).

– Couples with history of recurrent fetal loss (see p. 167) or with family history of congen ital abnormalities (genetic, chromosomal or

structural) are investigated and counseled appropriately. There may be some untreatable facto rs (p. 493).

The counseling should be done by primary health care providers. The help of an obste trician, physician and geneticist may be required

and should be extended.

LIMITATIONS: Unfortunately, only a small percentage of women take the advantage of preconceptual care. The important reasons

are: (i) Lack of public awareness (ii) Many pregnancies are unplanned.

SUMMARY OF ANTENATAL (PRENATAL) CARE

• Careful history taking

• Thorough clinical examination (general and obstetric)

• Investigations (routine and special)

• Advice—diet (nutrition), hygiene, specific to any problem

• Subsequent visits: Every 4 weeks until 28 weeks then every 2 weeks until 36 weeks and weekly thereafter A. Maternal health:

Weight, BP, Pallor, Symptom analysis (nausea, dysuria, etc.). Any other abnormality

• Identification of high risk factor(s)

B. Fetal health: Fetal growth, fundal height, fetal heart rate, amniotic flu id volume, presentation and fetal activity

• Couple education, counseling and advice

• Preparation for child birth: Couple is informed about labor course, de livery, the need of operations, anesthesia and

the complications.

Antenatal Assessment of Fetal Well Being

Majority (80%) of fetal deaths occur in the antepartum period. The important ca uses of deaths are—(i) Chronic fetal hypoxia (IUGR).

(ii) Maternal complications, e.g. diabetes, hypertension, infection. (iii) Fetal congenital malforma tion and (iv) Unexplained cause.

There is progressive decline in maternal deaths all over the world. Currently more inter est is focussed to evaluate the fetal health. The

primary objective of antenatal fetal assessment is to avoid fetal death. As s uch simultaneously with good maternal care during

pregnancy and labor, the fetal health in utero should be supervised with equal vigilance.

Aims of antenatal fetal monitoring:

• To ensure satisfactory growth and well being of the fetus throughout pregna ncy.

• To screen out the high risk factors that affect the growth of the fetus.

Common indications for antepartum fetal monitoring :

• Pregnancy with obstetric complications: IUGR, Multiple pregnancy, Polyhydramnios or

Oligohydramnios, Rhesus alloimmunization.

• Pregnancy with medical complications: Diabetes mellitus, Hypertension , Epilepsy, Renal or Cardiac

disease, Infection (Tuberculosis), SLE.

• Others: Advanced maternal age (> 35 years), previous still birth or recurrent abortio n, previous birth of

a baby with structural (anencephaly, spina bifida) or chromosomal (autosomal trisomy) abnormalities.

• Routine antenatal testing.

Box 1: Rationality of antenatal fetal tests

• Tests must provide information superior to that of clinical evaluation

• Test results should be helpful in management to improve perinatal outcome .

• Benefits of tests must outweight the potential risks and the costs.

Box 2: The measures that can be taken when a fetus is found compromised

• Bed rest • Fetal surveillance • Drug therapy

• Urgent delivery of the fetus—term or preterm

• Neonatal intensive care (NIC)

• Termination of pregnancy for fetal congenital anomaly

CLINICAL EVALUATION OF FETAL WELL BEING AT ANTENATAL CLIN IC At First Visit

The initial antenatal examination should be carried out in the first trimester. At this examin ation a record is kept of the size of the uterus

following bimanual examination or by ultrasonography. This is of immense help in estimating the correct duration of gestation in the last

trimester.

Fetal well being depends on satisfactory maternal health throughout pregnancy. After a thorough clinical examination of the mother, the

investigations are initiated as early as possible (see p. 98). At Subsequent Visits

At every antenatal visit, the following clinical parameters are taken into account for asse ssment of satisfactory progress of gestation.

1. Maternal weight gain: During the second half of pregnancy, the average weigh t gain is 1 kg a fortnight. Any excess weight gain may

be due to excess fluid retention and could be the first sign of pre-eclampsia. If the weig ht gain is less than normal, stationary or even

falling, one should be on the look out for intrauterine growth restriction.

2. Blood pressure: Initial recording of blood pressure prior to 12 weeks helps to diff erentiate a pre-existing chronic hypertension from a

pregnancy induced hypertension developing later on. Hypertension, pre-existing or pr egnancy induced may impair the fetal growth (p.

226).

3. Assessment of the size of the uterus and height of the fundus: In early weeks, the size of the uterus is of great value in confirming

the calculated duration of gestation. The height of the fundus should be documented at each visit. The top of the uterine fundus is

measured from the superior border of the symphysis pubis (bladder should be empt y) using a tape. After 24 weeks of pregnancy the

distance measured in cm normally corresponds to the period of gestation in weeks . A variation of 1–2 cm is acceptable.

Provided the patient is sure about her date of last no rmal menstrual period a measurement of symphysis-fundal height in later month

of pregnancy is an useful screening test for further investigation. The measurement is compared to t he expected distance plotted on a

chart (Fig. 11.1). If the measurement falls below the 10th centile, fetal growth restriction is su spected and more specific investigation

should be done.

4. Clinical assessment of excess liquor should be recorded, as well as any scan ty liquor in the last trimester. Evidence of scanty liquor

may indicate placental insufficiency and the need for undertaking other placental functi on tests.

5. Documentation of the girth of the abdomen in the last trimester of pregnancy should form a routine part of abd ominal

examination. This is measured at the lower border of the umbilicus. Normally, the girth increases steadily up to term. If the girth

gradually diminishes beyond term or earlier, it arouses suspicion of placental insufficiency . This is of particular value in suspecting

placental insufficiency in the high risk cases such as pre-eclampsia, chronic hyp ertension and IUGR.

SPECIAL INVESTIGATIONS

About 30 percent of antepartum fetal deaths are due to asphyxia (IUGR, post dates), 3 0 percent due to maternal complications (pre-

eclampsia, placental abruption, diabetes mellitus), 15 percent to congenital malformations and chromosomal abnormalities and 5 percent

to infection. About 20 percent of stillbirths have no obvious cause. About 50 percent of first trimester spontaneous abortions and

about 5 percent of stillborn infants have chromosomal abnormalities.

Congenital abnormalities may be: (1) Chromosomal: numerical (47 XX X) or structural (translocations) (2) Single gene (cystic

fibrosis) (3) Polygenic and multifactorial (NTDs) and (4) Terato genic disorders (drugs).

Apart from clinical evaluation, biochemical and biophysical methods have also been used for the diagnosis. Some of these methods

carry risks to the mother and/or the fetus and are also expensive. Therefore, their application s hould provide definite benefits that

clearly outweighs the potential risks and the costs.

EARLY PREGNANCY

• Biochemical • Biophysical • Cytogenetic

Fig. 11.1: Gestational age chart estimated from symphysis fundal height

Antenatal assessment of fetal well being in early pregnancy is primarily designed to detec t fetal congenital abnormalities. Therefore, this

chapter should be read in conjunction with Chapter 32 (p. 492). The candidates for prenatal sc reening are mentioned in p. 493. Women

who are screen positive should be offered fetal karyotyping for confirmation.

BIOCHEMICAL: Maternal serum alpha fetoprotein (MSAFP): AFP is an oncofetal protein (Mo lecular weight 70,000). It is

produced by yolk sac and fetal liver. Highest level of AFP in fetal serum and amniotic fluid is reached around 13 weeks and thereafter it

decreases. Maternal serum level reaches a peak around 32 weeks. MSAFP leve l is elevated in a number of conditions: (a) wrong

gestational age (b) open neural tube defects (NTDs) (c) multiple pregnancy, Rh isoimmunization (d) IUFD (e) anterior abdominal wall

defects and (f) renal anomalies. Low levels are found in trisomies (Down’s syndrome), gestational trophoblastic disease.

Test is done between 15–20 weeks. MSAFP value of 2.5 multiples of the median (MOM ) when adjusted with maternal weight and

ethnicity, is taken as cut off point. Elevated MSAFP detects 85% of all neural tube defec ts. Cases with such high values are considered

for high resolution ultrasound imaging and/or amniocentesis.

Triple test: It is a combined biochemical test which includes MSAFP, hCG and UE3 ( unconjugated estriol). Maternal age in relation to

confirmed gestation age is also taken into account. It is used for detection of Down’s syndr ome. In an affected pregnancy, level of

MSAFP and UE

tend to be low while that of hCG is high. It is performed at 15–18 weeks. It gi ves a risk ratio and for confirmation

amniocentesis has to be done. The result is considered to be screen positive if the risk ratio is 1:250 or greater.

Acetylcholine esterase: (AChE) Amniotic fluid AChE level is elevated in most cases of open neural tube defects. It has got better

diagnostic value than AFP.

Inhibin A is a dimeric glycoprotein. It is produced by the corpus luteum and the placenta. Serum level of inhibin A is raised in women

carrying a fetus with Down’s syndrome.

First trimester screening (↑ hCG, ↓ MSAFP, ↓ PAPP) can detect trisomy 21 in 85% with a false positive rate of 5%. When nasal bone

detection is combined together, the detection rates rise to 97%. Second trimester screening (15–18 weeks): Triple test (↓ MSAFP, ↓

, ↑ Total hCG) and quadruple test (↓ MSAFP, ↓ UE

, ↑ Total hCG, ↑ Inhibin A) can detect trisomy 21 in 70% and 80% of affected

pregnancies respectively.

Prenatal genetic diagnosis—can be made directly from fetal tissue obtained by amniocentesis, chorion villus sampling (CVS) or by

cordocentesis.

Structural chromosomal abnormalities (translocations , inversions, mutations) can be detected by Fluorescence In Situ

Hybridization (FISH). Chromosome specific probes can be used to detect the unkno wn DNA.

Amniocentesis (genetic) is an invasive procedure. It is performed be tween 14 and 16 weeks under ultrasonographic guidance (see p.

651). The fetal cells obtained in this procedure are subjected for cytogenetic an alysis.

• Cytogenetic analysis—The desquamated fetal cells in the amniotic fluid, obtai ned by amniocentesis or trophoblast cells from CVS or

fetal blood cells obtained by cordocentesis are cultured, G banded and examined to make a diagnosis of chromosomal anomalies, e.g.

trisomy 21 (Down’s syndrome), monosomy X (Turner’s syndrome) and others.

• DNA analysis—Single gene disorders (cystic fibrosis, Tay-Sachs disease) can be diagnosed using specific DNA probes. DNA

amplification is done by polymerase chain reaction (PCR). The specific chromosomal region c ontaining the mutated gene can be

identified.

• Biochemical—Amniotic fluid AFP level is high when the fetus suffers from open neura l tube defects. This is also confirmed by

ultrasound scanning. The normal AFP concentration in liquor amnii at the 16th week is about 20 mg/liter. Amniotic fluid level of 17

hydroxy progesterone is raised in congenital adrenal hyperplasia.

Early amniocentesis has been carried out at 12–14 weeks gestation. Amnifiltration has been used to increase the cell yield.

Chorionic villus sampling (CVS) is performed for prenatal diagnosis of genetic disorders. It is carrie d out transcervically between 10–

12 weeks and transabdominally from 10 weeks to term. Diagnosis can be obtained by 24 hours, and as such, if termination is considered,

it can be done in the first trimester safely. A few villi are collected from the chorio n frondosum under ultrasonic guidance with the help

of a long malleable polyethylene catheter introduced transcervically along the extraovul ar space. While it provides earlier diagnosis than

amniotic fluid studies, complications like fetal loss (1–2%), oromandibular limb d eformities or vaginal bleeding are higher. False

positive results (2–3%) are there due to placental mosaics and maternal cell contaminatio n. In such a situation, amniocentesis should be

performed to confirm the diagnosis. Limb Reduction Defects (LRD) are high when CVS was performed at less than 10 weeks of

gestation. CVS when performed between 10 and 12 weeks of gestation are safe and accurate a s that of amniocentesis. Anti-D

immunoglobulin 50 µg IM should be administered following the procedure to a Rh nega tive woman. The information obtained by CVS

are same as discussed under amniocentesis.

PRENATAL DIAGNOSIS: CVS, AMNIOCENTESIS AND CORDOCENTESIS

Time

Materials for study

Chorion villus sampling

Transcervical 10–12 weeks, Transabdominal 10 weeks to term Trophoblast cells

Karyotype Result

Fetal loss Accuracy

Termination of

pregnancy when

indicated

Maternal effects

following termination of pregancy

• Direct preparation—24–48 hours.

• Culture—10–14 days

0.5–1%

Accurate; may need amniocentesis for confirmation

1st trimester—safe

Amniocentesis

14–16 weeks (early 12–14 weeks)

• Fetal fibroblasts

• Fluid for biochemical

study (p. 646)

• Culture

3–4 weeks

0.5%

Highly accurate

Cordocentesis 18–20 weeks

• Fetal white blood cells (others—infection and biochemical study)

• Culture

24–48 hours

1–2%

Highly accurate

2nd trimester—risky 2nd trimester—risky

Very little

More traumatic; physically and psychologically

FETAL BLOOD SAMPLING Cordocentesis (Percutaneous umbilical blood sampling)

Same as amniocentesis

A 22 gauze spinal needle 13 cm in length is inserted through the maternal abdominal an d uterine wall under real time ultrasound

guidance using a curvilinear probe. The needle tip is progressed carefully and it punctu res the umbilical vein approximately 1–2 cm.

from the placental insertion. Generally, 0.5 to 2 mL. of fetal blood is collected. It is performed under local anesthetic usually from 18

weeks gestation.

RISKS: This invasive procedure may lead to abortion, preterm labor and intrauterine fetal dea th. These may be due to bleeding, cord

hematoma formation, infection (amnionitis), fetomaternal hemorrhage or preterm ru pture of membranes. Overall fetal loss is 1–4%.

Anti-D immunoglobulin 100 µg IM should be given to Rh negative, yet unimmunized wo man.

All the information as obtained in amniocentesis or chorion villus sampling, could be gat hered. Additional values are mentioned below,

Hematological —

Fetal infections — Fetal blood gas and — acid base status

Fetal therapy —

For fetal anemia (see p. 333), bleeding disorders (auto immune thrombocytopenia), Rh esus disease (see p. 331) and hemoglobinopathies

Toxoplasmosis, viral infections (see p. 297)

In fetal growth restriction (see p. 462)

Blood transfusion (p. 338), drug therapy (see p. 497) BIOPHYSICAL: Ultrasonographic exam ination of the fetus in the early (10–14

weeks) pregnancy can detect fetal anomalies. Crown-Rump Length (CRL) smaller than the gestational age is associated with the risk

of chromosomal anomalies (trisomy or triploidy). Increased nuchal translucency (NT) at 10-14 we eks is associated with many

chromosomal abnormalities (trisomy, monosomy, triploidy—see Fig. 40.8). Detection rate is about 70–80% with a false positive rate of

5–6%. Absence of nasal bone (NB) on USG at 10–12 weeks is associated with fetal Down’ s syndrome. When NB and NT were

combined detection rate of trisomy 21 was 92% with a false positive rate of 3.5% . For details of prenatal diagnosis see p. 493 and

biophysical markers see p. 650.

ANTEPARTUM FETAL SURVEILLANCE (LATE PREGNANCY)

OBJECTIVES ARE (ACOG-2007) —(1) prevention of fetal death and (2) avoidanc e of unnecessary interventions. METHODS:•

Clinical • Biochemical • Biophysical

CLINICAL: The clinical assessment of fetal growth can be evaluated by the parameters men tioned earlier in

the chapter. They may be useful as screening test for further investigation.

BIOCHEMICAL: Biochemical tests are mainly done for assessment of pulmonary maturity (see p. 110). BIOPHYSICAL:

Principle—Biophysical profile is a screening test for utero-placental insufficiency. The fetal

biophysical activities are initiated, modulated and regulated through fetal nervous system . The fetal CNS is very much sensitive to

diminished oxygenation. Hypoxia → metabolic acidosis → CNS depression → changes in fetal biophysical activity.

The following biophysical tests are used:

(1) Fetal movement count

(4) Fetal biophysical profile (BPP) (7) Contraction stress test (CST) (2) Cardiotocograp hy (3) Non-stress test (NST) (5) Dopper

ultrasound (6) Vibroacoustic stimulation test (8) Amniotic fluid volume

Fetal movement count —Any of the two methods can be applied:

• Cardif ‘count 10’ formula: The patient counts fetal movements starting at 9 am. The counting comes to an end as soon as 10

movements are perceived. She is instructed to report the physician if—(i) less than 10 movements occur during 12 hours on 2

successive days or (ii) no movement is perceived even after 12 hours in a single day.

• Daily fetal movement count (DFMC): Three counts each of one hour duration (morning, noon and evening) are recommended. The

total counts multiplied by four gives daily (12 hour) fetal movement count (DFMC). If there is diminution of the number of ‘kicks’ to

less than 10 in 12 hours (or less than 3 in each hour), it indicates fetal comprom ise.

• Mothers perceive 88% of the fetal movements detected by Doppler Imaging. The count should be performed daily starting at 28

weeks of pregnancy.

Loss of fetal movements is commonly followed by disappearance of FHR within next 24 hours. In eithe r of the above methods, if the

result is ominous, the candidate is subjected to NST. Maternal hypoglycemia is ass ociated with increased fetal movements. Maternal

perception of fetal movements may be reduced with fetal sleep (quiet), fetal anomalies (CNS ), anterior placenta, hydramnios, obesity,

drugs (narcotics), chronic smoking and hypoxia.

Non-stress test (NST): In non-stress test, a continuous electronic monitoring of the fe tal heart rate along with recording of fetal

movements (cardiotocography) is undertaken. There is an observed association of FH R acceleration with fetal movements, which

when present, indicates a healthy fetus. It can reliably be used as a screenin g test. The accelerations of the FHR associated with fetal

movements are presumably reflex mediated. It should be emphasized that the tes t is valuable to identify the fetal wellness rather than

illness.

Interpretation

• Reactive (Reassuring)—When two or more accelerations of more th an 15 beats per minute above the baseline and longer than 15

seconds in duration are present in a 20 minute observation (see p. 611).

• Non-reactive (Non-reassuring)—Absence of any fetal reactivity.

A reactive NST is associated with perinatal death of about 5 per 1000. But perinat al death is about 40 per 1000 is when the NST is

nonreactive. Testing should be started after 30 weeks and frequency should be twice weekly. The test has a false negative rate of 0.5%

and false positive rate of 50%.

Vibroacoustic stimulation (VAS) is used (see p. 612) to change the fetal sleep state fr om quiet (non-REM) to active (REM) sleep. A

reactive NST after VAS indicates a reactive fetus. The procedure is harmless.

Biophysical Profile Scoring (Manning—1992) Observation for 30 minutes Normal sc ore = 2 Abnormal = 0

BPP Scoring, interpretation and management

Parameters

• Non-stress Test (NST)

• Fetal breathing movements

• Gross body

movements

• Fetal muscle tone

• Amniotic fluid

Minimal normal criteria Score Reactive pattern (p. 108) 2

≥ 1 episode lasting 2

> 30 second

≥ 3 discrete body/limb 2

movements

≥ 1 episode of extension (limb or 2

trunk) with return of flexion

≥ 1 pocket measuring 2 cm in 2

two perpendicular planes (2 × 2

cm pocket)

BPP Score Interpretation 8–10 No fetal asphyxia

6 Suspect chronic asphyxia

4 Suspect chronic asphyxia

0–2 ↓

Strongly suspect asphyxia

Management

Repeat testing at

weekly interval or

If > 36 weeks →

deliver; but If L/S < 2.0 repeat test in 4–6 hours

If ≥ 36 weeks deliver, if < 32 weeks repeat testing in 4–6 hours Test for 120 minutes → persistent score ≤ 4→ deliver regardless of

gestational age

Fetal Biophysical Profile (BPP) —considers several parameters (see Table). BPP using real time ultrasonography has a high predictive

value.

Indication—Non-reactive NST, High risk pregnancy. Test frequency weekly after a no rmal NST, and twice weekly after an abnormal

test.

Modified Biophysical Profile consists of NST and ultrasonographically determined amniotic fluid index (AFI). Modified BPP is

considered abnormal (nonreassuring) when the NST is non-reactive and/or the AFI is < 5.

Fetal Cardiotocography (CTG): A normal tracing after 32 weeks, would s how base line heart rate of 110–150 beats per minute (bpm)

with an amplitude of base line variability 5–25 bpm. There should be no deceleration or there may be early deceleration of very short

duration. Importantly, there should be two or more accelerations during a 20-m inute period (see p. 611).

Ultrasonography: IUGR can be diagnosed accurately with serial measurement o f BPD, AC, HC, FL and amniotic fluid volume. AC is

the single measurement which best reflects fetal nutrition. The average increase of biparie tal diameter beyond 34 weeks is 1.7 mm

per week. When the HC/AC ratio is elevated (> 1.0) after 34 weeks, IUGR is suspec ted (see p. 463).

Doppler Ultrasound Velocimetry:

Doppler flow velocity wave forms are obtained from arterial and venous beds in the fe tus. Arterial Doppler waveforms are helpful to

assess the downstream vascular resistance. The arterial Doppler waveform is used to measure the peak systolic(s), peak diastolic (D) and

mean (M) volumes. From these values S/D ratio, pulsatility index (PI) [PI = (S-D)/M] or Resistance Index (RI) [RI = (S-D)/S] are

calculated.

In a normal pregnancy the S/D ratio , PI and RI decreases as the gestational age advances. Higher values greater than 2 SDs above

the gestational age mean indicates reduced diastolic velocities and increased placental vas cular resistance. These features are at increased

risk for adverse pregnancy outcome.

Venous Doppler parameter provide information about cardiac forward functio n (cardiac compliance, contractility and after load).

Fetuses with abnormal cardiac function show pulsatile flow in the umbilical vein (UV). Norma l UV flow is monophasic (see Table 11.1).

B(i)

B(ii) B(iii) Figs 11.2A and B: Umbilical artery flow velocity waveform: (A) N ormal; (B) Abnormal—(i) Reduced end-diastolic flow (ii)

Absent end-diastolic flow (iii) Reversed end-diastolic flow

Contraction stress test (CST) is based to observe the response of the fetus at risk for utero placental insufficiency in relation to uterine

contractions (see p. 501).

Amniotic fluid volume (AFV): Amniotic fluid volume is primarily dependent u pon the fetal urine, output, pulmonary fluid production

and fetal swallowing. Decreasing AFV may be the result of fetal hypoxia and placental insufficiency. A vertical pocket of amniotic fluid

> 2 cm is considered normal. Amniotic fluid index (AFI) is the sum of vertical pocke ts from four quadrant of uterine cavity (see p. 39).

AFI < 5 is associated with increased risk of perinatal mortality and morbidity.

Table 11.1: Antenatal Doppler ultrasound changes and the suggestive features of a compromised fetus Clinical significance

↑ resistance in fetoplacental circulation → IUGR,

pre-eclampsia

‘Brain Sparing’ effect in response to hypoxemia Fetal acidemia

Fetal acidemia

Pathophysiological. basis Failure of villous trophoblast invasion (see p. 32)

Vessel Change

A. Umbilical artery (UA) Reduced or absent or reversed end diastolic flow (Fig . 11.2)

B. Middle cerebral artery ↑ Diastolic velocity; (MCA) ↓ S/D or PI

C. Ductus venosus (DV) ↑ Doppler index*; Absent/

Reversed flow (a-wave) D. Umbilical vein (UV) ↑ Doppler index; Pulsatile flow

* Increased Doppler indices means there is increased vascular flow resistance.

OTHER INVESTIGATIONS IN LATE PREGNANCY

Dilatation of cerebral vessels

↑ Central venous pressure (CVP)

↑ CVP or

↓ Cardiac compliance

Amniocentesis in late pregnancy:

• Test for fetal pulmonary maturity • Assessment of severity of Rh iso-immunizat ion Pulmonary maturity: Confirmation of lung

maturation reduces the incidence of respiratory distress

syndrome (RDS) in the newborn . The risk of RDS (p. 474) is high for infants that are de livered preterm (< 37 weeks). RDS is caused

by the deficiency of pulmonary surfactant (see p. 468), which is synthesized by the type II alveolar cells. Surfactant is packaged in

lamellar bodies → discharged in the lung alveoli → carried in the pulmonary flu id → carried into the amniotic fluid.

Assessment of fetal pulmonary maturity

1. Estimation of pulmonary surfactant by Lecithin/Sphingomyelin (L/S) ratio. Amniotic fluid L/S ratio at 31–32 weeks is 1; at 35

weeks L/S ratio is 2. L/S ratio > 2 indicates pulmonary maturity.

2. Shake test or Bubble test (Clement’s): This is a useful bed side test, rapidly perform ed with a fair degree of accuracy. The test is

based on the ability of pulmonary surfactant to form a foam or bubble, on shaking which remains stable for at least 15 minutes.

Increasing dilutions of amniotic fluid are mixed with 96 percent ethanol, shak en for 15 seconds and inspected after 15 minutes for the

presence of a complete ring of bubbles at the meniscus. If it is present , the test is positive and indicates maturity of the fetal lungs.

3. Foam Stability Index (FSI) is based on surfactant detection by shake test (see above). FSI is calcula ted by utilizing serial dilutions of

amniotic fluid to quantitate the amount of surfactant present. FSI >47 virtually exclu des the risk of RDS.

4. Presence of phosphatidyl glycerol (PG) in amniotic fluid reliably indicates lu ng maturation. PG is tested by thin layer

chromatography similar to L: S measurement.

5. Saturated phosphatidyl choline > 500 ng/mL indicates pulmonary m aturity.

6. Fluorescence polarization: This test utilizes polarized light to quantitate surfacta nt in the amniotic fluid. The ratio of surfactant to

albumin is measured by an automatic analyzer. Presence of 55 mg of surfact ant per gram of albumin indicates fetal lung maturity.

7.Amniotic fluid optical density at 650 mµ greater than 0.15 indicates lung maturity.

8. Lamellar bodyis the storage form of surfactant in the amniotic fluid. They can be counted as the size is same as that of platelets. A

lamellar body count > 30,000/µL indicates pulmonary maturity.

9. Orange colored cells—desquamated fetal cells obtained from the centrifu ged amniotic fluid are stained with 0.1% Nile blue sulfate.

Presence of orange coloured cells > 50% suggests pulmonary maturity.

10.Amnioticfluidturbidity: During first and second trimesters, amniotic fluid is y ellow and clear. At term it is turbid due to vernix.

Assessment of severity of Rh–isoimmunization is done by amniocentesis for estimation of bilirubin in the amnio tic fluid by

spectophotometric analysis. The optical density difference at 450 nm gives the prediction of the severity of fetal hemolysis (see p. 336).

KEY POINTS

h Approximately 3 percent of liveborn infants have a major birth defc ect. Majority (80%) of fetal deaths occur antenatally.

h Birth defect may be—(a) Chromosomal : numerical or structural, (b) Single gene disor der (c) Polygenic or multifactorial or (d)

Teratogenic disorder (drugs). About half of chromosomal abnormalities are due to autosomal tris omy and remaining half is due to sex

chromosomal abnormalities (see p. 492).

h Screening for prenatal diagnosis should be offered to all pregnancies. MSAFP estimation is done between 15–18 weeks. Value of 2.5

MOM, adjusted with maternal age is taken as cut off point. Elevated level can detect 85% of all open NTDs (see p. 106).

h Triple test (MSAFP, hCG, UE

) is used for detection of Down’s syndrome. It is done between 15 and 18 weeks.

h First trimester screening with biochemical (↓ MSAFP, ↓ PAPP – A and ↑ hCG) and USG can improve detection rate (80%) of

Down’s syndrome (p. 106). For confirmation prenatal genetic study (amniocentesis, C VS or cordocentesis) has to be performed.

h Invasive procedures carry risks (see p. 494). CVS is comparable to amniocente sis in terms of fetal loss rate and diagnostic accuracy.

To avoid the problems of LRD, CVS should be done at 10 weeks or beyond. The com plications of cordocentesis appears to be 1–2%

(see p. 107).

h Single gene disorders can be detected by enzymatic analysis and or by molecular genetics. Direct analysis is done when gene

sequence is known otherwise linkage analysis is done.

h PGD can be done by (see p. 494) removing a single cell from the em bryo. Molecular genetics including FISH can detect genetic or

chromosomal disorder accurately and safely. Currently implantation rate is only 20–30% in most IVF centers. After genetic screening,

implantation rate increases by 50%.

h Fetal cells have been recovered from maternal circulation. Genetic and c hromosomal disorders are detected from a fetal cell using

DNA probes and FISH (see p. 494).

h Fetal movement count by the mother is an ideal first line screening test b oth for high risk and low risk patients. A healthy fetus should

have minimum 10 movements in 12 hour period. Count should be done daily beginning at 28 weeks (p. 108). Mothers perceive 88% of

fetal movements detected by sonography.

h Fetal cardiac accelerations are associated with fetal m ovements in more than 85 percent of the time. A reactive NST requires at least

two accelerations of FHR in 20 minutes of monitoring (p. 108).

h At term a fetus spends approximately 25% of its time in quiet sleep s tate (NREM) and 70% in active sleep state (REM).

h Vibroacoustic stimulation (VAS) can change fetal state from quiet (non-REM) s leep to active (REM) sleep and it is harmless. A

reactive NST after VAS indicates a healthy fetus (see p. 109).

h NST should be done twice weekly in complicated pregnancies (diabetes mellit us, IUGR). NST has a low false negative rate (< 1%) but

a high false positive rate (> 50%) — p. 109.

h Ultrasound examination is an essential tool for : pregnancy dating, detecting structural an d/or chromosomal anomalies, growth profile

and well being of the fetus (p. 645)

h Fetal BPP includes NST, Fetal breathing, Gross body movement. Fetal m uscle tone and Amniotic fluid. volume. Management is based

on total score (see p. 109). A score of 6 is suspicious and should be repeated.

hModified BPP includes NST and AFI. It takes less time. BPP has lower false positive rate than NST and high positive predictive value

(p. 109).

h Cardiotocography is the cornerstone of antenatal fetal assessment (see p. 610). A normal trace should have a base line of 110–160

bpm, variability of 5–25 bpm and at least two accelerations in a 20 minute period.

h In a normal pregnancy the S/D ratio and the pulsatility index (PI) decrease as pregnancy advances (p.109).

hAbsent or reversed end-diastolic flow velocity in the umbilical artery is associated w ith an increase in perinatal mortality and

morbidity (p. 110).

Normal Labor

DEFINITION : Series of events that take place in the genital organs in an effort to ex pel the viable products of conception out of

the womb through the vagina into the outer world is called Labor. It may occur prior to 37 completed weeks, when it is called

preterm labor. Expulsion of a previable live fetus occurs through the same process but in a mini ature form and is called mini-labor. A

parturient is a patient in labor and parturition is the process of giving birth. Delivery is the expulsion or extraction of a viable fetus out of

the womb. It is not synonymous with labor; delivery can take place without labor as in elective c esarean section. Delivery may be

vaginal, either spontaneous or aided or it may be abdominal.

NORMAL LABOR (EUTOCIA) : Labor is called normal if it fulfils the following criteria . (1) Spontaneous in onset and at term. (2)

With vertex presentation. (3) Without undue prolongation. (4) Natural termination with minim al aids. (5) Without having any

complications affecting the health of the mother and/or the baby.

ABNORMAL LABOR (DYSTOCIA) : Any deviation from the definition of normal labo r is called Abnormal labor. Thus, labor in

a case with presentation other than vertex or having some complications even with verte x presentation affecting the course of labor or

modifying the nature of termination or adversely affecting the maternal and/or fetal progn osis is called abnormal labor.

DATE OF ONSET OF LABOR : It is very much unpredictable to foretell precisely the exact date of onset of lab or. It not only varies

from case to case but even in different pregnancies of the same individual. Calculation b ased on Naegele’s formula can only give a rough

guide. Based on the formula, labor starts approximately on the expected date in 4%, one week on either side in 50%, 2 weeks earlier

and 1 week later in 80%, at 42 weeks in 10% and at 43 weeks plus in 4%.

CAUSES OF ONSET OF LABOR

The precise mechanism of initiation of human labor is still obscure. Endocrine, biochem ical and mechanical stretch pathways as obtained

from animal experiments, however, put forth the following hypotheses.

Fig. 12.1: Initiation of parturition

• Uterine distension:Stretching effect on the myometrium by the growing fetus and liquor amnii can explain the onset of labor at least in

twins or polyhydramnios. Uterine stretch increases gap junction proteins, receptors for oxytocin and specific contraction associated

proteins (CAPS).

• Fetoplacental contribution: Cascade of events activate fetal hypothalamic pit uitary adrenal axis prior to onset of labor → increased

CRH → increased release of ACTH → fetal adrenals → increased cortisol secretion → accelera ted production of estrogen and

prostaglandins from the placenta (see Fig. 12.1).

• Estrogen—the probable mechanisms are:

— Increases the release of oxytocin from maternal pituitary.

— Promotes the synthesis of myometrial receptors for oxytocin (by 100–200 fold s), prostaglandins and increase in gap junctions in

myometrial cells.

— Accelerates lysosomal disintegration in the decidual and amnion cells resulting in incre ased prostaglandin (PGF

2α

) synthesis.

— Stimulatesthe synthesis of myometrial contractile protein—actomyosin through cAM P.

— Increases the excitability of the myometrial cell membranes.

• Progesterone: Increased fetal production of dehydroepiandrosterone sulfat e (DHEA-S) and cortisol

inhibits the conversion of fetal pregnenolone to progesterone. Progesterone levels there fore fall

before labor. It is the alteration in the estrogen: progesterone ratio rather than the fall in the absolute

concentration of progesterone which is linked with prostaglandin synthesis.

• Prostaglandins:Prostaglandins are the important factors which initia te and maintain labor. The major

sites of synthesis of prostaglandins are—amnion, chorion, decidual cells and my ometrium. Synthesis

is triggered by—rise in estrogen level, glucocorticoids, mechanical stretching in late pregnancy, increase

in cytokines (IL–1, 6, TNF), infection, vaginal examination, separation or rupture of th e membranes.

Prostaglandins enhance gap junction (intermembranous gap between two cells through which stimulus

flows) formation.

Biochemical mechanisms involved in the synthesis of prostaglandins

Ph ospholipase A

in the lysosomes of the fetal membranes near term → esterified arachidonic acid → fo rmation of free arachidonic

acid →synthesis of prostaglandins through prostaglandin synthetase. Prostaglandins (E

and F

2α

) diffuse in the myometrium → act

directly at the sarcoplasmic reticulum →inhibit intracellular cAMP generation → increase local free calcium ions → uterine contraction.

Once the arachidonic acid cascade is initiated, prostaglandins themselves will activate lyso somal enzyme systems. The prostaglandin

synthesis reaches a peak during the birth of placenta probably contributing to its e xpulsion and to the control of postpartum hemorrhage.

• Oxytocin and myometrial oxytocin receptors: (i) Large number of oxytocin receptors are p resent in the fundus compared to the lower

segment and the cervix. (ii) Receptor number increases during pregnancy reaching maximum during labor. (iii) Receptor

sensitivity increases during labor. (iv) Oxytocin stimulate synthesis and release of PGs (E

and F

2α

) from amnion and decidua. Vaginal

examination and amniotomy cause rise in maternal plasma oxytocin level (Ferguson refl ex). Fetal plasma oxytocin level is found

increased during spontaneous labor compared to that of mother. Its role in human labor is not yet established.

• Neurological factor: Although labor may start in denervated uterus, labor may also be in itiated through nerve pathways. Both α and β

adrenergic receptors are present in the myometrium; estrogen causing the α receptors a nd progesterone the β receptors to function

predominantly. The contractile response is initiated through the α receptors of the postga nglionic nerve fibers in and around the cervix

and the lower part of the uterus. This is based on observation that onset of labor occurs following stripping or low rupture of the

membranes.

CONTRACTILE SYSTEM OF THE MYOMETRIUM

The basic elements involved in the uterine contractile systems are—(a) actin (b) myosin (c) adenosine triphosphate (ATP) (d) the

enzyme myosin light chain kinase (MLCK) and (e) Ca

Structural unit of a myometrial cell is myofibril which contains the proteins— ac tin and myosin. The interaction of myosin and actin is

essential for muscle contraction. The key process in actin–myosin interaction is myosin li ght chain phosphorylation. This reaction is

controlled by myosin light chain kinase (MLCK). Oxytocin acts on myometrial receptor s and activates phospholipase C → increases

intracellular calcium level. Calcium is essential for the activation of MLCK and b inds to the kinase as calmodulin–calciumcomplex.

Intracellular calcium levels are regulated by two general mechanisms : (a) Influx across the cell membrane and (b) Release from

intracellular storage sites. Calcium is stored within the cells in the sarcoplasmic reticulum and in m itochondria. Progesterone and cAMP

promote calcium storage at these sites. PGF

2α

, E

and oxytocin on the other hand stimulate its release.

• Intracellular Ca

→ Calmodulin Ca

→ MLCK → Phosphorylated Myosin + Actin → Myometrial contraction.

• Decease of intracellular Ca

(oritsshifttothestoragesites)→ dephosphorylation of myosin light chain→ inactivation of myosin light

chain kinase → Myometrial relaxation.

Uterine muscles have two types of adrenergic receptors— (a) α receptors, which on stimulation produce a decrease in cyclic AMP

(adenosine monophosphate) and result in contraction of the uterus and (b) β receptors , which on stimulation produce rise in cyclic AMP

and result in inhibition of uterine contraction.

FALSE PAIN : (Syn: false labor, spurious labor): It is found more in primigra vidae than in parous women. It usually appears prior to

the onset of true labor pain, by 1 or 2 weeks in primigravidae and by a few days in multip arae. Such pains are probably due to stretching

of the cervix and lower uterine segment with consequent irritation of the neighboring g anglia.

PRELABOR (Syn: premonitory stage): The premonitory stage may begin 2–3 weeks before the onset of true labor in primigravidae and

a few days before in multiparae. The features are inconsistent and may consist of the following:

• “Lightening”: Few weeks prior to the onset of labor specially in primigravidae, the pr esenting part sinks into the true pelvis. It is due

to active pulling up of the lower pole of the uterus around the presenting part. It signifies in corporation of the lower uterine segment into

the wall of the uterus. This diminishes the fundal height and hence minimizes the p ressure on the diaphragm (Fig. 12.2). The mother

experiences a sense of relief from the mechanical cardiorespiratory embarrassment. Th ere may be frequency of micturition or

constipation due to mechanical factor—pressure by the engaged presenting part. It is a welcome sign as it rules out cephalopelvic

disproportion and other conditions preventing the head from entering the pelvic inlet .

• Cervical changes: Few days prior to the onset of labor, the cervix becomes ripe. A ripe cervix is soft, less than 1.5 cm in length,

admits a finger easily and is dilatable.

• Appearance of false pain (see below).

True labor pains are characterized by :(i) Uterine contractions at regular intervals (ii) Frequency of contraction s increase gradually

(iii) Intensity and duration of contractions increase progressively (iv) Associated with “ show” (v) Progressive effacement and dilatation

of the cervix (vi) Descent of the presenting part (vii) Formation of the “bag of forewaters” (viii) Not relieved by enema or sedatives.

False labor pains are : (i) Dull in nature (ii) Confined to lower abdomen and groin (iii) Not associated wi th hardening of the uterus (iv)

They have no other features of true labor pains as discussed above (v) Usually r elieved by enema or sedative.

Labor pains : Throughout pregnancy, painless Braxton Hicks contractions with simu ltaneous hardening of the uterus occur. These

contractions change their character, become more powerful, intermittent and are associated with pain. The pains are more often felt in

front of the abdomen or radiating toward the thighs.

Show : With the onset of labor, there is profuse cervical secretion. Simultaneously, there is slight oozing of blood from rupture of

capillary vessels of the cervix and from the raw decidual surface caused by separation of the membranes due to stretching of the lower

uterine segment. Expulsion of cervical mucus plug mixed with blood is called “show”.

A B

Figs 12.2A and B:Showing phenomenon of ‘lightening’. (A) before a nd (B) after lightening

Dilatation of internal os : With the onset of labor pain, the cervical canal begins to dilate more in the upper part than in the lower, the

former being accompanied by corresponding stretching of the lower uterine segment.

Formation of “bag of waters” : Due to stretching of the lower uterine segment, the membranes are de tached easily because of its loose

attachment to the poorly formed decidua. With the dilatation of the cervical canal, the low er pole of the fetal membranes becomes

unsupported and tends to bulge into the cervical canal. As it contains liquor which has p assed below the presenting part, it is called “bag

of waters”. During uterine contraction with consequent rise of intra-amniotic pressure, this bag becomes tense and convex. After the

contractions pass off, the bulging may disappear completely. This is almost a certain sign of onset of labor. However, in some cases

the membranes are so well applied to the head that the finding may not be detected.

STAGES OF LABOR : Conventionally, events of labor are divided into three stages:

• First stage: It starts from the onset of true labor pain and ends with full dilatatio n of the cervix. It is, in other words, the “cervical

stage” of labor. Its average duration is 12 hours in primigravidae and 6 hour s in multiparae.

• Second stage: It starts from the full dilatation of the cervix (not from the ruptu re of the membranes) and ends with expulsion of the

fetus from the birth canal. It has got two phases—(a) The propulsive phase – starts f rom full dilatation upto the descent of the presenting

part to the pelvic floor. (b) The expulsive phase is distinguished by maternal b earing down efforts and ends with delivery of the baby. Its

average duration is 2 hours in primigravidae and 30 minutes in multiparae.

• Third stage:It begins after expulsion of the fetus and ends with expulsion of the place nta and membranes (after-births). Its average

duration is about 15 minutes in both primigravidae and multiparae. The duration is, how ever, reduced to 5 minutes in active

management.

• Fourth stage:It is the stage of observation for at least 1 hour after expulsion of th e after-births. During this period, general condition of

the patient and the behavior of the uterus are to be carefully monitored.

PHYSIOLOGY OF NORMAL LABOR

During pregnancy there is marked hypertrophy and hyperplasia of the uterine muscle and the enlargement of the uterus. At term, the

length of the uterus measures about 35 cm including cervix. The fundus is wider both transversely and anteroposteriorly than the lower

segment. The uterus assumes pyriform or ovoid shape. The cervical canal is occluded by a thic k, tenacious, mucus plug.

UTERINE CONTRACTION IN LABOR : Throughout pregnancy there is irregular involuntary spasmodic uterine contractions which

are painless (Braxton-Hicks) and have no effect on dilatation of the cervix (see p. 47) . The character of the contractions change with the

onset of labor. The pacemaker of the uterine contractions is situated in the region of the tubal ostia fr om where waves of contractions

spread downwards. While there are wide variations in frequency, intensity and duratio n of contractions, they remain usually within

normal limits in the following patterns.

— There is good synchronization of the contraction waves from both halves of the ute rus.

— There is fundal dominance with gradual diminishing contraction wave through midz one down to lower segment which takes about

10–20 seconds.

— The waves of contraction follow a regular pattern.

— Intra-amniotic pressure rises beyond 20 mm Hg during uterine contraction.

— Good relaxation occurs in between contractions to bring down the intra-amniotic pr essure to less than 8 mm Hg. Contractions of the

fundus last longer than that of the midzone.

During contraction, uterus becomes hard and somewhat pushed anteriorly to make the long axis of the uterus in line with that of pelvic

axis. Simultaneously, the patient experiences pain which is situated more on the hypogas tric region, often radiating to the thighs.

Probable causes of pain are: (a) Myometrial hypoxia during contractions (as in angina). (b) Str etching of the peritoneum over the

fundus. (c) Stretching of the cervix during dilatation. (d) Compression of the nerve ga nglion. The pain of uterine contractions is

distributed along the cutaneous nerve distribution of T

to L

. Pain of cervical dilatation and stretching is referred to the back

through the sacral plexus.

Tonus: It is the intrauterine pressure in between contractions.During p regnancy, as the uterusisquiescent (inactive), the tonus is of

2–3 mm Hg. During the first stage of labor, it varies from 8–10 mm Hg. It is inversely proportional to relaxation. The factors which

govern the tonus are—(1) Contractility of uterine muscles (ii) Intra-abdominal press ure (iii) Overdistension of uterus as in twins and

hydramnios.

Intensity : The intensity of uterine contraction describes the degree of uterine systole. The intensity gradually increases with

advancement of labor until it becomes maximum in the second stage during delivery of the baby. Intensity is initially influenced

probably by hormones but subsequently depend on multiple origin of contractions. Intr auterine pressure is raised to 40–50 mm Hg

during first stage and about 100–120 mm Hg in second stage of labor during contr actions. In spite of diminished pain in third

stage, the intrauterine pressure is probably the same as that in the second stage. The diminished pain is due to lack of stretching

effect.

Duration: In the first stage, the contractions last for about 30 seconds initially but gradually increase in d uration with the progress of

labor. Thus in the second stage, the contractions last longer than in the first stage.

Frequency: In the early stage of labor, the contractions come at intervals of 10–15 minutes. Th e intervals gradually shorten with

advancement of labor until in the second stage, when it comes every 2–3 minutes.

It is important to note that all the features of uterine contractions mentioned are very effective only when they are in

combination.

RETRACTION: Retraction is a phenomenon of the uterus in labor in which the muscl e fibers are permanently shortened. Unlike

any other muscles of the body, the uterine muscles have this property to become shortene d once and for all. Contraction is a

temporary reduction in length of the fibers, which attain their full length during relaxatio n. In contrast, retraction results in permanent

shortening and the fibers are shortened once and for all (Fig. 12.3). The net effects of r etraction in normal labor are:

— Essential property in the formation of lower uterine segment and dilatation and effacemen t of the cervix.

Fig. 12.3: Showing phenomenon of contraction and retraction of uterine muscle fibers during labor

— To maintain the advancement of the presenting part made by the uterine contractions and to help in ultimate expulsion of the fetus.

— To reduce the surface area of the uterus favoring separation of placenta.

— Effective hemostasis after the separation of the placenta.

EVENTS IN FIRST STAGE OF LABOR

The first stage is chiefly concerned with the preparation of the birth canal so as to facilitate expulsion of the fetus in the second stage.

The main events that occur in the first stage are—(a) dilatation and efface ment of the cervix and (b) full formation of lower uterine

segment.

DILATATION OF THE CERVIX :Prior to the onset of labor, in the prelabor phase (Phase-1) there may be a certain amount of

dilatation of cervix, specially in multiparae and in some primigravidae. Important structu ral components of the cervix are—(a) smooth

muscle (5–20%) (b) collagen and (c) the ground substance. Predisposing factors wh ich favor smooth dilatation are—(a) softening of

the cervix (b) fibromusculoglandular hypertrophy (c) increased vascularity (d) accum ulation of fluid in between collagen fibers and (e)

breaking down of collagen fibrils by enzymes collagenase and elastase (f) change in th e various glycosaminoglycans (e.g. increase in

hyaluronic acid, decrease in dermatan sulfate) in the matrix of the cervix. These are un der the action of hormones—estrogen,

progesterone and relaxin. Too much fibrosis as in chronic cervicitis or prolapse or org anic lesion in the cervix as in carcinoma, results in

deficiency of these factors. As a result, cervix may fail to dilate.

ACTUAL FACTORS RESPONSIBLE ARE:

• Uterine contraction and retraction —The longitudinal m uscle fibers of the upper segment are attached with circular muscle fibers of

the lower segment and upper part of the cervix in a bucket holding fashion (Fig.12.4). Thus, with each uterine contraction, not only the

canal is opened up from above down but it also becomes shortened and retracted. The re is some co-ordination between fundal

contraction and cervical dilatation called “polarity of uterus”. While the upper segment contrac ts, retracts and pushes the fetus, the

lower segment and the cervix dilate in response to the forces of contraction of upper se gment.

A B

Figs 12.4A and B: Diagrammatic representation showing dilatation of the cervix b y the pull of the longitudinal muscles of the uterus—

(A) Before labor (B) After labor

• Bag of membranes —The membranes (amnion and chorion) are attached loosely to the decidua lining the uterine cavity except over

the internal os. In vertex presentation, the girdle of contact of the head (that part of the circumference of the head which first comes in

contact with the pelvic brim) being spherical, may well fit with the wall of the lower uter ine segment. Thus, the amniotic cavity is

divided into two compartments (Fig. 12.5). The part above the girdle of contact contains th e fetus with bulk of the liquor called

hindwaters and the one below it containing small amount of liquor called forewater s. With the onset of labor, the membranes attached

to the lower uterine segment are detached and with the rise of intrauterine pressure during cont ractions there is herniation of the

membranes through the cervical canal. There is ball-valve like action by the well flexed head. Uterine contractions generate hydrostatic

pressure in the forewaters that in turn dilate the cervical canal like a wedge. Whe n the bag of forewater is absent (PROM) the pressure of

the presenting part pushes the cervix centrifugally.

• Fetal axis pressure: In labor with longitudinal lie, there is a tendency of straightening out of the fetal vertebral column due to

contraction of circular muscles of the body of uterus. This allows the fundal contraction to transmit through the podalic pole into the fetal

axis and hence allows mechanical stretching of the lower segment and opening up of th e cervical canal. With each uterine contraction,

there is elongation of the uterine ovoid and decrease in the transverse diameter. In trans verse lie fetal axis pressure is absent.

• Vis-a-tergo: The final phase of dilatation and retraction of the cervix is achieve d by downward thrust of the presenting part of the fetus

and upward pull of the cervix over the lower segment. This phenomenon is lacking in tra nsverse lie where a thin cervical rim fails to

disappear.

EFFACEMENT OR TAKING UP OF CERVIX :Effacement is the process by which the muscular fi bers of the cervix are pulled

upward and merges with the fibers of the lower uterine segment. The cervix becomes t hin during first stage of labor or even before that in

primigravidae. In primigravidae, effacement precedes dilatation of th e cervix, whereas in multiparae, both occur simultaneously

(Fig.12.6). Expulsion of mucus plug is caused by effacement.

LOWER UTERINE SEGMENT : Before the onset of labor, there is no complete anatomical or functional division of the uterus.

During labor, the demarcation of an active upper segment and a relatively passive lowe r segment is more pronounced. The wall of the

upper segment becomes progressively thickened with progressive thinning of the lower segment (Fig. 12.7). This is pronounced in late

first stage, specially after rupture of the membranes and attains its maximum in seco nd stage. A distinct ridge is produced at the junction

of the two, called physiological retraction ring which should not be confused with the pathologica l retraction ring—a feature of

obstructed labor (p. 363). Lower segment of uterus is characterized by following featu res:

Figs 12.5A to C: (A) Formation of bag of membranes and forewaters,(B) Well fittingpresentingp artdividingtheforewater from hindwater,

(C) Ill fitting presenting part allows the hindwaters to force into the bag of membran es during contraction which may lead to its early

rupture

LOWER SEGMENT OF UTERUS AND THE CLINICAL SIGNIFICANCE An atomical features

1. It is developed from the isthmus of the (nonpregnant)

uterus which is bounded above anatomical and below by histological internal os.

Clinical significance

1. The phenomenon of receptive relaxation enables expulsion of the fetus by formation of c omplete birth canal along with the fully

dilated cervix (Fig. 12.17).

2. In labor it is bounded above by the physiological retraction ring (p. 121) and below by the fibro muscular junction of cervix and

uterus.

3. This segment is formed maximally during labor and the peritoneum is loosely attached an teriorly.

4. It measures 7.5–10 cm when fully formed and becomes cylindrical during the secon d stage of labor (Figs 12.7B, C).

5. The wall becomes gradually thin due to: (i) Relaxation of the muscle fibers to allow elongation. (ii) The muscle fibers are drawn up by

the muscle fibers of the upper uterine segment by contraction and retraction during labor (p. 118). (iii) Descent of the presenting part

causes further stretching and thinning out of wall (see p. 121).

6. This segment has got poor retractile property compared 2. Implantation of place nta in lower segment is known as placenta previa (p.

241).

3. It is through this segment that cesarean section is performed.

4. Poor decidual reaction in this segment facilitates morbid adherent placenta (p. 24 7), once the placenta is implanted here.

5. In obstructed labor, the lower segment is very much stretched and thinned o ut and ultimately gives way (ruptures) specially in

multiparae (p. 362).

6. It is entirely the passive segment of the uterus. Because of poor retractile property, the re is chance of postpartum hemorrhage if

placenta is implanted over the area.

to the upper segment.

(a) (a)

(b)

A (d) B (d)

Figs 12.6A and B: Diagrammatic representation of the dilatation and “taking up” o f the cervix in (A) primigravida and (B) multipara.

(A) a – cervix before labor; b, c – progressive ‘taking up’ of the cervix without much dilatation; d – cervix completely taken up with

external os still remaining undilated. (B) a – cervix before labor, to note the patulous ce rvix; b, c – progressive and simultaneous

dilatation and ‘taking up’ of the cervix; d – taking up and dilatation of the external os oc cur simultaneously

A B C Figs 12.7A to C: Sequence of development of the active and passive segments of the uterus. (A) Uterus at term, (C) In early

labor, (D) Late second stage

EVENTS IN SECOND STAGE OF LABOR

The second stage begins with the complete dilatation of the cervix and ends with the exp ulsion of the fetus. This stage is concerned

with the descent and delivery of the fetus through the birth canal.

Second stage has two phases : (A) Propulsive—from full dilatation until head touches the pel vic floor. (B) Expulsive—since the time

mother has irresistable desire to ‘bear down’ and push until the baby is delivered.

With the full dilatation of the cervix, the membranes usually rupture and there is escape of good amount of liquor amnii. The volume of

the uterine cavity is thereby reduced. Simultaneously, uterine contraction and retraction become stronger. The uterus becomes elongated

during contraction, while the antero-posterior and transverse diameters are reduced. Th e elongation is partly due to the contractions of

the circular muscle fibers of the uterus to keep the fetal axis straight.

Delivery of the fetus is accomplished by the downward thrust offered by uterine contr actions supplemented by voluntary contraction of

abdominal muscles (Fig.12.8) against the resistance offered by bony and soft tissues of the birth canal. There is always a tendency to

push the fetus back into the uterine cavity by the elastic recoil of the tissue of the vagina and the pelvic floor. This is effectively

counterbalanced by the power of retraction. Thus, with increasing contraction and retrac tion, the upper segment becomes more and

more thicker with corresponding thinning of lower segment. Endowed with power of retraction, the fetus is gradually expelled from

the uterus against the resistance offered by the pelvic floor. After the expulsion of the fetus , the uterine cavity is permanently reduced

in size only to accommodate the after-births.

The expulsive force of uterine contractions is added by voluntary contraction of the ab dominal muscles called “bearing down” efforts.

For details see p. 130.

Fig. 12.8: Diagram showing the expulsive forces in thesecond stage. Increased intra-abdominal p ressure augments the downward

expulsive force of uterine contraction

EVENTS IN THIRD STAGE OF LABOR

The third stage of labor comprises the phase of placental separation; its descent to the lower se gment and finally its expulsion with

the membranes.

PLACENTAL SEPARATION : At the beginning of labor, the placental attachme nt roughly corresponds to an area of 20 cm (8") in

diameter. There is no appreciable diminution of the surface area of the placental attachm ent during first stage. During the second stage,

there is slight but progressive diminution of the area following successive retractions, which attains its peak immediately following the

birth of the baby.

After the birth of the baby, the uterus measures about 20 cm (8") vertically and 10 cm (4") antero-posteriorly, the shape becomes discoid.

The wall of the upper segment is much thickened while the thin and flabby lower segment is thrown into folds. The cavity is much

reduced to accommodate only the afterbirths.

Mechanism of separation : Marked retraction reduces effectively the surface area at the placental s ite to about its half. But as the

placenta is inelastic, it cannot keep pace with such an extent of diminution resulting in its buckling (Fig. 12.9). A shearing force is

instituted between the placenta and the placental site which brings about its ultimate separa tion. The plane of separation runs through

deep spongy layer of decidua basalis so that a variable thickness of decidua covers the maternal surface of the separated placenta.

There are two ways of separation of placenta (Fig. 12.10).

(1) Central separation (Schultze): Detachment of placenta from its uterine attac hment starts at the center resulting in opening up of few

uterine sinuses and accumulation of blood behind the placenta (retroplacental hematoma ). With increasing contraction, more and more

detachment occurs facilitated by weight of the placenta and retroplacental blood until wh ole of the placenta gets detached.

(2) Marginal separation (Mathews-Duncan): Separation starts at the ma rgin as it is mostly unsupported. With progressive uterine

contraction, more and more areas of the placenta get separated. Marginal separation is f ound more frequently.

Separation of the membranes : The membranes which are attached loosely in the active part are thrown into multiple folds. Those

attached to the lower segment are already separated during its stretching. The sepa ration is facilitated partly by uterine contraction and

mostly by weight of the placenta as it descends down from the active part. The membranes so se parated carry with them remnants of

decidua vera giving the outer surface of the chorion its characteristic roughn ess.

EXPULSION OF PLACENTA : After complete separation of the placenta, it is forced down into the f labby lower uterine segment or

upper part of the vagina by effective contraction and retraction of the uterus. Thereaft er, it is expelled out by either voluntary contraction

of abdominal muscles (bearing down efforts) or by manual procedure (p. 140).

A B

Figs 12.9A and B: Diagram showing area of placental site— (A) Before the deliv ery of the baby, (B) After the delivery of the baby.

Note the reduction of the surface area of the placental site resulting in buckling of the place nta. PS = Placental surface

A B

Figs 12.10A and B: Types of separation of the placenta— (A) Schultze method, (B) Mathews-Duncan method

A B Figs 12.11A and B: Blood vessels: (A) Running through the interlacing muscle fibers are (B) Literally clamped due to effective

retraction of the uterine muscles

Mechanism of control of bleeding : After placental separation, innumerable torn sinuses which have free circulation of blood from

uterine and ovarian vessels have to be obliterated. The occlusion is effected by comple te retraction where by the arterioles, as they pass

tortuously through the interlacing intermediate layer of the myometrium, are literally clam ped (Fig. 12.11). It (living ligature) is the

principal mechanism of hemostasis. However, thrombosis occurs to occlud e the torn sinuses, a phenomenon which is facilitated by

hypercoagulable state of pregnancy. Apposition of the walls of the uterus following expulsion of the placenta (myotamponade) also

contributes to minimize blood loss.

MECHANISM OF NORMAL LABOR

DEFINITION : The series of movements that occur on the head in the process of adaptat ion, during its journey through the

pelvis, is called mechanism of labor. It should be borne in mind that while the principal movements are t aking place in the head, the

rest of the fetal trunk is also involved in it, either participating in or initiating the movement.

MECHANISM : In normal labor, the head enters the brim more commonly through the available tr ansverse diameter (70%) and to a

lesser extent through one of the oblique diameters. Accordingly, the position is either occipitola teral or oblique occipitoanterior. Left

occipitoanterior is little commoner than right occipitoanterior as the left oblique diameter is encroached by the rectum. The engaging

antero-posterior diameter of the head is either suboccipito-bregmatic 9.5 cm (3¾") or in slight deflexion—the suboccipitofrontal 10 cm

(4"). The engaging transverse diameter is biparietal 9.5 cm (3 ¾"). As the occipitolateral position is the commonest, the

mechanism of labor in such position will be described. The principal movements are: (1) Engagement (2) Descent (3) Flexion (4)

Internal rotation (5) Crowning (6) Extension (7) Restitution (8) External rotation and ( 9) Expulsion of the trunk. Although the various

movements are described separately but in reality, the movements at least some , may be going on simultaneously.

Engagement : Head brim relation prior to the engagement as revealed by imaging st udies show that due to lateral inclination of the head,

the sagittal suture does not strictly correspond with the available transverse diameter of the inlet. I nstead, it is either deflected anteriorly

toward the symphysis pubis or posteriorly towards the sacral promontory (Fig. 12.12). Such deflection of the head in relation to the

pelvis is called asynclitism. When the sagittal suture lies anteriorly, the posterior parietal bone be comes the leading presenting part and

is called posterior asynclitism or posterior parietal presentation. This is more frequently found in primigravid ae because of good

uterine tone and a tight abdominal wall. In others, the sagittal suture lies more posteriorly with the result that the anterior parietal bone

becomes the leading presenting part and is then called anterior parietal presentation or anter ior asynclitism. It is more commonly

found in multiparae. Mild degrees of asynclitism are common but severe degrees indica te cephalopelvic disproportion.

Posterior lateral flexion of the head occurs to glide the anterior parietal bone past the sym physis pubis in posterior parietal presentation.

Lateral flexion in the reverse direction occurs to glide the posterior parietal bone past th e sacral promontory in anterior parietal

presentation. After this movement which occurs early in labor, not only the head ente rs the brim but synclitism occurs. However,

in about 25% of cases, the head enters the brim in synclitism, i.e. the sagittal suture corres ponds to the diameter of engagement.

In primigravidae, engagement occurs in a significant number of cases before the o nset of labor while in multiparae, the same may

occur in late first stage with rupture of the membranes.

A B C Figs 12.12A to C:Head brim relation prior to engagemen t—(A) Anterior parietal presentation, (B) Head in synclitism, (C)

Posterior parietal presentation

Descent :Provided there is no undue bony or soft tissue obstruction, descent is a continuous process. I t is slow or insignificant in first

stage but pronounced in second stage. It is completed with the expulsion of the fetus. In primigravidae, with prior engagement of the

head, there is practically no descent in first stage; while in multiparae, descent starts with engagement. Head is expected to reach the

pelvic floor by the time the cervix is fully dilated. Factors facilitating descent are —(1) uterine contraction and retraction, (2) bearing

down efforts and (3) straightening of the fetal ovoid specially after rupture of the mem branes.

Flexion : While some degree of flexion of the head is noticeable at the beginning of labor but complete flexion is rather uncommon. As

the head meets the resistance of the birth canal during descent, full flexion is achieved. T hus, if the pelvis is adequate, flexion is

achieved either due to the resistance offered by the unfolding cervix, the walls of t he pelvis or by the pelvic floor. It has

been seen that flexion precedes internal rotation or at

least coincides with it. Flexion is essential for descent,

since it reduces the shape and size of the plane of the

advancing diameter of the head.

Flexion is explained by the two arm lever theory —

the fulcrum represented by the occipitoallantoid joint

of the head, the short arm extends from the condyles

to the occipital protuberance and the long arm

extends from condyles to the chin. When resistance is

encountered, by ordinary law of mechanics, the short

arm descends and the long arm ascends resulting in

flexion of the head (Fig. 12.13).

Internal rotation : It is a movement of great

importance without which there will be no further

descent. The mechanism of internal rotation is very

complex although easy to describe. The theories

which explain the anterior rotation of the occiput are:

A B

Figs 12.13A and B: Lever action producing flexion of the head reducing the eng aging diameter of the head from—(A) Occipitofrontal to

(B) Suboccipito bregmatic — Slope of pelvic floor: Two halves of levator ani form

a gutter and viewed from above, the direction of the fibers is backwards and toward the midline. Th us, during each contraction, the

head, occiput in particular, in well flexed position, stretches the levator ani, particularly th at half which is in relation to the occiput. After

the contraction passes off, elastic recoil of the levator ani occurs bringing the occiput fo rward toward the midline. The process is

repeated until the occiput is placed anteriorly. This is called rotation by law of pelvic floor (Hart’s rule).

— Pelvic shape: Forward inclination of the side walls of the cavity, narrow bispinous diameter and long anteroposterior diameter of the

outlet result in putting the long axis of the head to accommodate in the maximum available diameter, i.e. anteroposterior diameter of the

outlet leaving behind the smallest bispinous diameter.

— Law of unequal flexibility (Sellheim and Moir): The internal rotation is primarily due to inequalitie s in the flexibility of the

component parts of the fetus.

Fig. 12.14:Degree of internal rotation, restitution and external rotation of the head in left occipitola teral position

In occipitolateral position, there will be anterior rotation by 2/8th of a circle of the occipu t (Fig. 12.14) whereas in oblique anterior

position, rotation will be 1/8th of a circle forward, placing the occiput behind the symph ysis pubis. There is always an accompanying

movement of descent with internal rotation. Thus, prerequisites of anterior in ternal rotation of the head are well flexed head,

efficient uterine contraction, favourable shape at the midpelvic plane and tone of the levator ani muscles.

The level at which internal rotation occurs is variable. Rotation in the cervix although fa vorable is a less frequent occurrence. In

majority of cases, rotation occurs at the pelvic floor. Rarely, it occurs as late as crowning of the head.

Torsion of the neck: Torsion of the neck is an inevitable phenomenon during internal rotation of the head. If the shoulders remain in the

anteroposterior diameter, the neck has to sustain a torsion of 2/8th of a circle correspon ding with the same degree of anterior rotation of

the occiput. But the neck fails to withstand such major degree of torsion and as such the re will be some amount of simultaneous rotation

of the shoulders in the same direction to the extent of 1/8th of a circle placing the should ers to lie in the oblique diameter with 1/8th of

torsion still left behind. Thus, the shoulders move to occupy the left oblique diamete r in left occipitolateral position and right

oblique diameter in right occipitolateral position. In oblique occipitoanterior position, there is no movement of the shoulders from

the oblique diameter as the neck sustains a torsion of only 1/8th of a circle.

Crowning : After internal rotation of the head, further descent occurs until the subocciput lies underneath the pubic arch. At this stage,

the maximum diameter of the head (biparietal diameter) stretches the vulval outlet witho ut any recession of the head even after

the contraction is over—called “crowning of the head”.

Extension : Delivery of the head takes place by extension through “co uple of force” theory. The driving force pushes the head in a

downward direction while the pelvic floor offers a resistance in the upward and forwa rd direction. The downward and upward forces

neutralize and remaining forward thrust helping in extension (Fig. 12.15). The succ essive parts of the fetal head to be born through the

stretched vulval outlet are vertex, brow and face. Immediately following the release of the chin through the anterior margin of the

stretched perineum, the head drops down, bringing the chin in close proximity to the m aternal anal opening.

Restitution : It is the visible passive movement of the head due to untwisting of the neck su stained during internal rotation.

Movement of restitution occurs rotating the head through 1/8th of a circle in the directio n opposite to that of internal rotation (Fig.

12.14). The occiput thus points to the maternal thigh of the corresponding side to which it originally lay (Fig. 12.25).

C D

Figs 12.15A to D: Lateral view showing mechanism of labor in left occipitolateral position. (A and B) Posterior parietal presentation,

posterior lateral flexion of the head and engagement. (C and D) Internal rotation of the head with movement of the shoulders; descent

and delivery of the head by extension

External Rotation : It is the movement of rotation of the head visible externally du e to internal rotation of the shoulders. As the

anterior shoulder rotates toward the symphysis pubis from the oblique diameter, it carr ies the head in a movement of external rotation

through 1/8th of a circle in the same direction as restitution. The shoulders now lie in the antero-posterior diameter. The occiput points

directly towards the maternal thigh corresponding to the side to which it originallyd irected at the time of engagement (Fig. 12.14

and Fig. 12.25).

A B

Figs 12.16A and B: Delivery of the shoulders by lateral flexion. (A) Anterior sho ulder (B) Posterior shoulder

Birth of Shoulders and Trunk (Fig. 12.16) : After the shoulders are positioned in anteroposterior diameter of the outlet, further descent

takes place until the anterior shoulder escapes below the symphysis pubis first. By a moveme nt of lateral flexion of the spine, the

posterior shoulder sweeps over the perineum. Rest of the trunk is then expelled out by lateral flex ion.

ANATOMY OF LABOR

As labor advances, the body of the uterus, the cervix and the vagina together form an uniformly curved canal called the birth canal.

Normally, at the onset of labor when the head is not engaged, the pelvic structures ante rior to the vagina are urethra and bladder and

those posterior to the vagina are the pouch of Douglas with coils of intestine, rectum, anal canal , perineum and anococcygeal raphe.

As the head descends down with progressive dilatation of the vagina, it displaces the an terior structures, upwards and forwards and the

posterior structures, downwards and backwards, as if the head is passing through a sw ing door (Fig.12.17). The bladder which remains a

pelvic organ throughout the first stage becomes an abdominal organ in the second stage of labor. However, there is no stretching of the

urethra as was previously thought. Rather, the urethra is pushed anteriorly, with the neck of th e bladder still lying in the vulnerable

position behind the symphysis pubis. The changes in the posterior structures due to dow nward and backward displacement are marked

when the head is sufficiently low down and in the stage of “crowning”. The perineum which is a triangular area of about 4 cm thickness

becomes a thinned out, membranous structure of less than 1 cm thickness. The anus, from bei ng a closed opening, becomes dilated to the

extent of 2–3 cm. The anococcygeal raphe is also thinned and stretched. Thus, the posterior wall of the birth canal becomes about 23 cm

(9") in length; 11.5 cm (4 1/2") for the depth of the sacrum and 11.5 cm (4 1/2") for the stretched soft tissue, while its anterior wall

remains the same 4 cm (1 1/2"), in length. The canal becomes almost a semicircle.

B C

Figs 12.17A to C: (A) The relative position of the bladder, urethra and the genital organs at the beginning of labor. (B) Formation of

birth canal with the cervix fully dilated. Note the forward displacement of t he urethra and bladder neck behind the pubis. (C)

Marked stretching with downward and backward displacement of the posterior wall of the canal as the head descends down

CLINICAL COURSE OF FIRST STAGE OF LABOR

The first symptom to appear is intermittent painful uterine contractions followed by expu lsion of blood stained mucus (show) per

vaginam. Only few drops of blood mixed with mucus is expelled and any excess shoul d be considered abnormal.

PAIN: The pains are felt more anteriorly with simultaneous hardening of the uterus. Initially, the pains are not strong enough to cause

discomfort and come at varying intervals of 15–30 minutes with duration of about 30 s econds. But gradually the interval becomes

shortened with increasing intensity and duration so that in late first stage the contraction c omes at intervals of 3–5 minutes and lasts for

about 45 seconds. The relation of pain with uterine contraction is of great clinical signifi cance. In normal labor, pains are usually felt

shortly after the uterine contractions begin and pass off before complete relaxation of t he uterus. Clinically, the pains are said to be

good if they come at intervals of 3–5 minutes and at the height of contraction the uter ine wall cannot be indented by the fingers.

Fig. 12.18A: Composite partographic representation of different phases of labor showin g progressive cervical dilatation, descent and

rotation of the head

DILATATION AND EFFACEMENT OF THE CERVIX :Progressive anatomical ch anges in the cervix such as dilatation and

effacement are recorded following each vaginal examination. Cervical dilatation relat es with dilatation of the external os and

effacement is determined by the length of the cervical canal in the vagina. In primi gravidae, the cervix may be completely effaced,

feeling like a paper although not dilated enough to admit a finger tip. It may be mistaken for one that is fully dilated. While in

multiparae, dilatation and taking up occur simultaneously which are more abrupt follow ing rupture of the membranes. The anterior lip

of the cervix is the last to be effaced. The first stage is said to be completed only when the cerv ix is completely retracted over the

presenting part during contractions.

Cervical dilatation is expressed either in terms of fingers— 1, 2, 3 or fully dilated or better in terms of centimeters (10 cm when fully

dilated). It is usually measured with fingers but recorded in centimeters. One finger equ als to 1.6 cm on average. Simultaneously,

effacement of the cervix is expressed in terms of percentage, i.e. 25%, 50% or 100% (cervix less than 0.25 cm thick). The term ‘rim’is

used when the depth of the cervical tissue surrounding the os is about 0.5–1 cm.

Partograph (Fig. 34.4):Freidman (1954) first devised it. Partograph is a composite graphical record of cervical dilatation and descent of

head against duration of labor in hours. It also gives information about fetal and matern al condition, which are all recorded on a single

sheet of paper (details see p. 531). Cervical dilatation is a sigmoid curve and the first sta ge of labor has got two phases—a latent phase

and an active phase (Fig. 12.18A). The active phase has got three components .

(i) Acceleration phase with cervical dilatation of 2.5–4 cm.

B C

Figs 12.18B and C :(B) Head is palpable5/5th abovethesymphisis pubis. He ad is mobile, free and not engaged. (C) Head is palpable

2/5th above and 3/5th has gone down the brim. Head is engaged. See also Fig. 12.20

(ii) Phase of maximum slope of 4–9 cm dilatation. (iii) Phase of deceleration of 9–10 cm dilatation.

In primigravidae, the latent phase is often long (about 8 hours) during which effaceme nt occurs; the cervical dilatation averaging only

0.35 cm/h. In multiparae, the latent phase is short (about 4 hours) and effacement and d ilatation occur simultaneously. Because of

variable duration of latent phase, it is difficult to plot the cervical dilatation along the graph. But it h as got a distinct advantage to sort out

the cases of delay in labor, specially after the latent phase is over (cervix 3 cm dilated). Dilatation of the c ervix at the rate of 1 cm/h

in primigravidae and 1.5 cm in multigravidae beyond 3 cm dilatation (active phase of labor) is considered satisfactory.

STATUS OF THE MEMBRANES : Membranes usually remain intact until full dilatation of the cervix or sometimes even beyond, in

the second stage. However, it may rupture any time after the onset of labor but b efore full dilatation of cervix—when it is called early

rupture. When the membranes rupture before the onset of labor, it is called premat ure rupture (p. 317). As it has got some influence

on the obstetric outcome, it is discussed elsewhere (see ch. 21).

An intact membrane is best felt with fingers during uterine contraction when it becomes tense and bulges out through the cervical

opening. In between contractions, the membranes get relaxed and lies in contact with th e head. With the rupture of the membranes,

variable amounts of liquor escape out through the vagina and often there is acceleration of uterine contractions.

MATERNAL SYSTEM: General condition remains unaffected, although, a feeling of transie nt fatigue appears following a strong

contraction. Pulse rate is increased by 10–15 beats per minute during contraction which settles down to its previous rate in between

contractions. Systolic blood pressure is raised by about 10 mm Hg during contraction. Tem perature remains unchanged.

FETAL EFFECT : As long as the membranes are intact, there is hardly any adverse effect on the fetu s(Fig. 12.19). However, during

contraction, there may be slowing of fetal heart rate by 10–20 beats per minute which soon returns to its normal rate of about 140 per

minute as the intensity of contraction diminishes provided the fetus is not compromised.

Fig. 12.19: Generalized intra-amniotic pressure with intact membranes. Placental circulation is almo st unaffected during uterine

contraction

CLINICAL COURSE OF SECOND STAGE OF LABOR

Second stage begins with full dilatation of the cervix and ends with expulsion of the f etus. PAIN: The intensity of the pains

increases. The pain comes at intervals of 2–3 minutes and lasts for about 1–1½ minutes. It becomes successive with increasing intensity

in the second stage.

BEARING DOWN EFFORTS : It is the additional voluntary expuls ive efforts that appear during the second stage of labor

(expulsive phase). It is initiated by nerve reflex (Ferguson Reflex) set up due to stre tching of the vagina by the presenting part. In

majority, this expulsive effort start spontaneously with full dilatation of the cervix. Alon g with uterine contraction, the woman is

instructed to exert downward pressure as done during straining at stool. Sustained push ing beyond the uterine contraction is

discouraged. Premature (in the first stage) bearing down efforts may suggest uterine dysfunction. There may be slowing of the FHR

during pushing and it should come back to normal once the contraction is over.

MEMBRANES STATUS :Membranesmay rupturewith a gush ofliquor pervaginam. Ruptu remay occasionally be delayed till the head

bulges out through the introitus. Rarely, spontaneous rupture may not take place at all, allowing the baby to be “born in a caul”.

DESCENT OF THE FETUS : Features of descent of the fetus are eviden t from abdominal and vaginal examinations. Abdominal

findings are—progressive descent of the head, assessed in relation to the brim (Fig. 12.20), r otation of the anterior shoulder to the

midline and change in position of the fetal heart rate— shifted downwards and medially . Internal examination reveals—descent of the

head in relation to ischial spines and gradual rotation of the head evidenced by position o f the sagittal suture and the occiput in relation

to the quadrants of the pelvis (Fig. 12.21).

Abdominal assessment of progressive descent of the head (using fifth formula)

Progressive descent of the headcan be usefully assessedabdominally by estimating the n umber of ‘fifths’of the head above the pelvic

brim (Crichton): The amount of head felt suprapubically in finger breadth is assessed b y placing the radial margin of the index finger

above the symphysis pubis successively until the groove of the neck is reached. When one-fifth above, only the sinciput can be felt

abdominally and nought-fifths represents a head entirely in the pelvis with no poles f elt abdominally (Fig. 12.20).

Advantages over “station of the head” in relation to ischial spines

1. It excludes the variability due to caput and moulding or by a different depth of the p elvis.

2. The assessment is quantitative and can be easily reproduced.

3. Repeated vaginal examinations are avoided.

Fig. 12.20: Progressive descent of the head, assessed ‘in fifths’ palpable above the brim (s ee also Figs 12.18B and C)

VAGINAL SIGNS : As the head descends down, it distends the perineum, the vulv al opening looks like a slit through which the scalp

hairs are visible. During each contraction, the perineum is markedly distended with the o verlying skin tense and glistening and the vulval

opening becomes circular (expulsive phase). The adjoining anal sphincter is stretched and stool comes out during contraction. The head

recedes after the contraction passes off but is held up a little in advance because of retra ction. Ultimately, the maximum diameter of the

head (biparietal) stretches the vulval outlet and there is no recession even after the contr action passes off. This is called ‘crowning’ of

the head. The head is born by extension. After a little pause, the mo ther experiences further pain and bearing down efforts to expel the

shoulders and the trunk. Immediately thereafter, a gush of liquor (hind waters) follows, often tinged with blood.

MATERNAL SIGNS : There are features of exhaustion. Respiration is, however, slowed down w ith increased perspiration. During the

bearing down efforts, the face becomes congested with neck veins prominent. Immedi ately following the expulsion of the fetus, the

mother heaves a sigh of relief.

FETAL EFFECTS: Slowing of FHR during contractions is observed which comes back to normal before the next contraction.

CLINICAL COURSE OF THIRD STAGE OF LABOR

Third stage includes separation, descent and expulsion of the placenta with its membranes. PAIN: For a short time, the patient

experiences no pain. However, intermittent discomfort in the lower abdomen reappears , corresponding with the uterine contractions.

BEFORE SEPARATION: Per abdomen—Uterus becomes discoid in shape, f irm in feel and non-ballottable. Fundal height reaches

slightly below the umbilicus.

Per vaginam —There may be slight trickling of blood. Length of the umbilical cord as visible from outside, remains static.

AFTER SEPARATION: It takes about 5 minutes in conventional management for the placenta to separate.

Per abdomen—Uterus becomes globular, firm and ballottable. The fundal height is slightly raised as the separated placenta comes

down in the lower segment and the contracted uterus rests on top of it. There may be slight bulging in the suprapubic region due to

distension of the lower segment by the separated placenta.

Per vaginam—There may be slight gush of vaginal bleeding. Permanent lengthening of t he cord is established. This can be elicited

by pushing down the fundus when a length of cord comes outside the vulva which remains permanent, even after the pressure is

released. Alternatively, on suprapubic pressure upwards by fingers, there is no indrawing of the cord and the same lies unchanged outside

the vulva.

EXPULSION OF PLACENTA AND MEMBRANES: The expulsion is achieved either by voluntary bearing down efforts or more

commonly aided by manipulative procedure. The “after-birth” delivery is soon followe d by slight to moderate bleeding amounting to

100–250 mL.

MATERNAL SIGNS: There may be chills and occasional shivering. Slight transient hypotension is not unusual.

PLACE OF DELIVERY

Although in about 85% of cases, the delivery remains uncomplicated and uneventful b ut in the remaining, unforeseen complications may

arise which require urgent and skilled management. Effective antenatal care redu ces the hazards of delivery significantly but to get an

optimum outcome, adequate supervised intranatal care is mandatory (p. 104). Thus ideally, a ll women should have institutional

delivery. The national sociodemographic goals and the Millennium Development Go als (MDG 4 & 5) aim by 2015 to achieve

100% deliveries conducted by skilled birth attendant (SBA) and to reduce materna l mortality ratio below 100 and perinatal

death rate below 30 (see p. 602).

In the developed countries, there is a growing demand to have delivery at home (in low risk cases) with minimal intervention (natural

birth). Every woman should have one midwife (named midwife) for the continuit y of care during pregnancy and labor, e.g.

community-based care.

Changing child birth stressed the importance of community based care with the integratio n of community and hospital. There should

be agreed protocols for referral and ease of transport between community and hospita l.

Screening of high risk mothers (see p. 631) needs careful check up of all pregnant wo men at regular interval. However, in the under

privileged sector the vast majority are forced to have home delivery either on choice or by compulsion. They are delivered by “dais” or

even by relatives. Thus, the teaching hospitals and the district or sub-divisional hospit als are mostly being utilised as referral hospitals

where most of the neglected cases are rushed late and in a bad shape.

FLYING SQUAD : The squad consists of a team of experienced obstetrician, anesthetist and nursing staff, equipped with

sterilized packs of equipments and containers with stored blood. Ambulance car with the squadisru shedtothespot oncall,mostly

inthenatureofantepartumhemorrhageorpost-partumhemorrhage or eclampsia. Manual r emoval of placenta and resuscitation of the patient

at home or during transport to the referral hospital are the common procedures employ ed.

MANAGEMENT OF NORMAL LABOR

General considerations : Labor events have got great psychological, emotional and so cial impact to the woman and her family. She

experiences stress, physical pain and fear of dangers. The caregiver should be tactful, sensitive and respectful to her. The woman is

allowed to have her chosen companion (family member). Privacy must be maintained. S he is explained about the events from time to

time. Comfortable environment, skill and confidence of the caregiver and the emotional support (see p. 529) are all essential so that a

woman can give birth with dignity.

Management of normal labor aims at maximal observation with minimal active intervention. The idea is to maintain the normalcy and

to detect any deviation from the normal at the earliest possible moment.

ANTISEPTICS AND ASEPSIS: Scrupulous surgical cleanliness and asepsi s on the part of the patients and the attendants involved in

the delivery process are to be maintained.

Patient care: Shaving or hair clipping of the vulva is done. The vulva and the perin eum are washed liberally with soap and water and

then with 10% Dettol solution or Hibitane (chlorhexidine) 1 in 2000.

The woman should take a shower or bath, wear laundered gown and stay mobile. Thr oughout labor she is given continued

encouragement and emotional support. Antiseptic and aseptic precautions are t o be taken during vaginal examination and during

conduction of delivery.

VAGINAL EXAMINATION IN LABOR: First vaginal examination shou ld be done by a senior doctor to be more reliable and

informative. The examination is done with the patient lying in dorsal position.

PRELIMINARIES: (1) Toileting—The hands and forearms should be washed wit h soap and running water, a scrubbing brush be used

for the finger nails. The procedure should take at least 3 minutes. (2) Sterile pair of gloves is donned. (3) Vulval toileting is performed.

Vulva should once more be swabbed from before backwards with antiseptic lotion like 10% Dettol or Hibitane 1 in 2000. The same

solution is poured over the vulva by separating the labia minora by the fingers of left hand. (4) Gloved middle and index fingers of the

right handsmeared liberally with antiseptic cream like Cetavlon (cetrimide IP 0.5% W/W and hib itane 0.1% W/W) are introduced into

the vagina after separating the labia by two fingers of the left hand. (5) Complete examinati on should be done before fingers are

withdrawn. (6) Vaginal examination should be kept as minimum as possible to avoid risk s of infection.

The following information are to be noted and recorded carefully (Partograph — see p. 529):

— Degree of cervical dilatation in centimetres. It is marked with a cross (x) on the partograph at 4 cm dilatation. Alert line (p. 403,

530) starts at 4 cm of cervical dilatation and continued to the point of full dilatation (10 cm) at t he rate of 1 cm/h. Action line (p. 403,

530) is drawn parallel and 4 hours to the right of the alert line.

—Degree of effacement of cervix (p. 129).

— Status of membranes and if ruptured— colour of the liquor. Color of t he liquor in the partograph is recorded as—I:

Fig. 12.21:Station of the head in relation to ischial spines

membranes intact; R: membranes ruptured; C: liquor clear; M: Liquor meconium stained ; B: Liquor blood stained.

— Presenting part and its positionby noting the fontanelles and sagittal suture in relation to the quadrants of the pelvis.

— Caput or moulding of the head and if present, to note its degree. Moulding 1: Sutures apposed; 2: Sutures overlapped but reducible;

3: Sutures overlapped but not reducible.

— Station of the head in relation to ischial spines (Fig. 12.21).

Spines are the most prominent bony projections felt on internal examination and the bisp inous diameter is the shortest diameter of the

pelvis in transverse plane being 10.5 cm. The level of ischial spines (see Fig. 12.21) is the halfway between the pelvic inlet and outlet.

This level is known as station zero (0). The levels above and below the spines ar e divided into fifths to represent centimeters. The station

is said to be ‘O’if the presenting part is at the level of the spines. The station is stated in minus figu res, if it is above the spines (–1 cm, –

2 cm, –3 cm –4 cm and –5 cm) and in plus figures if it is below the spines (+1 cm. +2 cm. +3 cm +4 cm and +5 cm).

—Assessment of the pelvis specially in primigravidae is to be done and elasticity of the p elvic floor and presence of vulval varicosity, if

any, are to be noted.

INDICATIONS OF VAGINAL EXAMINATION:

Whatever aseptic technique is employed, there is always some chance of introducing in fection specially after rupture of the membranes.

Hence vaginal examination should be restricted to a minimum.

— At the onset of labor—To confirm the onset of labor and to detect precisely the pres enting part and its position. Pelvic assessment

specially in primigravidae should be done during the initial examination.

— The progress of labor can be judged on periodic examinations noting the dilatation o f the cervix and descent of the head in relation

to the spines (station). Generally it is done at an interval of 3–4 hours.

— Following rupture of the membranes to exclude cord prolapse specially where the head is not yet engaged.

— Whenever any interference is contemplated.

—To confirm the actual coincidence of bearing down efforts with complete dilatation o f the cervix and to diagnose precisely the

beginning of second stage.

MANAGEMENT OF THE FIRST STAGE

PRINCIPLES : (1) Non-interference with watchful expectancy so as to prepare the patient for natural birth. (2) To mo nitor

carefully the progress of labor, maternal conditions and fetal behavior so as to detect any intrap artum complication early.

PRELIMINARIES :Thisconsistsofbasicevaluationofthecurrent clinicalcondition.Enqu iry istobemadeabout the onset of labor pains or

leakage of liquor, if any. Thorough general and obstetrical examinations including vaginal examination are to be carried out and

recorded. Records of antenatal visits, investigation reports and any specific treatment given, if available, are to be reviewed.

ACTUAL MANAGEMENT:

• General—(a) Antiseptic dressing are as described before (p. 133).(b) Encouragement, emoti onal support and assurance are given

to keep up the morale. (c) Constant supervision is ensured.

• Bowel—An enema with soap and water or glycerine suppository is traditio nally given in early stage. This may be given if the rectum

feels loaded on vaginal examination. But enema neither shortens the duration of labor nor reduces the infection rate.

• Rest and ambulation—If the membranes are intact, the patient is allowed to walk about. This attitude prevents venacaval compression

and encourages descent of the head. Ambulation can reduce the duration of labor, nee d of analgesia and improves maternal comfort. If,

however, labor is monitored electronically or analgesic drug (epidural analgesia ) is given, she should be in bed.

• Diet—There is delayed emptying of the stomach in labor. Low pH of the gastric contents is a real danger if aspirated following general

anesthesia when needed unexpectedly (see p. 520). So food is withheld during act ive labor. Fluids in the form of plain water, ice chips

or fruit juice may be given in early labor. Intravenous fluid with ringer solution is starte d where any intervention is anticipated or the

patient is under regional anesthesia.

• Bladder care—Patient is encouraged to pass urine by herself as full bladder often inhibits uteri ne contraction and may lead to infection.

If the woman cannot go to the toilet, she is given a bed pan. Privacy must be maintained and co mfort must be ensured. If the patient fails

to pass urine specially in late first stage, catheterization is to be done with strict asep tic precautions.

• Relief of pain—The detail of analgesia in labor is discussed in chapter 33. For practical purp oses, the common analgesic drug used is

pethidine 50-100 mg intramuscularly when the pains are well established in the active ph ase of labor. If necessary, it is repeated after 4

hours. Pethidine is an effective analgesic as well as a sedative. Metoclopramide 10 mg IM is commonly given to combat vomiting due to

pethidine. Pethidine crosses the placenta and is a respiratory depressant to the neonate . The drug should not be given if delivery is

anticipated within two hours (For antidote see p. 472).

• Assessment of progress of labor and partograph recording.

Pulse is recorded every 30 minutes and is marked with a dot (.) in the partograph. Blood pressure is recorded at every 1 hours and is

marked with arrows ( ) p. 530. Temperature is recorded every 2 h ours. Urine ouput is recorded for volume, protein or a cetone. Any

drug (oxytocin or other) when given is recorded in the partograph.

Abdominal palpation—(a) Uterine contractions: as regard the frequency, intensity and d uration are assessed. The number of

contractions in 10 minutes and duration of each contraction in seconds are recorde d in the partograph (see p. 402, 530).

Partograph is charted every half an hour (p. 530) as: contraction duration < 20 seconds ; between 20 and 40 secs and > 40 secs .

(b) Pelvic grip: Gradual disappearance of polesof the head(sinciput and occiput) which were felt previously, (usually occur in labor).

Abdominal palpation for descent of the fetal head in terms of fifths felt above the brim is to be used (Figs. 12.18B and 12.18C).

To note the fetal well being:

•Fetalheart rate (FHR) along with its rhythm and intensity should be noted every half hour in the first stage and every 15 minutes in

second stage or following rupture of the membranes. To be of value, the observatio n should be made immediately following uterine

contraction. The count should be made for 60 seconds. For routine clinical observation, ordinary stethoscope is quite suit able. Doppler

ultrasonic cardiography (Dopplex), however, is helpful in the case of obesity and poly hydramnios (see Fig. 41.32). To avoid confusion

of maternal and fetal heart rates, maternal pulse should be counted. Otherwise maternal tachycardia may be wrongly treated as fetal

heart rate. Normal fetal heart rate ranges from 110–150 per minute.

CONTINUOUS ELECTRONIC FETAL MONITORING (Fig. 34.4): The device consists of simultaneous recording of fetal heart

action by fetal electrocardiography and uterine contraction by tocography (details in p. 610). It is commonly used for high risk

pregnancies.

Vaginal examination — (a) Dilatation of the cervix in centimeters in relation to hours of l abor is a reliable index to note the progress of

labor. (b) To note the position of the head and degree of flexion. (c) To note the st ation of the head in relation to the ischial spines. (d)

Color of the liquor (clear or meconium stained) if the membranes are ruptured (e) Degree of mouldi ng of the head—Moulding occurs

first at the junction of occipitoparietal bones and then between the parietal bones (see p. 86). (f) Caput formation—Progressive increase

is more important than its mere presence (p. 86).

EVIDENCES OF FETAL DISTRESS: (See intrapartum fetal monitoring p. 609).

TO WATCH THE MATERNAL CONDITION: Routine check up includes: (a) to record 2 hourly pulse, blood pressure and

temperature; (b) to observe the tongue periodically for hydration (see partograph p. 53 0) and (c) to note the urine output, urine for

acetone, glucose and (d) IV fluids, drugs.

Evidence of maternal distress are:

 Anxious look with sunken eyes  Rising pulse rate of 100 per minute or more  Dehydration, dry tongue  Hot, dry vagina often with

offensive discharge  Acetone smell in breath  Scanty high colored urine with presence of acetone

MANAGEMENT OF THE SECOND STAGE

The transition from the first stage to the second stage is evidenced by the following features : t Increasing intensity of uterine

contractions t Appearance of bearing down efforts t Urge to defecate w ith descent of the presenting part

t Complete dilatation of the cervix as evidenced on vaginal examination

PRINCIPLES: (1) To assistin the natural expulsion of the fetus slowly and steadily, (2) To prevent perineal injuries.

GENERAL MEASURES:

— The patient should be in bed.

— Constant supervision is mandatory and the FHR is recorded at every 5 minutes.

— To administer inhalation analgesics, if available, in the form of Gas N

O and O

to relieve pain during contractions.

— Vaginal examinationis done at the beginning of the second stage not only to confirm its onset but to d etect any accidental cord

prolapse. The position and the station of the head are once more to be reviewed and th e progressive descent of the head is ensured.

PREPARATION FOR DELIVERY

— Position—Positions of the woman during delivery may be lateral or partial sitting. Dorsal position with 15° left lateral tilt is

commonly favored as it avoids aortocaval compression and facilitates pushing effort.

— The accoucheur scrubs up and puts on sterile gown, mask and gloves and stands o n the right side of the table.

— Toileting the external genitaliaandinner side of the thighsisdone with cotton swabssoak edin Savlon or Dettol solution. One sterile

sheet is placed beneath the buttocks of the patient and one over the abdomen. Sterilized leggings are to be used. Essential aseptic

procedures are remembered as 3 ‘C’s: (a) Clean hands, (b) Clean surfac e and (c) Clean cutting and ligaturing of the cord.

— To catheterize the bladder, if it is full.

CONDUCTION OF DELIVERY: The assistance required in spontaneous delivery is divided into three phases :

• Delivery of the head • Delivery of the shoulders • Delivery of the trunk

Delivery of the head: The principles to be followed are to maintain flexion of the head, to prevent its early extensio n and to regulate its

slow escape out of the vulval outlet.

— The patient is encouraged for the bearing down efforts during uterine contractions. This facilitates descent of the head.

— When the scalp is visible for about 5 cm in diameter, flexion of the head is maintaine d during contractions. This is achieved by

pushing the occiput downwards and backwards by using thumb and index fingers of the left ha nd while pressing the perineum by the

right palm with a sterile vulval pad. If the patient passes stool, it should be cleaned and th e region is washed with antiseptic lotion.

— The process is repeated during subsequent contractions until the sub-occiput is place d under the symphysis pubis. At this stage, the

maximum diameter of the head (biparietal diameter) stretches the vulval outlet witho ut any recession of the head even after the

contraction is over and it is called “crowning of the head” (Fig. 12.22). The purpose of incre asing the flexion of the head is to ensure

that the small suboccipito-frontal diameter 10 cm (4") distends the vulval outlet instead of larger occipitofrontal diameter 11.5 cm (4

1/2") (Fig. 12.23).

— When the perineum is fully stretched and threatens to tear specially in primigravid ae, episiotomy is done at this stage after prior

infiltration with 10 mL of 1% lignocaine. Bulging thinned out perineum is a better crit erion than the visibility of 4–5 cm of scalp to

decide the time of performing episiotomy (details in chapter 36). Episiotomy is done selectively an d not as a routine (see p. 568).

— Slow delivery of the head in between the contractions is to be regulated. This is done when the sub-occipito frontal diameter

emerges out. This is accomplished by pushing the chin with a sterile

Fig. 12.22: Crowning of the head

Fig. 12.23: Sub-occipitofrontal diameter distending the vulval outlet

towel covered fingers of the right hand placed over the anococcygeal region while the left hand exerts pressure on the occiput (Ritzen

maneuver Fig. 12.24). The forehead, nose, mouth and the chin are thus born successively o ver the stretched perineum by

extension.

Care following delivery of the head:

— Immediately following delivery of the head, the mucus and blood in the mouth and pha rynx are to be wiped with sterile gauze

piece on a little finger. Alternatively, mechanical or electrical sucker may be used . This simple procedure prevents the serious

consequence of mucus blocking the air passage during vigorous inspiratory efforts.

— The eyelids are then wiped with sterile dry cotton swabs using one for each eye starting from the medial to the lateral canthus to

minimize contamination of the conjunctival sac.

Fig. 12.24: Assisted deliveryof thehead byextension,exerting an upward pressure to the chin by th e right hand placed over the anoco-

ccygeal raphe (Ritzen maneuver)

— The neck is then palpated to exclude the presence of any loop of cord (20–25%). If it is found and if loose enough, it should be

slipped over the head or over the shoulders as the baby is being born. But if it is sufficiently t ight enough, it is cut in between two pairs

of Kocher’s forceps placed 1 inch apart.

PREVENTION OF PERINEAL LACERATION: More attention sh ould be paid not to the perineum but to the controlled delivery of

the head.

— Delivery by early extension is to be avoided. Flexion of the the sub-occ iput comes under the symphysis pubis so that lesser sub-

occipitofrontal 10 cm (4") diameter emerges out of the introitus.

— Spontaneous forcible delivery of the head is to be avoided by assuring the patient not to bear down during contract ions.

— To deliver the head in between contractions.

— To perform timely episiotomy (when indicated).

— To take care during delivery of the shoulders as the wider bisacromial diameter (12 cm) emerges out of the introitus.

Delivery of the shoulders: Not to be hasty in delivery of the shoulders. Wait for the uterine contractions to come and for the

movements of restitution and external rotation of the head to occur (Fig. 12.25). This in directly signifies that the bisacromial diameter is

placed in the anteroposterior diameter of the pelvis. During the next contraction, the anterior shoulder is born behind the symphysis. If

there is delay, the head is grasped by both hands and is gently drawn posteriorly u ntil the anterior shoulder is released from under the

pubis. By drawing the head in upward direction, the posterior shoulder is delivered ou t of the perineum (Fig. 12.26). Traction on the

head should be gentle to avoid excessive stretching of the neck causing injury to the bra chial plexus, hematoma of the neck or fracture

of the clavicle.

Delivery of the trunk: After the delivery of the shoulders, the fore finger of each hand are inserted under the axillae and the trunk is

delivered gently by lateral flexion.

IMMEDIATE CARE OF THE NEWBORN

• Soon after the delivery of the baby, it should be placed on a tray covered with clean dry linen with the head slightly downwards

(15°). It facilitates drainage of the mucus accumulated in the tracheobronchial tree by gravity. The tray is placed between the legs of the

mother and should be at a lower level than the uterus to facilitate gravitation of blood from the placenta to the in fant.

C D

Figs 12.25A to D:(A) Head is born by extension. (B) Head drops down with the face clo se to the anus. (C) Restitution. (D) External

rotation

• Air passage (oropharynx) should be clearedof mucus and liquor by gentle s uction.

• Apgar rating at 1 minute and at 5 minutes is to be recorded.

• Clamping and ligature of the cord—The cord is clamped by two Kocher’s forcep s, the near one is placed 5 cm away from the

umbilicus and is cut in between. Two separate cord ligatures are applied with sterile cotto n threads 1 cm apart using reef-knot, the

proximal one being placed 2.5 cm away from the navel. Squeezing the cord with fingers prior to applying ligatures or plastic cord

clamps (see Fig. 41.30), prevents accidental inclusion of embryonic remnants (see p . 39). Leaving behind a length of the cord attached

to the navel not only prevents inclusion of the embryonic structure, if present, but also f acilitates control of primary haemorrhage due to

a slipped ligature. The cord is divided with scissors about 1 cm beyond the ligatures taki ng aseptic precautions so as to prevent cord

sepsis. Presence of any abnormality in cord vessels (single umbilical artery) is to be noted. The cut end is then covered with sterile

gauze piece after making sure that there is no bleeding. The purpose of clam ping the cord on the maternal end is to prevent soiling of

the bed with blood and to prevent fetal blood loss of the second baby in undiagnosed m onozygotic twin.

Delay in clamping for 2–3 minutes or till cessation of the cord pulsation facilitates transfer of 80-1 00 mL blood from the compressed

placenta to a baby when placed below the level of uterus. This is beneficial to a mature baby but may be deleterious to a pre-term or a

low birth weight baby due to hypervolemia. But early clamping should be done in cases of Rh-incompatibility (to prevent antibody

transfer from the mother to the baby) or babies born asphyxiated or one of a dia betic mother.

A B

Figs 12.26A and B: Assisted delivery of the shoulders—(A) Anterior shoulder. ( B) Posterior shoulder

t Quick check is made to detect any gross abnormality and the baby is wrapped w ith a dry warm towel. The identification tape is tied

both on the wrist of the baby and the mother. Once the management of third stage is over (us ually 10–20 minutes), baby is given to the

mother or to the nurse.

MANAGEMENT OF THE THIRD STAGE

Third stage is the most crucial stage of labor.Previously uneventful first and secon d stage can become abnormal within a minute with

disastrous consequences.

The principles underlying the management of third stage are to ensure strict vigilance and to follo w the management guidelines

strictly in practice so as to prevent the complications, the important one being postpartum hemorrhage.

STEPS OF MANAGEMENT: Two methods of management are currently in practice.

t Expectant management t Active management (preferred)

Expectant management (traditional):

In this management, the placental separation and its descent into the vagina are allowe d to occur spontaneously. Minimal assistance

may be given for the placental expulsion if it needed. t Constant watch is mandato ry and the patient should not be left alone.

t If the mother is delivered in the lateral position, she should be changed to dorsal positio n to note

features of placental separation and to assess the amount of blood loss.

t A hand is placed over the fundus—(a) to recognise the signs of separation of p lacenta, (b) to note

the state of uterine activity—contraction and relaxation and (c) to detect, though rare, cupping of the

fundus which is an early evidence of inversion of the uterus.

Desire to fiddle with the fundus or massage the uterus is strongly to be condemned .Placenta is separated within m inutes following

the birth of the baby. A watchful expectancy can be extended up to 15–20 minutes. In so me institutions, ‘no touch’ or ‘hands off’ policy

is employed. The patient is expected to expel the placenta within 20 minutes with the aid of gravi ty.

t Expulsion of the placenta: Only when the features of placental separation and its descent into the lower segment are confirmed,

the patient is asked to bear down simultaneously with the hardening of the uterus. The raise d intra-abdominal pressure is often adequate

to expel the placenta. If the patient fails to expel, one can wait safely upto 10 minutes if t here is no bleeding. As soon as the placenta

passes through the introitus, it is grasped by the hands and twisted round and round with g entle traction so that the membranes are

stripped intact. If the membranes threaten to tear, they are caught hold of by sponge ho lding forceps and in similar twisting movements

the rest of the membranes are delivered. Gentleness, patience and care are prerequ isites for complete delivery of the membranes. If

the spontaneous expulsion fails or is not practicable, because of delivery under anes thesia, any one of the following methods can be used

to expedite expulsion.

Fig. 12.27:Expression of the placenta by controlled cord traction

Fig. 12.28:Expression of the placenta by fundal pressure

Assisted expulsion : (a) Controlled cord traction (modified Brandt-Andrews method) —The palmar surface of the fingers of the left

hand is placed (above the symphysis pubis) approximately at the junction of upper and lower uterine segment (Fig. 12.27). The body of

the uterus is pushed upwards and backwards, toward the umbilicus while by the right hand steady tension (but not too strong traction) is

given in downward and backward direction holding the clamp until the placen ta comes outside the introitus. It is thus more an uterine

elevation which facilitates expulsion of the placenta. The procedure is to be adopted only when the uterus is hard and contracted.

(b) Fundal pressure—The fundus is pushed downwards and backwards after placing four fingers behind the fundus and the thumb

in front using the uterus as a sort of piston (Fig. 12.28). The pressure must be giv en only when the uterus becomes hard. If it is not,

then make it hard by gentle rubbing. The pressure is to be withdrawn as soon as the pla centa passes through the introitus. If the baby is

macerated or premature, this method is preferable to cord traction as th e tensile strength of the cord is much reduced in both the

instances.

The cord may be accidentally torn which is not likely to cause any problem. The sterile gloved hand should be introduced and the

placenta is to be grasped and extracted.

— The uterus is massaged to make it hard, which facilitates expulsion of retain ed clots if any. Injection of oxytocin (5–10 units) IV

slowly or methergin 0.2 mg is given intramuscularly. Oxytocin is more stable and has lesser side e ffects compared to ergometrine

(nausea, vomiting, rise of BP). See p. 503.

— Examination of the placenta membranes and cord: The placenta is placed on a tray and is washed out in running tap water to

remove the blood and clots. The maternal surface is first inspected for its comple teness and anomalies. The maternal surface is

covered with greyish decidua (spongy layer of the decidua basalis). Normally the cotyledons are placed in close approximation and any

gap indicates a missing cotyledon. The membranes—chorion and amnion are to be examined carefully for completeness and presence

of abnormal vessels indicative of succenturiate lobe. The amnion is shin y but the chorion is shaggy. The cut end of the cord is

inspected for number of blood vessels. Normally, there are two umbilical arteri es and one umbilical vein. An oval gap in the

chorion with torn ends of blood vessels running upto the margin of the gap indicates a missing succenturiate lobe. The absence of

a cotyledon or evidence of a missing succenturiate lobe or evidence of significant missin g membranes demands exploration of the uterus

urgently.

— Vulva, vagina and perineum are inspected carefully for injuries and to be repa ired, if any. The episiotomy wound is now sutured.

The vulva and adjoining part are cleaned with cotton swabs soaked in antiseptic solution . A sterile pad is placed over the vulva.

— Fourth stage— Pulse, blood pressure, behavior of the uterus and any abn ormal vaginal bleedings, is to be watched at least for 1 hour

after delivery. When fully satisfied that the general condition is good, pulse and b lood pressure are steady, the uterus is well contracted

and there is no abnormal vaginal bleeding, the patient is sent to the ward.

Active management of third stage:

The underlying principle in active management is to excite powerful uterine contr actions within one minute of delivery of the baby

(WHO) by giving parenteral oxytocic. This facilitates not only early separation of the placenta but also produces effective uterine

contractions following its separation.

The advantages are — (a) to minimize blood loss in third stage approximately to 1/5th and (b) to shorten the duration of third stage to

half. The only disadvantage is slight increased incidence of retained placenta ( 1–2%) and consequent increased incidence of manual

removal. Of course, accidental administration during delivery of the first baby in undiagnosed twins produces grave danger to the unborn

second baby caused by asphyxia due to tetanic contraction of the uterus. Thus , it is imperative to limit its use in twins only following

delivery of the second baby.

Procedures: Injection oxytocin 10 units IM (preferred) or methergin 0.2 mg IM is given within 1 minute of delivery of the baby (WHO).

The placenta is expected to be delivered soon following delivery of the baby. If the pla centa is not delivered thereafter, it should be

delivered forthwith by controlled cord traction (BrandtAndrews) technique after clamp ing the cord while the uterus still remains

contracted. If the first attempt fails, another attempt is made after 2–3 minutes failing wh ich another attempt is made at 10 minutes. If

this still fails, manual removal is to be done. Oxytocic may be given with crowning of the head, with delivery of the anterior shoulder of

the baby or after the delivery of the placenta. If the administration is mistimed as might hap pen in a busy labor room, one should

not be panicky but conduct the third stage with conventional watchful expe ctancy.

Limitation: To be effective, it should be administered in proper time and followed by rapid delivery of the placenta. Thus, it may be an

ideal procedure while conducting delivery in an equipped surroundings and the attenda nt is conversant with the management. Even if it

cannot be extended routinely to all cases, it is certainly of value, for cases likely to develop postpartum hemorrhage. These are cases

delivered vaginally under anesthesia, anemia, hydramnios, twins, grand multiparae and previous history of PPH. It should not be used in

cardiac cases or severe pre-eclampsia, for fear of precipitating cardiac overload in the former and aggravation of blood pressure in the

latter.

KEY POINTS

h Labor involves a series of changes in the genital organs. De livery is not synonymous with labor as it can take place without labor.

Normal labor should fulfil some defined criteria (p. 113).

h Onset of laboris difficult to understand (p. 113). Role of Estrogen, Progesterone, Prostag landins, Oxytocin and the fetus have been

explained (p. 114).

h Labor events are conventionally divided into three stages (p . 116).

hMain events in the first stage of labor are: (a) Dilatation and (b) Effacement of the cervix (p. 118). Second s tage events are (a)

Descent and (b) Delivery of the fetus. Second stage is characterized by two phases: (a) propulsive and (b) expulsive (bear down) to

deliver the fetus (p. 121). Third stage events are sepa ration of placenta and expulsion of placenta (p. 122).

h Lower uterine segmentis formed mainly during the first stage of labor. Clinica l importance of lower uterine segment are many (p.

119).

h Mechanism of normal labor involves a series of movements on the head in the proce ss of adaptation during its passage through the

pelvis (p. 123).

h Diagnosis of labor (true labor pains) includes regular painful uterine contractions, pr ogressive cervical dilatation and effacement and a

show (p. 116).

h Progressive descent of fetal head is assessed abdominally in terms of ‘fifth s’(crichton) Fig. 12.18B, C and 12.20 and also on vaginal

examination.

h Successful labor and deliveryis dependent on complex interactions of three variable s (three ‘P’s): the Power (uterine contractions),

the Passenger (fetus) and the Passage (pelvis).

h Partograph is used to record labor events (p. 129, 530). Electronic fetal mo nitoring is used for high risk cases (p. 609).

KEY POINTS

FIRST STAGE OF LABOR:

First stage of labor starts from the onset of true labor pain and ends with full dilatation of the cervix. Its average duration is about 12

hours in primigravidae and 6 hours in multiparae. First stage consists of latent phase (upto 3 cm of cer vical dilatation) and active

phase(upto10cm).Thestageischiefly concernedwithdilatationandeffacement of the cervix. The stage is clinically manifestedby

progressive uterine contraction, dilatation and “effacement” of the cervix and ulti mate rupture of the membranes. Maternal and fetal

conditionsremain unaffected except during uterine contraction. Management consi sts of: (1) Non-interference with watchful

expectancy. (2) Women is given encouragement, emotional support and adequate pain relief during th e entire course of labor. (3) To

monitor carefully the progress of labor, maternal condition and fetal behavior so as to d etect any deviation from the normal. (4)

Partograph is maintained (see p. 530).

SECOND STAGE OF LABOR:

The second stage of labor starts from full dilatation of the cervix and ends with expulsion of the fetus. Its average duration is two

hours in primigravidae and 30 minutes in multiparae. The stage concerns with the de scent and delivery of the fetus through the birth

canal. The stage isclinically manifested by increased freque ncy and intensity of uterine contractions with appearance of “bearing down”

efforts which result in expulsion of the fetus. The mother may show features of exhaus tion. The principles in management are: (1) To

assist in the natural expulsion of the fetus slowly and steadily (2) To prevent perineal injurie s. During conduction of delivery, head is

delivered slowly in between contractions. Flexion is maintained althrough so that smaller diameter o f the head stretches the perineum.

This, along with timely performed episiotomy (selective) prevents perineal laceration. Sh oulders are delivered slowly with next

contraction. Immediate care of the newborn includes clearing of the air passage and eyes, clamping and ligaturi ng of the umbilical cord

and Apgar scoring.

THIRD STAGE OF LABOR:

The third stage begins after the expulsion of the fetus and ends with expulsion of the placenta and membranes. Its average duration is

15 minutes. The stage concerns with placental separation and its expulsion. The separ ation is achieved by marked reduction in the

uterine surface area of the placental site following delivery due to retraction. The placenta b einginelastic shears off its attachment

through the deep spongy decidual layer. There are two ways of separation —central (Schultze) and marginal (Mathews-Duncan). The

bleeding is controlled by effective myometrial contraction and retraction (living ligature) an d by thrombosis. The expulsion may occur

through “bearing down” efforts or more commonly, with assistance. The management is either by employing watchful expectancy or by

active management (WHO) in cases where oxytocin 10 units IV (slowly) or IM/mether gin 0.2 mg IV is administered within one minute

following the delivery of the baby. The placenta and the membranes should be examined f ollowing their expulsion.

Normal Puerperium

DEFINITION

Puerperium is the period following childbirth during which the body tissues, specially the pelvic organs revert back

approximately to the prepregnant state both anatomically and physiologically . The retrogressive changes are mostly confined to the

reproductive organs with the exception of the mammary glands which in fact show features of activity. Involution is the process

whereby the genital organs revert back approximately to the state as they were b efore pregnancy. The woman is termed as a

puerpera.

DURATION: Puerperium begins as soon as the placenta is expelled and lasts for approxim ately 6 weeks when the uterus becomes

regressed almost to the non-pregnant size. The period is arbitrarily divided into — (a) immed iate – within 24 hours; (b) early – up to 7

days and (c) remote – up to 6 weeks. Similar changes occur following abortion but takes a shorter period for the involution to

complete.

Fourth trimester is the time from delivery until complete physiolgical involution and ps ychological adjustment.

INVOLUTION OF THE UTERUS

ANATOMICAL CONSIDERATION

Uterus: Immediately following delivery, the uterus becomes firm and retract with alternate hardening and softening. The uterus

measures about 20 × 12 × 7.5 cm (length, breadth and thickness) and weighs about 10 00 gm (Fig. 13.1). At the end of 6 weeks, its

measurement is almost similar to that of the non-pregnant state and weighs about 6 0 gm. The decrease in size of the uterus and cervix has

been shown with serial MRI (Fig. 13.2). The placental site contracts rapidly presenting a raised surface with measures about 7.5 cm

and remains elevated even at 6 weeks when it measures about 1.5 cm.

Lower uterine segment: Immediately following delivery, the lower segm ent becomes a thin, flabby and collapsed structure. It takes a

few weeks to revert back to the normal shape and size of the isthmus, i.e. the part between the b ody of the uterus and internal os of the

cervix.

Cervix: The cervix contracts slowly; the external os admits two fingers for a few da ys but by the end of first week, narrows down to

admit the tip of a finger only. The contour of the cervix takes a longer time to regain (6 weeks) and the external os never reverts back to

the nulliparous state.

PHYSIOLOGICAL CONSIDERATION

The physiological process of involution is most marked in the body of the uterus. Chan ges occur in the following components: (1)

Muscles (2) Blood vessels (3) Endometrium.

Muscles: There is marked hypertrophy and hyperplasia of muscle fibers dur ing pregnancy and the individual muscle fiber enlarges to the

extent of 10 times in length and 5 times in breadth. During puerperium , the number of muscle fibers is not decreased but there is

substantial reduction of the

Fig. 13.1: Sagittal section showing uterus five days after delivery

myometrial cell size . Withdrawal of the steroid hormones, estrogen and progesteron e, may lead to increase in the activity of the uterine

collagenase and the release of proteolytic enzyme. Autolysis of the protoplasm occurs b y the proteolytic enzyme with liberation of

peptones which enter the blood stream. These are excreted through the kidneys as urea and creatinine. This explains the increased

excretion of the products in the puerperal urine. The connective tissues also und ergo the same type of degeneration. The conditions

which favors involution are — (a) efficacy of the enzymatic action and (b) relative an oxia induced by effective contraction and

retraction of the uterus.

Blood vessels: The changes of the blood vessels are pronounced at the placent al site. The arteries are constricted by contraction of its

wall and thickening of the intima followed by thrombosis. During the first week, the arteries undergo thrombosis, hyalinization and

fibrinoid end arteritis. The veins are obliterated by thrombosis, hyalinization and endoph lebitis. New blood vessels grow inside the

thrombi.

Endometrium: Following delivery, the major part of the decidua is cast off with the expulsio n of the placenta and the membranes, more

at the placental site. The endometrium left behind varies in thickness from 2–5 mm. The s uperficial part containing the degenerated

decidua, blood cells and bits of fetal membranes becomes necrotic and is cast off in the lo chia. Regeneration starts by 7th day. It

occurs from the epithelium of the uterine gland mouths and interglandular s tromal cells. Regeneration of the epithelium is

completed by 10th day and the entire endometrium is restored by the day 16, except at the placental site where it takes about 6

weeks.

CLINICAL ASSESSMENT OF INVOLUTION

The rate of involution of the uterus can be assessed clinically by noting the height of the fundus of the uterus in relation to the symphysis

pubis. The measurement should be taken carefully at a fixed time every day, preferably by the same observer. Bladder must be emptied

before hand and preferably the bowel too, as the full bladder and the loaded bowel may r aise the level of the fundus of the uterus. The

uterus is to be centralized and with a measuring tape, the fundal height is measured abo ve the symphysis pubis. Following delivery,

the fundus lies about 13.5 cm (5 1/2”) above the symphysis pubis. During the first 24 hours, the level remains constant; thereafter,

there is a steady decrease in height by 1.25 cm (1/2”) in 24 hours, so that by the end of second week the uterus becomes a pelvic

organ. The rate of involution thereafter slows down until by 6 weeks, the uterus becomes almo st normal in size.

The involution may be affected adversely and is called subinvolution. Sometimes, the inv olution may be continued in women who are

lactating so that the uterus may be smaller in size — superinvolution. The uterus, howev er, returns to normal size if the lactation is

withheld.

Fig. 13.2: MRI — sagittal view of the uterus and cervix showing large size and thick walls after 6 days of delivery

INVOLUTION OF OTHER PELVIC STRUCTURES

Vagina: The distensible vagina, noticed soon after birth takes a long time (4-8 weeks) to inv olute. It regains its tone but never to the

virginal state. The mucosa remains delicate for the first few weeks and submucous ven ous congestion persists even longer. It is the

reason to withhold surgery on puerperal vagina. Rugae partially reappear at third week but never to the same degree as in prepregnant

state. The introitus remains permanently larger than the virginal state. Hymen is lacerated and is represented by nodular tags — the

carunculae myrtiformes.

Broad ligaments and round ligaments require considerab le time to recover from the stretching and laxation. Pelvic floor and pelvic

fascia take a long time to involute from the stretching effect during parturition.

LOCHIA It is the vaginal discharge for the first fortnight during puerperium. The disch arge originates from the uterine body,

cervix and vagina.

Odor and reaction: It has got a peculiar offensive fishy smell. Its reaction is alkaline tending to b ecome acid towards the end.

Color: Depending upon the variation of the color of the discharge, it is named as: (1) Lochia rubra (red) 1-4 days. (2) Lochia serosa

(5-9 days) — the color is yellowish or pink or pale brownish. (3) Lochia alba — (pale white) — 10-1 5 days.

Composition: Lochia rubra consists of blood, shreds of fetal membranes and decidua, vernix c aseosa, lanugo and meconium.

Lochia serosa consists of less RBC but more leukocytes, wound exudate, mucus from the cervix and microorganisms (anaerobic

streptococci and staphylococci). The presence of bacteria is not pathognom onic unless associated with clinical signs of sepsis.

Lochia alba contains plenty of decidual cells, leukocytes, mucus, cholestrin crystals, fatty and gr anular epithelial cells and

microorganisms.

Amount: The average amount of discharge for the first 5–6 days, is estimated to be 250 mL.

Normal duration: The normal duration may extend up to 3 weeks. The red lochia may pers ist for longer duration especially in women

who get up from the bed for the first time in later period. The discharge may be scanty, especially following premature labors or may be

excessive in twin delivery or hydramnios.

Clinical importance: The character of the lochial discharge gives useful information about the abnorm al puerperal state. The vulval

pads are to be inspected daily to get information:

• Odor: If malodorous, indicates infection.Retai ned plug or cotton piece inside the vagina should be kept in mind.

• Amount: Scanty or absent — signifies infection or lochiometra. If excessive — ind icates infection.

• Color: Persistence of red color beyond the normal limit signifies subinvolution or reta ined bits of conceptus.

• Duration: Duration of the lochia alba beyond 3 weeks suggests lo cal genital lesion.

GENERAL PHYSIOLOGICAL CHANGES

PULSE: For a few hours after normal delivery, the pulse rate is likely to be raised, w hich settles down to normal during the second day.

However, the pulse rate often rises with after-pain or excitement.

TEMPERATURE: The temperature should not be above 37.2°C (99°F) within the first 24 hours. There may be slight reactionary rise

following delivery by 0.5°F but comes down to normal within 12 hours. On the 3rd da y, there may be slight rise of temperature due to

breast engorgement which should not last for more than 24 hours. However, genito urinary tract infection should be excluded if there

is rise of temperature.

URINARY TRACT: The bladder mucosa becomes edematous and hyperemic an d often shows evidences of submucous extravasation of

blood. The bladder capacity is increased. The bladder may be over distended without a ny desire to pass urine. The common urinary

problems are: over distension, incomplete emptying and presence of residual urine. Urina ry stasis is seen in more than 50% of women.

The risk of urinary tract infection is, therefore, high. Dilated ureters a nd renal pelves return to normal size within 8 weeks. There is

pronounced diuresis on the second or third day of the puerperium. Only ‘clean catch’ sample of uri ne should be collected and sent for

examination and contamination with lochia should be avoided.

GASTROINTESTINAL TRACT: Increased thirst in early puerperium is due to loss of fluid during labor, in the lochia, diuresis and

perspiration. Constipation is a common problem for the following reasons: delayed GI motility, mi ld ileus following delivery, together

with perineal discomfort. Some women may have the problem of anal incontinence.

WEIGHT LOSS: In addition to the weight loss (5–6 kg) as a consequence of the expulsion of the fe tus, placentae, liquor and blood loss,

a further loss of about 2 kg (5 lb) occurs during puerperium chiefly caused by diuresis. This weight loss may continue up to 6 months of

delivery.

FLUID LOSS: There is a net fluid loss of at least 2 liters during the first week and an a dditional 1.5 liters during the next 5 weeks. The

amount of loss depends on the amount retained during pregnancy, dehydratio n during labor and blood loss during delivery. The loss of

salt and water are larger in women with preeclampsia and eclampsia.

BLOOD VALUES: Immediately following delivery, there is slight decrease of blood volume due to blood loss and dehydration. Blood

volume returns to non-pregnant level by the second week. Cardiac output rises soon after delivery to about 80% above the pre-labor

value but slowly returns to normal within one week.

RBC volume and hematocrit values returns to normal by 8 weeks postpartum after the hydremia disappears. Leukocytosis to th e

extent of 25,000 per cumm occurs following delivery probably in response to stress of labor. Platelet count decreases soon after the

separation of the placenta but secondary elevation occurs, with increase in platele t adhesiveness between 4-10 days. Fibrinogen level

remains high up to the second week of puerperium. A hypercoagulable state persists fo r 48 hours postpartum and fibrinolytic activity is

enhanced in first 4 days. The secondary increase in fibrinogen, factor VIII and platele ts in the first week increases the risk for

thrombosis. The increase in fibrinolytic activity after delivery acts as a protective mechanism.

MENSTRUATION AND OVULATION: The onset of the first menstrual period foll owing delivery is very variable and depends on

lactation. If the woman does not breastfeed her baby, the menstruation returns by 6th week following delivery in about 40% and by

12th week in 80% of cases.

In non-lactating mothers , ovulation may occur as early as 4 weeks and in lactat ing mothers about 10 weeks after delivery. In

lactating mothers the mechanism of amenorrhea and anovulation are depicted schematic ally above. A women who is exclusively

breastfeeding, the contraceptive protection is about 98% up to 6 months of postpartum. Thus, lactatio n provides a natural method

of contraception (see p. 537). However,

ovulation may precede the first menstrual period in about one-third and it is possibl e for the patient to become pregnant before

she menstruates following her confinement. Non-lactating mother should use contraceptiv e measures in 3rd postpartum week and the

lactating mother in 3rd postpartum month.

LACTATION

For the first two days following delivery, no further anatomic changes in the breasts oc cur. The secretion from the breasts called

colostrum which starts during pregnancy becomes more abundant during the period.

COMPOSITION OF THE COLOSTRUM: It is deep yellow serous fluid, alkaline in reaction. It has got a higher specific gravity; a

high protein, vitamin A, sodium and chloride content but has got lower carbohydrate, f at and potassium than the breast milk. It contains

antibody (IgA) produced locally.

Microscopically: It contains fat globules, colostrum Table 13.1: Percentage composition of colostrum and

corpuscles and acinar epithelial cells. The

colostrum

corpuscles are large polynuclear leukocytes, oval or

round in shape containing numerous fat globules.

Advantages: (1) The antibodies (IgA, IgG, IgM) and

Colostrum

humoral factors (lactoferrin) provides immunogical

Breast milk

breast milk

Protein Fat Carbohydrate Water 8.6 2.3 3.2 86

1.2

3.2 7.5 87 defense to the new born (see p. 451). (2) It has laxative

action on the baby because of large fat globules.

PHYSIOLOGY OF LACTATION

Although, lactation starts following delivery, the preparation for effective lactation starts during pregnancy. The physiological basis of

lactation is divided into four phases:

(a) Preparation of breasts (mammogenesis).

(b) Synthesis and secretion from the breast alveoli (lactogenesis).

(d) Maintenance of lactation (galactopoiesis).

The endocrine control in relation to different phases of lactation has been depicted in Fi gure 6.2.

• Mammogenesis: Pregnancy is associated with a remarkable growth of both t he ductal and lobuloalveolar systems. An intact nerve

supply is not essential for the growth of the mammary glands during pregnancy .

• Lactogenesis: Though some secretory activity is evident (colostrum) during pregnan cy and accelerated following delivery, milk

secretion actually starts on 3rd or 4th postpartum day. Around this time, the breasts become engorged, tense, tender and feel warm.

Inspite of a high prolactin level during pregnancy, milk secretion is kept in abeyance. P robably, the steroids — estrogen and

progesterone circulating during pregnancy make the breast tissues unresponsive to pro lactin. When the estrogen and progesterone are

withdrawn following delivery, prolactin begins its milk secretory activity in previously

Fig. 13.3: Lactation reflex arc and the role of prolactin and oxytocin

fully developed mammary glands. Prolactin and glucocorticoids are the im portant hormones in this stage. The secretory activity is

enhanced directly or indirectly by also growth hormone, thyroxine and insulin. For milk secretion to occur, nursing effort is not

essential.

• Galactokinesis: Discharge of milk from the mammary glands depends no t only on the suction exerted by the baby during suckling but

also on the contractile mechanism which expresses the milk from the alveoli into the duc ts. Oxytocin is the major galactokinetic

hormone.

DURING SUCKLING, A CONDITIONED REFLEX IS SET UP (Fig. 13.3): T he ascending tackle impulses from the nipple and

areola pass via thoracic sensory (4, 5 and 6) afferent neural arc to the paraventricular and supraoptic nuclei of the hypothalamus to

synthesize and transport oxytocin to the posterior pituitary (see Fig. 13.3). Oxytocin (ef ferent arc via blood), is liberated from the

posterior pituitary, produces contraction of the myoepithelial cells of the alveoli and the du cts containing the milk. This is the “milk

ejection” or “milk let down”reflex whereby the milk is forced down into the ampulla of the lactiferous ducts, wher e from it can be

expressed by the mother or sucked out by the baby. Presence of the infant or infant’s cry can induce let down without suckling. A

sensation of rise of pressure in the breasts by milk experienced by the mother at the beginning of sucking is called “draught”. This can

also be produced by injection of oxytocin.

The milk ejection reflex is inhibited by factors such as pain, breast engorgement or a dverse psychic condition. The ejection reflex may

be deficient for several days following initiation of milk secretion and results in breast en gorgement.

• Galactopoiesis: Prolactin appears to be the single most important galactop oietic hormone. For maintenance of effective and

continuous lactation, suckling is essential. It is not only essential for the rem oval of milk from the glands, but it also causes the release

of prolactin. Secretion is a continuous process unless suppressed by congestion or e motional disturbances. Milk pressure reduces the rate

of production and hence periodic breastfeeding is necessary to relieve the pressure wh ich in turn maintains the secretion.

• MILK PRODUCTION: A healthy mother will produce about 500-800 mL of milk a day to feed her infant. This requires about 700

Kcal/day for the mother, which must be made up from diet or from her body store. For this purpose a store of about 5 kg of fat during

pregnancy is essential to make up any nutritional deficit during lactation.

STIMULATION OF LACTATION: Mother is motivated as regard the benefits of b reastfeeding (see p. 449) since the early

pregnancy. No prelacteal feeds (honey, water) are given to the infant. Following delivery important steps are: (i) To put the baby to the

breast at 2–3 hours interval from the first day. (ii) Plenty of fluids to drink. (iii) To avoi d breast engorgement. Early (

– 1 hour) and

exclusive breastfeeding in correct position (see p. 450) are encouraged.

INADEQUATE MILK PRODUCTION (Lactation failure): It may be due to infrequent suckling or due to endogenous suppression of

prolactin (ergot preparation, pyridoxin, diuretics or retained placental bits). Pain, anxiety and ins ecurity may be the hidden reasons.

Unrestricted feeding at short interval (2–3 hours) is helpful.

DRUGS TO IMPROVE MILK PRODUCTION (Galactogogues): Metoclopramide (10 mg thrice daily) increases milk volume (60-

100%) by increasing prolactin levels. Sulpuride (dopamine antagonist) has also been fo und effective. Intranasal oxytocin contracts

myoepithelial cells and causes milk let down.

Lactation suppression: It may be needed for women who cannot breastfeed for per sonal or medical reasons. Lactation is suppressed

when the baby is born dead or dies in the neonatal period or if breastfeeding is c ontraindicated. Methods commonly used are: (i) To stop

breastfeeding (ii) To avoid pumping or milk expression (iii) To wear breast support (iv ) Ice packs to prevent engagement (v) Analgesics

(aspirin) to relieve pain (vi) A tight compression bandage is applied for 2–3 days. The na tural inhibition of prolactin secretion will result

in breast involution.

Medical methods of suppression with estrogen, androgen or bromocriptine is not reco mmended. The side effects of bromocriptine are:

hypotension, rebound secretion, seizures, myocardial infarction and puerperal stroke.

Breast milk for premature infant is beneficial by many ways (psychological, nutritional and immu nological). Metabolic disturbances

like azotemia, hyperamnioacidemia and metabolic acidosis are less with breast milk co mpared to formula. It gives immunological

protection to the premature infant. There are methods for collection (manual expression or electric pumps), and milk preservation.

MANAGEMENT OF NORMAL PUERPERIUM

The principles in management are: (1) To restore the health of the mother. (2) To prevent infection. (3) To take c are of the breasts,

including promotion of breastfeeding. (4) To motivate the mother for c ontraception.

Immediate attention: Immediately following delivery, the patient should be closely observed as outlined in the management of the

fourth stage of labor (see p. 141). She may be given a drink of her choice or somethin g to eat, if she is hungry. Emotional support is

essential. Usually the first feeling of mother is the sense of happiness and relief, w ith the birth of a healthy baby. The woman needs

emotional support when she suffers from postpartum blues or stress due to newborn’s prematu rity, illness, congenital malformation or

death.

REST AND AMBULANCE: Early ambulation after delivery is beneficial. Af ter a good resting period, the patient becomes fresh and

can breastfeed the baby or moves out of bed to go to the toilet. Early ambulatio n is encouraged. Advantages are: (1) Provides a sense

of well-being (2) Bladder complications and constipation are less (3) Facilitates uterine d rainage and hastens involution of the uterus (4)

Lessens puerperal venous thrombosis and embolism. Following an uncomplicated delive ry, climbing stairs, lifting objects, daily

household work, cooking may be resumed.

HOSPITAL STAY: Early discharge from the hospital is an almost universal pro cedure. If adequate supervision by trained health

visitors is provided, there is no harm in early discharge. Most women are discharged fi t and healthy after 2 days of spontaneous vaginal

delivery with proper education and instructions. Early discharge may be done in a few selecte d women. Some need prolonged

hospitalization due to morbidities (infections of urinary tract, or the perineal wound, pain, o r breastfeeding problems).

DIET: The patient should be on normal diet of her choice. If the patient is lactating , high calories, adequate protein, fat, plenty of

fluids, minerals and vitamins are to be given (see p. 100). However, in non-lactating mothers, a diet as in non-pregnant is enough.

CARE OF THE BLADDER: The patient is encouraged to pass urine following de livery as soon as convenient. At times, the patient

fails to pass urine and the causes are — (1) Unaccustomed position and (2) Reflex pain from the perineal injuries. This is common

after a difficult labor or a forceps delivery. If the patient still fails to pass urine, c atheterization should be done. Catheterization is

also indicated in case of incomplete emptying of the bladder evidenced by the presence of residual urine of more than 60 mL.

Continuous drainage is kept until the bladder tone is regained. The underlying princ iple of the bladder care is to ensure adequate

drainage of urine so that infection and cystitis are avoided.

CARE OF THE BOWEL: The problem of constipation is much less because of early a mbulation and liberalization of the dietary

intake. A diet containing sufficient roughage and fluids is enough to move the bowel. If necessary, mild laxative such as isabgol husk 2

teaspoons may be given at bed time.

SLEEP: The patient is in need of rest, both physical and mental. So she sho uld be protected against worries and undue fatigue. Sleep

is ensured providing adequate physical and emotional support. If there is any discomfo rt, such as after pains or painful piles or engorged

breasts, they should be dealt with adequate analgesics (Ibuprofen).

CARE OF THE VULVA AND EPISIOTOMY WOUND: Shortly after delivery, the vu lva and buttocks are washed with soap water

down over the anus and a sterile pad is applied. The patient should look after personal cleanliness of the vulval region. The perineal

wound should be dressed with spirit and antiseptic powder after each act of micturition a nd defecation or at least twice a day. The nurse

should use sterilised gloves during dressing. Cold (ice) sitz baths relieve pain. W hen the perineal pain is persistent, a vaginal and rectal

examination is done to detect any hematoma, wound gaping or infection. For pain Ibuprofen is safe for nursing mothers.

CARE OF THE BREASTS: The nipple should be washed with sterile water before each feeding . It should be cleaned and kept dry

after the feeding is over. A nursing brassiere provides comfortable support. Nipple soreness is avoided by frequent short feedings rather

than the prolonged feeding, keeping the nipples clear and dry. Candida infection may b e another cause (see p. 439).

Nipple confusion is a situation where the infant accepts the artificial nipple but refuses the mother’s nipple. This is avoided by making

the mother’s nipple more protractile and not offering any supplemental fluids to the infant.

MATERNAL–INFANT BONDING (ROOMING-IN): It starts from first few moments after birth. This is manifested by f ondling,

kissing, cuddling and gazing at the infant. The baby should be kept in her bed or in a c ot besides her bed. This not only establishes the

mother-child relationship but the mother is conversant with the art of baby care so that she can ta ke full care of the baby while at home.

Baby, friendly hospital initiative (see p. 449) promotes parent-infant-bonding, baby roo ming with the mother and breastfeeding.

ASEPSIS AND ANTISEPTICS: Asepsis must be maintained especially duri ng the first week of puerperium. Liberal use of local

antiseptics, aseptic measures during perineal wound dressing, use of clean bed linen and clothings are positive steps. Clean surroundings

and limited number of visitors could be of help in reducing nosocomial infect ion.

IMMUNISATION: (i) Administration of anti–D–gamma globulin to unimmunized Rh–negativ e mother bearing Rh–positive baby (see

details in chapter 22). (ii) Women who are susceptible to rubella can be vaccinated safe ly with live attenuated rubella virus. Mandatory

postponement of pregnancy for at least two months following vaccination can easily be achieve d. (iii) The booster dose of tetanus toxoid

should be given at the time of discharge, if it is not given during pregnancy.

MANAGEMENT OF AILMENTS

• After pain— It is the infrequent,spasmodic pain felt in t he lower abdomen after delivery for a variable period of 2–4 days.

Presence of blood clotsor bits of the after births lead to hypertonic contractions of the uterus in an attemp t to expel them out. This is

commonly met in primipara. The pain may also be due to vigorous uterine contrac tion especially in multipara. The mechanism of pain is

similar to cardiac anginal pain induced by ischemia. Both the types are excited during br eastfeeding. The treatment includes massaging

the uterus with expulsion of the clot followed by administration of analgesics (Ibuprofe n) and antispasmodics.

• Pain on the perineum: Never forget to examine the perineum when analgesic is given to relieve pain. Early detection of vulvo-

vaginal hematoma can thus be made. Sitz baths (hot or cold) can give additional pain re lief.

• Correction of anemia: Majority of the women in the tropics remain in an anemic state following delivery. Supplementary iron therapy

(ferrous sulfate 200 mg) is to be given daily for a minimum period of 4–6 weeks.

• Hypertension is to be treated until it comes to a normal limit. The physician should be consulted if proteinuria persists.

TO MAINTAIN A CHART (Fig.13.4): A progress chart is to be maintained notin g the following: (1) Pulse, respiration and

temperature recording 6 hourly or at least twice a day (2) Measurement of the height o f the uterus above the symphysis pubis once a day

in a fixed time with prior evacuation of the bladder and preferably the bowel too (3) C haracter of the lochia (4) Urination and bowel

movement.

POSTPARTUM EXERCISE: The objectives of postpartum exercises are: (1) To improv e the muscle tone, which are stretched

during pregnancy and labor especially the abdominal and perineal muscles. (2) To edu cate about correct posture to be attained when the

patient is getting up from her bed. This also includes the correct principle of lif ting and working positions during day-to-day activities.

Advantages gained thereby are: (1) To minimize the risk of puerperal venous thrombosis by promoting arterial circulation and

preventing venous stasis (2) To prevent backache (3) To prevent genital prolapse and stress i ncontinence of urine.

PROCEDURE: (1) Initially, she is taught breathing exercise and leg movemen ts lying in bed. (2) Gradually, she is instructed to tone up

the abdominal and perineal muscles and to correct the postural defects. These can well b e taught by a trained physiotherapist. The

exercise should be continued for at least 3 months. The common exercises presc ribed are: (a) To tone up the pelvic floor muscles:

The patient is asked to contract the pelvic muscles in a manner to withhold the

Fig. 13.4: A composite chart to note the important clinical events in the puerperium

act of defecation or urination and then to relax. The process is to be repeated as often a s possible each day. (b) To tone up the

abdominal muscles: The patient is to lie in dorsal position with the knees bent and the feet flat on t he bed. The abdominal muscles are

contracted and relaxed alternately and the process is to be repeated several times a day. (c) To tone up the back muscles: The patient is

to lie on her face with the arms by her side. The head and the shoulders are slowly mov ed up and down. The procedure is to be repeated

3–4 times a day and gradually increased each day.

Physical activity should be resumed without delay. Sexual activity may be resume d (after 6 weeks) when the perineum is comfortable

and bleeding has stopped. Some women may get “flaring response of some autoimmun e disorders due to rebound effect of the immune

suppression during pregnancy (see p. 636).

CHECK-UP AND ADVICE ON DISCHARGE: A thorough check-up of the mother a nd the baby is mandatory prior to discharge of

the patient from the hospital. Discharge certificate should have all the important informat ion as regard the mother and baby.

Advices include: (1) Measures to improve her general health. Continuance of supplementary i ron therapy (2) Postnatal exercises (3)

Procedures for a gradual return to day-to-day activities (4) Breastfeeding and care of the newborn (5) Avoidance of intercourse for a

reasonable period of 4–6 weeks until lacerations or episiotomy wound are well healed (6) Fam ily planning advice and guidance —

Non-lactating women should practice some form of contraceptive meas ures after 3 weeks and the lactating women should start 3

months after delivery (7) To have postnatal check up after 6 weeks.

The method of contraception will depend upon breastfeeding status, state of h ealth and number of children (see p. 537). Natural

methods cannot be used until menstrual cycles are regular. Exclusive breastfeedin g provides 98% contraceptive protection for 6 months.

Barrier methods (see p. 534) may be used. Steroidal contraceptions — combined preparations are suitable for nonlactating women

and should be started 3 weeks after. In lactating women it is avoided due to its suppressive effects (see p. 549). Progestin only pill may

be a better choice for them. Other progestins (DMPA, Levonorgestrel implants (see p. 550) m ay be used. IUDs are also a satisfactory

method irrespective of breastfeeding status. Sterilization (puerperal) is suitable for those who have compl eted their families.

POSTNATAL CARE

Postnatal care includes systematic examination of the mother and the baby and appropriate advice given to the mother during

postpartum period. The first postnatal examination is done and the advice is given on discharge of the patient from the hospital. This

has already been discussed. The second routine postnatal care is conducted a t the end of 6th week postpartum.

AIMS AND OBJECTIVES:

• To assess the health status of the mother. Medical disorders like diabetes, hype rtension should be reassessed.

• To detect and treat at the earliest any gynecological condition arising out of ob stetric legacy.

• To note the progress of the baby including the immunization schedule for the infant (see p. 455).

• To impart family planning guidance (discussed above).

PROCEDURE:• Examination of the mother • Advice given to th e mother • Examination of the baby and advice Examination of

the Mother:

• Routine examination includes recording weight, pallor, blood pressure and tone of the abdominal muscles and examination of the

breasts.

• Pelvic examination should be done only when indicated. The following should be noted: A ce rvical smear may be taken for

exfoliative cytological examination if this has not been done previously and insertion o f intrauterine contraceptive device may be done

when desired.

• Laboratory investigations (e.g. hemoglobin) depending on the clinical need may be advised.

Examination of the baby: This should be conducted by a pediatrician. In this respect, an att ached well baby clinic to the postpartum

unit is an absolute necessity. The progress of the baby is evaluated and preventive or curative steps are to be taken. Immunization to the

baby is started (see p. 455).

Advices given: General — (1) If the patient is in sound health she is allowed to do her u sual duties. (2) Postpartum exercises may be

continued for another 4–6 weeks. (3) To evaluate the progress of the baby periodical ly and to continue breastfeeding for 6 months.

Family planning counseling and guidance — (discussed above and also see p. 558).

Management of ailments: Additional investigation and appropriate therapy is given acco rding to the abnormalities detected during

check up. Management of some common gynecological problems are given below. Some wome n need psychological support also

(see p. 442).

• Irregular vaginal bleeding:It is not uncommon to encounter irregular o r at times, heavy bleeding after 4–6 weeks following an

uneventful period after delivery. This is usually the first period especially in non-lactatin g women and simple assurance is enough.

Persistence of bleeding dating back from childbirth is likely due to retained bits of conce ptus and usually requires ultrasound examination

followed by dilatation and curettage operation.

• Leukorrhea: Profuse white discharge might be due to ill health, vaginitis , cervicitis or subinvolution. Improvement of the general

health and specific therapy cure the condition.

• Cervical ectopy (erosion) met during this period without any symptom should not be tr eated surgically. Hormone induced ectopy

during pregnancy takes a longer time (about 12 weeks) to regress. Thus, asymptomatic ectop y should be examined again after 6

weeks and if it still persists, cauterization is to be considered.

• Backache: It is mostly due to sacroiliac or lumbosacral strain. Backache situated over the sacrum is likely due to pelvic pathology,

but if it is over the lumbar region, it might be due to an orthopedic condition and is often relieved by physiotherapy.

• Retroversion seldom produces backache. If associated with subinvolutio n with symptoms, a pessary is inserted after correcting the

position and is to be kept about 2 months.

• Slight degree of uterine descentwith cystocele, stress incontinence and relaxe d perineum are the common findings at this stage. These

can be cured by effective pelvic floor exercise. However,if the prolapse is marke d, effective surgery should be done after three

months.

Vomiting in Pregnancy

Vomiting is a symptom which may be related to pregnancy or may be a manifestation o f some medicalsurgical-gynecological

complications, which can occur at any time during pregnancy. The former is by far the commonest one and is called vomiting of

pregnancy. The causes of vomiting in pregnancy can be classified as follows:

A. Early pregnancy:

I. Related to pregnancy (vomiting of pregnancy)

(i) Simple vomiting (morning sickness, emesis

gravidarum)

(ii) Hyperemesis gravidarum (pernicious vomiting)

II. Associated with pregnancy (see table below)

B. Late pregnancy:

I. Related to pregnancy

(i) Continuation or reappearance of simple vomiting of pregnancy

(ii) Acute fulminating preeclampsia

II. Associated with pregnancy (see table below)

(i) Medical-surgical-gynecological causes in early

pregnancy (ii) Hiatus hernia

Medical

(i) Intestinal infestation

(ii) Urinary tract infection

(iii) Hepatitis

(iv) Ketoacidosis of diabetes

(v) Uremia

Surgical Gynecological (i) Appendicitis (i) Twisted ovarian tumor (ii) Peptic ulcer (ii) Red degener ation of fibroid (iii) Intestinal

obstruction

(iv) Cholecystitis

VOMITING IN PREGNANCY

The vomiting is related to the pregnant state and depending upon the severity, it is classif ied as: (i) Simple vomiting of pregnancy or

milder type (ii) Hyperemesis gravidarum or severe type.

SIMPLE VOMITING (Syn: morning sickness, emesis gravidarum) : The patient complains of nausea and occasional sickness on rising

in the morning. Slight vomiting is so common in early pregnancy (about 50%) that it is considered as a symptom of pregnancy. It may,

however, occur at other times of the day. The vomitus is small and clear or bile stained . It does not produce any impairment of health or

restrict the normal activities of the women. The feature disappears with or without trea tment by 12-14th week of pregnancy. High level of

serum human chorionic gonadotropin, estrogen and altered immunological states are co nsidered responsible for initiation of the

manifestation, which is probably aggravated by the neurogenic factor.

Management: Assurance is important. Taking of dry toast or biscuit and avoidance of fatty and spicy foods are enough to relieve the

symptoms in majority. If the simple measures fail, antiemetic drugs — trifluoperazine (E spazine) 1 mg twice daily and phenobarbitone

30-60 mg tab at bed time are quite effective. Patient is advised to take plenty of fluids (2.5 L in 24 hours) and fruit juice.

HYPEREMESIS GRAVIDARUM

DEFINITION: It is a severe type of vomiting of pregnancy which has got deleterious effect on the health of the mother and/or

incapacitates her in day-to-day activities. The adverse effects of severe vomiting are— dehy dration, metabolic acidosis (from

starvation) or alkalosis (from loss of hydrochloric acid), electrolyte imbalance (hypoka lemia) and weight loss.

INCIDENCE: There has been marked fall in the incidence during the last 30 years . It is now a rarity in hospital practice (less than 1 in

1000 pregnancies). The reasons are — (a) Better application of fa mily planning knowledge which reduces the number of unplanned

pregnancies, (b) early visit to the antenatal clinic and (c) potent antihistaminic, antiemetic drugs.

ETIOLOGY: The etiology is obscure but the following are the known facts: (1) It is mostly limited to the first trimester (2) It is

more common in first pregnancy, with a tendency to recur again in subsequent pregna ncies (3) It has got a familial history — mother and

sisters also suffer from the same manifestation (4) It is more prevalent in hydatidiform mole and multiple pregnancy (5) It is more

common in unplanned pregnancies but much less amongst illegitimate ones.

THEORIES: (1) Hormonal—(a) Excess of chorionic gonadotropin or higher biological activity of hCG is associated. This is proved by

the frequency of vomiting at the peak level of hCG and also the increased association w ith hydatidiform mole or multiple pregnancy

when the hCG titer is very much raised (b) High serum level of estrogen (c) Progester one excess leading to relaxation of the cardiac

sphincter and simultaneous retention of gastric fluids due to impaired gastric motility. Oth er hormones involved are: thyroxin, prolactin,

leptin and adrenocortical hormones.

(2) Psychogenic: It probably aggravates the nausea once it begins. But neur ogenic element sometimes plays a role, as evidenced by its

subsidence after shifting the patient from the home surroundings. Conversion disorder, somatization, excess perception of sensations by

the mother are the other theories.

(3) Dietetic deficiency: Probably due to low carbohydrate reserve, as it happens after a night without food. Deficiency of vitamin B

, Vit

and proteins may be the effects rather than the cause.

(4) Allergic or immunological basis. (5) Decreased gastric motility is found to cause nausea.

Whatever may be the cause of initiation of vomiting, it is probably aggravated by the ne urogenic element. Unless it is not quickly

rectified, features of dehydration and carbohydrate starvation supervene and a vicious cycle of vomiting appears — vomiting →

carbohydrate starvation → ketoacidosis → vomiting.

PATHOLOGY: There is no specific morbid anatomical findings. The changes in the various organs as described by Sheehan are the

generalized manifestations of starvation and severe malnutrition.

Liver: There is centrilobular fatty infiltration without necrosis.

Kidneys: Usually normal with occasional findings of fatty change in the cells of fir st convoluted tubule, which may be related to acidosis.

Heart: A small heart is a constant finding. There may be subendocardial hem orrhage.

Brain: Small hemorrhages in the hypothalamic region giving the manifestation of Wernicke’s encephalopathy. The lesion may be related

to vitamin B

deficiency.

METABOLIC, BIOCHEMICAL AND CIRCULATORY CHANGES: The changes are due to the combined effect of dehydration

and starvation consequent upon vomiting.

Metabolic: Inadequate intake of food results in glycogen depletion. For the energy supp ly, the fat reserve is broken down. Due to low

carbohydrate, there is incomplete oxidation of fat and accumulation of ketone bodies in the blood. The acetone is ultimately excreted

through the kidneys and in the breath. There is also increase in endogenous tissue prote in metabolism resulting in excessive excretion of

non-protein nitrogen in the urine. Water and electrolyte metabolizm are seriously affect ed leading to biochemical and circulatory

changes.

Biochemical: Loss of water and salts in the vomitus results in fall in plasma sodium, po tassium and chlorides. The urinary chloride may

be well below the normal 5 g/liter or may even be absent. Hepatic dysfunction results in acidosis and ketosis with rise in blood urea and

uric acid; hypoglycemia; hypoproteinemia; hypovitaminosis and rarely hyperbilirubinem ia.

Circulatory: There is hemoconcentration leading to rise in hemoglobin percentage, R BC count and hematocrit values. There is slight

increase in the white cell count with increase in eosinophils. There is concomitant reducti on of extracellular fluid.

156 TEXTBOOK OF OBSTETRICS CLINICAL COURSE

From the management and prognostic point of view, the cases are grouped into:

• Early • Late (moderate to severe)

The patient is usually a nullipara, in early pregnancy. The onset is insidious.

EARLY: Vomiting occurs throughout the day. Normal day-to-day activities are curtailed. There is no evidence of dehydration or

starvation.

LATE: (Evidences of dehydration and starvation are present).

Symptoms: Vomiting is increased in frequency with retching. Urine quantity is dimin ished even to the stage of oliguria. Epigastric pain,

constipation may occur. Complications may appear (see below) if not treated.

Signs: Features of dehydration and ketoacidosis: Dry coated tongue, sunken eye s, acetone smell in breath, tachycardia, hypotension,

rise in temperature may be noted, jaundice is a late feature. Such late cases are rarely se en these days. Vaginal examination and/or

ultrasonography is done to confirm the diagnosis of pregnancy.

Investigations:

• Urinalysis: (1) Quantity—small (2) Dark color (3) High specific gra vity with acid reaction (4) Presence of acetone, occasional

presence of protein and rarely bile pigments (5) Diminished or even absence of chloride.

• Biochemical and circulatory changes: The changes are mentioned previously. Ro utine and periodic estimation of the serum

electrolytes (sodium, potassium and chloride) is helpful in the management of the case.

• Ophthalmoscopic examination is required if the patient is seriously ill. Retinal hemor rhage and detachment of the retina are the most

unfavorable signs.

• ECG when there is abnormal serum potassium level.

DIAGNOSIS: The pregnancy is to be confirmed first. Thereafter, all the associated cause s of vomiting (enumerated before) are to be

excluded. Ultrasonography is useful not only to confirm the pregnancy but also to exclude other, obstetric (hydatidiform mole, multiple

pregnancy), gynecological, surgical or medical causes of vomiting (see p. 155).

Differential diagnosis: When vomiting is persistent in spite of usual treatment other causes of sev ere vomiting (medical or surgical)

should be considered (p. 154) and investigated.

COMPLICATIONS: The majority of the clinical manifestations are due to the effects of dehydration and starvation with resulting

ketoacidosis. Leaving aside those symptomatology, the following complications may occur which are fortunately rare now-a-days. (1)

Neurologic complications — (a) Wernicke’s encephalopathy due to thiamine deficiency (b) Pon tine myelinolysis (c) Peripheral neuritis

(d) Korsakoff’s psychosis. (2) Stress ulcer in stomach (3) Esophageal tear (Mallory-W eiss syndrome) (4) Jaundice (5) Convulsions and

(6) Coma and (7) Renal failure.

PREVENTION: The only prevention is to impart effective management to correct sim ple vomiting of pregnancy.

MANAGEMENT

The principles in the management are:

• To control vomiting

• To correct the fluids and electrolytes imbalance

• To correct metabolic disturbances (acidosis or alkalosis)

• To prevent the serious complications of severe vomiting • Case o f pregnancy.

Hospitalization: Whenever a patient is diagnosed as a case of hyperemesis gravida rum, she is admitted. Surprisingly, with the same diet

and drugs used at home, the patient improves rapidly. The relatives may be too sympathetic or too indifferent.

Fluids: Oral feeding is withheld for at least 24 hours after the cessation of vomiting. Du ring this period, fluid is given through

intravenous drip method. The amount of fluid to be infused in 24 hours is calculated as f ollows: The total amount of fluid

approximates 3 liters, of which half is 5% dextrose and half is Ringer’s solution. Extra amo unt of 5% dextrose equal to the amount of

vomitus and urine in 24 hours, is to be added. With thisregime — dehydration, ketoa cidosis, water andelectrolyteimbalance are likely

tobe rectified.Serum electrolyte should be estimated and corrected if there is any abnorm ality. Enteral nutrition through nasogastric tube

may also be given.

Drugs:

(a) Antiemetic drugs promethazine (Phenergan) 25 mg or prochlorperazine (Stemetil) 5 mg or trifluopromaz ine (Siquil) 10 mg may

be administered twice or thrice daily intramuscularly. Trifluoperazine (Espazine) 1 mg twice daily intramuscularly is a potent antiemetic

therapy. Vitamin B

and doxylamine are also safe and effective. Metoclopramide stimulates gastric and intestinal m otility without

stimulating the secretions. It is found useful.

(b) Hydrocortisone 100 mg IV in the drip is given in a case with hypo tension or in intractable vomiting. Oral method prednisolone is

also used in severe cases.

, Vit B

, Vit C and Vit B

are given.

Nursing care: Sympathetic but firm handling of the patient is essential. Social and psychological support should be extended.

Hyperemesis progress chart is helpful to assess the progress of patient while in hospi tal. Daily record of pulse, temperature, blood

pressure at least twice daily, intake-output, urine for acetone, protein, bile, blood biochemistry and ECG (when serum potassium is

abnormal) are important.

Clinical features of improvement are evidenced by — (a) subsidence of vomiting (b) feeling of hunger (c) better lo ok (d)

disappearance of acetone from the breath and urine (e) normal pulse and blood pressu re and (f) normal urine output.

Diet: Before the intravenous fluid is omitted, the foods are given orally. At first, dry ca rbohydrate foods like biscuits, bread and toast are

given. Small but frequent feeds are recommended. Gradually full diet is restored.

Termination of pregnancy is rarely indicated. Intractable hyperemesis gravidarum inspite of the rapy is rare these days.

SUMMARY

Excessive vomiting of pregnancy incapacitating the day-to-day activities and/or de teriorating the health of the mother is called

hyperemesis gravidarum. It is rare now-a-days (1 in 1000). It is common in first birth a nd limited to early pregnancy. The exact cause

is not known but once vomiting starts, probably neurogenic elements aggravate the state. The morbid pathological changes are due to

starvation. The clinical manifestations are due to the effect of dehydration, starvation and ketoacidosis. If not rectified promptly,

the condition may turn fatal. Management consists of hospitalisation, sym pathetic but firm handling of the patient, antiemetic drugs,

replacement of fluids by infusion, correction of electrolyte imbalance and supply of glu cose to protect the liver and vitamin supplement.

Intractable hyperemesis gravidarum in spite of therapy is rare these days. Termination o f pregnancy is rarely indicated.

Hemorrhage in Early Pregnancy

The causes of bleeding in early pregnancy are broadly divided into two groups:

• Those related to the pregnant state: This group relates to abortion (95%) , ectopic pregnancy, hydatidiform mole and implantation

bleeding.

• Those associated with the pregnant state: The lesions are unrelated to pregnancy—either pre-exist ing or aggravated during

pregnancy. Cervical lesions such as vascular erosion, polyp, ruptured varicose veins and malignancy are important causes. These

gynecological lesions in relation to pregnancy are discussed in chapter 20.

SPONTANEOUS ABORTION (MISCARRIAGE)

DEFINITION: Abortion is the expulsion or extraction from its mother of an embryo or fetus weighing 500 g or less when it is not

capable of independent survival (WHO). This 500 g of fetal development is attained ap proximately at 22 weeks (154 days) of

gestation. The expelled embryo or fetus is called abortus. The term miscarriage is the recomme nded terminology for spontaneous

abortion.

INCIDENCE: The incidence of abortion is difficult to work out but probably 10–2 0% of all clinical pregnancies end in miscarriage and

another optimistic figure of 10% are induced illegally. 75% abortions occur b efore the 16th week and of these, about 75% occur

before the 8th week of pregnancy.

CLASSIFICATION OR VARIETIES:

ETIOLOGY

The etiology of miscarriage is often complex and obscure. The following factors (embr yonic or parental) are important: • Genetic

• Immunological

• Endocrine and metabolic • Anatomic • Infection

• Antifetal antibodies • Thrombophilias • Others

GENETIC FACTORS: Majority (50%) of early miscarriages are due to ch romosomal abnormality in the conceptus. Autosomal

trisomy is the commonest (50%) cytogenetic abnormality. Trisomy for every chromosome has been reported. The most common

trisomy is trisomy 16 (30%). Polyploidy has been observed in about 22% of abortuses. (Po lyploidy refers to the presence of three or

more multiples of a haploid number of chromosome, e.g. 3n = 69, 4n = 92. Triploidy is more common than tetraploidy). Monosomy X

(45X) is the single most common chromosomal abnormality in miscarriages (20%). Struct ural chromosomal rearrangements are

observed in 2–4% of abortuses. These includes translocation, deletion, inversion a nd ring formation.Other chromosomal abnormalities

like mosaic, double trisomy, etc. are found in about 4% of abortuses.

ENDOCRINE AND METABOLIC FACTORS (10–15%): Luteal P hase Defect (LPD) results in early miscarriage as implantation

and placentation are not supported adequately. Deficient progesterone secret ion from corpus luteum or poor endometrial response to

progesterone is the cause. Thyroid abnormalities: Overt hypothyroidism or hyperthyroidism are asso ciated with increased fetal loss.

Thyroid auto antibodies are often increased. Diabetes mellitus when po orly controlled causes increased miscarriage.

ANATOMICAL ABNORMALITIES (10–15%)

• Cervicouterine factors: These are related mostly to the second trimester abortio ns. (1) Cervical incompetence, either congenital or

acquired is one of the commonest cause of midtrimester and recurrent abortion. (2) Congenital malformation of the uterus in the form

of bicornuate or septate uterus may be responsible for midtrimester recurrent abortion. Causes of fetal loss are: (i) Reduced intrauterine

volume (ii) Reduced expansile property of the uterus (iii) Reduced placental vascularity when implanted on the septum (iv) Increased

uterine irritability and contractility. (3) Uterine (fibroid) specially of the submucous variety migh t be responsible not only for infertility

but also for abortion. This is due to distortion or partial obliteration of the uterine cav ity. Other causes are: decreased vascularity at the

implantation site, red degeneration of fibroid and increased uterine irritability. (4) Intrauter ine adhesions (synechiae) interfere with

implantation, placentation and fetal growth. Depending on the severity of adhesions, e.g. total (A sherman’s syndrome), corporal or

cervicoisthmic, patient suffers from amenorrhea, hypomenorrhea, infertility or recurren t abortion.

INFECTIONS (5%) —are the accepted causes of late as well as earl y abortions. Transplacental fetal infections occur with most

microorganisms and fetal losses could be caused by any. Infections could be—(i) Viral: Rubella, cytomegalo, variola, vaccinia or HIV.

(ii) Parasitic: Toxoplasma, Malaria. (iii) Bacterial: Ureaplasma, chlamydia, brucella. Spiroch etes hardly cause abortion before 20th

week because of effective thickness of placental barrier.

IMMUNOLOGICAL DISORDERS (5–10%) —Both autoimmune and alloimmune factors can cause miscarriage (p. 634).

• Autoimmune disease—can cause miscarriage usually in the second tri mester. These patients form antibodies against their own tissue

and the placenta. These antibodies ultimately cause rejection of early pregnancy. Antibo dies responsible are: (i) Antinuclear antibodies

(ANAs); (ii) Anti-DNA antibodies (double or single stranded); (iii) Antiphospholipid an tibodies includes lupus anticoagulant (LAC) and

anticardiolipin antibodies (aCL). Spiral artery and placental intervillous thrombosis, place ntal infarction and fetal hypoxia is the ultimate

pathology (p. 342) to cause abortion.

• Alloimmune disease (see p. 167, 342, 634). Paternal antigens which are foreign to the mother invoke a protective blocking antibody

response. These blocking antibodies prevent maternal immune cells from recognizing th e fetus as a foreign entity. Therefore, the fetal

allograft containing foreign paternal antigens are not rejected by the mother. Paternal h uman leukocyte antigen (HLA) sharing with the

mother leads to diminished fetal-maternal immunologic interaction and ultimately fetal rejection (abortion).

• Antifetal antibodies are deleterious to cause fetal loss as found in cases with Rh-negative women with anti-D antibodies. T-helper 1

(Th-1) cytokines (tumor necrosis factor), Interleukin (IL-2), and Interferon (gamma) (IFNγ) are deleterious whereas T-helper 2 cytokines

(IL-4, 5, 6, 10) are not. Down regulation of Th-1 cytokines by progesterone may imp rove fetal outcome. Activated NK cells damage the

placental trophoblast cells to cause abortion (p. 36).

• Maternal medical illness (see p. 260): Cyanotic heart disease, hemoglobinopathie s are associated with early abortion.

BLOOD GROUP INCOMPATIBILITY: Incompatible ABO group matings may b e responsible for early pregnancy wastage and often

recurrent but Rh incompatibility is a rare cause of death of the fetus before 28th week . Couple with group ‘A’ husband and group

‘O’ wife have got higher incidence of abortion.

PREMATURE RUPTURE OF THE MEMBRANES inevitably leads to abortion.

Paternal factors : Sperm chromosomal anomaly (translocation) can cause miscarriage. S ome women who miscarry recurrently may

have normal pregnancies following marriage with a different man.

Thrombophilias:Inherited thrombophilia (see p. 275, 343, 439) causes both early and late mis carriages due to intravascular

coagulation. Protein C resistance (factor V Leiden mutation) is the most common cause. Other conditions are: Protein C deficien cy

and hyperhomocysteinemia (p. 167).

ENVIRONMENTAL FACTORS: Conclusions relating to environmental f actors are difficult to establish.

Cigarette smoking—increases the risk due to formation of carboxy hemoglobin and decreased oxygen transfer to the fetus. Alcohol

consumption should be avoided or minimized during pregnancy. X-Irradiation and an tineoplastic drugs are known to cause abortion. X-

ray exposure upto 10 rad is of little risk. Contraceptive agents—IUD in situ i ncreases the risk whereas oral pills do not. Drugs,

chemicals, noxious agents—anesthetic gases, arsenic, aniline, lead, formaldeh yde increase the risk. Miscellaneous—Exposure to

electromagnetic radiation from video display terminals (VDTs) does not increase the risk . Women can use hair dyes, watch television

and fly in airlines during pregnancy (p. 100).

UNEXPLAINED (40–60%): Inspite of the numerous factors mentioned, it is indeed diffic ult, in the majority, to pinpoint the exact

cause of miscarriage. Too often, more than one factor is present. However, risk of abo rtion increases with increased maternal age. About

22% of all pregnancies detected by urinary hCG (periimplantation) are lost, before the clinical diagnosis.

COMMON CAUSES OF MISCARRIAGE:

First trimester: (1) Genetic factors (50%). (2) Endocrine disorders (LPD, thyroid abnormali ties, diabetes). (3) Immunological disorders

(Autoimmune and Alloimmune). (4) Infection and (5) Unexplained.

Second trimester: (1) Anatomic abnormalities—(a) Cervical incompetence (congenita l or acquired). (b) Mullerian Fusion defects

(Bicornuate uterus, septate uterus). (c) Uterine synechiae. (d) Uterine fibroid. (2) Maternal medical illness and (3) Unexplained.

MECHANISM OF MISCARRIAGE: In the early weeks, death of the ovum occurs first, followed by its expulsion. In the later weeks,

maternal environmental factors are involved leading to expulsion of the fetus which ma y have signs of life but is too small to survive.

• Before 8 weeks: The ovum, surrounded by the villi with the decidual coverings, is expelled ou t intact. Sometimes, the external os fails

to dilate so that the entire mass is accommodated in the dilated cervical canal and is called ce rvical miscarriage (Fig. 15.1).

Fig. 15.1: Cervical miscarriage

• 8–14 weeks: Expulsion of the fetus commonly occurs leaving behind the placenta and the membranes. Apart of it may be partially

separated with brisk hemorrhage or remains totally attached to the uterine wal l.

• Beyond 14th week: The process of expulsion is similar to that of a “mini labor”. Th e fetus is expelled first followed by expulsion of the

placenta after a varying interval.

THREATENED MISCARRIAGE

DEFINITION:It is a clinical entity where the process of miscarriage has started but ha s not progressed to a state from which

recovery is impossible [Fig. 15.2A].

CLINICAL FEATURES:

The patient, having symptoms suggestive of pregnancy, complains of:

(1) Bleeding per vaginam is usually slight and may be brownish or bright re d in color. On rare occasion, the bleeding may be brisk,

specially in the late second trimester. The bleeding usually stops spontaneously.

(2) Pain: Bleeding is usually painless but there may be mild backache or dull pain i n lower abdomen. Pain appears usually following

hemorrhage.

Pelvic examination should be done as gently as possible. (a) Speculum examination reveals— bleeding if any, escapes through the

external os. Differential diagnosis includes cervical ectopy, polyps or carcinoma, ec topic pregnancy and molar pregnancy. (b) Digital

examination reveals the closed external os (Fig. 15.2A). The uterine size corresponds to the period of amenorrhea. The uterus and cervix

feel soft. Pelvic examination is avoided when ultrasonography is available (see below) .

INVESTIGATIONS:

Routine investigations include : (1) Blood—for hemoglobin, hematocrit, ABO and R h grouping. Blood transfusion may be required if

abortion becomes inevitable and anti-D gamma globulin has to be given in Rh negative non-immunized women. (2) Urine for

immunological test of pregnancy is not helpful as the test remains positive for a v ariable period even after the fetal death.

Ultrasonography (TVS) findings may be: (1) A well formed gestation ring with central ec hoes from the embryo indicating healthy fetus

(see p. 625) (2) Observation of fetal cardiac motion. With this, there is 98% chance of continuation of pregnancy (3) A blighted ovum is

evidenced by loss of definition of the gestation sac, smaller mean gestational sac diameter, a bsent fetal echoes and absent fetal cardiac

movements (Fig. 15.1A).

Serum progesterone value of 25 ng/mL or more generally indicates a viable pregnancy in about 95% of cases. Serial serum chorionic

gonadotropin (hCG) level is helpful to assess the fetal well being. Ectopic pregnancy mus t be ruled out during investigations (p. 182).

TREATMENT:

Rest : The patient should be in bed for few days until bleeding stops. Prolonged restriction of activity has got no therapeutic value.

Drugs: Relief of pain may be ensured by diazepam 5 mg tablet twice daily.

There is no evidence that treatment with natural progesterone or synthetic progestins imp roves the prognosis, on the contrary, there is a

probability of having a missed abortion. Initial study suggests that use of hCG improves pregnancy outcome.

ADVICE ON DISCHARGE: The patient should limit her activities for at least two weeks an d avoid heavy work. Coitus is avoided

during this period. She should be followed up with repeat sonography at 3–4 weeks tim e. The following indicates unfavorable

outcome: falling serum βhCG, decreasing size of the fetus, irregular shape of the gestational sac or decreasing feal heart rate.

PROGNOSIS: The prognosis is very unpredictable. In isolated spontaneous th reatened miscarriage, the following events may

occur. (1) In about two-third, the pregnancy continues beyond 28 weeks. (2) In the rest, it terminates either as inevitable or missed

miscarriage. If the pregnancy continues, there is increased frequency of preterm labor, placenta previa, intrauterine growth

restriction of the fetus and fetal anomalies.

Blighted ovum (silent miscarriage Fig. 15.1A): It is a sonographic diagnosis. There is absence of fetal pole in a gestational sac with

diameter of 3 cm or more. Uterus is to be evacuated once the diagnosis made.

Fig. 15.1A: Ultrasonographic picture of blighted ovum

INEVITABLE MISCARRIAGE

DEFINITION:It is the clinical type of abortion where the changes have progressed to a state from where continuation of

pregnancy is impossible.

CLINICAL FEATURES: The patient, having the features of threatened misca rriage, develops the following manifestations. (1)

Increased vaginal bleeding (2) Aggravation of pain in the lower abdomen which may be colicky in nature (3) Internal examination

reveals dilated internal os of the cervix through which the products of conception are felt (F ig. 15.2). On occasion, the features may

develop quickly without prior clinical evidence of threatened miscarriage. In the second trimester, however, it may start with rupture of

the membranes or intermittent lower abdominal pain (mini labor).

MANAGEMENT is aimed: (a) to accelerate the process of expulsion (b) to maintain strict asepsis (p. 563). General measures:

Excessive bleeding should be promptly controlled by administering methergin 0.2 mg if the cervix is dilated and the size of the uterus is

less than 12 weeks. The blood loss is corrected by intravenous fluid therapy and blood transfu sion.

Active Treatment:

• Before 12 weeks:(1) Dilatation and evacuation followed by curettage of the uter ine cavity by blunt curette using analgesia or under

general anesthesia (2) Alternatively, suction evacuation followed by curettage i s done.

• After 12 weeks: (1) The uterine contraction is accelerated by oxytocin drip (10 units in 500 mL of normal saline) 40–60 drops per

minute. If the fetus is expelled and the placenta is retained, it is removed by ovum force ps, if lying separated. If the placenta is not

separated, digital separation followed by its evacuation is to be done under general anes thesia.

COMPLETE MISCARRIAGE

DEFINITION:When the products of conception are expelled en masse, it is called complete miscarriage .

CLINICAL FEATURES: There is history of expulsion of a fleshy mass per vaginam followed by: (1) Subsidence of abdominal pain.

(2) Vaginal bleeeding becomes trace or absent (3) Internal examination reveals: (a) Uterus i s smaller than the period of amenorrhea

and a little firmer (b) Cervical os is closed (c) Bleeding is trace. (4) Examination of the expelled fleshy mass is found complete.

MANAGEMENT: Transvaginal sonography is useful to see that uterine cavity is empty, otherwise evacuation of uterine curettage

should be done.

Rh-NEGATIVE WOMEN: A Rh—negative patient without antibody in her system shou ld be protected by Anti-D gamma globulin-50

microgram or 100 microgram intramuscularly in cases of early miscarriage or late misca rriage respectively within 72 hours. However,

Anti-D may not be required in a case with complete miscarriage before 12 weeks gesta tion where no instrumentation has been done.

A B C

Figs 15.2A to C: (A) Threatened miscarriage; (B) Inevitable miscarriage; (C) Incomplete miscarriage

INCOMPLETE MISCARRIAGE

DEFINITION: When the entire products of conception are not expelled, instead a pa rt of it is left inside the uterine cavity, it is

called incomplete miscarriage. This is the commonest type met amongst women, hospitalized f or miscarriage complications.

CLINICAL FEATURES: History of expulsion of a fleshy mass per vaginam followed by: (1) Continuation of pain lower abdomen (2)

Persistence of vaginal bleeding (3) Internal examination reveals—(a) uterus smaller than the period of amenorrhea (b) patulous

cervical os often admitting tip of the finger and (c) varying amount of bleeding (4) on examination, the expelled mass is found

incomplete (Fig. 15.2C).

COMPLICATIONS: The retained products may cause: (a) profuse bleeding (b) sepsis or (c) place ntal polyp. MANAGEMENT: In

recent cases—Evacuation of the retained products of conception (ERCP) is done. She should be re suscitated before any active

treatment is undertaken.

• Early abortion: Dilatation and evacuation under analgesia or general anesthesia is to be done .

• Late abortion: The uterus is evacuated under general anesthesia and the products are rem oved by ovum forceps or by blunt curette. In

late cases, dilatation and curettage operation is to be done to remove the bits of tissues left behind. The removed materials are

subjected to a histological examination.

Medical management of incomplete miscarriage may be done. Tablet Misoprostol 200 µg is used vaginally every 4 hours. Compared to

surgical method, complications (p. 176), are less with medical method.

MISSED MISCARRIAGE

DEFINITION: When the fetus is dead and retained inside the uterus for a variable per iod, it is called missed miscarriage or

early fetal demise.

PATHOLOGY: The causes of prolonged retention of the dead fetus in the uterus is not clear . Beyond 12 weeks, the retained fetus

becomes macerated or mummified. The liquor amnii gets absorbed and the placenta bec omes pale, thin and may be adherent. Before 12

weeks, the pathological process differs when the ovum is more or less completel y surrounded by the chorionic villi.

CARNEOUS MOLE (Syn: blood mole, fleshy mole): It is the pathological variant of missed miscarriage af fecting the fetus before 12

weeks. Small repeated hemorrhages in the choriodecidual space disrupt the villi from its attachments. The bleeding is slight, so it does

not cause rupture of the decidua capsularis. The clotted blood with the contained ovum is known as a blood mole. By this time, the ovum

becomes dead and is either completely absorbed or remains as a rudimentary structure. Gradually, the fluid portion of the blood

surrounding the ovum gets absorbed and the wall becomes fleshy, hence the term fleshy or carneous mole (Fig. 15.3).

CLINICAL FEATURES: The patient usually presents with features of threate ned miscarriage followed by: (1) Persistence of brownish

vaginal discharge (2) Subsidence of pregnancy symptoms (3) Retrogression of b reast changes (4) Cessation of uterine growth which in

fact becomes smaller in size (5) Nonaudibility of the fetal heart sound even with Dopple r ultrasound if it had been audible before (6)

Cervix feels firm (7) Immunological test for pregnancy becomes negative (8) Real ti me ultrasonography reveals an empty sac early in

the pregnancy or the absence of fetal motion or fetal cardiac movements.

COMPLICATIONS: The complications of the missed miscarriage are those mentione d in intrauterine fetal death (see Ch. 21). Blood

coagulation disorders are less likely to occur in missed miscarriage.

Fig. 15.3: Expulsion of decidual cast following missed miscarriage (Ref. p. 181)

MANAGEMENT: • Expectant • Medical • Surgical

• Uterus is less than 12 weeks: (i) Expectant management—Many women expel the conceptus sp ontaneously (Fig. 15.3) (ii) Medical

management: Prostaglandin E

(Misoprostol) 800 mg vaginally in the posterior fornix is given and repeated after 24 hours if needed.

Expulsion usually occurs within 48 hours (iii) Suction evacuation or dilatation an d evacuation is done either as a definitive treatment or it

can be done when the medical method fails. The risk of damage to the uterine walls and brisk hemorrhage during the operation should be

kept in mind.

• Uterus more than 12 weeks: The same principles of the management as advocated in th e intrauterine fetal death are to be followed (see

ch.21). Induction is done by the following methods: Prostaglandins are more effective t han oxytocin in such cases. The methods used

are:

a. Prostaglandin E

analogue (misoprostol) 200 µg tablet is inserted into the posterior vaginal fornix every 4 hou rs for a maximum of

5 such.

b. Oxytocin—10–20 units of oxytocin in 500 mL of normal saline at 30 drops per minute is started. If fails, escalating dose of oxytocin

to the maximum of 200 mlU/min, may be used with monitoring.

c. Many patients need surgical evacuation following medical treatment. Following medic al treatment, ultrasonography should be done to

document empty uterine cavity. Otherwise evacuation of the retained products of conception (ERPC) should be done.

d. Dilatation and evacuationis done once the cervix becomes soft with use of PGE

. Otherwise cervical canal is dilated using the

mechanical dilators or by laminaria tent (p. 564). Evacuation of the uterine cavity is done ther eafter slowly.

SEPTIC ABORTION

DEFINITION: Any abortion associated with clinical evidences of infection of the uteru s and its contents, is called septic

abortion. Although clinical criteria vary, abortion is usually considered septic when there are : (1) rise of temperature of at least

100.4°F (38°C) for 24 hours or more (2) offensive or purulent vaginal discharge and (3) other evidences of pelvic infection such as lower

abdominal pain and tenderness.

INCIDENCE: It is difficult to work out the overall incidence of septic abortion. Ab out 10% of abortions requiring admission to hospital

are septic. The majority of septic abortion are associated with incomplete abortion. While in the majority of cases the infection occurs

following illegal induced abortion but infection can occur even after spontaneous abo rtion.

MODE OF INFECTION: The microorganisms involved in the sepsis are usually tho se normally present in the vagina (endogenous).

The microorganisms are: (a) Anaerobic—Bacteroides group (fragilis), anaerobic Streptococci, Cl. welchii, and tetanus bacillus (b)

Aerobic—Escherichia coli (E. coli), Klebsiella, Staphylococcus, Pseudomonas and hemolytic Strep tococcus (usually exogenous). Mixed

infection is more common. The increased association of sepsis in illegal induced abortion is du e to the fact that: (1) proper

antiseptic and asepsis are not taken (2) incomplete evacuation and (3) inadvertent injury to the genital organs and adjacent structures,

particularly the bowels.

PATHOLOGY: In the majority (80%), the organisms are of endogenous origin and the infe ction is localized to the conceptus without

any myometrial involvement. In about 15%, the infection either produces localized endom yometritis surrounded by a protective

leucocytic barrier, or spreads to the parametrium, tubes, ovaries or pelvic peritoneum. In a bout 5%, there is generalized peritonitis and/or

endotoxic shock.

CLINICAL FEATURES: Depending upon the severity and the extent of infe ction, the clinical picture varies widely. History of illegal

termination by an unauthorized person is mostly concealed.

• Pyrexia is an important clinical manifestation. Associated chills and rigors suggest bloo d stream spread of infection. However, if

hypothermia is present, it is an ominous feature of endotoxic shock.

• Pain abdomen of varying degrees is almost a constant feature.

• A rising pulse rateof 100–120/min or more is a s ignificant finding than even pyrexia. It indicates spread of infection beyond the

uterus.

• Variable systemic and abdominal findings depending upon the spread of in fection (see below).

• Internal examinationreveals offensive purulent vaginal discharge or a tender uteru s usually with patulous os or a boggy feel of the

uterus associated with variable pelvic findings depending upon the spread of infection.

CLINICAL GRADING: Grade–I: The infection is localiz ed in the uterus. Grade–II: The infection spread s beyond the uterus to the

parametrium, tubes and ovaries or pelvic peritoneum. Grade–III: Ge neralized peritonitis and/or endotoxic shock or jaundice or acute

renal failure.

Grade-I is the commonest and is usually associated with spontaneous abortion. Grade-II I is almost always associated with illegal

induced abortion.

INVESTIGATIONS: Routine investigations include: (1) Cervical or high vagina l swab is taken prior to internal examination

for—(a) culture in aerobic and anaerobic media to find out the dominant micro-organisms (b) s ensitivity of the microorganisms to

antibiotics and (c) smear for Gram stain.Gram-negative organisms are— E. coli, Pseudom onas, Bacteroides, etc. Gram-positive

organisms are—Staphylococci, anaerobic Streptococci, Cl. welchii, Cl. tetani, etc. (2) Blood for hemoglobin estimation, total and

differential count of white cells, ABO and Rh grouping. (3) Urine analysis including culture.

Special investigations—(1) Ultrasonography of pelvis and abdomen to detect i ntrauterine retained products of conception, physometra,

foreign body—intrauterine or intra-abdominal, free fluid in the peritoneal cavity or in the pou ch of Douglas. (2) Blood—(a) Culture—if

associated with spell of chills and rigors (b) Serum electrolytes—as an adjunct to the ma nagement protocol of endotoxic shock (c)

Coagulation profile. (3) Plain X-ray—(a) Abdomen—in suspected cases of bowel in jury (b) Chest—for cases with pulmonary

complications (atelectasis).

COMPLICATIONS:

Immediate: Most of the fatal complications are associated with illegally induced abortions of grade II I type.

• Hemorrhagerelated due to abortion process and also due to the injury inflicte d during the interference.

• Injury may occur to the uterus and also to the adjacent structures particularly gut.

• Spread of infection leads to: (a) Generalized peritonitis—The infec tion reaches through: (i) the uterine tubes (ii) perforation of the

uterus (iii) bursting of the microabscess in the uterine wall and (iv) injury to the gut. (b) Endotoxic shock—mostly due to E. coli or Cl.

welchii infection. (c) Acute renal failure— Multiple factors are involved pro ducing patchy cortical necrosis or acute tubular necrosis. It

is common in infection with Cl. welchii. (d) Thrombophlebitis.

All these lead to increased maternal deaths, the magnitude of which is to the extent of ab out 20–25% as per hospital statistics.

Remote: The remote complications include: (a) Chronic debility (b) Chronic pelvic pain and backache (c) Dyspareunia (d) Ectopic

pregnancy (e) Secondary infertility due to tubal blockage and (f) Emotional depression .

PREVENTION: (1) To boost up family planning acceptance in order to curb the un wanted pregnancies (2) Rigid enforcement of

legalized abortion in practice and to curb the prevalence of unsafe abortions. Education, m otivation and extension of the facilities are

sine-qua-non to get the real benefit out of it (see p. 562) (3) To take antiseptic and aseptic precau tions either during internal examination

or during operation in spontaneous abortion (outlined in p. 563).

MANAGEMENT

GENERAL MANAGEMENT:

• Hospitalization is essential for all cases of septic abortion. The patient is kept in isolation.

• To take high vaginal or cervical swab for culture, drug sensitivity test and G ram stain.

• Vaginal examination is done to note the state of the abortion process and extension of the in fection.

• Overall assessment of the case and the patient is levelled in accordance with the clinical grading.

• Investigation protocols as outlined before are done.

• Principles of management are: (a) To control sepsis (b) To remove the source of infection (c) To give

supportive therapy to bring back the normal homeostatic and cellular metabolism (d) To assess the response of treatment.

GRADE–I

Drugs:

(1) Antibiotics (see below).

(2) Prophylactic anti-gas-gangrene serum of 8000 units and 3 000 units of antitetanus serum intramuscularly are given if there is a

history of interference.

(3) Analgesics and sedatives, as required, are to be prescribed.

Blood transfusion is given to improve anemia and body resistance.

Evacuation of the uterus: As abortion is often incomplete, evacuation should be p erformed at a convenient time within 24 hours

following antibiotic therapy. Excessive bleeding is, of course, an urgent indication for evacuatio n. Early emptying not only minimizes

the risk of hemorrhage but also removes the nidus of infection. The procedure should be gentle to avoid injury to the uterus.

GRADE–II

Drugs: Antibiotics—Mixed infections including Gram-positive, Gram-negative and ana erobic organisms are common. Ideal antibiotic

regimens should cover all of them.

A. For Gram-positive aerobes: (i) Aqueous penicillin G 5 million units IV every 6 hours, or (ii) Ampicillin 0.5–1 g IV every 6 hours.

B. Gram-negative aerobes: (i) Gentamicin 1.5 mg/kg IV every 8 hours ( serum level to be monitored in a case with renal failure and

dose to be adjusted accordingly), or (ii) Ceftriaxone IG, IV every 12 hours. C. For anaerobes: Metronidazole 500 mg IV every 8 hours,

or Clindamycin 600 mg IV every 6 hours.

Antibiotic regimens have to be modified according to the culture and sensitivity report a s obtained later on. Analgesic, AGS and ATS

are given as in Grade-I. Blood transfusion, in adequate amount, is more often needed than in Grade-I cases.

Clinical monitoring: To note pulse, respiration, temperature, urinary output and progress of the pain, tenderness and mass in lower

abdomen.

Surgery: (1)Evacuation of the uterus—Evacuation should be withheld for at least 48 hou rs when the infection is controlled and is

localized, the only exception being excessive bleeding. (2) Posterior colpotomy— When the in fection is localized in the pouch of

Douglas pelvic abscess is formed. It is evidenced by spiky rise of temperature, rectal tenes mus (frequent loose stool mixed with mucus)

and boggy mass felt through the posterior fornix. Posterior colpotomy and drainage of the pus relieve the symptoms and improve the

general outlook of the patient.

GRADE–III

Antibiotics are discussed above. Clinical monitoring is to be conducted as outlined in Grade- II. Supportive therapy is directed to treat

generalized peritonitis by gastric suction and intravenous saline infusion. Management o f endotoxic shock or renal failure, if present, is

to be conducted as described in the chapter 38. Patient may need intensive care unit management (see p. 620).

Active Surgery:

Indications are—(1) Injury to the uterus (2) Suspected injury to bowel (3) Presence of foreign bo dy in the abdomen as evidenced by the

sonography or X-ray or felt through the fornix on bimanual examination (4) Unresponsive per itonitis suggestive of collection of pus (5)

Septic shock or oliguria not responding to the conservative treatment (6) Uterus too big to be safely evacuated per vaginam.

The laparotomy should be done by experienced surgeon with a skilled anesthetist . Rem oval of the uterus should be done

irrespective of parity. Adnexa is to be removed or preserved according to the pathology found. T horough inspection of the gut and

omentum for evidence of any injury is mandatory. Even when nothing is found o n laparotomy, simple drainage of the pus is

effective.

UNSAFE ABORTION is defined as the procedure of termination of unwanted pregna ncy either by persons lacking the necessary skills

or in an environment lacking the minimal standards or both. 90% of unsafe abortions a re in the developing countries comprising 13% of

all maternal deaths (WHO 1998). All the complications (see p. 165) are preventable if it is performed in a safe manner with proper

postabortion care services (p. 564).

RECURRENT MISCARRIAGE

DEFINITION: Recurrent miscarriage is defined as a sequence of three or more conse cutive spontaneous abortion before 20 weeks.

Some however, consider two or more as a standard. It may be primary or secondary ( having previous viable birth). A woman procuring

three consecutive induced abortion is not a habitual aborter.

INCIDENCE: This distressing problem is affecting approximately 1% of all women of reproductive age. The risk increases with each

successive abortion reaching over 30% after three consecutive losses. ETIOLOGY

The causes of recurrent abortion are complex and most often obscure. More than one factor may operate in a case. Factors may be

recurrent or non-recurrent. There are known specific factors which are responsible f or early or late abortion and they are grouped

accordingly.

FIRST TRIMESTER ABORTION:

• Genetic factors (3–5%): Parental chromosomal abnormalities is a proven cause of r ecurrent abortion. The most common

abnormality is a balanced translocation. Risk of miscarriage in couples with a balanced translocation is > 25%. However, the chance

of a successful pregnancy even without treatment is 40–50%.

• Endocrine and Metabolic: (1) Poorly controlled diabetic patients do have an increased incidence of early pregnancy failure. (2)

Presence of thyroid autoantibodiesis often associated with an increased risk but it is likely tha t this finding is secondary to a generalized

autoimmune abnormality rather than a specific endocrine dysfunction. Thyroid function is usually normal. (3) Luteal phase defect

(LPD) with less production of progesterone is too often related but whether the diminished progesterone level is the cause or effect is not

clear (see p. 159). (4) Hypersecretion of luteinizing hormone as seen in PCO S casesis associated with subfertility and higher

miscarriage. This is due to the adverse effects of LH on (i) the oocyte and (ii) on the endo metrium via excess androgen secretion. There

is suboptimal implantation as the endometrial prostaglandin secretion (↓PGI

, ↑TXA

) is also altered.

• Infection: Infection in the genital tract may be responsible for sporad ic spontaneous abortion but its relation to recurrent fetal wastage

is inconclusive (see p. 171). Transplacental fetal infection can occur with mos t microorganisms (p. 159).

• Inherited thrombophilia (see p. 276, 439) causes both early and late miscarriages due t o intravascular (spiral artery), and placental

intervillous thrombosis. Protein C resistance (factor V Leiden mutation) is the most common cause. Protein C is the natural inhibitor of

coagulation. Hyperhomocystinemia (autosomal recessive disorder) is also a risk factor for re current miscarriage (see p. 343).

• Immunological cause:

Autoimmunity —Presence of autoantibodies cause rejection of early pregnancy (15%) in the second trimesters mainly. Antibodies

responsible are: Antinuclear antibodies, Anti-DNA antibodies (double or single stranded ) and Antiphospholipid antibodies (Lupus

anticoagulant, anticardiolipin antibodies). APA positive women demonstrate a tendency to miscar ry at progressively lower gestational

ages. Spiral artery thrombosis, placental vascular atherosis, intervillous thrombosis and d ecidual vasculopathy with fibrinoid necrosis are

the immediate pathology for fetal loss (details see p. 342, 636). Alloimmunity (p. 159 )—There is failure of maternal recognition of

trophoblast lymphocyte cross-reactive antigen (TLX). Consequently there is lack of pro duction of blocking antibodies by the mother.

This is due to sharing of Human Leucocyte Antigen (HLA) between the partners (see p. 635). Parenteral HLA typing is not

recommended.

• Unexplained: In the majority, the cause remains unknown (see p. 160).

SECOND TRIMESTER MISCARRIAGE:

Anatomic abnormalities are responsible for 10–15% of recurrent abortion. The causes may be congenital or

acquired . Congenital anomalies may be due to defects in the mullerian duct fusion or resorption (e.g. unicornuate, bicornuate, septate or

double uterus). Congenital cervical incompetence is rare. Acquired anomalies are: intrauterine adhesions, uterine fibroids and

endometriosis and cervical incompetence. The pathology of abortion have been discussed in p. 159.

Defective Mullerian fusion —such as double uterus, septate or bicornuate uterus (F igs 15.4A and B). The association is about 12% cases

of recurrent abortion. Abortions tend to recur beyond 12 weeks and the successive pr egnancies are carried longer. Implantation on the

septum leads to defective placentation. The diagnosis is confirmed either by hysterograp hy or hysteroscopy combined with laparoscopy

in non-pregnant state or during digital exploration following abortion.

Case history (Fig. 15.4B) : The patient had three consecutive midtrimester abortions. Hysterography revealed bicornuate uterus.

Metroplasty was done. Pregnancy occurred one year later, which was delivered by ce sarean section at 39 weeks.

a b

Fig. 15.4A: Diagrammatic representation of—(a) septate and (b) double uteru s with double cervix and septate vagina

OTHER CAUSES OF SECOND TRIMESTER MISCARRIAGE:

• Chronic maternal illness—such as uncontrolled diabetes with arteri osclerotic changes, hemoglobinopathies, chronic renal disease.

Inflammatory bowel disease, systemic lupus erythematosus.

• Infection—Syphilis, toxoplasmosis and listeriosis may be responsible in some cases.

• Unexplained.

CERVICAL INCOMPETENCE (CERVICAL INSUFFICIENCY)—20%

Causes : The retentive power of the cervix (internal os) may be impaired functionally and/ or ana tomically due to the following

conditions: (a) Congenital Uterine anomalies, (b) Acquired (i atrogenic)—common, following: (i) D and C operation (ii) induced

abortion by D and E (10%) (iii) vaginal operative delivery through an undilated cervix and (iv) amputation of the cervix or cone biopsy.

(c) Others—Multiple gestations, prior preterm birth. Cervical incompetence is consi dered as a biological continuum of spontaneous

preterm birth syndrome (p. 314).

Diagnosis of Cervical Incompetence:

• History—Repeated mid trimester painless cervical dilatation (without apparent cause) and escape of liquor amnii followed by painless

expulsion of the products of conception is very much suggestive.

Fig. 15.4B: Hysterosalpingography showing bicornuate uterus

A B

Fig. 15.5A and B: Diagrammatic representation of the hysterographic shadow obtained in the premenstrual phase. (A) A normally

competent cervix (B) Incompetent cervix showing funnelling. (FW = Funnel width, FL = Funnel length, CL = Cervical length).

• Internal examination: (i) Interconceptional period— Bimanual examination reveals presence o f unilateral or bilateral tear and /or

gaping of the cervix upto the internal os.

INVESTIGATIONS:

Interconceptional period : (i) Passage number 6–8 Hegar dilator beyond the internal os without any resista nce and pain and absence

of internal os snap on its withdrawal specially in premenstrual period indicate incomp etence.

(ii) Premenstrual hysterocervicography shows funnel shaped shadow (Fig. 15.5). The internal os is supposed to be tight due to action

of progesterone during this phase of cycle. Similar funnel shaped shadow may be found if hysterography is done in the proliferative

phase even with a competent cervix.

(iii) During pregnancy—(a) Clinical digital: Painless cervical shortenin g and dilatation. (b) Sonography: Short cervix < 25 mm;

Funnelling of the internal Os > 1 cm. (c)

Speculum examination : Detection of dilatation of internal os with herniation of the me mbranes (Fig. 15.6). INVESTIGATIONS

A thorough medical, surgical and obstetric history with meticulous clinical examination sh ould be carried out to find out the possible

cause or causes as mentioned previously. Careful history taking should include—(i) Th e nature of previous abortion process (ii)

Histology of the placenta or karyotyping of the conceptus, if available (iii) Any chronic illness.

Diagnostic tests : (1) Blood-glucose (fasting and post- prandial), VDRL, Thyroid function test, ABO and Rh grouping (husband and

wife), Toxoplasma antibodies IgG and IgM (2) Autoimmune screening—lupus anticoa gulant and anticardiolipin antibodies (3) Serum

LH on D

of the cycle (4) Ultrasonography—to detect congenital malformation of uterus, polycy stic ovaries and uterine fibroid (5)

Hysterosalpinography in the secretory phase to detect—cervical incompetence, u terine synechiae and uterine malformation (6) This is

supported by hysteroscopy and or laparoscopy (7) Karyotyping (husband and wife) (8) Endocervical swab to detect chlamydia,

mycoplasma and bacterial vaginosis.

TREATMENT

INTERCONCEPTIONAL PERIOD:

• To alleviate anxiety and to improve the psychology—W hile counseling the couple, they should be assured that even after 3

consecutive miscarriages, the chance of a successful pregnancy is high (70%). Howe ver, the success rate depends on the underlying

etiology as well as the age of the woman.

• Hysteroscopic resection of uterine septa, synechae and submucous myomas imp roves the pregnancy outcome. Uterine unification

operation (metroplasty) is done for cases with bicornuate uterus.

• Chromosomal anomalies—If chromosomal abnormality is detected in the couples or in the abortus, genetic counseling is undertaken.

Karyotyping of the products of conception from future miscarriage is mandatory. Coupl es with chromosomal translocations or inversion

is counseled for preimplantation genetic diagnosis (PGD) (see p. 493) or prenatal diagnosis (amnioc entesis or CVS) in subsequent

pregnancy or pregnancy with donor gametes (sperm or oocyte).

• Hypersecretion of LH as seen in PCOS cases, is suppressed with GnRH analogu e therapy. Subsequently ovulation induction with

gonadotropins improves the pregnancy outcome.

• Endocrine dysfunction: Control of diabetes and thyroid disorders are done (see p. 2 81, 287). Subclinical diabetes and or thyroid

disease need not be treated.

• Genital tract infections are treated appropriately following culture of cervical an d vaginal discharge. Empirical treatment with

doxycycline or erythromycin is cost effective.

DURING PREGNANCY:

• Reassurance and tender loving care are very much helpful. Probably this removes the stress and improves uterine blood flow.

• Ultrasoundshould be used at the earliest to detect a viable pregnancy. This will influ ence further management. If the fetus is viable

ultrasonographically at 8–9 weeks, only 2 to 3% are lost thereafter and similarly fetal lo ss is only 1% after 16 weeks of viable fetus.

• Rest—Patient should take adequate rest, avoid strenous activities, intercourse and traveling.

• Luteal Phase Defect (LPD) cases are treated with natural micronized progesterone 100 mg daily as vaginal suppository. It is started

2 days after ovulation. If the period is missed and pregnancy is confirmed, progesterone supplem entation is continued until 10–12 weeks

gestation. hCG therapy is thought to improve the pregnancy outcome. hCG s timulates corpus luteum to produce progesterone. LPD is a

questionable entity and the benefits of both the hormonal treatments are uncertain (RCO G– 2003).

• Antiphospholipid antibody syndrome (APS): Women are treated with low dose a spirin (50 mg/day), or low dose aspirin and heparin

(5000 units SC twice daily) upto 34 weeks.

• Circlage operation (Fig. 15.6) for cervical incompetence is to be performed (see below).

• Chromosomal anomaly—Prenatal diagnosis by CVS or a mniocentesis (p. 107) is done. Preimplantation genetic diagnosis in

blastomere stage is another option (p. 494). Only then the few balanced embryos are tra nsferred and there is successful pregnancy.

• Alloimmune disorders: Intravenous Immune Globulin (IVIG) infusion resulted in s uccessful pregnancy. It reduces the cytotoxic

activity of the NK cells by its immunosuppressive properties. Leucocyte immunizationby injectio n of paternal leucocyte into the mother

has been found to be ineffective. Progesterone is also used intravaginally for its immun osuppressive effects.

• Inherited thrombophilias (p. 275): Antithrombotic therapy improv es the pregnancy outcome. Heparin (5000 IU SC twice daily)

or low molecular weight heparin SC once daily (preferred) is effective. Heparin is give n upto 34 weeks.

• Medical complications in pregnancy: Hemoglobinopathies, SLE, cyanotic heart disease are advised to delay pregnancy until the

disease is optimally treated. During pregnancy specific management is continue d (p. 271).

• Unexplained: Despite differentinvestigations about40–60% of recurrentabortions remain unexplained. However, ‘tender loving care’

(TLC) and some supportive therapy improves the pregnancy outcome by 70%.

MANAGEMENT OF CERVICAL INCOMPETENCE

Circlage operation : Two types of operation are in current use during pregnancy each claimin g an equal success rate of about 80–90%.

The operations are named after Shirodkar (1955) and McDonald (1963).

Principle: The procedure reinforces the weak cervix by a non-absorbable tape, placed around t he cervix at the level of internal os.

Time of operation: In a proven case, prophylactic circlage should be done around 14 weeks of pregnancy or at least two weeks earlier

than the lowest period of previous wastage, as early as the 10th week. Emergency circlage can be done when the cervix is dilated and

there is bulging of the membranes. Case selection: Circlage operation is done mainly in cases where careful history and physical

examination suggest cervical incompetence as it remains a diagnosis of exclusion. Clini cal observation is supported with

sonographically detected short cervical length, with or without funnelling of the internal os. Prio r to operation, fetal growth and anatomy

is assessed by sonography.

STEPS OF SHIRODKAR’S OPERATION (Fig. 15.7)

Step—I: The patient is put under light general anesthesia and placed in lithotomy position with good exp osure of the cervix by a

posterior vaginal speculum. The lips of the cervix are pulled down by sponge holding f orceps or Allis tissue forceps.

A B C

Figs 15.6A to C:Principles of encirclage operation—(A) Competent cervix; (B) Incompe tent cervix with herniation of the membranes;

Step—II : A transverse incision is made anteriorly below the base of the bladder on the vaginal wall and the bladder is pushed up to

expose the level of the internal os. A vertical incision is made posteriorly on the cervicov aginal junction.

Step—III : The non-absorbable suture material—Mersilene (Dacron) or Ethibond tape is p assed submucously with the help of an

aneurysm needle or cervical needle so as to bring the suture ends through the posterior incision.

Step—IV: The ends of the tapes are tied up posteriorly by a reef knot. The bulging membrane s, if present, must be gently reduced

beforehand into the uterine cavity. The anterior and posterior incisions are repaire d by interrupted stitches using chromic catgut.

McDONALD’S OPERATION (see Fig.15.7)

The non-absorbable suture (Mersilene) material is placed as a purse string suture as hig h as possible (level of internal os) at the junction

of the rugose vaginal epithelium and the smooth vaginal part of the cervix below the level of the b ladder. The suture starts at the anterior

wall of the cervix. Taking successive deep bites (4–5 sites) it is carried around the l ateral and posterior walls back to the anterior wall

again where the two ends of the suture are tied.

The operation is simple having less blood loss, and has got a good success rate. There is less formation of cervical scar and hence less

chance of cervical dystocia during labor.

Postoperative care: (1) The patient should be in bed for at least 2–3 days (2) Weekly injections of 17α hydroxy progesterone caproate

500 mg IM is given in women with history of prior preterm delivery (3) Isoxsuprine (tocolyti cs) 10 mg tablet may be given thrice daily

to avoid uterine irritability.

Advice on discharge: (a) Usual antenatal advice (b) To avoid intercourse (c) To avoid rough jour ney (d) To report if there is vaginal

bleeding or abdominal pain (e) Periodic ultrasonographic monitoring of the fetus an d the cervix.

Removal of stitch: The stitch should be removed at 37th week or earlier if labor pain starts or features of abortion appear. If the stitch

is not cut in time, uterine rupture or cervical tear may occur. If the stitch is cut prior to t he onset of labor, it is preferable to cut it in

operation theater as there is increased chance of cord prolapse specially in the cases with floa ting head.

Contraindications: (i) Intrauterine infection (ii) Ruptured membranes (iii) History of vaginal ble eding (iv) Severe uterine irritability (v)

Cervical dilatation > 4 cm.

Complications: (i) Slipping or cutting through the suture (ii) Chorioamnionitis (iii) Rupture of th e membranes (iv) Abortion/preterm

labor (v) Cervical lacerations during delivery (vi) Cervical scarring and dystocia requi ring cesarean delivery.

Abdominal circlage: A mersilene tape is placed at the level of the isthmus between the uterine wall and the uterine vessels. The tape is

tied anteriorly. This is done between 11 and 13 weeks following laparotomy. Disadvan tages are: (i) Increased complications during

operation (ii) Subsequent laparotomy for delivery or removal of the tape (if needed). Indication s are: cases where cervix is hypoplastic

or where prior vaginal circlage has failed. A similar procedure can be done laparoscop ically during the non-pregnant state.

A B

Figs 15.7A and B:Circlage operation—(A) McDonald technique; (B) Shirodkar’ s technique.

Alternative to cervical circlage —(non-surgical), may be bed rest alone to avoid pressure on the cervix. In jection of 17α OH

progesterone caproate 500 mg IM weekly is given as cervical incompotence is conside red as a continum of preterm birth syndrome.

PROGNOSIS OF RECURRENT MISCARRIAGE

The prognosis of recurrent miscarriage is not so gloomy as it was previously thought. T he overall risk of recurrent miscarriage is about

25–30% irrespective of the number of previous spontaneous miscarriage. The overall prognosis is good even without therapy. The

chance of successful pregnancy is about 70–80% with an effective therapy. Reassu rance and tender loving care are very much

helpful.

INDUCTION OF ABORTION

Deliberate termination of pregnancy either by medical or by surgical method befor e the viability of the fetus is called induction

of abortion. The induced abortion may be legal or illegal (criminal). There are many c ountries in the globe where the abortion is not yet

legalized. In India, the abortion was legalized by “Medical Termination of Pregna ncy Act” of 1971, and has been enforced in the year

April 1972. The provisions of the act have been revised in 1975.

MEDICAL TERMINATION OF PREGNANCY (MTP)

Since legalization of abortion in India, deliberate induction of abortion by a registered m edical practitioner in the interest of mother’s

health and life is protected under the MTP Act. The following provisions are laid down:

• The continuation of pregnancy would involve serious risk of life or grave in jury to the physical and mental health of the pregnant

woman.

• There is a substantial risk of the child being born with serious physical and me ntal abnormalities so as to be handicapped in life.

• When the pregnancy is caused by rape, both in cases of major and minor gir l and in mentally imbalanced women.

• Pregnancy caused as a result of failure of a contraceptive.

In practice , the following are the indications for termination under the MTP Act:

• To save the life of the mother (Therapeutic or Medical termination): The indications are limited and scarcely ju stifiable now-a-days

except in the following cases: (i) Cardiac diseases (Grade-III and IV) with history of decom pensation in the previous pregnancy or in

between the pregnancies (ii) Chronic glomerulonephritis (iii) Malignant hypertension (iv) In tractable hyperemesis gravidarum (v)

Cervical or breast malignancy (vi) Diabetes mellitus with retinopathy (vii) Epilepsy or psych iatric illness with the advice of a

psychiatrist.

• Social indications: This is almost the sole indication and is covered under the provision “to prevent grave injury to the physical

and mental health of the pregnant woman”. In about 80%, it is limited to parous women having unplanned pregnancy with low

socioeconomic status. Pregnancy caused by rape or unwanted pregnancy caused due to failure of any contraceptive device also falls in

this category (20%).

• Eugenic: This is done under the provision of “substantial risk of the child being born with serious physical and mental abnormalities so

as to be handicapped in life”. The indication is rare.

i. Structural (Anencephaly), chromosomal (Down’s syndrome) or genetic (Hemophilia) abnormalities of the fetus. i i. When the fetus is

likely to be deformed due to action of teratogenic drugs (warfarin) or radiation exposure (> 10 rads) in early preg nancy.

iii. Rubella, a viral infection affecting in the first trimester, is an indication for termination (p. 299).

RECOMMENDATIONS

• In the revised rules, a registered medical practitioner is qualified to perform a n MTP provided: (a) One has assisted in at least 25 MTP

in an authorized center and having a certificate. (b) One has got six months hous e surgeon training in obstetrics and gynecology. (c) One

has got diploma or degree in obstetrics and gynecology.

• Termination can only be performed in hospitals, established or maintained by the government or places approved by the government.

• Pregnancy can only be terminated on the written consent of the woman. Hus band‘s consent is not required.

• Pregnancy in a minor girl (below the age of 18 years) or lunatic cannot be te rminated without written consent of the parents or legal

guardian.

• Termination is permitted upto 20 weeks of pregnancy. When the pregnancy exceeds 12 weeks, opinion of two medical practitioners

is required.

• The abortion has to be performed confidentially and to be reported to the Dir ector of Health Services of the State in the prescribed

form.

METHODS OF TERMINATION OF PREGNANCY

First Trimester (Up to 12 Weeks)

Medical

• Mifepristone

• Mifepristone and Misoprostol (PGE

)

• Methotrexate and Misoprostol

• Tamoxifen and Misoprostol

Surgical

• Menstrual regulation (p. 567)

• Vacuum Aspiration (MVA/EVA) p. 567

• Suction evacuation and/or curettage

• Dilatation and evacuation:

i. Rapid method

Second Trimester (13–20 Weeks)

• Prostaglandins PGE

(Misoprostol), 15 methyl

PGF

α (Carboprost), PGE

(Dinprostone) and their analogues (used-intravaginally, intramuscularly or intraamniotica lly)

• Dilation and evacuation (13–14 weeks)

• Intrauterine instillation of hyperosmotic solutions a. Intra-amniotic hypertonic ur ea (40%), saline (20%)

b. Extra-amniotic—Ethacrydine lactate, Prostaglandins (PGE

, PGF

α)

• Oxytocin infusion high dose used along with either of the above two methods

ii. Slow method

• Hysterotomy (abdominal)— less commonly done

FIRST TRIMESTER TERMINATION OF PREGNANCY

MEDICAL METHODS OF FIRST TRIMESTER ABORTION: Mifepristone (RU-486) and Mis oprostol: Mifepristone an analog

of progestin (norethindrone) acts as an antagonist, blocking the effect of natural proge sterone. Addition of low dose prostaglandins

(PGE

) improves the efficiency of first trimester abortion. It is effective upto 63 days and is h ighly successful when used within 49 days

of gestation.

PROTOCOL: 200 mg of mifepristone orally is given on day 1. On day 3, misopro stol (PGE

) 400 µg orally or 800 µg vaginally is

given. Patient remains in the clinic for 4 hours during which expulsion of the conceptus (95%) often occurs. Patient is re-examined after

10–14 days. Complete abortion is observed in 95%, incomplete in about 2% of cases and about 1% do not respond at all. Oral

mifepristone 200 mg (1 tablet) with vaginal misoprostol 800 µg (4 tablet, 200 µg each) after 6–48 ho urs is equally effective. This

combipack (1+4) is approved by DGHS, Government of India for MTP up to 63 day s of pregnancy. Medical methods are safe, effective,

noninvasive and have minimal or no complications.

Methotrexate and Misoprostol —Methotrexate 50 mg/m

IM (before 56 days of gestation) followed by 7 days later misoprostol 800 µg

vaginally is highly effective. Misoprostol may have to be repeated after 24 hours if it fa ils. If the procedure fails, ultrasound examination

is done to confirm the failure. Then suction evacuation should be done. Methotrexate and misoprostol regimen is less expensive but

takes longer time than Mifepristone and Misoprostol. Misoprostol has less side effects and is stable at room temperative unlike other

PGs, which must be refrigerated (see p. 505).

Contraindications—Mifepristone should not be used in women aged over 35 years, heavy smok ers and those on longterm

corticosteroid.

SURGICAL METHODS OF FIRST TRIMESTER ABORTION:

 MENSTRUAL REGULATION: See p. 567

 VACUUM ASPIRATION (MVA/EVA) is done upto 12 weeks with minimal cervical dilata tion. It is

performed as an outpatient procedure using a plastic disposable cannula (up to 12 mm size) and a 60 mL plastic (double valve) syringe

(Fig. 41.20). It is quicker (15 minutes), effective (98–100%), less traumatic and safer than dilatation, evacuation and curettage (details

see p. 567).

 SUCTION EVACUATION AND/OR CURETTAGE:

This improvised method consists of a suction machine fitted with a cannula either plastic (Karman) or metal available in various sizes.

The details of its technique are described in the chapter of operative obstetrics (p. 566).

Advantages : (1) It is done as an outdoor procedure (2) Hazards of general anesthesia are absent as it is done, at best, under paracervical

block anesthesia (3) Ideal for termination for therapeutic indications (4) Blood loss is m inimal (5) Chance of uterine perforation is much

less specially with the plastic cannula.

Drawbacks : (1) The method is not suitable with bigger size uterus of more than 10 weeks as chance of retained products is more (2)

Requires electricity to operate and the machine is costly.

 DILATATION AND EVACUATION:• Rapid method • Slow meth od

• Rapid method: This can be done as an outdoor procedure with diazepam sedation and paracervical block anesthesia. The details are

described in p. 563.

Advantages: (1) As it can be done as an outdoor procedure, the patient can go home after t he sedative effect is over. (2) Chance of

sepsis is minimal.

Drawbacks: (1) Chance of cervical injury is more (2) Uterus should not be m ore than 6–8 weeks of pregnancy. (3) All the drawbacks of

D and E (see p. 565).

• Slow Method: Slow dilatation of the cervix is achieved by inserting laminaria tents (hygroscopic osmotic dilators) into the cervical

canal (synthetic dilators like Dilapan, Lamicel are also used). This is followed by evacuation of the uterus after 12 hours. Vaginal

Misoprostol (PGE

) 400 µg 3 hours before surgery is equally effective for cervical ripening. The detai ls are described in p. 566.

Advantages: (1) Chance of cervical injury is minimal (2) Suitable in cases of therapeutic indi cations. Drawbacks: (1) Hospitalization is

required at least for one day (2) Chance of introducing sepsis (3) All the complications of D an d E (see p. 565).

MID TRIMESTER TERMINATION OF PREGNANCY

MEDICAL METHODS:

PROSTAGLANDINS: Prostaglandins and their analogues are very much effective . They are used extensively, specially in the

second trimester. They act on the cervix and the uterus. The PGE (dinoprostone, sulpro stone, gemeprost, misoprostol) and PGF

(carboprost) analogues are commonly used. PGEs are preferred as they have more se lective action on the myometrium and less side

effects.

(i) Misoprostol (PGE

analogue), 400–800 µg of misoprostol given vaginally at an interval of 3–4 ho urs is most effective as the

bioavailability is high. Alternatively, first dose of 600 µg misoprostol given vaginally, the n 200 µg, orally every 3 hours are also found

optimum. This regimen reduces the number of vaginal examinations. Recently 400 µg m isoprostol is given sublingually every 3 hours

for a maximum of five doses. This regimen has got 100% success in second trimester abo rtion. The mean induction—abortion interval is

11–12 hours.

(ii) Gemeprost (PGE

analogue): 1 mg vaginal pessary every 3–6 hours for five doses in 24 hours has go t about 90% success. The

mean induction-abortion interval was 14–18 hours.

(iii) Mifepristone and prostaglandins: Mifepristone 200 mg oral, followed 36–48 hou rs later by misoprostol 800 µg vaginal; then

misoprostol 400 µg oral every 3 hours for 4 doses is used. Success rate of abortion is 9 7% and median induction delivery interval is 6.5

hours. Pretreatment with mifepristone reduces the induction— abortion interval significa ntly compared to use of misoprostol alone.

(iv)Dinoprostone (PGE

analogue): 20 mg is used as a vaginal suppository every 3–4 hours (maximum for 4–6 doses ). When used

along with osmotic dilators, the mean induction to abortion interval is 17 hours. PGE

is thermolabile (needs refrigeration) and is

expensive.

(v) Prostaglandin F

(PGF

2α

), carboprost tromethamine—250 µg IM every 3 hours for a maximum 10 doses can be used. The success

rate is about 90% in 36 hours. Side effects of PGF

2α

(nausea, vomiting, diarrhea and pain at injection site) are more. It is contraindicated

in cases with bronchial asthma.

OXYTOCIN:High dose oxytocin as a single agent can be used for second trimester abortion . It is effective in 80% of cases. It can be

used with intravenous normal saline along with any of the medications used either in tra-amniotic or extra-amniotic space in an attempt to

augment the abortion process (see below). The drip rate can be increased upto 50 milli units or more per minute. Currently high dose

(upto 300 units in 500 mL of dextrose saline) is favored.

SURGICAL METHODS:

It is difficult to terminate pregnancy in the second trimester with reasonable safety as in f irst trimester. The following surgical methods

may be employed.

Between 13 and 15 weeks

• Dilatation and Evacuation in the midtrimester is less commonly do ne. Pregnancies at 13 to 14 menstrual weeks are evacuated. In all

midtrimester abortion cervical preparation must be used (WHO 1997) to make the proc ess easy and safe. Intracervical tent (Laminaria

osmotic dilator), mifepristone or misoprostol are used as the cervical priming agents. The procedure may need to be performed under

ultrasound guidance to reduce the risk of complications (p. 566). Simultaneous use of oxyt ocin infusion is useful.

Between 16 and 20 weeks: INTRAUTERINE INSTILLATION OF HYPER TONIC SOLUTION:

• Intra-amniotic • Extra-amniotic

• Intra-amniotic:Intra-amniotic instillation of hypertonic saline (20% ) is less commonly used now. It is instilled through the

abdominal route.

Procedure: Preliminary amniocentesis is done as described in p. 651 by a 15 cm 18 gauge needle. The amount of saline to be instilled

is calculated as number of weeks of gestation multiplied by 10 mL. The amount is to be infused slowly at the rate of 10 mL/min.

Contraindications : It should not be used in presence of cardiovascular or renal lesion or in sev ere anemia because of sodium load.

Precautions: (1) To be sure that the needle is in the amniotic cavity evidenced b y clear liquor coming out. If there is a bloody tap, the

needle should be pushed further or change the direction until clear liquor comes out. If fails, the procedure is to be abandoned. (2) The

instillation should be a slow process (10 mL/min). (3) Vital signs should be checked imm ediately after the instillation and she should be

kept at bed rest for at least 1 hour. (4) To stop the procedure if the untoward s ymptoms like acute abdominal pain, headache, thirst or

tingling in the fingers appear (feature of intravascular injection of the hypertonic saline) . A rapid infusion of 1000 mL dextrose in

water along with intravenous diuretics is indicated in such cases. (5) Strict vigila nce is taken during and following instillation till

expulsion occurs. (6) Routine antibiotic is given such as ampicillin 500 mg thrice daily fo r 3–5 days.

Mode of action: There is liberation of prostaglandins following necrosis of the amniotic epithelium and the decidua. This in turn excites

uterine contraction and results in the expulsion of the fetus.

Success rate: The method is effective in 90–95% cases with induction-abortion inte rval of about 32 hours. The method failure (end

point) is considered when abortion fails to occur within 48 hours. If the method fa ils, some other method may be employed.

Complications: The complications include—(a) minor complaints like fever, headache, nausea, vomiting, abdominal pain (b) cervical

tear and laceration (c) retained products for which exploration has to be done (d) infe ction (e) hypernatremia, cardiovascular collapse—

due to intravascular injection (f) pulmonary and cerebral edema (g) renal failure (h) d isseminated intravascular coagulopathy. The

incidence of death rate varies from 0–5 per 1000 instillations.

Intra-amniotic instillation of hyperosmotic urea: Intra-amniotic instillation of 40% urea solu tion (80 g of urea in 200 mL distilled

water) along with syntocinon drip is effective with less complications. Combination of in tra-amniotic hyperosmotic urea and 15 methyl

PGF

2α

reduces the induction abortion interval to 13 hours.

• Extra-amniotic:Extra-amniotic instillation of 0.1% ethacrydine lacta te (estimated amount is 10 mL per week) is done

transcervically through a number 16 Foley‘s catheter. The catheter is passed up the cer vical canal for about 10 cm above the internal os

between the membranes and myometrium and the balloon is inflated (10 mL) with saline. It is removed after 4 hours. The success rate is

similar to saline instillation but is less hazardous. It can be used in cases contraindicated for saline instillation. Stripping the membranes

with liberation of prostaglandins from the decidua and dilatation of the cervix by the cat heter are some of the known factors for initiation

of the abortion.

HYSTEROTOMY: The operation is performed through abdominal route. The steps are giv en in chapter 36.

Indications: (i) Prior failed medical termination of pregnancy (TOP) (ii) Cases wh ere D and E cannot be safely done: (a) Fibroid in the

lower uterine segment (b) Uterine anomalies (c) Patients with repeated scarred uterus with placenta accreta or percreta. It is less

commonly done these days. The operation should be combined with sterilization oper ation.

Hazards:Immediate: (i) Hemorrhage and shock (ii) Anesthetic complications (iii) Peritonitis (iv) Intestinal obstruction.

Remote: (1) Menstrual abnormalities (2) Scar endometriosis (1%) (3) Incisional hernia (4) If pregn ancy occurs, chance of scar rupture.

Rh-NEGATIVE WOMEN: In non-immunized women, intramuscular administration of 1 00 µg anti-D immunoglobulin is given within

72 hours of abortion.

COMPLICATIONS OF MTP

There is no universally safe and effective method which is applicable to all cases. Howe ver, the complications are much less (5%) if

termination is done before 8 weeks by MVA or suction evacuation/currette. The compl ications are about five times more in mid-

trimester termination. Use of PG analogues and mifepristone has made second trimester MTP effective and safe. The complications are

either related to the methods employed or to the abortion process.

IMMEDIATE: (1) Injury to the cervix (cervical lacerations) (2) Uterine perforation d uring D and E (p. 565) (3) Hemorrhage and shock

due to trauma, incomplete abortion, atonic uterus or rarely coagulation failure (4) Thro mbosis or embolism (5) Postabortal triad of pain,

bleeding and low grade fever due to retained clots or products. Antibiotics should be co ntinued, may need repeat evacuation (6) Related

to the methods employed:

• Prostaglandins—intractable vomiting, diarrhea, fever, uterine pain and cervicouterine injury.

• Oxytocin—water intoxication and rarely convulsions • Hysterotomy (v ide supra)

• Saline—hypernatremia, pulmonary edema, endotoxic shock, DIC, rena l failure, cerebral hemorrhage

REMOTE: The complications are grouped into: • Gynecological • Obstetrica l

• Gynecological complications include—(a) menstrual disturbances (b) chronic pelvic inf lammation (c) infertility due to cornual block

(d) scar endometriosis (1%) and (e) uterine synechiae leading to secondary amenorrh ea.

• Obstetrical complications include—(a) recurrent midtrimester abortion due to cervic al incompetence, (b) ectopic pregnancy (three-

fold increase), (c) preterm labor, (d) dysmaturity, (e) increased perinatal loss, (f) ru pture uterus, (g) Rh isoimmunization in Rh-negative

women, if not prophylactically protected with immunoglobulin, (h) failed abortion and c ontinued pregnancy.

Failed abortion, continued pregnancy and ectopic pregnancy: Pregnancy may continue following MVA (inspite of histologically

proven villi). When no chorionic villi are found on tissue examination ectopic pregnanc y need to be excluded by quantitative serum hCG

and vaginal ultrasound. Failed MTP is defined when there is a failure to achieve TOP w ithin 48 hours. Failed second trimester MTP with

PG analogues and the rate of live birth is 4–10%.

MORTALITY: First trimester: The maternal death is lowest (about 0.6/100,000 procedures) in first trimester termination specially

with MVA and suction evacuation. Concurrent tubectomy even by abdominal route do ubles the mortality rate.

Midtrimester: The mortality rate increases 5–6 times to that of first trimester. Con trary to the result of the advanced countries, the

mortality from saline method has been found much higher in India compared to termina tion by abdominal hysterotomy with tubectomy.

ECTOPIC PREGNANCY

Ectopic pregnancy still contributes significantly to the cause of maternal mortality and mo rbidity. While there has been about four fold

increase in incidence over the couple of decades, but the mortality has been slashed down by 80%. Recognition of high-risk cases (p.

180), early diagnosis (even before rupture) with the use of TVS, serum β hCG and laparosco py have significantly improved the

management of ectopic pregnancy.

DEFINITION: An ectopic pregnancy is one in which the fertilized ovum is implanted an d develops outside the normal

endometrial cavity.

SITES OF IMPLANTATION:

TUBAL PREGNANCY

FREQUENCY: The incidence has increased. The reasons are: increased prev alence of chronic pelvic inflammatory disease, tubal plastic

operations, ovulation induction and IUD use. Secondly, early diagnosis helps to detect s ome cases, that in the past, may have resolved

spontaneously. Early diagnosis and therapy has helped to reduce maternal deaths du e to ectopic pregnancy. The incidence varies

from 1 in 300 to 1 in 150 deliveries.

ETIOLOGY:

• Salpingitis and pelvic inflammatory disease (PID) increases the risk of ectop ic pregnancy by 6–10 fold. (a) Loss of cilia of the lining

epithelium and impairment of muscular peristalsis. (b) Narrowing of the tubal lumen. (c ) Formation of pockets due to adhesions between

mucosal folds. (d) Peritubal adhesions resulting in kinking and angulation of the tube . Chlamydia trachomatis infection is the most

common risk factor. Salpingitis isthmica nodosa also increases the risk.

• Iatrogenic:

I. Contraception failure:Women using any form of contraception have significantly reduced chance of having a ectopic pregnancy. But

in selected contraception failure, there is increased incidence of ectopic pregnancy. (a) IUD—It prevents intrauterine pregnancy

effectively, tubal implantation to a lesser extent and the ovarian

pregnancy not at all. There is relative increase in tubal pregnancy (7 times m ore) should pregnancy occur with IUD in situ. CuT

380A and levonorgestrel devices have got the lowest rate of ectopic whereas progestas ert has got the highest one. Whether tubal infection

or abnormal tubal mobility in post-fertilization period is the cause is not clear.

(b) Sterilization operation—There is 15–50% chance of being ectopic, if pregna ncy occurs. This is due to sterilization failure. The

risk is highest following laparoscopic bipolar coagulation.

(c) Use of progestin only pill or postcoital estrogen preparations increases the chance of tubal p regnancy probably by impaired tubal

motility.

II. Tubal Surgery—Tubal reconstructive surgery

to improve fertility, increases the risk of tubal

pregnancy significantly. Pre-existing tubal pathology,

impaired tubal motility, kinking of the tube or

terminal stricture are the contributing factors. III. Intrapelvic adhesions following pelvic surgery. IV. ART—Tubal pregnancy is

increased following

ovulation induction and IVF-ET and GIFT

procedures. The risk of ectopic is 5–7% and that of

heterotypic pregnancy is 1% in contrast to 1 in 5000

in spontaneous pregnancy.

V. Others:

Table 15.1: Risk factors of ectopic pregnancy

History of PID

History of tubal ligation

Contraception failure

Previous ectopic pregnancy

Tubal reconstructive surgery

History of infertility

ART particularly if the tubes are patent but damaged

IUD use

Previous induced abortion

Tubal endometriosis

• Previous ectopic pregnancy: There is 10–15% chances of repeat ecto pic pregnancy.

• Prior induced abortion significantly increases the risk.

• Developmental defects of the tube: (a) Elongation, (b) Diverticulum, (c) Access ory ostia.

• Transperitoneal migration of the ovum— contralateral presence of corpus luteum is n oticed in tubal pregnancy in about 10% cases.

Factors facilitating nidation in the tube: (i) Early resumption of the tro phoblastic activity is probably due to premature degeneration of

the zona pellucida, (ii) Increased decidual reaction, (iii) Tubal endometriosis.

The reasons for rising incidence of ectopic pregnancies are— (i) Rise in the incid ence of STIs and salpingitis, (ii) Rise in the

incidence of pregnancy following ART procedures, (iii) Increased tubal surgery (eithe r sterilization or tuboplasty procedure), (iv) Early

detection of cases that were otherwise destined to undergo spontaneous absorption.

MORBID ANATOMY

CHANGES IN THE TUBE: (i) Implantation in the tube occurs more common ly in intercolumnar fashion, i.e. in

between two mucosal folds. (ii) Decidual change at the site of impla ntation is minimal. The muscles undergo limited hyperplasia and

hypertrophy but more stretching. Blood vessels are engorged. (iii) The blastocyst bur rows through the mucous membrane and lies

between the lumen and the peritoneal covering—so-called intramuscular implantation. (iv) A pseudocapsule is formed consisting of

fibrin, lining epithelium and few muscle fibers. (v) Blood vessels are eroded by the chorionic villi and blood accumulates in between the

blastocyst and the serous coat. (vi) The tube on the implantation site is distended and the wa ll is thinned out. (vii) Blood may sp ill from

the fimbriated end and may cause hemoperitoneum. (viii) The stretching of the p eritoneum over the site of implantation results in

episodic pain. Finally, tubal rupture occurs when the muscles and the serosa are maximally stre tched and undergo necrosis. (ix)

Hemoperitoneum is found in all cases of ruptured tubal ectopic pregnancy. (x) The trophoblasts of ectopic pregnancy do not usually

grow as that of a normal pregnancy. As a result hCG production is inadequate comp ared to a normal pregnancy.

Changes in the uterus : Under the influence of estrogen, progesterone from corpus luteum and cho rionic gonadotrophin, there is varying

amount of enlargement of the uterus with increased vascularity. The decidua develops all t he characteristics of intrauterine

pregnancy except that it contains no evidence of chorionic villi. When progesterone lev el falls due to fall in the level of hCG,

endometrial growth is no longer maintained. Endometrium sloughs out causing uterine b leeding. Sometimes entire decidua is expelled as

a single piece through the cervix. This is known as decidual cast that may be c onfused with a spontaneous abortion.

MODE OF TERMINATION

Because of the unfavorable environment, early interruption of pregnancy is inevitable within 6–8 weeks. Earliest interruption occurs in

the isthmial implantation whereas pregnancy may continue up to 3–4 months in interstitia l implantation. However, genuine cases are on

record of gestation continuing to term in the Fallopian tube. The modes of termination ar e as follows:

Tubal mole (Fig. 15.8) : The formation of the tubal mole is similar to that formed in uterine pregnancy. Repeate d small hemorrhages

occur in the chorio-capsular space, separating the villi from their attachments. The fate of th e mole is either—(a) complete absorption or

(b) expulsion through the abdominal ostium as tubal abortion with a variable amount of internal h emorrhage. The encysted blood so

collected in the pouch of Douglas, is called pelvic hematocele.

Fig. 15.8:Modes of Termination of Tubal Pregnancy

Tubal abortion (Fig. 15.8): This is the common mode of term ination, if implantation occurs in the ampulla or infundibulum.

Muscular contraction enhances separation and facilitates its expulsion through the abdom inal ostium.

Tubal rupture: Tubal rupture is predominantly common in isthmic and interstitial implantation . As the isthmic portion is narrow and

the wall is less distensible, the wall may be easily eroded by the chorionic villi. Isthmic ruptu re usually occurs at 6–8 weeks, the

ampullary one at 8–12 weeks and the interstitial one at about 4 months .

Depending upon the site of rupture , it is known as: (1) Intraperitoneal rupture: This type of r upture is common. The rent is situated

on the roof or sides of the tube. The bleeding is intraperitoneal. (2) Extra-peritoneal r upture (intraligamentary): This is rare and occurs

when the rent lies on the floor of the tube where the broad ligament is attached. It is com monly met in isthmic implantation.

Secondary abdominal pregnancy : The pre-requisites for the continuation of fetal growth outside the tube are: (1) Perforation of the

tubal wall should be a slow process, (2) Amnion must be intact, (3) Placental chorion should esca pe injury from the rupture, (4)

Herniation of the amniotic sac with the living ovum and the placenta should occur through the r ent, (5) Placenta gets attached to the

neighboring structures and new vascular connection should be re-established. The fibrin is deposited over the exposed amnion to

constitute a secondary amniotic sac, (6) Intestine, omentum and adjacent structures get adherent to the secondary sac.

Secondary broad ligament pregnancy : Rarely pregnancy may continue in the same process as in abdo minal pregnancy between the two

layers of the peritoneum.

Arias-Stella reaction : This is characterized by a typical adenomatous change of t he endometrial glands. Intraluminal budding together

with typical cell changes (loss of polarity of cells, pleomorphism, hyperchromatic nuclei , vacuolated cytoplasm and occasional mitosis)

are collectively referred to as Arias-Stella reaction. This is strikingly due to proge sterone influence. It is present in about 10–15% cases

of ectopic pregnancy. It is not, however, specific for ectopic pregnancy but rather the blig htning of conceptus either intrauterine

or extrauterine.

Source of vaginal bleeding: Levels of progesterone secreted by the corpus luteum falls as th ere is insufficient level of hCG.

Endometrial growth and function is no longer maintained and if then sloughs out. On ra re occasion, the bleeding may be due to tubal

abortion through the uterine ostium in interstitial pregnancy.

FATE OF SECONDARY ABDOMINAL PREGNANCY

• Death of the blastocyst→ complete absorption

• Massive intraperitoneal hemorrhage due to placental

separation

• Infection→ fistulous communication with intestine, bladder,

umbilicus

• Fetal death→ mummification, suppuration, adipocere

formation, calcification (lithopaedion)

• Continue to term pregnancy (Rare – 1.0%) (risk of fetal

malformation and deformation)

CLINICAL FEATURES OF ECTOPIC PREGNANCY

Very few clinical conditions exhibit so varied features like that of disturbed tubal pregna ncy. The clinical types are correlated with the

morbid pathological changes in the tube subsequent to implantation and the amount of intra peritoneal bleeding. However, clinically three

distinct types are described:

• Acute • Unruptured • Sub-acute (chronic or old)

ACUTE ECTOPIC: An acute ectopic is fortunately less common (about 30%) and it is as sociated with cases of tubal rupture or tubal

abortion with massive intraperitoneal hemorrhage.

Patient profile: (1) The incidence is maximum between the age of 20 and 30 years, being the max imum period of fertility, (2) The

prevalence is mostly limited to nulliparity or following long period of infertility.

Mode of onset: The onset is acute. The patients, however, have got persistent unilateral unea siness in about one-third of cases before the

acute symptoms appear.

Symptoms: The classic triad of symptoms of disturbed tubal pregnancy are : abdominal pain (100%), preceded by amenorrhea

(75%) and lastly, appearance of vaginal bleeding (70%).

• Amenorrhea: Short period of 6–8 weeks (usually); there may be delayed period or h istory of vaginal spotting. Amenorrhea may be

absent even.

• Abdominal pain is the most constant feature. It is acute, agonising or colicky. Otherwise it m ay be a vague soreness. Pain is located at

lower abdomen: unilateral, bilateral or may be generalized. Shoulder tip pain (25% ) (referred pain due to diaphragmatic irritation from

hemoperitoneum) may be present.

• Vaginal bleeding (see p. 180) may be slight and continuous. Expulsion of dec idual cast (5%) may be there (Fig. 15.3) p. 163.

• Vomiting, fainting attack. Syncopal attack (10%) is due to reflex vasomo tor disturbances following peritoneal irritation from

hemoperitoneum.

SIGNS:

• General look (diagnostic): The patient lies quiet and conscious, perspi res and looks blanched.

• Pallor: Severe and proportionate to the amount of internal hemorrhage.

• Features of shock: Pulse – rapid and feeble, hypotension, extremities—cold clammy.

• Abdominal examination: Abdomen (lower abdomen)—tense, tumid, tender. N o mass is usually felt, shifting dullness present, bowels

may be distended. Muscle guard – usually absent.

• Pelvic examination is less informative due to extreme tenderness and it may precip itate more intraperitoneal hemorrhage due to

manipulation.The findings are: (i) Vaginal mucosa—blanched white (ii) Uterus seems normal in size or slightly bulky (iii) Extreme

tenderness on fornix palpation or on movement of the cervix (75%) (iv) No mass is usu ally felt through the fornix (v) The uterus floats

as if in water. Caution: Vaginal examination may precipitate more hemorrhage due to man ipulation.

UNRUPTURED TUBAL ECTOPIC PREGNANCY

High degree of suspicion and an ectopic conscious clinician can only diagnose the entity at its prerupture state. There is a high frequency

of misdiagnosis and physician delay. The physician should include ectopic pregnanc y in the differential diagnosis when a sexually

active female has abnormal bleeding and/or abdominal pain. This is specially so when th e woman has got some risk factors (p.

178).

Symptoms:• Presence of delayed period or spotting with features suggestive of pregnancy . • Uneasiness on one side of the flank which is

continuous or at times colicky in nature.

Signs: Bimanual examination: (i) Uterus is usually soft showing evidence of early pregnancy (ii) A pulsatile small, well

circumscribed tender mass may be felt through one fornix separated from the ute rus. The palpation should be gentle, else rupture

may precipitate and massive intraperitoneal hemorrhage when shock and collapse may oc cur dramatically.

Investigations: With the advent of transvaginal sonography (TVS), highly sensitive radioimmunoassa y of β hCG and laparoscopy

(see below), more and more ectopics are now diagnosed in unruptured state.

CHRONIC OR OLD ECTOPIC:

Onset: The onset is insidious. The patient had previous attacks of acute pain from which she h ad recovered or she had chronic features

from the beginning.

Symptoms:

• Amenorrhea: Short period of 6-8 weeks is usually present.

• Lower abdominal pain is present with varying degrees. It starts as an acute one a nd gradually becomes dull or colicky in nature.

• Vaginal bleeding appears sooner or later following the pain. It is scanty, sanguinous o r dark-colored and continuous in nature.

Expulsion of decidual cast may be present (see Fig.15.3).

• Other symptoms: There may be features of bladder irritation —dysuria, frequency or even retention of urine. Rectal tenesmus may

appear specially following infected hematocele. Rise of temperature may be due to infecti on or due to absorption of the products of

degenerated blood accumulated in the abdomen.

On examination (signs): • Bimanual examination is painful and reveals: (i) Va ginal

• The patient looks ill

mucosa—pale (ii) Uterus seems to be normal in size or

•

Pallor

varying degree is present

bulky, often incorporated in the mass occupying the pelvis

(iii) Extreme tenderness on movement of the cervix (iv) An

• Pulse persistently high even during rest—a conspicuous ill-defined, boggy an d extremely tender mass is felt

finding

through the

posterolateral fornix extending to the pouch

•

Features of shock

are absent

of Douglas. The mass may push the uterus to the opposite

side

• Temperature may be slightly elevated to 38°C • Rectal examinati on corroborates the pelvic findings

• Abdominal examination: (i) Tenderness and muscle guard

• Examination under anesthesia (EUA) is helpful to evaluate

on the lower abdomen specially on the affected side is a

the pelvic findings but accidental tubal rupture may be

striking feature (ii) A mass in the lower abdomen may be

provoked during manipulation. Moreover, the diagnostic

felt which is irregular and tender

(iii) Cullen‘s sign—Dark

features of pain on examination and tenderness on moving the cervix (cervical excitat ion pain) cannot be elicited.

bluish discoloration around the umbilicus, if found, suggests

intraperitoneal hemorrhage

DIAGNOSIS OF ECTOPIC PREGNANCY

ACUTE ECTOPIC: The classic history of acute abdominal catastrophe with fainting attack and collapse associated with features

of intra-abdominal hemorrhage in a woman of child bearing age points to a certain diagnosis of acute ectopic.

No time should be wasted for investigations other than estimation of hemoglobin and blo od grouping (ABO and Rh).

Ecamination under anesthesia: Extreme tenderness on vaginal examination, which is of signific ance, cannot be elicited by EUA.

Moreover, at times, it proves risky as the manipulation may provoke further bleeding. I n any case, laparotomy is indicated by its own

merit even though it may be proved otherwise.

Differential diagnosis of acute ectopic pregnancy are: (1) acute appendicitis (2) ruptured corpus luteum. Clinic al presentation is

similar to ruptured tubal ectopic pregnancy— pregnancy test is negative (3) twisted ova rian tumor (4) ruptured chocolate cyst and (5)

perforated peptic ulcer. Considering the fact that all the clinical conditions require urgen t laparotomy, there is no possibility of acute

ectopic being overlooked.

SUBACUTE (CHRONIC) ECTOPIC:It is indeed difficult at times to diagnose old ectopic s because of vagaries of clinical features

mentioned earlier.Increased awareness on the part of the clinicians is the sheet anchor in the diagnosis of old ectopic. The

confusing features are: (1) Absence of amenorrhea (2) Absence of vaginal bleeding (3) Vaginal bleeding followed by pain (4)

Apparently normal general condition (5) Presence of bilateral mass on internal examina tion (6) Previous history of tubectomy operation

or IUD insertion.

Investigations for the diagnosis of tubal ectopic pregnancy

• Blood examination should be done as a routine for: (i) Hemoglobin (ii) ABO and R h grouping (iii) Total white cell count and

differential count (iv) ESR. There may be varying degrees of leucocytosis and raised ESR.

• Culdocentesis is simple and safe. Where sensitive TVS or laparoscopy is not rea dily available, culdocentesis is still a diagnostic

alternative. Unfortunately negative culdocentesis does not rule out an ectopic pregnancy neither a positive result is very specific.

Through a 18 gauze lumbar puncture needle fitted with a syringe, the posterior fornix ispunc turedtogain

accesstothepouchofDouglas.Aspirationofnonclotting bloodwith hematocrit > 15% signif ies ruptured ectopic pregnancy.

• Estimation of β hCG: Urine pregnancy test—ELISA is sensitive to 10-50 mIU/ml and are positive in 95% of ectopic pregnancies. A

single estimation of β hCG level either in the serum or in urine confirms pregnancy but cannot determ ine its location. The

suspicious findings are: (1) Lower concentration of β hCG compared to normal intraut erine pregnancy (2) Doubling time in plasma fails

to occur in 2 days.

• Sonography: Transvaginal sonography (TVS) is more informative. The diagnostic features are: (1) Absence of intrauterine

pregnancy with a positive pregnancy test. (2) Fluid (echogenic) in the pouch of Douglas. (3) Adnexal mass clearly separated from the

ovary. (4) Rarely cardiac motion may be seen in an unruptured tubal ectopic pregnancy. Color Do ppler Sonography: (TV–CDS)—can

identify the placental shape (ring-of-fire pattern) and enhanced blood flow pattern outside th e uterine cavity.

• Combination of quantitative β hCG values and sonography : TVS provides visualization of a well formed intrauterine gestational

sac as early as 4-5 weeks from the last menstrual period. The lowest level of se rum β hCG at which a gestational sac is consistently

visible using TVS (discriminatory zone) is 1500 IU/L. The corresponding valu e of serum β hCG for TAS is 6000 IU/L. (1) When the β

hCG value is greater than 1500 IU/L and there is an empty uterine cavity, ectopic pr egnancy is more likely. (2) Failure to double the

value of β hCG by 48 hours along with an empty uterus is very much suggestive.

• Laparoscopyoffers benefit in cases of confusion with other pelvic lesions . It should be employed only when the patient is

hemodynamically stable. Advantages are:(i) Confirmation of diagnosis ( ii) Removal of the ectopic mass using operative procedures at

the same time (iii) Direct injection of chemotherapeutic agents into the ectopic mass—when med ical management is decided (see p.

189). However, laparoscopy runs the risk of false positive or false negative diagn osis in 2–5% of cases.

• Dilatation and curettage—Identification of decidua without villi structure is ve ry much suggestive. Chorionic villi that float in normal

saline as lacy fronds, is diagnostic of intrauterine pregnancy.

• Serum progesterone—Level greater than 25 ng/ml is suggestive of viable intra uterine pregnancy whereas level less than 5 ng/ml

suggests an ectopic or abnormal intrauterine pregnancy.

• Laparotomyoffers benefit when in doubt. The old axiom, “open and see” holds good specially when the patient is hemo dynamically

unstable. One should not be ashamed of having a negative abdominal exploration, rat her to be disgraced for the mistake in

diagnosis with the eventual fatality. Differential diagnosis of subacute ectopic pregnancy :

1. Incomplete abortion: (i) Bleeding appears prior to pain (ii) Absence of fainting attack (iii) Ble eding is bright-red and at times profuse

(iv) General condition proportionate with visible blood loss (v) No features of intraperi toneal bleeding (vi) Fornix palpation gives

negative findings (vii) D & C relieves the symptoms (viii) Histological examinatio n shows presence of villi. Persistence of symptoms

even after thorough uterine curettage, makes one suspicious of ectopic.

2. Salpingitis: (i) Previous history of similar attacks of pain (ii) The pain is of burning nature (iii) Amenorrhea is absent although slight

bleeding may appear (iv) Rise of temperature is more (v) The patient is tossin g in bed (vi) Pallor is absent, rather the face is flushed

(vii) Pelvic examination reveals—bilateral tenderness or mass (viii) Leucocytosis.

3. Appendicitis: (1) Pain and tenderness settles down to the McBurney’s point (2) Muscle gu ard and rigidity are characteristic. (3) Pelvic

findings are negative.

4. Twisted ovarian tumor: (1) History of presence of previous swe lling (2) Fainting attack is absent (3) Vaginal bleeding may appear

confusing the picture (4) General condition remains unaffected (5) Internal examinatio n reveals a cystic mass felt separated from the

uterus.

5. Ruptured chocolate cyst of the ovary.

6. Ruptured corpus luteum: Clinical presentation is similar to tubal rupture but pregnancy test is negative.

INTERSTITIAL PREGNANCY (FIG. 15.9)

It is the rarest variety of tubal pregnancy . Because of the thick an d vascular musculature of the uterine wall with greater

distensibility, the fetus grows dissecting the muscle fibres for a longer period (12-14 we eks) before termination occurs. The usual

termination is rupture. It is associated with massive intraperitoneal hemorrh age due to its combined vascularization by the uterine

and ovarian arteries. On rare occasion, abortion occurs through the uterine cavity.

The diagnosis before rupture is very difficult. Asymmetrical enlargement of the uterus specially detected during active contraction is a

conspicuous finding. It is usually confused with lateral flexion of a gravid uterus, pregn ancy associated with fibroid or pregnancy in

bicornuate uterus or with angular pregnancy. β hCG, high

Fig. 15.9A:Interstitial pregnancy Fig. 15.9B:Ruptured interstitial pregnancy— subtotal hysterectomy done

resolution sonography and laparoscopy can lead to early diagnosis. However, the diag nosis is revealed on laparotomy following

termination as rupture. Hysterectomy is commonly done.

MANAGEMENT OF ECTOPIC PREGNANCY

Over the past decade, the management of ectopic pregnancy (in uncommon locations) has evolved from a radical operative approach

(salpingectomy) to a more conservative surgical or medical treatment. This has be en possible due to early diagnosis, advanced

laparoscopic techniques and ability to monitor the patient after conservative surgical or m edical treatment. However, the type of

treatment must be individualized and depends more on clinical presentation.

ACUTE

Principle : The principle in the management of acute ectopic is resuscitation and laparotomy and not resuscitation followed by

laparotomy.

Anti-shock treatment: Anti-shock measures are to be taken energetically with simultaneou s preparation for urgent laparotomy.

• Ringer’s solution (crystalloid) is started, if necessary with venesection.

• Arrangement is made for blood transfusion. Even if blood is not availab le, laparotomy is to be done desperately. When the blood is

available, it is better to be transfused after the clamps are placed to occlude the b leeding vessels on laparotomy, as it is of little help to

transfuse when the vessels are open.

• After drawing the blood, samples for grouping and cross matching, volume replacement with colloids (hemaccel) is to be done.

Laparotomy: Indications of Laparotomy are—(i) Patient hemodynamically unstable (ii) Lapar oscopy contraindicated (iii) Evidence of

rupture. The principle in laparotomy is ‘quick in quick out’.

Steps:

• Abdomen is opened by infraumbilical longitudinal incision.

• To grasp the uterus and draw it up under vision.

• The tubes and ovaries of both the sides are quickly inspected to find out the s ide of rupture.

• Salpingectomy (Fig. 15.10) is the definitive surgery. The excised tube should be s ent for histological examination.

• The ipsilateral ovary and its vascular supply is preserved. Oophorectomy i s done only if the ovary is damaged beyond salvage

or is pathological.

• Place of subtotal hysterectomy (Fig. 15.9B): In interstitial pregnancy, the rupture rent is so big and the general condition is so low

that, most often, a quick subtotal hysterectomy is done. However, if the condition permi ts and the uterine conservation is desirable,

resection of the uterus may be attempted.

Fig. 15.10: Salpingectomy. Note the placement of the clamps.

Place of auto transfusion : Its routine use is not advocated because of its adverse reaction. In case, where donated blo od is not available,

the fresh blood from the peritoneal cavity may be collected for auto transfusion. The co llection is done through strainer consisting of 4-5

layers of sterile gauze pieces into a bottle containing citrate soluton (3.8%) in the propor tion of five parts of blood to one part of citrate

solution.

CHRONIC ECTOPIC: All cases of chronic or suspected ectopic are to be admitted as an emerg ency. The patient is kept under

observation, investigations are done and the patient is put up for laparotomy at the ear liest convenient time. Usually a pelvic hematocele

is found. Blood clots are removed. The affected tube is identified and salping ectomy is commonly done as described previously.

Resumption of ovulation and contraception: About 15% of women ovulate by 19 days and about 25% ovulate by the 30th

postoperative day. Contraception should ideally be commenced at the time of hospital di scharge.

UNRUPTURED TUBAL PREGNANCY

Management: • Expectant • Conservative • Salpingectomy

Expectant management : Where only observation is done hoping spontaneous resolution.Ind ications are: (i) Initial serum hCG level <

1000 IU/L and the subsequent levels are falling (ii) Gestation sac size < 4 cm (iii) No fetal heart beat on TVS. (v) No evidence of

bleeding or rupture.

A B C

Figs 15.11A to C: Laparoscopic linear salpingostomy for unruptured tubal pregnan cy—(A) Linear incision on the antimesenteric

border (B) Gestationsac is removed(C) Incisionmargins left unsutured.Above: Schema tic andBelow: operation.

Conservative management may be either medical or surgical. Otherwise salpingectomy is done.

The advantages of conservative management are: (1) Significant reduction in operativ e morbidity, hospital stay as well as cost (2)

Improved chance of subsequent intrauterine pregnancy (3) Less risk of recurrence.

Medical management: Number of chemotherapeutic agents have been used either sys temic or direct local (under sonographic or

laparoscopic guidance) as medical management of ectopic pregnancy. The dr ugs commonly used for salpingocentesis are:

methotrexate, potassium chloride, prostaglandin (PGF

2α

), hyperosmolar glucose or actinomycin. The patient must be (i)

hemodynamically stable (ii) Serum hCG level should be < 3000 IU/L (iii) tubal diameter should be less than 4 cm without any fetal

cardiac activity (iv) There should be no intra-abdominal hemorrhage. For systemic therapy, a sin gle dose of methotrexate (MTX) 50 mg/

is given intramuscularly.

Monitoring is done by measuring serum β hCG on D

and D

. When the decline in hCG between (i) D

and D

is > 15%, patient is

followed up weekly with serum hCG until hCG < 10 mIU/ml. If the decline is < 15%, a second dose of MTX 50 mg/M

is given on D

Variable dose methotrexate (MTX) includes: MTX – 1 mg/kg IM on D

1,3,5,7

and Leukovorin 0.1 mg/kg IM on D

2,4,6&8

. Serum β

hCG is monitored weekly until < 5.0 mIU/ml.

Conservative Surgery: The procedure can be done either laparoscopically or by microsurgical lap arotomy.

1. Linear Salpingostomy: A longitudinal incision is made on the antimesenteric border directly over the site of ectopic pregnancy. After

removing the products (by fingers, scalpel handle or by suction), the incision line is kep t open to be healed later on by secondary

intention. Hemostasis is achieved by electrocautery or laser (Fig. 15.11).

2. Linear Salpingotomy: The procedures are the same as those of salpingostomy. But the incision line is closed in 2 layers with 7-0

interrupted vicryl sutures. This is not commonly done.

3. Segmental Resection: This is of choice in isthmic pregnancy. End to end anasto mosis can be done immediately or at a later date after

appropriate counselling of the patient.

4. Fimbrial Expression: This is ideal in cases of distal ampullary (fimbrial) pregnancy and is done digitally. Salpingectomy is done

when (i) whole of the affected tube is damaged (ii) contralateral tube is normal or (iii) f uture fertility is not desired.

Following conservative surgery or medical treatment, estimation of β-hCG should be do ne weekly till the value becomes < 5.0 mlU/ml.

Additional monitoring by TVS is preferred. Following laparoscopic salpingostomy, pers istent ectopic pregnancy ranges between 4-20%.

Persistent ectopic pregnancy is due to incomplete removal of trophoblast. It is high after fimbr ial expression and in cases where initial

serum β hCG level is > 3000 IU/L. Prophylactic single dose MTX (1 mg/kg) I.M. is effective to resolve the problem.

Rh-NEGATIVE WOMEN: In Rh-negative women not yet sensitized to Rh antigen, anti- D gamma globulin— 50 microgram (if

gestation < 12 weeks) or 300 µg (if > 12 weeks) intramuscularly is administered soon following operation to prevent isoimmunization.

PROGNOSIS OF TUBAL PREGNANCY: Immediate prognosis so far as maternal mortality is concerned has been markedly reduced

(0.05%) due to early diagnosis, adequate blood replacement and surgery even in desp arately ill patient. An ectopic mother has got every

chance of a viable birth in 1 in 3 and a chance of recurrence of ectopic in 1 in 10. Patient is asked to report after she misses her period to

confirm and to locate the new pregnancy.

PREVENTION OF RECURRENCE OF TUBAL PREGNANCY: Incidence of subsequent intrauterine pregnancy (IUP) is 60-70%,

in women with unruptured tubal ectopic pregnancy treated by conservative surgery. T he incidence of subsequent ectopic pregnancy is

about 10-20% and successful conception is about 60%.

Salpingostomy done for unruptued tubal ectopic pregnancy does not increase the risk o f ectopic pregnancy compared to salpingectomy.

Conservative surgery for unruptured tubal ectopic pregnancy is beneficial.

Future advice: Main concern is the risk of recurrence. Whenever there is amenorrh ea, pregnancy test is done and if positive, hig h

resolution TVS is done to know the site of pregnancy.

ABDOMINAL PREGNANCY

PRIMARY: Primary implantation of the fertilized ovum on the peritoneum is s o rare that its existence is questionable. However, the

criteria laid down by Studiford to diagnose primary abdominal pregnancy are : (1) Both the tubes and ovaries are normal without

evidence of recent injury (2) Absence of uteroperitoneal fistula (3) Presence of a pregnan cy related exclusively to the peritoneal surface

and young enough to eliminate the possibility of secondary implantation following primary nidation in the tube.

SECONDARY: Abdominal pregnancy is almost always secondary, the primar y sites being tube, ovary or even the uterus—the

conceptus escapes out through the rent in the uterine scar. The morbid pathological pro cess and the fate of the pregnancy have been

described previously (p. 180). The average incidence is about 1 in 3000 pregnancie s. With the use of ART incidence is found rising.

Symptoms: (1) History suggestive of disturbed tubal pregnancy during early months (pain l ower abdomen and vaginal bleeding) is often

present (2) Minor ailments of normal uterine pregnancy are often exaggerated, such as na usea, vomiting, constipation, pain abdomen and

increased fetal movements.

Signs in advanced pregnancy: (1) Uterine contour is not well defined even by massaging the abdominal wall, as the Braxton-Hicks

contraction is absent in abdominal pregnancy (2) Fetal parts are felt easily and persistent ab normal attitude and position of the fetus

on repeated examination is quite common. While abnormal high position of the fetus is c ommonly found in intraperitoneal pregnancy,

the fetus is lying low in intraligamentary pregnancy.

Internal examination : The uterus is difficult to separate from the abdominal mass. If it does, it is enla rged (12-16 weeks) but the cervix

is not typically soft and is usually displaced depending upon the position of the sac.

Imaging Studies:

Sonography : It is commonly performed. Suggestive features are—absence of uterine wall ar ound the fetus, abnormally high position of

fetus with abnormal attitude, fetal parts with close approximation to maternal abdominal wall and visualization of the uterus separately.

Diagnostic error could be even up to 40%.

Magnetic Resonance Imaging (MRI) can confirm the diagnosis and may be very ac curate.Computed tomography is diagnostic and is

superior to MRI. CT has the risk of radiation.

X-ray examination: Straight X-ray reveals—(a) Abnormally high position of the fetus w ith absence of outline of uterine shadow (b)

Superimposition of gas shadow on the fetal skeleton (c) Lateral X-ray on standing posi tion shows superimposition of fetal skeleton

shadow with the maternal spinal shadow.

DIAGNOSIS: Its rarity, variegated clinical pictures and not keeping in mind the possibility , lead to confusion in diagnosis. To give a

positive diagnosis, the clinician should be conscious of the entity. Highly suggestive features: (1) Repeated failu re of induction for

intrauterine fetal death (2) During induction of labor by oxytocin, uterine contraction c ould not be excited. Surest evidence is on

laparotomy.

MANAGEMENT: Once the diagnosis is made, the opinion is almost crystallized in favor o f urgent laparotomy irrespective of period

of gestation. The risks of continuation of pregnancy are: (1) Catastrophic hemorrhage (2) Fe tal death (3) Increased fetal malformation

(4) Increased neonatal loss (50%). Thus continuation of pregnancy for few weeks ho ping the baby to become mature enough to survive

can only be justified in exceptional circumstances. The patient and her relatives should b e explained about the eventuality. During the

period, the patient should be in the hospital.

Laparotomy: The ideal surgery is to remove the entire sac-fetus, the placenta and the membra nes. This may be achieved if the placenta

is attached to a removable organ like uterus or broad ligament. If however, the pla centa is attached to vital organs, it is better to take out

the fetus and leave behind the placenta and the sac, after tying and cutting the cord flus hed with its placental attachment. In such a

situation, placental activity is to be monitored by quantitative serum β-hCG level and ultrasound. Complete absorption of the left behind

placenta occurs through aseptic autolysis. Complications include secondary he morrhage, intestinal obstruction and infection.

Prognosis : Because of the risk mentioned before maternal mortality is less than 5% but m orbidity is high. Perinatal mortality

approximates 90%. Fetal malformation could be as high as 50%. Normal infants have b een reported in 10% of cases.

OVARIAN PREGNANCY

Spiegelberg‘s criteria in diagnosis of ovarian pregnancy are— (1) Tube on the affected side must be intact (2) Th e gestation sac must

be in the position of the ovary (3) The gestation sac is connected to the uterus by the ov arian ligament (4) The ovarian tissue must be

found on its wall on histological examination.

The embedding may occur intrafollicular or extrafollicular. In either types, rupture is an inevitable phenomenon and salpingo-

oophorectomy is the definite surgery. Ovarian resection could be done whe n the diagnosis is made early.

CORNUAL PREGNANCY

Pregnancy occurring in rudimentary horn of a bicornuate uterus, is called cornual p regnancy (Fig. 15.12) . The horn does not

usually communicate with the uterine cavity. The impregnation is presumed to occur by a spermatozoa which passes through the normal

half of the uterus and tube. It then fertilizes an ovum either in the peritoneal cavity or in the tube connected to the rudimentary horn. The

concerned ovum is usually shed from the ovary on the same side of the rudimentary ho rn.

The general and local reactions are similar to those in the tubal pregnancy. But these are intensified and pregnancy may continue for

longer time. Termination by rupture is inevitable between 12 and 20 weeks with massive intraper itoneal hemorrhage.

The diagnosis is seldom done before the catastrophe. The condition is com monly diagnosed as fibroid or ovarian tumor with

pregnancy. Even on laparotomy, the exact position is confused with interstitial pregnancy. Position o f the round ligament which is

attached to the sac and the long pedicle by which it is attached to the uterus are the diagno stic points. Surgery includes removal of

the rudimentary horn. If the pedicle is short and the attachment is wide, hysterectomy m ay have to be done.

Fig. 15.12: Cornual pregnancy

CERVICAL PREGNANCY

This is a rare (1 in 16,000 pregnancies) variant of ectopic pregnancy when the implantation occurs in th e cervical canal at or below

the internal os. Erosion of the walls by the trophoblasts occurs resulting in thinnin g and distension of the canal. The condition is

commonly confused with cervical abortion. In cervical pregnancy, the bleeding is painless and the ute rine body lies above the

distended cervix. Intractable bleeding following evacuation or expulsion of the products brings about suspicion. The morbidity and

mortality is high because of profuse hemorrhage. Clinical diagnostic criteria (Rubin–1 983) for cervical pregnancy are—(a) Soft,

enlarged cervix equal to or larger than the fundus (b) Uterine bleeding following amen orrhea, without cramping pain (c) Products of

conception entirely confined within and firmly attached to endocervix (d) A closed inte rnal cervical os and a partially opened external os

(Fig. 15.13). Sonography reveals the pregnancy in the cervical canal and an e mpty uterine cavity. Hysterectomy is often required to stop

bleeding. An attempt to preserve the uterus may be made by intracervical pluggin g. Methotrexate therapy has been considered both

systemic and direct local as an alternative or adjunct to hysterectomy. Uterine artery emb olization with gelfoam can control hemorrhage.

Confirmation is done by histological evidence of the presence of villi inside the cervic al stroma.

Pregnancy of unknown location : No sign of either intra or extrauterine pregnancy or retained prod ucts of conception in a woman with

a positive pregnancy test.

Pregnancy of uncertain viability: Intrauterine gestation sac (< 20 mm mean diamete r) with no obvious yolk sac or fetus or fetal echo <

6 mm crown-rump length with no obvious fetal heart activity. In order to confirm or refute viab ility, a repeat scan at a minimal interval of

1 week is necessary.

A B C

Figs 15.13A to C: Cervical pregnancy—hysterectomy done (showing Rubin’s diagnostic criteria): (A) Globular cervix with partially

opened external os (B) Uterus cut opened through the anterior wall to show the huge h emorrhagic mass occupying the cervical canal

with empty uterine cavity (C) When the mass was dissected, the cervical wall showed m acroscopic evidence of invasion of trophoblastic

tissue (confirmed on histology)

Heterotopic pregnancy: Incidence is about 1 in 8000 pregnancies at present. It is more common following ART procedures.

Intrauterine pregnancy may be coexistent with tubal or rarely with cervical or ovarian p regnancy. Diagnosis is difficult. Absence of

vaginal bleeding in the presence of signs and symptoms of an ectopic pregnancy is suspicious. Ab normally rising hCG level and

ultrasonography may be helpful.

GESTATIONAL TROPHOBLASTIC DISEASES (GTD)

DEFINITION: Gestational Trophoblastic Disease (GTD) encompasses a spectrum of prol iferative abnormalities of trophoblasts

associated with pregnancy. Persistent GTD (persistently raised βhCG) is referred as ges tational trophoblastic neoplasia (GTN).

CLASSIFICATION: Classification and terminology of GTD is extensive and at times co nfusing. Morphological classification of GTD

is less important. Because at present management is largely medical irrespective of histology. Follow up of patients with GTD again

depends on hCG than on histologic diagnosis.Immunohistochemical and molecular st udies are thought to be more important.

The conventional histological classification , includes—hydatidiform mole (complete and partial), invasive mole, choriocarcinoma and

placental site trophoblastic tumor (PSTT). Modified WHO (1998) classification on GTD has been given here (p. 191). Metastatic disease

may be A. Low risk or B. High risk group.

Non-gestational trophoblastic disease occurs as a primary chorioc arcinoma of the ovary and is probably a teratomatous tumor.

HYDATIDIFORM MOLE (Syn: Vesicular mole)

TYPES: • Complete • Incomplete (partial)

The types are categorized on the basis of gross morphology, histopathology and karyo type (see table p.

198). However, unless specified, molar pregnancy relates one with complete mole.

DEFINITION:It is an abnormal condition of the placenta where there are partly dege nerative and partly

proliferative changes in the young chorionic villi. These result in the formatio n of clusters of small cysts of

varying sizes. Because of its superficial resemblance to hydatid cyst, it is named as hyda tidiform mole. It is

best regarded as a benign neoplasia of the chorion with malignant potential.

INCIDENCE: There is wide range of geographical and ethnic variation of the pre valence of the condition. The

molar pregnancy is common in Oriental countries—Philippines, China, Indonesia, Japan , India, Central and

Latin America and Africa. The highest incidence is in Philippines being 1 in 80 pregnancies and lowest in

European countries 1 in 752 and USA being about 1 in 2000. The incidence, in India, is about 1 in 40 0. ETIOLOGY: The cause is not

definitely known,

but it appears to be related to the ovular defect as

it sometimes affects one ovum of a twin pregnancy.

However, the following factors and hypotheses have

been forwarded:

— Its prevalence is highest in teenage pregnancies and in those women over 35 years of age.

— The prevalence appears to vary with race and ethnic origin.

— Faulty nutrition caused by inadequate intake of protein, animal fat could partly e xplain its preva-lence in the Oriental Countries. Low

dietary intake of carotene is associated with increased risk.

— Disturbed maternal immune mechanisms suggested by—(a) Rise in gammaglobulin l evel in absence of hepatic disease (b) Increased

association with AB blood group which possesses no ABO antibody.

— Cytogenetic abnormality—In general, complete moles have a 46, XX kar yotype

CLASSIFICATION OF GTD

• Hydatidiform mole: – Complete – Partial

• Invasive mole

• Placental site trophoblastic tumor

• Choriocarcinoma

Non metastatic disease (confined to the uterus) Metastatic disease:

A. Low risk (good prognosis)

– Disease is present < 4 months duration – Initial serum hCG level < 40,000 mIU/ml – Metastasis limited to lung and vagina

– No prior chemotherapy

– No preceding term delivery

B. High risk (poor prognosis)

– Long duration of disease (> 4 months) – Initial serum hCG > 40,000 mIU/ml

– Brain or liver metastasis

– Failure of prior chemotherapy

– Following term pregnancy

– WHO score > 8

(85%) , the molar chromosomes are derived entirely from the father. The ovum nucleus may be either absent (empty ovum) or

inactivated which has been fertilized by a haploid sperm. It then duplicates its ow n chromosomes after meiosis. This phenomenon is

known as androgenesis. Infrequently, the chromosomal pattern may be 46, XY or 45, X.

— The higher the ratio of paternal: maternal chromosomes, the greater is the molar cha nge. Complete moles show 2: 0 paternal/maternal

ratio whereas partial mole shows 2: 1 ratio.

— History of prior hydatidiform mole increases the chance of recurrence (1 to 4%).

PATHOLOGY OF HYDATIDIFORM MOLE

It is principally a disease of the chorion . Death of the ovum or failure of the embr yo to grow is essential to develop complete (classic)

hydatidiform mole. The secretion from the hyperplastic cells and transferred substances from the maternal blood accumulate in the

stroma of the villi which are devoid of blood vessels. This results in distension of the vill i to form small vesicles. The distension may

also be due to edema and liquefaction of the stroma. Vesicle fluid is interstitial fluid an d is almost similar to ascitic or edema fluid,

but rich in hCG.

Naked eye appearance (Fig. 15.14): The mass filling the uterus is made of multiple chains and clusters of cysts of varying sizes. There

is no trace of embryo or the amniotic sac. Hemorrhage, if occurs, takes place in the decidual sp ace.

Microscopic appearance (Fig. 15.15): The basic findings are—(1) There is marked prolife ration of the syncitial and cytotrophoblastic

epithelium (2) Marked thinning of the stromal tissue due to hydropic degeneration (3) There is absence of blood vessels in the villi which

seems primary rather than due to pressure atrophy (4) The villus pattern is distinc tly maintained.

Ovarian changes : Bilateral lutein cysts are present in about 50%. These are due to excessive pr oduction of chorionic gonadotropin and

they are also observed in multiple pregnancy. These regress spontaneously within two m onths after expulsion of mole. The contained

fluid is rich in chorionic gonadotropin. It also contains estrogen and progesterone.

Fig. 15.14: Hydatidiform mole showing clusters of vesicles of varying sizes

Fig. 15.15: Histological section of hydatidiform mole showing hydropic degeneration of the villus stroma w ith absence of blood vessels

and trophoblastic proliferation (Dr S K Dutta)

CLINICAL FEATURES

Age and parity: It is prevalent amongst teenaged and elderly patients w ith high parity. The patient gives history of amenorrhea of 8–12

weeks with initial features suggestive of normal pregnancy but subsequently presents with the following manifestations (often confused

with abortion).

SYMPTOMS

— Vaginal bleeding:Vaginal bleeding is the commonest presentation (90%). Often the symptom s mimic an incomplete or theratened

abortion. The blood may be mixed with a gelatinous fluid from ruptured cysts giving the appearance of discharge “white currant in red

currant juice”.

— Varying degree of lower abdominal pain may be due to—(a) Over stretching of th e uterus (b) Concealed hemorrhage (c) Rarely

perforation of the uterus by the invasive mole (d) Infection or (e) Uterine contractions to ex pel out the contents.

— Constitutional symptoms: (a) The patient becomes sick withou t any apparent reason (b) Vomiting of pregnancy becomes

excessive to the stage of hyperemesis in 15% cases. It is probably related to excess chorionic gonadotr opin (c) Breathlessness due to

pulmonary embolization of the trophoblastic cells (2%) (d) Thyrotoxic features of tremors or tachycardia are present on occasion (2%).

It is probably due to increased chorionic thyrotropin.

— Expulsion of grape like vesicles per vaginam is diagnostic of vesicular mole. Actually, in ap proximately 50% of cases the mole is

not suspected until it is expelled in part or whole.

— History of quickening is absent.

SIGNS

— Features suggestive of early months of pregnancy are evident.

— The patient looks more ill than can be accounted for.

— Pallor is present and may be unusually out of proportion to the visible blood lo ss. This may be due to concealed hemorrhage. It is

mostly due to iron deficiency but may be megaloblastic due to folic acid deficiency.

Classical Clinical Features of a Complete Mole

Abnormal vaginal bleeding

t Lower abdominal pain

t Hyperemesis gravidarum

Features of early onset pre-eclampsia < 20 weeks

Uterus > dates (50%)

Absent fetal parts and FHS

t Expulsion of vesicular tissues (Fig. 15.17)

t Thecalutein cyst of ovaries (25%) > 6 cm

Hyperthyroidism (rare)

Serum hCG > 100,000 mIU/mL

USG: snowstorm appearance

— Features of pre-eclampsia (hypertension, edema and/or proteinuria) are present in about 50%. O n rare

occasion, convulsion may occur.

Per abdomen:

— The size of the uterus is more than that expected for the period of amenorrh ea in 70%, corresponds with the period of amenorrhea in

20% and smaller than the period of amenorrhea in 10%. The frequent findings of undu e enlargement of the uterus is due to exuberant

growth of the vesicles andthe concealed hemorrhage.

— The feel of the uterus is firm elastic (doughy). This is due to the absence of the amniotic fluid sac. — Fetal parts are n ot felt, nor

any fetal movements. External ballottement cannot be elicited. — Absence of fetal heart soundwhich cannot be detected even by the

Doppler effect cardioscope.

The negative abdominal signs are of value when these signs should have been present depending on the size of the uterus presented in

the particular case.

Vaginal examination:

— Internal ballottement cannot be elicited.

— Unilateral or bilateral enlargement (theca lutein cyst) of the ovary may be p alpable in 25–50% of cases. The enlarged ovary may

not be palpable due to the enlarged uterus.

— Finding of vesicles in the vaginal discharge is pathognomonic of hydatidiform mole.

— If the cervical os is open, instead of the mem-branes, blood clot or the vesicles may be felt.

Investigations:

t Full blood count, ABO and Rh grouping.

t Hepatic, renal and thyroid function tests are carried out.

t Sonography: Characteristic features of molar pregnancy is ‘snowstorm’ appearance (Fig. 15.16). Sometimes confusion arises with

the missed abortion, partial mole or the degenerated fibroid. Doppler USG, sonograph y of liver, kidneys and spleen is also carried out.

t Quantitative estimation of chorionic gonadotropin: High hCG titre in urine (positive pregnancy test) diluted up to 1 in 200 to 1 i n

500 beyond 100 days of gestation is very much suggestive. Rapidly increasing value o f serum hCG (hCG > 100,000 mIU/mL), are usual

with molar pregnancies. Normal pregnancy value reaches a peak at about 10 –14 weeks and rarely it is more than 100,000 mIU/mL.

Serum hCG value > 2 MOM for corresponding gestational age is of value.

t Plain X-ray abdomen: If the uterine size is more than 16 weeks, a negative fetal shado w may be of help. Straight X-ray of the chest

should also be carried out as a routine for evidence of pulmonary embolizatio n even in benign mole.

t CT and MRI: Routine use of computed tomography or magnetic resonance imaging for diagnosis or to detect metastatic disease is not

recommended.

 Definitive diagnosis is made by histological examination of the products of conception ( Fig. 15.15).

DIFFERENTIAL DIAGNOSIS: The following conditions are often confused with molar pregnancy: Estimation of serum hCG and

ultrasonography are diagnostic.

• Threatened abortion: Persistence of dark-colored vaginal bleeding with mist aken date showing disproportionate increase in size of the

uterus is quite confusing on clinical examination.

• Fibroid or ovarian tumor with pregnancy: Disproportionate enlargement of th e uterus is the confusing point.

• Multiple pregnancy: Presence of pre-eclampsia in early months, disp roportionate enlargement of the uterus and unusually high hCG

titre in the urine are confusing features. Twin pregnancy with one norm al fetus and placenta and the other with complete mole is

differentiated from partial mole by cytogenetic and high resolution USG studies.

Fig. 15.16:‘Snowstorm’ appearance of Hydatidiform mole

COMPLICATIONS OF MOLAR PREGNANCY

Immediate: (1) Hemorrhage and shock—The causes of hemorrhage are: (a) Separation of the vesicles from its attachment to the

decidua. The hemorrhage may be concealed or revealed. (b) Massive intraperitoneal h emorrhage which may be the first feature of a

perforating mole. (c) During evacuation of the mole due to—(i) atonic uterus or ( ii) uterine injury.

(2) Sepsis: The increased risk of sepsis is due to: (a) As there are no prote ctive membranes, the vaginal organisms can creep up into

the uterine cavity. (b) Presence of degenerated vesicles, sloughing decidua and old blood favors nidation of bacterial growth. (c)

Increased operative interference.

(3) Perforation of the uterus: The uterus may be injured due to: (a) Perforating mole—which may produce massive intraperitoneal

hemorrhage (b) During vaginal evacuation specially by conventional (D & E) method o r during curettage following suction evacuation.

(4) Pre-eclampsia with convulsion on rare occasion. (5)Acute pulmonary insufficiency due to pulmonary embolization of the

trophoblastic cells with or without villi stroma. Symptoms usually begins within 4–6 hour s following evacuation.

(6) Coagulation failure due to pulmonary emboliza-tion of trophoblastic ce lls as they cause fibrin and platelets deposition within the

vascular tree (see p. 626).

Late: The development of choriocarcinoma follow-ing hydatidiform mole ranges between 2 and 10%. The known risk factors are

recorded in the box above which are more likely to be associated with the maligna nt change.

PROGNOSIS:Immediate risk from hemorrhage and sepsis ar e markedly diminished due to early diagnosis, blood transfusion and

treatment. About 15-20% of complete moles progress to persistent GTD where there is a plateau or re-elevation of the hCG level. In

about 5% cases, metastatic disease develops. The risk of recurrence of hydatidiform mole in future pregnancy is about 1–4%.

However, chance of fetal malformation is not increased following chemotherapy. The improvement and long term prognosis may

be attributed to the following factors: (i) Recognition of high risk factors related to chorioca rcinoma (ii) Careful follow up with serum

β-hCG (iii) Use of cytotoxic drug at the optimum time and in the right case.

RISK FACTORS FOR MALIGNANT CHANGE

• Patient’s age≥ 40 or < 20 years irrespective of parity

• Parity≥ 3. Age is more important than the parity

• Serum hCG > 100,000 mIU/mL

• Uterine size > 20 weeks

• Previous history of molar pregnancy

• Thecaleutin cysts: large (> 6 cm diameter)

MANAGEMENT

With the use of ultrasonography and sensitive hCG testing, diagnosis is made early in m ajority of the cases.

The principles in the management are: t Suction evacuation (SE) of the uterus as early as the diagnosis is made.

t Supportive therapy: Correction of anemia and infection, if there is any.

t Counseling for regular follow-up (p. 196).

The patients are grouped into two:

 Group A: The mole is in process of expulsion (Fig. 15.17)—less common.

 Group B:The uterus remains inert (early diagnosis with ultrasonography).

Fig. 15.17: Hydatidiform mole in the process of expulsion showing clusters of vesicles of varying sizes

By courtesy: Dr Subrata Bhattacharya, Silchar

SUPPORTIVE THERAPY: The patient usually presents with variable amoun t of bleeding and often they are anemic and associated

with infection. (i) IV infusion with Ringer’s solution is started (ii) Blood transfusion is given if the patient is anemic (iii) Parenteral

antibiotic is given if there is associated infection. (iv) Blood is kept reserved during th e evacuation as there is risk of hemorrhage.

DEFINITIVE MANAGEMENT:Suction evacuation (SE) is the method of treatment . It is safe, rapid and effective in almost all

cases. Suction evacuation can safely be done even when the uterus is of 28 weeks gest ation.  Group A: Cervix is favorable —(a) The

preferred method is suction evacuation. A negative pressure is applied up to 200–250 mm Hg. The procedure can be performed under

diazepam sedation or general anesthesia.

(b) Alternatively, conventional dilatation of the cervix followed by evacuation is done. D uring evacuation procedure patient should

ideally be monitored by pulse oximeter (oxygen saturation). 500 mL Ringer’s solution I V infusion is set up. Risk of hemorrhage is high

specially when the uterus is large. Senior surgeon should be present during the SE p rocedure. Use of oxytocin helps the expulsion of

moles and reduces blood loss but its routine use is not recommended due to the risks of embolization (see below).

(c) Digital exploration and removal of the mole by ovum forceps under general anesth esia may also be an alternative procedure.

After the evacuation is completed, methergin – 0.2 mg is given intramuscularly.

 Group B: Cervix is tubular and closed—Prior slow dilatation of the cervix is done by introducing laminaria tent followed by suction

and evacuation. Alternatively, vaginal misoprostol (PGE

) 400 µg, 3 hours before surgery may be used.

Complications of vaginal evacuation —Apart from the injury to the uterus, hemorrhage and shock, there are two more rare but

fatal complications—(1) Acute pulmonary insufficiency due to pulmonary embolization of the trophoblastic cells. Symptoms of acute

chest pain, tachycardia, tachypnea and dyspnea develop about 4–6 hours following ev acuation. Medical induction (oxytocin infusion)

before evacuation may increase the risk of pulmonary insufficiency (RCOG). Arterial PO

is monitored. Patient may need ventilatory

assistance and intensive care unit management. (2) Thyroid storm—In pres ence of hyperthyroid state when evacuation is done under

general anesthesia, the acute features such as hyperthermia, delirium, convulsion s, coma and cardiovascular collapse develop. The

condition can be managed by administration of beta adrenergic blocking agents.

• Hysterectomy is indicated in: (i) Patients with age over 35 (ii) Patient complete d her family irrespective of age (iii) Uncontrolled

hemorrhage or perforation during surgical evacuation. Hysterectomy reduces the ris k of GTN by five-fold.

• Hysterotomy is rarely done these days. It may be done in cases with (i) Profuse vaginal bleeding (ii) Cervix is unfavorable for

immediate vaginal evacuation (iii) Accidental perforation of the uterus during surgical e vacuation.

It should be remembered that following hysterectomy, persistent GTD is observed in 3– 5% cases. As such, it does not eliminate the

necessity of follow up. The enlarged ovaries (theca lutein cysts) found during operatio n should be left undisturbed as they will regress

following removal of mole. But, if complication arises, like torsion, rupture or infarction , they should be removed. The uterus following

hysterectomy should be sent for histopathological examination.

Following evacuation Anti. D immunoglobulin should be given to the Rh-negative nonim munized patient (see p. 334).

PLACE OF CURETTAGE FOLLOWING VAGINAL EVACUATION: Routine c urettage is not recommended. It is done in

selected cases with persistent vaginal bleeding (persistent GTN). Gentle curettage may be done 5–7 days following evacuation. At this

time the uterine wall gets thicker, firmer and the cavity becomes smaller so that effective curettage can be done without risk of damaging

the uterus. The objective of curettage is to remove the necrosed decidua and the attache d vesicles so as to accelerate involution and to

reduce the irregular bleeding. The materials should be sent for histology to note the degree of trophoblastic hyperplasia and to see

whether the villus structure is present or not.

FOLLOW-UP: Routine follow-up is mandatory for all cases for at least 1 year. The occurrence of choriocarcinoma is mostly

confined to this period. The prime objective is to diagnose persistent trophoblastic diseas e (20-30%) that is considered malignant.

However, hCG levels following evacuation should regress to normal within 3 months time.

Intervals : Initially, the check up should be at an interval of one week till the serum hCG level becomes negative. This usually

happens by 4–8 weeks. Once negative within 56 days, the patient is followed u p at every one month interval for 6 months. Women who

undergo chemotherapy should be followed up for one year after hCG has been normal. The patient must not become pregnant during the

period of follow-up.

Follow-up protocols: The follow-up protocols includes: (i) history and clinical examination (ii) hCG assay.

Methods employed in each visit : (1) Enquire about relevant symptoms like irregular vagin al bleeding, persistent cough, breathlessness

or hemoptysis.

(2) Abdominovaginal examination to note: (i) involution of the uterus (ii) ovarian size (iii) mali gnant deposit if any, in the anterior

vaginal wall. The lutein cysts usually regress within two months. Pelvic examination is done after one week of molar evacuation.

(3)Investigations: (i) Detection of hCG in urine or serum—Urine or serum assays are carried out at every visit. Initially, the less

sensitive and less costly immunological test may be carried out until the test becomes negative. Thereafter, it is preferable to use a more

sensitive serum hCG level by radioimmunoassay. (ii) Chest X-ray: If the pre- evac uation chest radiograph shows metastasis, it should be

repeated at 4 weeks interval, until remission is confirmed. It is then repeated at 3 mo nths interval during the rest of the follow-up period.

When pre-evacuation chest X-ray is normal, it is repeated only when the hCG titer plateaus or rises.

PROPHYLACTIC CHEMOTHERAPY: Eighty percent of patients unde rgo spontaneous remission. Sensitive βhCG assay can

identify the rest that develop malignancy. Moreover the drugs used are toxic. These dru gs in young females increase the risk of

premature ovarian failure and menopause. So it is not appropriate to treat all patients as a routine prophylactically. However, it is used

with advantages in the following circumstances:

(i) If the hCG level fails to become normal by the stipulated time (10-12 weeks) or ther e is re-elevation at 4-8 weeks (ii) Rising β hCG

level after reaching normal levels (iii) Post evacuation hemorrhage (presence of trophoblastic activity) (iv) Where follow up facilities are

not adequate (v) Evidences of metastases irrespective of the level of hCG (vi) In ca ses, where the malignant sequelae is higher as judged

by the risk factors (see p. 194) and where proper follow-up facilities are not avai lable. Prophylactic chemotherapy in such cases is

better than no follow-up. Prophylactic chemotherapy is useful in high risk grou p of women as it prevents metastasis and reduces

morbidity.

Regimes: Methotrexate, 1 mg/kg/day IV or IM is given on Days 1, 3, 5 and 7 with Folinic acid 0.1 mg/kg IM on Days 2, 4, 6 and 8. It is

to be repeated every 7 days. A total 3 courses are given. β hCG level should decrease by at least 15%, 4-7 days after methotrexate.

Alternatively, intravenous actinomycin D 12 µg/kg body weight daily for 5 days may b e given. It is less toxic than methotrexate. (See

author’s Text Book of Gynecology, for details of Chemotherapy, Chapter 22).

CONTRACEPTIVE ADVICE: The patient is traditionally advised not to be pregnant for at least one year. A rise in hCG titers

might cause confusion between a fresh pregnancy or persistent GTD. However, with v aginal probe ultrasound scan, pregnancy can be

diagnosed even as early as 5–6 weeks. Thus, if the patient so desires, she m ay be pregnant after a minimum of 6 months, following

the negative hCG titer. But pregnancy is delayed at least up to one year for gestational troph oblastic neoplasia and up to 2 years if there

is metastasis.

Use of contraception: IUD is contraindicated, because of its frequent association of irregular bleeding — a feature often coexists with

choriocarcinoma. Combined oral pills can be used after the hCG value has become normal. Inj DMPA can be used safely (see p. 548).

Barrier method of contraception can also be used. Surgical sterilization is another alternative when she has completed her family.

Unfavorable manifestations: (1) Persistent ill health (2) Irregular vaginal bleeding or continuing amenorrhea (3) Appearance of

respiratory symptoms (4) Sub-involution (5) Appearance of secondary metastasis in th e vagina (6) Chest radiograph showing positive

finding of “cannon ball” shadow (7) hCG titers remain elevated or there is re-elevation after a negative report.

hCG levels should be checked 3 weeks after the end of any pregnancy, subsequent to a molar o ne.

PARTIAL OR INCOMPLETE MOLE

I n partial hydatidiform mole, the affection of the chorionic villi is focal. There is a fetus or at least an amniotic sac.

The karyotype is triploid either 69, XXY or 69, XYY with one maternal but usually tw o paternal haploid chromo-somes. Microscopic

examination of the dilated chorionic villi shows predominant hyperplasia of the syncyt iotro-phoblast and presence of fetal blood

vessels with fetal red blood cells. The fetus, if present, dies in early first trimester. Rarely, the baby may be born which is growth

retarded with multi-system abnormalities (Fig. 15.18).

The clinical picture does not differ markedly from complete mole and too often confuse d with threatened or missed abortion. The hCG

titre is not markedly raised. With wider use of sonography, more and more cases are bein g revealed. In partial mole, uterus is generally

not large for dates and malignant potential is very low.

Once the diagnosis is made and the fetus is not alive, termination of pregnancy is to be done. Even if the fetus is alive, the patient should

be warned about the risks involved to the fetus if pregnancy is continued.

Post-termination follow-up protocol should be the same as outlined in complete mole. As the chance of malignancy is much less,

the follow up for 3–6 months is to be continued after hCG level returns to norma l.

Fig. 15.18: Partial mole with a stillborn baby. Courtesy: Dr Chandana Das, Professor, NRS Medic al College, Kolkata

IMPORTANT FEATURES OF COMPLETE AND PARTIAL MOLES Features

• Embryo/Fetus

• Hydropic degeneration of villi

• Trophoblast hyperplasia

• Uterine size

• Theca lutein cysts

• Karyotype

• β hCG

• Classic clinical symptoms

• Risk of persistent GTD

Complete mole

Absent

Pronounced and diffused Diffuse

More than the date (30-60%) Common (25-50%)

46 XX (85%), Paternal in origin High (> 50,000)

Common

20%

< 5%

Partial mole

Present

Variable and focal

Focal

Less than the date

Uncommon

Triploid (90%) diploid (10%) Slight elevation (< 50,000) Rare

PLACENTAL SITE TROPHOBLASTIC TUMOR (PSTT)

It is a rare histological diagnosis. Syncytotrophoblastic cells are generally absent. So ther e is persistent low level of serum or urinary

hCG. The tumor arises from the intermediate trophoblasts of the placental bed and is comp osed mainly of cytotrophoblastic cells. Patient

presents with vaginal bleeding. Local invasion into the myometrium and lymphatics occ urs. PSTT is not responsive to chemotherapy.

Hysterectomy is the preferred treatment.

PERSISTENT GESTATIONAL TROPHOBLASTIC DISEASE

DEFINITION: Persistent GTD is defined where there is persistence of trophoblastic activit y as evidenced by clinical, imaging,

pathological and or hormonal study following initial treatment. This may be following tre atment of hydatidiform mole, invasive mole,

choriocarcinoma or placental site trophoblastic tumor. A postmolar GTD may be b enign or malignant. But a GTD after non-molar

pregnancy is always a choriocarcinoma. Overall incidence of persistent GTN after comple te hydatidiform moles is 15–20%.

Approximately, 50% of the cases develop following a hydatidiform mole, 25% followi ng an abortion or ectopic pregnancy and another

25% following normal pregnancy.

DIAGNOSIS: This state is diagnosed during post-evacuation follow-up period. The diagno stic features are:

t Continued vaginal bleeding

t Persistent theca lutein cysts

t Persistently soft and enlarged uterus

t hCG titers either fail to become negative or remain plateau or there is re-elevation after a initial f all by 8 weeks post-molar evacuation.

Local or systemic metastases should always be excluded (X-ray chest, CT, MRI of brain and liver). Asymptomatic patients, with a

normal chest X-ray, is unlikely to have brain or other visceral metastasis.

t Pathologically this may be due to invasive mole, choriocarcinoma or placental site trophoblastic tu mor.

Regardless of the histological diagnosis, the therapeutic approach is almost the same. The prognosis is usually good.

TREATMENT: Patients are classified into low or high risk categories (WHO Prognostic Scorin g—see Author’s Gyne Text p. 351).

Low risk group receive single agent chemotherapy (usually methotrexate). High ri sk group receive combination chemotherapy

(usually EMA-CO).

Hysterectomy—This is justified in women approaching 40 and/or who has completed her family. Following hysterectomy or

chemotherapy, regular follow-up is essential.

Invasive mole, choriocarcinoma, PSTT and the rest of the gestational trophoblastic neop lasia have been described in author’s Textbook of

Gynecology (Chapter 22).

REFERENCES

1. The investigation and treatment of couples with recurrent miscarriage; Royal College of Obstetricians and Gynecologists, Guideline

17; Revised 2004.

2. Immunological testing and interventions for reproductive failure; Royal College of O bstetricians and Gynecologists, Scientific

Advisory Committee Opinion; Paper 5, 2004.

3. The Management of Tubal Pregnancies; Royal College of Obstetricians and Gyneco logist, Guideline 21; 2004.

4. American College of Obstetricians and Gynecologists: Medical Management of ectop ic pregnancy, Practice bulletin No. 94, June

2008.

5. Comprehensive abortion care: NRHM—Ministry of health and family welfare, Gov t. of India; 2010.

6. The Management of Gestational Trophoblastic neoplasia; Royal College of Obstetricia ns and Gynecologists, Guideline: 38; 2010.

7. American College of Obstetricians and Gynecologists: Diagnosis and treatment of ges tational trophoblastic disease, Obstet Gynecol.

103:365:2004.

Multiple Pregnancy, Hydramnios and Abnormalities of Placenta and C ord

When more than one fetus simultaneously develops in the uterus , it is called multiple pregnancy. Simultaneous development of

two fetuses (twins) is the commonest; although rare, development of three fetuses (triple ts), four fetuses (quadruplets), five fetuses

(quintuplets) or six fetuses (sextuplets) may also occur.

TWINS

Simultaneous development of two fetuses in the uterus is the commonest variety of multi ple pregnancy. VARIETIES: (1) Dizygotic

twins—It is the mostcommon (80%) and results from the fertilization of two ova

(2) Monozygotic twins (20%) results from the fertilization of a single ovum.

GENESIS OF TWINS: Dizygotic twins 80% (Syn: fraternal, binovular) result from fertilization of tw o ova, most

likely ruptured from two distinct Graafian follicles usually of the same or one from each ovary, by two sperms

during a single ovarian cycle. Their subsequent implantation and development differ littl e from those of a

single fertilized ovum. The babies bear only fraternal resemblance to each other (that of brothers and sisters

from different births) and hence called fraternal twins.

In Monozygotic twins 20% (Syn: identical, uniovular), the twinning may occur a t different periods

after fertilization and this markedly influences the process of implantation and the forma tion of the fetal

membranes.

On rare occasion, the following possibilities may occur:

• If the division takes place within 72 hours after fertiliz ation (prior to morula stage) the resulting embryos will have two separate

placenta, chorions and amnions (diamniotic-dichorionic or D/D – 30%).

• If the division takes place between the 4th and 8th day after the formation of inner cell mass when chorion has already developed

—diamniotic monochorionic twins develop (D/M – 66%).

• If the division occurs after 8th day of fertilization, when the amn iotic cavity has already formed, a monoamniotic-monochorionic twin

develops (M/M – 3%).

• On extremely rare occasions, division occurs after 2 weeks of the d evelopment of embryonic disc resulting in the formation of

conjoined twin (<1%) called—Siamese twin. Four types of fusion may occur: (i) Thoracopagus (mostcommon), (ii) pyopagus

(posterior fusion), (iii) craniopagus (cephalic) and (iv) Ischiopagus (caudal).

Zygosity refers to the genetic makeup of twin pregnancy and chorionicity indicates th e pregnancy’s membrane status.

DETERMINATION OF ZYGOSITY: With the advent of organ transplantation, the identific ation of the zygosity

of the multiple fetuses has assumed much importance.

• Examination of placenta and membranes:

Dizygotic twins: (i) There are two placentae, either completely separated or mor e commonly fused at

the margin appearing to be one (9 out of 10). There is no anastomosis between the two fetal vessels (ii) Each

fetus is surrounded by a separate amnion and chorion (iii) As such, the intervening mem branes consist of 4

layers—amnion, chorion, chorion and amnion. Infact in early pregnancy the decid ua capsularis of each sac

may be identified under the microscope in between the chorionic layers (Fig. 16.1).

Monozygotic twins: (i) The placenta is single. There is varying degree of free a nastomosis between the two fetal vessels (ii) Each fetus

is surrounded by a separate amniotic sac with the chorionic layer common to both (diam niotic—monochorionic)

A B C D

Figs 16.1A to D: Twin placenta. Dizygotic twins (A, B) have two placentae (D/D): (A) separate d and (B) fused without any vascular

communications; intervening membranes consist of 4 layers (D/D). Monozygotic twins; (B) two placentae (D/D); (C) one placenta with

free internal vascular anastomosis; the intervening membranes consist of 2 layers (D/M) ; (D) same as (C) but without any intervening

membranes (M/M)

(iii) As such the intervening membranes consist of two layers of amnion only (Fig. 16.1). However, o n rare occasions, the uniovular

twins may be diamniotic-dichorionic or monoamniotic-monochorionic.

• Sex: While twins having opposite sex are almost always binovular and twins of the s ame sex are not always uniovular but the uniovular

twins are always of the same sex.

• If the fetuses are of the same sex and have the same genetic features (dominant blood group), monozygosity is likel y.

• A test skin graft—Acceptance of reciprocal skin graft is almost a certain proof of monozygosity.

• DNA microprobe techniqueis most definitive.

• Follow up study between 2–4 years—showing almost similar physical a nd behavioral features suggestive of monozygosity.

Placenta Commu

nicating vessels

Intervening membranes Sex

Monozygotic One 2 (amnions) Present

Dizygotic Two (most often fused)

Table 16.1: Summary of determination of zygosity

4 (2 amnions Absent Always

identical

May differ Genetic

features

(dominant

blood group) DNA finger printing

Same

Skin grafting (Reciprocal) Follow up

Acceptance

Differ Rejection Usually identical Not

2 chorions)

identical

INCIDENCE: The incidence varies widely. It is highest in Nigeria being 1 in 20 an d lowest in Far Eastern countries being 1 in 200

pregnancies. In India, the incidence is about 1 in 80. While the incidence of monozygo tic twins remains fairly constant throughout the

globe being 1 in 250, it is the dizygotic twins which are responsible for the wide variatio n of the incidence.

According to Hellin’s (1895) rules, the mathematical frequency of multiple birth is, twin s 1 in 80 pregnancies, triplets 1 in 80

quadruplets 1 in 80

and so on.

The actual incidence of multiple pregnancy has increased significantly at present. This is due to early detection by ultrasound as well as

increasing use of induction of ovulation and assisted reproductive techniques (ART).

ETIOLOGY: The cause of twinning is not known. The frequency of monozygotic twins remains constant throughout the globe and

is probably related to maternal environmental factors. It is the wide variation in the prevalence of binovular twins which is responsible

for the fluctuation in the overall incidence of twins in different populations.

Prevalence of dizygotic twins is related to :

Race: The frequency is highest amongst Negroes, lowest amongst Mongols and interm ediate amongst Caucasians. Hereditary: There is

hereditary predisposition likely to be more transmitted through the female (maternal side) . Advancing age ofthe mother: Increased

incidence of twinning is observed with the advancing age of the mother, the maximum

being between the age of 30–35 years . The incidence of twins is markedly reduced thereafter.

Influence of parity: The incidence is increased with increasing parity specially from 5th gravida onwards. Iatrogenic: Drugs us ed for

induction of ovulation

may produce multiple fetuses to the extent of 20–40% following gonadotrophin therap y, although to a lesser extent (5–6%) following

clomiphene citrate.

• Superfecundation is the fertilization of two different ova released in the same cycle, by separate acts of coitus within a short period of

time.

• Superfetation is the fertilization of two ova released in different menstrual cycles. T he nidation and development of one fetus over

another fetus is theoretically possible until the decidual space is obliterated by 12 weeks of pregnancy.

• Fetus papyraceous or compressus is a state which occurs if one of the fetuses dies early. The dead fetus is flattened, mummified and

compressed between the membranes of the living fetus and the uterine wall. It may occu r in both varieties of twins, but is more common

in monozygotic twins and is discovered at delivery or earlier by sonography (see Fig. 16. 2).

• Fetus acardiacus occurs only in monozygotic twins. Part of one fetus remains amorphous and becom es parasitic without a heart (see

p. 212).

Fig. 16.2: Fetus papyraceous or compressus

• Hydatidiform mole (from one placenta) and a normal fetus and placenta (fro m the other conceptus) have been observed

ultrasonographically.

• Vanishing twin: Serial ultrasound imaging in multiple pregnancy since ear ly gestation has revealed occasional death of one fetus and

continuation of pregnancy with the surviving one. The dead fetus (if within 14 weeks) simply ‘vanishes’ by resorption. The rate of

disappearance could be to the extent of 40%.

MATERNAL PHYSIOLOGICAL CHANGES: Multiple pregnancy imposes physical changes o n the mother in excess of those seen in

singleton pregnancy. (1) There is increase in weight gain and cardiac output. (2) Plasm a volume is increased by an addition of 500 mL.

There is no corresponding increase in red cell volume resulting in exaggerated hemodil ution and anemia. (3) There is increased a

fetoprotein level, tidal volume and glomerular filtration rate.

LIE AND PRESENTATION: The mostcommon lie of the fetuses is longitudinal (90%) but malpresentations are quite common. The

combination of presentation of the fetuses are—(1) both vertex (50%) (2) first v ertex and second breech (30%) (3) first breech and

second vertex (10%) (4) both breech (10%) (5) first vertex and second transverse an d so on, but rarest one, being both transverse

when the possibility of conjoined twins should be ruled out.

DIAGNOSIS

HISTORY: (i) History of ovulation inducing drugs specially gonadotrophins, for inferti lity or use of ART. (ii) Family history of

twinning (more often present in the maternal side).

SYMPTOMS: Minor ailments of normal pregnancy are often exaggerated. Som e of the symptoms are related to the undue enlargement

of the uterus: (i) Increased nausea and vomiting in early months (ii) Cardiorespiratory embarrassment which is evident in the later

months—such as palpitation or shortness of breath (iii) Tendency of swelling of the legs, varicose veins and hemorrhoids is greater (iv)

Unusual rate of abdominal enlargement and excessive fetal movements may be noticed by a n experienced parous mother.

GENERAL EXAMINATION: (i) Prevalence of anemia is more than in singleton pregnancy (i i) Unusual weight gain, not explained by

preeclampsia or obesity, is an important feature (iii) Evidence of preeclampsia (25%) is a common association.

ABDOMINAL EXAMINATION:

Inspection: The elongated shape of a normal pregnant uterus is changed to a more “barrel sha pe” and the abdomen is unduly enlarged.

Palpation: (i) The height of the uterus is more than the period of amenorrhea. This discrepancy may only become evident from mid-

pregnancy onwards (ii) The girth of the abdomen at the level of umbilicus is more than the nor mal average at term (100 cm) (iii) Fetal

bulk seems disproportionately larger in relation to the size of the fetal head (iv) Palpation of to o many fetal parts (v) Finding of two

fetal heads or three fetal poles make the clinical diagnosis almost certain.

Auscultation: Simultaneous hearing of two distinct fetal heart sounds located at separate spots wit h a silent area in between by two

observers, gives a certain clue in the diagnosis of twins, provided the difference in he art rates is at least 10 beats per minute.

The abdominal palpation and auscultation may not be carried out so easily, as described , because of the presence of hydramnios.

Fig. 16.3A and B: (A) “Twin peak” sign. In dichorionic diamniotic t win gestations, the chorion and amnion for each twin reflect

awayfromthefused placenta to formtheintertwin membrane.A potentialspace exists in th e intertwin membrane, which is filled

byproliferatingplacental villi givingriseto thetwin peaksign. Twin peaksign appears as atrianglewith thebasea t thechorionic surfaceand

theapex in theintertwin membrane. (B) In monochorionic, diamniotic twins, the intertwin membrane is composed of two amnions only

= Amnion; C

= Chorion). (See Fig. 16.1)

Fig. 16.3C: ColorDopplerScan (TVS) showingtwin pregnancy. Thick intertwin membra ne (twin peak sign) of dichorionic, diamniotic

placenta is seen

INTERNAL EXAMINATION: In some cases, one head is felt deep in the pelvis, while the other one is located by abdominal

examination.

On occasions, the clinical methods fail to detect twins prior to the delivery of the first bab y.

INVESTIGATIONS

• Sonography: In multifetal pregnancy it is done to obtain the following informat ion: (i) Confirmation of diagnosis as early as 10th

week of pregnancy. (ii) Viability of fetuses, vanishing twin in the second trimester. (iii) Chorionicity (lambda or twin peak sign— see

fig. 16.3A, B & C) (iv) Pregnancy dating. (v) Fetal anomalies (vi) Fe tal growth monitoring (at every 3–4 weeks interval) for IUGR. (vii)

Presentation and lie of the fetuses. (viii) Twin transfusion (Doppler studies). (ix) Placental local isation. (x) Amniotic fluid volume.

Chorionicity of the placenta is best diagnosed by ultrasound at 6 to 9 weeks of gestation. In dicho rionic twins there is a thick septum

between the chorionic sacs. It is best identified at the base of the membrane, where a tria ngular projection is seen. This is known as

lamda or twin peak sign. Presence of lamda or twin peak sign indicates dichorionic placenta (see Fig. 16.3A, B & C).

• Biochemical tests: Maternal serum chorionic gonadotrophin, α fetoprotein and un conjugated estriol are approximately double than

those of singleton pregnancies. But their values cannot diagnose clearly a twin from a single fetus.

DIFFERENTIAL DIAGNOSIS includes: (1) Hydramnios (2) Big baby (3) Fibroi d or ovarian tumor with pregnancy (4) Ascites with

pregnancy.

COMPLICATIONS

MATERNAL : • Pregnancy • Labor • Puerperium FET AL: (p. 205)

MATERNAL — During pregnancy:

• Nausea and vomiting occurs with increased frequency and severity.

• Anemia is more due to increased iron and folate requirement by the two fetuses. D eficiency of folic acid

leads to increased incidence of megaloblastic anemia.

• Preeclampsia (25%) is increased three times over singleton pregnancy. Expo sure to superabundance of

chorionic villi is the possible explanation (see p. 220).

• Hydramnios (10%) is more common in monozygotic twins and usually in volves the second sac. It is

perhaps due to increased renal perfusion with consequent increased urinary output wh ich may accompany

the hypervolemia in the larger twin.

• Antepartum hemorrhage may occur with slight increased frequency. The incr eased incidence of

placenta previa is due to the bigger size of the placenta encroaching on to the lower segmen t. The separation

of normally situated placenta may be due to — (i) increased incidence of preeclam psia (ii) sudden escape

of liquor following rupture of the membranes of

the hydramniotic sac (iii) deficiency of folic acid

and (iv) following delivery of the first baby due to

sudden shrinkage of the uterine wall adjacent to

the placental attachment.

• Malpresentation is quite common in twins

compared to singleton pregnancies. In about 70%

cases, the first baby is presented by vertex and in

50%, both presented by vertex. Malpresentation

is thus more common in the second baby.

Fortunately, the babies are usually smaller and do

not pose much of a problem.

• Preterm labor (50%) frequently occurs

and the mean gestational period for twins is 37

weeks. Overdistension of the uterus, hydramnios

and premature rupture of the membranes are

responsible for preterm labor.

Fig. 16.4A: Ultrasonogram showing two fetal heads. BPDs are measured

• Mechanical distress such as palpitation, dyspnoea, varicosities and hemorrhoids may be increased compared to a singleton

pregnancy.

During Labor

• Early rupture of the membranes and cord prolapse are likely to be increased due to increased prevalence of malpresentation. Cord

prolapse is five times more common than in singleton pregnancy and is more common i n relation to the second baby.

• Prolonged labor though theoretically expected, is practically not met with. This is because of parous women with smaller babies.

• Increased operative interference is due to high prevalen ce of malpresentation with its associated complications.

• Bleeding (intrapartum) following the birth of the first baby, may at times be alarming and is due to separation of the placenta

following reduction of placental site.

• Postpartum hemorrhage is the real danger in twins. It is due to: (i) Atony of the uterine muscle due to overdistension of the uterus

(ii) A longer time taken by the big placenta to separate (iii) Bigger surface area of the placen ta exposing more uterine sinuses (iv)

Implantation of a part of the placenta in the lower segment which is less retrac tile.

During puerperium: There is increased incidence of: (1) Subinvolution—because of bigger size of the u terus (2) Infection— because

of increased operative interference, pre-existing anaemia and blood loss dur ing delivery (3) Lactation failure—this is minimized by

reassurance and giving her additional support.

FETAL:

• Miscarriage rate is increasedspecially with monozy gotic twins.

• Premature rate (80%) is very much increased and babies suffer from its hazards (see p. 458).

• Discordant twin growth (20%)— Some degree of discordant gro wth is normal in dizygotic twins. Cases of true pathological

discordance involve estimated weight difference of 25% or more. This may be due to t win–twin transfusion syndrome, placental

insufficiency,IUGRor fromstructural anomalies occurring in one fetus.

Fig. 16.4B: Acephalus, acardius fetus in a triplet pregnancy. By courtesy: Dr S Chaudhur y, Assoc. Prof, Dept Obs-Gyn, NRSMC

COMPLICATIONS OF MULTIFETAL PREGNANCY Fetal

• Abortion

• Vanishing twin/Fetus

papyraceous

• Preterm birth

• Fetal anomalies

• Discordant growth

• Intrauterine death of one fetus

• Twin transfusion syndrome

• Cord prolapse

• Locked twins

• (↑) Perinatal mortality

(complications are more in monozygotic twins, p. 206)

Maternal

• Nausea, Vomiting

• Anemia

• PIH and Pre-eclampsia

• Polyhydramnions/

oligohydramios

• Preterm Labor

• Malpresentation

• Antepartum hemorrhage

• Mechanical distress (dyspnea, palpitation)

• Prolonged labor

• Operative interference

• Post partum hemorrhage

• (↑) Postnatal support

• Intrauterine death of one fetus—is more in monozygotic one. If a loss occurs in f irst trimester, the affected fetus simply ‘Vanishes’

by resorption. If the death occurs during second trimester, a fetus papyraceous or compressus may form. If death occurs late in

pregnancy, there may be death of the other fetus in presence of vascular ana stomosis (see p. 206) or it may complicate the mother with

DIC. The deaths are due to cord compression, competition for no urishment or congenital malformation.

• Fetal anomalies are increased by 2-4% compared to a singleton pregnancy, more i n monozygotic twins. They are in the form of

anencephaly, hydrocephalus, microcephaly, cardiac anomalies or Down’s syndrome.

• Asphyxia and stillbirth are more common due to increased pr evalence of preeclampsia, malpresentation, placental abruption and

increased operative interferences. The second baby is more at risk. Complications are more in monochorionic twin pregnancies.

PROGNOSIS

Maternal mortality is increased in twins than in a singleton pregnancy. D eath is mostly due to hemorrhage (before, during and after

delivery), preeclampsia and anemia. Increased maternal morbidity is due to the prev alence of complications and increased operative

interference.

Perinatal mortality is markedly increased mainly due to prematurity. It is 4–5 times higher than in a singleton pregnancy. It is

extremely high in monoamniotic monozygotic twins due to cord entanglement. Onethird loss is due to stillbirth and two-third due to

neonatal death. During delivery the second baby is more at risk (50%) than the first on e due to— (i) retraction of uterus leading to

placental insufficiency (ii) increased operative interference and (iii) increased incidence of cord prolapse.

Because of increased risk to both the mother and the baby, compared to that of a single ton pregnancy, the twin pregnancy is considered

‘high risk’ and as such should be delivered in a hospital. COMPLICATIONS OF MONOCHORIONIC TWINS

(i) Twin-twin transfusion syndrome (TTTS) — It is a clinicopathological sta te, exclusively met with in monozygotic twins, where

one twin appears to bleed into the other through some kind of placental vascular anasto mosis. Clinical manifestations of twin transfusion

syndrome occur when there is hemodynamic imbalance due to unidirectional deep arter iovenous anastomoses. As a result the receptor

twin becomes larger with hydramnios, polycythemic, hypertensive and hypervolemic, at the ex pense of the donor twin which becomes

smaller with oligohydramnios, anemic, hypotensive and hypovolemic. The donor twin may appear “stuck” due to severe

oligohydramnios. Difference of hemoglobin concentration between the two, usually exceeds 5 gm% and estimated fetal weight

discrepancy is 25% or more.

Management: Antenatal diagnosis is made by ultrasound with doppler blood flow study in the placental vascular bed. (a) Repeated

amniocentesis to control polyhydramnios in the recipient twin is done. (b) Septostomy (m aking a hole in the dividing amniotic

membrane). (c) Laser photocoagulation to interrupt the anastomotic vessels on the chor ionic plate can give some success. (d) Selective

reduction (feticide) of one twin is done when survival of both the fetuses is at risk (see p. 213). The smaller twin generally has got better

outcome. The plethoric twin runs the risk of congestive cardiac failure and hydrops. Congenital abnormalities (neural tube defects,

holoprosencephaly) are high (2-3 times). Perinatal mortality in TTTS is about 70%. (Se e further, author’s “A guide to clinical Obstetrics

and Gynecology” p. 138).

(ii) Dead fetus syndrome—death of one twin (2–7% ) is associated with poor outcome of the cotwin (25%) specially in monochorionic

placenta. The surviving twin runs the risk of cerebral palsy, microcephaly, renal cortica l necrosis and DIC. This is due to thromboplastin

liberated from the dead twin that crosses via placental anastomosis to the living twin.

(iii) Twin reversed arterial perfusion (TRAP) is characterized by an ‘acardiac per fused twin’ having blood supply from a normal

cotwin via large arterio-arterial or vein to vein anastomosis (Fig. 16.4B). In majority the cotwin dies (in the perinatal period) due to high

output cardiac failure. The arterial pressure of the donor twin being high, the recipient twin receives the ‘used’ blood from the donor. The

perfused twin is often chromosomally abnormal. The anomalous twin may appear as a n amorphous mass. Management of TRAP is

controversial. Ligation of the umbilical cord of the acardiac twin under fetoscopic g uidance has been done.

(iv) Monoamniocity (2% of all twins) in monochorionic twins leads to high perina tal mortality due to cord problems (entanglement).

Sulindac, a prostaglandin synthase inhibitor has been used to reduce fetal urine output, creating borderline oligohydramnios and to reduce

the excessive movements.

(v) Conjoined twin is rare (1.3 per 100,000 births). Perinatal survival depends upon the type of joint (see p. 210, 409). Major

cardiovascular connection leads to high mortality.

ANTENATAL MANAGEMENT

The essence of successful outcome of a twin pregnancy is to make an early diagnos is. High index of clinical suspicion and thorough

ultrasound examination are the keys to the diagnosis. It is useful to make early diagnosi s and to detect chorionicity, amniocity, fetal

growth pattern and congenital malformations.

ADVICE

• Diet: Increased dietary supplement is needed for increased energy supply to the extent of 300 K cal per day, over and above that needed

in a singleton pregnancy. The increased protein demand is to be met with.

• Increased rest at home and early cessation of work is advised to prevent preterm labor and other complications.

• Supplement therapy: (i) Iron therapy is to be increased to the extent of 100–200 mg p er day. (ii) Additional vitamins, calcium and

folic acid (5 mg) are to be given, over and above those prescribed for a singleton preg nancy.

• Interval of antenatal visit should be more frequent to detect at the earliest, the evidences of a nemia, preterm labor or preeclampsia.

• Fetal surveillance is maintained by serial sonography at every 3–4 weeks interval. Assessment of fetal growth, amniotic fluid volume

and AFI (see p. 39), non-stress test and Doppler velocimetry (see p. 109) are carried out.

HOSPITALISATION

• Routine hospital admission only for bed rest is not essential. However, bed rest ev en at home from 24 weeks onwards, not only ensures

physical and mental rest but also improves uteroplacental circulation. This results in — ( i) increased birth weight of the babies (ii)

decreased frequency of pre-eclampsia (iii) prolongation of the duration of preg nancy.

To prevent preterm delivery, routine use of betamimetics or circlage operation h as got no significant benefit. Use of corticosteroids

to accelerate fetal lung maturation is given (single dose) to women with preterm labor <34 weeks. Twins develop pulmonary maturity

3-4 weeks earlier than singletons.

• Emergency: Development of complicating factors necessitates urgent admission irrespective of the period of gestation.

MANAGEMENT DURING LABOR

Place of delivery: As the twin pregnancy is considered a ‘high risk’, the patient should b e confined in an equipped hospital preferably

having an intensive neonatal care unit.

Vaginal delivery is allowed when both the twins are or at least the first twin is with vertex presen tation. FIRST STAGE: Usual

conduction of the first stage as outlined for a singleton fetus, is to be followed with addition al precautions:

• A skilled obstetrician should be present. An experienced anesthesist sh ould be made available.

• Presence of ultrasound in the labor ward is helpful. It makes both the external and internal ver sions less difficult by visualizing the

fetal parts.

• The patient should be in bed to prevent early rupture of the membranes.

• Use of analgesic drugs is to be limited as the babies are small and rapid delivery may oc cur. Epidural analgesia is preferred as it

facilitates manipulation of second fetus should it prove necessary.

• Careful fetal monitoring (preferably electronic) is to be done (see Ch. 38).

• Internal examination should be donesoon after the rupture of the membranes to exclud e cord prolapse.

• An intravenous line with ringer’s solution should be set up for any urgent intraveno us therapy, if required.

• One unit of compatible and cross matched blood should be m ade readily available.

• Neonatologist should be present at the time of delivery.

DELIVERY OF THE FIRST BABY: The delivery should be conducted in the same guide lines as mentioned in

normal labor. As the baby is usually small, the delivery does not usually pose any probl em. (i) Liberal episiotomy under local

infiltration with 1% lignocaine (ii) Forceps delivery, if needed, should be done preferably und er pudendal block anesthesia. General

anesthesia is better avoided, as the second baby may be subjected to the effects o f prolonged anesthesia (iii) Do not give intravenous

ergometrine with the delivery of the anterior shoulder of the first baby (iv) Clamp the cord at two places and cut in between, to

prevent exsanguination of the second baby through communicating placental circulation i n monozygotic twins (of course, it is an usual

procedure even in singleton birth) (v) At least, 8–10 cm of cord is left behind for administration of any dru g or transfusion, if required

(vi) The baby is handed over to the nurse after labeling it as number 1.

CONDUCTION OF LABOR AFTER THE DELIVERY OF THE FIRST BABY

Principles: The principle is to expedite the delivery of the second baby. The seco nd baby is put under strain due to placental

insufficiency caused by uterine retraction following the birth of the first baby.

Steps of management: Step – I: Following the birth of the first baby, the lie, presentation, size and FHS of the second baby sh ould

be ascertained by abdominal examination or if required by real time ultrasound. A vaginal examination is also to be made not only

to confirm the abdominal findings but to note the status of the membranes and to exclude cord pro lapse, if any.

Lie longitudinal: Step – I: Low rupture of the membranes is done after fixing the presentin g part on the brim. Syntocinon may be added

to the infusion bottle to achieve this. Internal examination is once more to be done to exclud e cord prolapse. More vigilance is employed

to watch the fetal condition.

Step – II: If the uterine contraction is poor, 5 units of oxytocin is added to the infusion bottle. The interval between deliveries should

ideally be less than 30 minutes.

Step – III: If there is still a delay (say 30 minutes), interference is to be done.

• Vertex:• Low down — Forceps are applied.

•High up — If the first baby is too small and the second one seems bigger, cep halopelvic disproportion should be ruled out. The

possibility of hydrocephalic head should be excluded by ultrasonography. If th ese are excluded, internal version followed by breech

extraction is performed under general anesthesia. Ventouse may be an effective alterna tive.

• Breech: The delivery should be completed by breech extraction.

Lie transverse: If the lie is transverse, it should be corrected by external version into a longitudinal lie preferably cephalic, if fails,

podalic. If the external version fails, internal version under general anesthesia should be done forthwith. As the fetus is small there is

no difficulty in performing internal version and it is the only accepted indication of internal version in present day obstetric practice

(p. 585).

Indications of urgent delivery of the second baby: (1) Severe (intrapartum) vaginal bleeding (2) Cord prolapse of the second baby (3)

Inadvertent use of intravenous ergometrine with the delivery of the anterior shoulder of the first baby (4) First baby delivered under

general anesthesia (5) Appearance of fetal distress.

Management: In all these conditions, the baby should be delivered quickly. A rational s cheme is given below which depends on the lie,

presentation and station of the head.

A. Head• If low down, delivery by forceps

• If high up, delivery by internal version under general anesthesia

B. Breech should be delivered by breech extraction

C. Transverse lie—internal version followed by breech extraction under general anesth esia.

If, however, the patient bleeds heavily following the birth of the first baby, immediate lo w rupture of the membranes usually succeeds in

controlling the blood loss.

Delayed delivery of the second twin have been recorded from 21 to 143 days. Delayed delivery may be associated wi th perinatal death

and maternal infection.

MANAGEMENT OF THE THIRD STAGE: The risk of postpartum hemorrh age can be minimized by routine administration of

0.2mgmetherginIVor oxytocin10IUIMwiththedelivery of theanterior shoulder of t he second baby. The placenta is to be delivered

by controlled cord traction. It is a sound practice to continue the oxytocin drip for at least one ho ur, following the delivery of the second

baby. A blood loss of more than average should be immediately replaced by blood tran sfusion, already kept at hand. The patient is to be

carefully watched for about 2 hours after delivery. Multiple birth puts an additional stress and strain on the mother as well as on the

family members. Mother should be given additional support at home to look after both the bab ies.

INDICATIONS OF CESAREAN SECTION:

The indications are broadly divided into:• Obstetric causes • For twins

Obstetric indication: (1) Placenta previa (2) Severe preeclampsia (3) Previous cesarean section (4) Cord

prolapse of the first baby (5) Abnormal uterine contractions (6) Contracted pelvis.

For twins : (i) Both the fetuses or even the first fetus with noncephalic (breech or transverse) pres entation (ii) Twins with complications:

IUGR, Conjoint twins (iii) Monoamniotic twins (iv) Monochorionic twins with TTS (v) Collis ion of both the heads at brim preventing

engagement of either head.

MANAGEMENT OF DIFFICULT CASES OF TWINS

Fortunately, abnormal conditions leading to difficult delivery are extremely rar e.

• Interlocking: The mostcommon one being the aftercoming head of the first baby getting locked with the forecoming

head of the second baby . Vaginal manipulation to separate the chins of the fetuses is done, failing which cesarean section is necessary.

Decapitation of the first baby if already dead, pushing up the decapitated head, followe d by delivery of the second baby and lastly,

delivery of the decapitated head, at least saves one baby.

• Occasionally, two heads of both vertex twins get locked at the pelvic brim preventing engagement of either of the head. The

possibility should be kept in mind and the diagnosis is confirmed by intranatal s onography/radiography. Disengagement of the higher

head can be possible under general anesthesia. If fails, cesarean section is the alternative , for fetal interest.

CONJOINED TWINS (see p. 409): It is extremely rare. Incidence varies fr om 1: 100,000 to 1: 50,000 births. In twin pregnancies the

incidence is from 1: 900 to 1: 650.

Diagnosis: Unfortunately conjoined twins are often diagnosed during delivery when the re is obstruction in the second stage. Failure of

traction to deliver the first twin in the second stage or inability to move one twin without moving the other suggest conjoined twins.

Presence of a bridge of tissue between the fetuses on vaginal examination confirms the diagnosis.

Antenatal diagnosis (see p. 409) is important. Benefits are: (i) Reduces matern al trauma and morbidity (ii) Improves fetal survival (iii)

Helps to plan the method of delivery (iv) Allows time to organise the paediatric sur gical team. Management (see p. 409) depends on (i)

Extent and site of union (ii) Possibility of surgical separation and (iii) Size of th e fetuses and possibility of survival.

TRIPLETS, QUADRUPLETS, ETC.

Triplets may develop from fertilization of a single ovum or two or even three ova; simila rly with quadruplets and quintuplets. Female

Fig. 16.5A: Ultrasonographic diagnosis of a triplet pregnancy

Fig. 16.5: Xiphopagus or omphalopagus fetuses are joined at the anterior abdominal wall from xip hi sternum to the level of umbilicus.

Congenital malformation (omphalocele) is seen

fetus usually outnumber the male one . The diagnosis is accidental following sonography, r adiography or during births. Clinical course

and complications are intensified compared to twins. Perinatal loss is markedly in creased due to prematurity. Preterm delivery is

common (50%) and usually delivery occurs by 32–34 weeks (mean 33.5 weeks) tim e. Discordance of fetal growth is more common

than twins. Perinatal loss is inversely related to birth weight. Management is sim ilar to that outlined in twins. Average time for delivery

in quadruplets is 30–31 weeks. To improve the fetal salvage, specially in quadruplets, it is advisab le to employ liberal cesarean section.

Selective reduction: If there are 4 or more fetuses, selective reduction of the fetuses leaving behin d only two is done to improve

outcome of the cofetuses. This can be done by intracardiac injection of potassium chlor ide between 11 and 13 weeks under ultrasonic

guidance. It is done transabdominally. Umbilical cord of the targeted twin is occluded b y fetoscopic ligation or by laser or by bipolar

coagulation, to protect the co-twin from adverse drug effect. Multiple pregnancy reduc tion improves perinatal outcome in women with

triplets or more.

Selective termination of a fetus with structural or genetic abnormality may be done in a dicho rionic multiple pregnancy in the second

trimester.

POLYHYDRAMNIOS (Syn: Hydramnios)

DEFINITION: Anatomically, polyhydramnios is defined as a state where liquo r amnii exceeds 2000 mL. Clinical definition states—

the excessive accumulation of liquor amnii causing discomfort to the patient and/or when an imaging help is needed to substantiate the

clinical diagnosis of the lie and presentation of the fetus. Sonographic diagnosis is made (see p. 464) when amniotic fluid index (AFI) is

more than 24 cm (>95th centile for gestational age) and a largest vertical pocket is >8 cm.

INCIDENCE: Because of different criteria used in the definition of polyhydramni os, the incidence varies from 1–2% of cases. It is more

common in multiparae than primigravidae. While minor degrees of hydramnios are fairly commo n, hydramnios sufficient to produce

clinical symptoms probably occurs in 1 in 1000 pregnancies.

ETIOLOGY

Because of wide gaps in the knowledge of the origin and excretion of the liquor amnii, the exact cause of excess accumulation of the

liquor is still speculative. It may be the result of deficient absorption as well as excessive produc tion of liquor amnii, which may be

temporary or permanent. While certain maternal or fetal factors are found to be a ssociated with hydramnios, yet the cause remains

unknown in about 60%. The composition of the liquor amnii, however, remains normal.

I. FETAL ANOMALIES: Congenital fetal malformations (structural and chromosomal) are asso ciated with polyhydramnios in about

20% cases.

• Anencephaly—Hydramnios is found in association with anencephaly in a bout 50% cases. The causes of excessive production of liquor

amnii may be due to—(a) transudation from the exposed meninges (b) absence of feta l swallowing reflex and (c) possible suppression of

fetal antidiuretic hormone leading to excessive urination.

• Open spina bifida—increased transudation from the meninges.

• Esophageal or duodenal atresia—preventing swallowing of the liquor. However, hydra mnios is associated only in about 15% cases

of esophageal atresia.

• Facial clefts and neck masses—by interfering normal sw allowing.

• Hydrops fetalisdue to Rhesus isoimmunisation, cardiothoracic an omalies and fetal cirrhosis are often associated with hydramnios.

• Aneuploidy.

II. PLACENTA: Chorioangioma of the placenta: Tumor growing from a single villus consisting of hyperpla sia of blood vessels and

connective tissue results in increased transudation.

III. MULTIPLE PREGNANCY: Multiple pregnancy is about 10 times more common than its o verall incidence. Hydramnios is more

common in monozygotic twins, usually affecting the second sac. In TTTS the r ecipient twin develops polydramnios.

IV. MATERNAL: (i) Diabetes—It is more common in hydramnio s. Hydramnios is associated with diabetes in about 30% cases.

However, with adequate supervision, the incidence of hydramnios can be lowered. It i s presumed that a raised maternal blood sugar →

raised fetal blood sugar → fetal diuresis → hydramnios. (ii) Cardiac or renal disea se — may lead to edema of the placenta leading to

increase in transudation.

V. IDIOPATHIC

CLINICAL TYPES: Depending on the rapidity of onset, hydramnios m ay be: (a) Chronic (mostcommon) — onset is insidious taking

few weeks. (b) Acute (extremely rare) — onset is sudden, within few days or ma y appear acutely on pre-existing chronic variety. The

chronic variety is 10 times commoner than the acute one.

CHRONIC POLYHYDRAMNIOS

In the majority of cases, the accumulation of liquor is gradual and as such, the patient is not very much inconvenienced.

SYMPTOMS: The symptoms are mainly from mechanical causes.

• Respiratory— The patient may suffer from dyspnea or even remain i n the sitting position for easier breathing.

• Palpitation

• Edema of the legs, varicosities in the legs or vulva and hemorrhoids.

SIGNS:

• The patient may be in a dyspneic state in the lying down position.

• Evidence of preeclampsia (edema, hypertension and proteinuria) may be pre sent.

ABDOMINAL EXAMINATION

Inspection:

• Abdomen is markedly enlarged, looks globul ar with fullness at the flanks.

• The skin is tense, shiny with large striae.

Palpation :

• Height of the uterus is more than the period of amenorrhea.

• Girth of the abdomen round the umbilicus is more than normal (Fig. 16.6).

• Fluid thrill can be elicited in all directions over the uterus.

• Fetal partscannot be well defined; so also

the presentation or the position. External ballotte-ment can be elicited more easily.

Auscultation: Fetal heart sound is not heard distinctly, although its presence can be picked up by Doppler ultrasound.

INTERNAL EXAMINATION: The cervix is pulled up, may be partially taken up or at times, dilated, to admit a finger tip through

which tense bulged membranes can be felt.

INVESTIGATIONS:

• Sonography: Sonography is helpful (Fig. 3.12)—(1) to detect abnormally large echo-fre e space between the fetus and the uterine wall

(largest vertical pocket >8 cm). Amniotic fluid index (AFI) is more than 25 cm (p. 464). (2) to exclude m ultiple fetuses (3) to note the

lie and presentation

Fig. 16.6:Abdominal girth round the umbilicus is more than normal

of the fetus (4) to diagnose any fetal congenital malformation. (Specially the central ner vous system, gastrointestinal system and

musculoskeletal system).

• Blood: (1) ABO and Rh grouping — Rhesus isoimmunisation may cause hydrops fetalis and fetal ascites. (2) Postprandial sugar and if

necessary glucose tolerance test.

• Amniotic fluid: Estimation of alpha fetoprotein which is markedly elevated in the presence of a fetus with an open neural tube defect.

DIFFERENTIAL DIAGNOSIS: (1) Twins (2) Pregnancy with huge ovarian cyst (3) Maternal ascites.

1. Twins: The diagnosis is often confused and difficult because of its associatio n with hydramnios. (i) Abdomen is markedly enlarged (ii)

Too many fetal parts (iii) Fluid thrill absent (iv) Straight X-ray or sonography confirms the diagnosis.

2. Pregnancy with huge ovarian cyst: (i) The gravid uterus can be felt separate fro m the cyst (ii) Internal examination shows the cervix

to be pushed down into the pelvis. In hydramnios, the lower segment has to ride above the pelv ic brim, so that the cervix is drawn up

(iii) X-ray of the abdomen or sonography is helpful.

3. Maternal ascites: (i) Presence of shifting dullness (ii) Resonance on the midline due to floating gut whereas in hydramnios, it becomes

dull (iii) Internal examination and palpation of the normal size uterus, if possible, can giv e the clue (iv) Straight X-ray of the abdomen or

sonography helps to exclude pregnancy.

COMPLICATIONS

The complications of hydramnios are grouped into: • Maternal • Fetal

Maternal: During pregnancy—There is increased incidence of: (1) Preeclampsia (25%). (2) Malpresentation and persistence of

floating head. (3) Premature rupture of the membranes. (4) Preterm labor either spontaneous or induced. (5) Accidental

hemorrhage due to decrease in the suface area of the emptying uterus beneath the plac enta, following sudden escape of liquor amnii.

During labor: (1) Early rupture of the membranes. (2) Cord prolapse . (3) Uterine inertia. (4) Increased operative delivery due to

malpresentation. (5) Retained placenta, postpartum hemorrhage and shock. The po stpartum hemorrhage is due to uterine atony.

Puerperium: (1) Subinvolution (2) Increased puerperal morbidit y due to infection resulting from increased operative interference and

blood loss.

Fetal: There is increased perinatal mortality to the extent of about 50%. The de aths are mostly due to pre-maturity and congenital

abnormality (40%). Other contributing factors are cord prolapse, hydrops fetalis, effec ts of increased operative delivery and accidental

hemorrhage.

MANAGEMENT

Recently there has been a falling trend in the incidence of hydramnios of severe magni tude. The reasons are: (1) Early detection and

control of diabetes. (2) Rhesus isoimmunisation is now preventable. (3) Genetic counse ling in early months and detection of fetal

congenital abnormalities with ultrasound and their termination, reduce their number in late pre gnancy.

Treatment of polyhydramnios is usually tailored according to the underlying cause. M ILD POLYHYDRAMNIOS: It is

commonly found in midtrimester and usually requires no treatment, except extra b ed rest for a few days. The excess liquor is expected to

be diminished as pregnancy advances.

SEVERE POLYHYDRAMNIOS: In view of the risks involved and the high perinatal mortality rate, the patient should be shifted in

a hospital equipped to deal with “high risk” patients.

Principles: (1) To relieve the symptoms (2) To find out the cause (3) To avoid and to deal with the comp lication.

• Supportive therapy includes bed rest, if necessary, with a back rest and treatment of the associated conditions like preeclampsia or

diabetes on the usual line. The use of diuretic is of little value. Indomethacin given orally to the mother (25 mg every 6 hours) has been

found to decrease amniotic fluid as it reduces fetal urine output.

• Investigations are done to exclude congenital fetal malformations with the avai lable gadgets and also to detect such complications like

diabetes or Rhesus isoimmunization.

• Further management depends on: (1) Response to treatment. (2) Period of gestat ion. (3) Presence of fetal malformation. (4)

Associated complicating factors.

Uncomplicated cases: (No demonstrable fetal malformation)

1. Response to treatment is good: The pregnancy is to be continued awaiting spontaneous delivery at term. 2. U nresponsive: (with

maternal distress)

(a) Pregnancy less than 37 weeks: An attempt is made to relieve the distress with a hope of continuation of pregnancy by

amniocentesis (amnio reduction—see p. 651).

Slow decompression is done at the rate of about 500 ml per hour and the amount o f fluid to be removed should be sufficient enough

to relieve the mechanical distress. Ordinarily, it should not exceed 1–1.5 liter. Becaus e of slow decompression, chance of accidental

hemorrhage is less but liquor amnii may again accumulate, for which the procedure may hav e to be repeated. Amniotic fluid can be

tested for fetal lung maturity.

(b) Pregnancy more than 37 weeks: Induction of labor is done (see p . 522). The following procedures may be helpful.

Amniocentesis → drainage of good amount of liquor → to check the favorable lie and presentation of the fetus → a stabilising oxytocin

infusion is started → low rupture of the membranes is done when the lie becomes stable and the presenting part gets fixed to the pelvis.

This will minimize sudden decompression with separation of the placenta, change in lie of the fetus and cord prolapse.

With congenital fetal abnormality: Termination of pregnancy is to be done irrespective of the duration of pregnancy.

Amniocentesis is done to drain good amount of liquor. Thereafter induction by vaginal PGE

gel insertion followed by low rupture of

membranes is done. If, accidentally, low rupture of the membranes occurs, escape of gush of liquor should be immediately controlled

by placing the palm over the introitus to avoid accidental hemorrhage. The lie should be checked and if found longitudinal, oxytocin

infusion may be started.

DURING LABOR: Usual management is followed as outlined in twin pregnancy. Internal examina tion should be done soon after the

rupture of the membranes to exclude cord prolapse. If the uterine contraction becomes sluggish, oxytocin infusion may be started, if not

contraindicated. To prevent postpartum hemorrhage, intravenous methergin 0.2 mg s hould be given with the delivery of the anterior

shoulder. One must remain vigilant following the birth of the baby for retained placenta, postp artum hemorrhage and shock. Baby

should be thoroughly examined for any congenital anomaly.

ACUTE POLYHYDRAMNIOS

Acute hydramnios is extremely rare. The onset is acute and the fluid accumulates within a few days. It usually occurs before 20 we eks

of pregnancy. It is usually associated with monozygotic twins with TTS or chorioangioma of the placenta. SYMPTOMS: Features of

acute abdomen predominate — such as abdominal pain, nausea and vomiting.

SIGNS: (i) The patient looks ill (ii) Absence of features of shock (iii) Edema of t he legs or presence of other associated features of

preeclampsia (iv) Abdomen is hugely enlarged more than the period of amen orrhea; the wall is tense with shiny skin (v) Fluid thrill is

present (vi) Fetal parts cannot be felt nor is the fetal heart sound audible ( vii) Internal examination reveals—taking up of the cervix or

even dilatation of the os through which the bulged membranes are felt (viii) Sonography shows multiple fetuses or at times fetal

abnormalities.

TREATMENT: Most often, spontaneous abortion occurs. In case with severe TTTS, repetitive amnioreduction until the AFI is normal,

may improve the perinatal outcome. Laser ablation may cure the cause of TTTS wherea s amnioreduction only treats the symptoms (p.

206).

OLIGOHYDRAMNIOS (Syn: Oligamnios )

DEFINITION: It is an extremely rare condition where the liquor amnii is deficient in amount to the extent ofless than 200 mL at

term. Sonographically, it is defined when the maximum vertical pocket of li quor is less than <2 cm or when amniotic fluid index (AFI)

is less than 5 cm (<10th centile). With AFI <8 cm (below 5th percentile) or >24 cm (ab ove 95th percentile) was considered abnormal at

gestational age, from 28–40 weeks.

ETIOLOGY

A. Fetal conditions: (i) Fetal chromosomal or structural anomalies (ii) Renal agenes is (iii) Obstructed uropathy (iv) Spontaneous rupture

of the membrane (v) Intrauterine infection (vi) Drugs: PG inhibitors, ACE inhibito rs (vii) Postmaturity (viii) IUGR (ix) Amnion

nodosum (failure of secretion by the cells of the amnion covering the placenta).

B. Maternal conditions: (i) Hypertensive disorders (ii) Uteroplacental insufficiency (iii) Deh ydration (iv) Idiopathic.

DIAGNOSIS: (1) Uterine size is much smaller than the period of amenorrhea (2) Less f etal movements (3) The uterus is “full of fetus”

because of scanty liquor (4) Malpresentation (breech) is common (5) Evidences

of intrauterine growth retardation of the fetus (6) Sonographic diagnosis is made when largest liquor pool is less than 2 cm. Ultrasound

visualization is done following amnioinfusion of 300 ml of warm saline solution (7) Vis ualization of normal filling and emptying of fetal

bladder essentially rules out urinary tract abnormality. (8) Oligohydramnios with fetal symmet ric growth restriction is associated

with increased chromosomal abnormality (see p. 462, 493).

COMPLICATIONS

Fetal: (1) Abortion (2) Deformity due to intra-amniotic adhesions or due to compress ion. The deformities include alteration in shape of

the skull, wry neck, club foot, or even amputation of the limb (3) Fetal pulmonary hypo plasia (may be the cause or effect) (4) Cord

compression (5) High fetal mortality.

Maternal: (1) Prolonged labor due to inertia (2) Increased operative interference due to malpresentatio n. The sum effect may lead to

increased maternal morbidity.

TREATMENT: Presence of fetal congenital malformation needs delivery irrespective of the pe riod of gestation. Isolated

oligohydramnios in the third trimester with a normal fetus may be managed conservative ly. Oral administration of water, increases

amniotic fluid volume. In labor, cord compression is common. Amnioinfusion (prophy lactic or therapeutic) for meconium liquor is found

to improve neonatal outcome.

ABNORMALITIES OF PLACENTA AND CORD

There is a marked variation in the morphology including size, shape and weight of the p lacenta. Variation of the cord is also quite

common. Only those of clinical importance are described.

PLACENTA SUCCENTURIATA (Fig. 16.7D, E & F)

Morphology: One (usual) or more small lobes of placenta, size of a cotyledon, may be plac ed at varying distances from the main

placental margin. A leash of vessels connecting the main to the small lobe traverse through the m embranes (Fig. 16.7D, E & F). The

accessory lobe is developed from the activated villi on the chorionic laeve. In cases o f absence of communicating blood vessels, it is

called placenta spuria. The incidence of placenta succenturiata is about 3% .

Diagnosis : Diagnosis is made following inspection of the placenta after its expulsion. (1) With intact lobe— the features have already

been described (2) With missing lobe: (a) there is a gap in the chorion and (b) torn end s of blood vessels are found on the margin of the

gap.

Clinical significance : If the succenturiate lobe is retained, following birth of the placenta, it may lead to: (1) Postpartum

hemorrhage which may be primary or secondary (2) Subinvolution (3) Uterine sepsis (4) Polyp formation.

TREATMENT: Whenever the diagnosis of missing lobe is made, exploration of the uterus and removal of the lobe under general

anesthesia is to be done.

PLACENTA EXTRACHORIALIS

Two types are described: (1) Circumvallate placenta (2) Placenta marginata

Development: The placenta of such type is due to the smaller chorionic plate than the basal p late. Recurrent marginal hemorrhage

as diagnosed on serial ultrasound is thought to be the cause. The chorionic plate does not ext end to the placental margin. The

membranes (amnion and chorion) are folded, rolled back upon itself to form a ring wh ich is reflected centrally. This leaves a rim of bare

placental tissue (extra chorial portion —fig. 16.7C).

Morphology: Circumvallate placenta (Fig. 16.7C)—(1) The fetal surface is divided into a central depressed zone surrounded by a

thickened white ring which is usually complete. The ring is situated at varying distances f rom the margin of the placenta. The ring is

composed of a double fold of amnion and chorion with degenerated decidua (vera ) and fibrin in between (2) Vessels radiate from the

cord insertion as far as the ring and then disappear from view (3) The peripheral zone outside the ring is thicker and the edge is elevated

and rounded (Fig. 16.7C).

Placenta marginata — A thin fibrous ring is present at the margin of the chorio nic plate where the fetal vessels appear to terminate.

Clinical significance: There is increased chance of: (1) Abortion. (2) Hydrorrhea gravidarum (exce ssive Figs 16.7A to D:Common

types of abnormal placentae of obstetric significance (A, B, C and D)

watery vaginal discharge). (3) Antepartum hemorrhage. (4) Growth retardation of the baby. (5) Preterm delivery. (6) Retained placenta

or membranes.

PLACENTA MEMBRANECAE: The placenta is unduly large and thin. The place nta not only develops from the chorion frondosum

but also from the chorion laeve so that the whole of the ovum is practically cov ered by the placenta.

Clinical significance: (1) Encroachment of some part over the lower segment leads to placenta previa . (2) Imperfect separation in the

third stage leads to postpartum hemorrhage. (3) Chance of retained placenta is more an d manual removal becomes difficult.

E F

Fig. 16.7: Placenta succenturiate (D, E & F)

(D) = diagrammatic; (E) = maternal surface; (F) = fetal surface with communicating ve ssels (see arrow).

CORD ABNORMALITIES

BATTLEDORE PLACENTA: The cord is attached to the margin of the placenta. If associated with low implantation of the

placenta, there is chance of cord compression in vaginal delivery leading to fetal anoxia or even death; otherwise, it has got little clinical

significance (Fig 16.7A).

VELAMENTOUS PLACENTA: The cord is attached to the membranes. The branch ing vessels traverse between the membranes for

a varying distance before they reach and supply the placenta. If the leash of blood ves sels happen to traverse through the membranes

overlying the internal os, in front of the presenting part, the condition is called vasa previa. Rupture of the membranes involving the

overlying vessels leads to vaginal bleeding. As it is entirely fetal blood, this may res ult in fetal exsanguination and even death

(Fig.16.7B).

MANAGEMENT: In the presence of fetal bleeding, urgent delivery is essential either vag inally or by cesarean section. The infant’s

hemoglobin should be estimated and if necessary, blood transfusion be carried out. If t he baby is dead, vaginal delivery is awaited.

ABNORMAL LENGTH: The cord may be unduly long (300 cm) or absent (aco rdia).

Short cord : The short cord may be true (less than 20 cm or 8”) or commonly relative due to entangle ment of the cord round any fetal

part. In exceptional circumstances, the cord may be absent and the placenta may be attached to the liver as in exomphalos.

Clinical significance — In either variety, it may cause: (1) Failure of external version (2) Prevent descent o f the presenting part

specially during labor (3) Separation of a normally situated placenta (4) Favor malpresentation (5) Fetal distress in labor.

Long cord : The clinical significance due to the presence of a long cord is that there is an increased chance of: (1) Cord prolapse (2)

Cord entanglement round the neck or the body. The condition may produce sufficient compression on the cord vessels so as to produce

fetal distress or rarely death (3) True knot is rare. Even with true knot the fetal vessels are pr otected from compression, by the

Wharton’s jelly. False knots are the result of accumulation of Wharton’s jelly or due to varices (Fig. 16.8).

Fig. 16.8: Abnormalities in the umbilical cord

SINGLE UMBILICAL ARTERY: Single umbilical artery is present in about 1–2% of cases. It may be due to failure of development

of one artery or due to its atrophy in later months. It is more common in twins and in babies b orn of women with diabetes, epilepsy,

oligohydramnios, hydramnios, pre-eclampsia and antepartum hemorrhage. It is frequ ently associated with congenital malformation of

the fetus (20–25%). Renal and genital anomalies, Trisomy 18 are common . There is increased chance of abortion, fetal aneuploidy,

prematurity, IUGR and increased perinatal mortality (Fig. 16.8).

Hypertensive Disorders in Pregnancy

Hypertension is one of the common medical complications of pregnancy and co ntributes significantly to maternal and perinatal

morbidity and mortality. Hypertension is a sign of an underlying pathology which may be pre existing or appears for the first time

during pregnancy. The identification of this clinical entity and effective management pla y a significant role in the outcome of pregnancy,

both for the mother and the baby. In the developing countries with inadequate ly cared pregnancy, this entity on many occasions remains

undetected till major complications supervene.

Classification of Hypertension in Pregnancy ( National High Blood Pressure Educat ion Program 2000) Disorder

Hypertension

Disorder

Chronic

hypertension

with super

imposed pre

eclampsia and

eclampsia

Definition

The common causes of chronic hypertension:

Proteinuria

Definition

BP ≥ 140/90 mm Hg measured 2 times

with at least a 6-hour interval

Urinary excretion of ≥ 0.3 gm

protein/24 hours specimen or 0.1

gm/L

BP ≥ 140/90 mm Hg for the first time

in pregnancy after 20 weeks, without

proteinuria

Gestational hypertension with

proteinuria

Women with pre-eclampsia

complicated with convulsions and/

or coma

Known hypertension before

pregnancy or hypertension diagnosed

first time before 20 weeks of

pregnancy

Occurrence of new onset of

(a) Essential hypertension (b) Chronic renal disease (reno vascular) (c) Coarctation of aorta

Gestational

hypertension

(d) Endocrine disorders (diabetes mellitus, pheochromocytoma, thyrotoxicosis

Pre-eclampsia (e) Connective tissue diseases (Lupus erythematosus).

Eclampsia t The criteria for diagnosis of super imposed pre-eclampsia: (i) N ew onset of proteinuria >0.5

Chronic

hypertension

gm/24 hours specimen. (ii) Aggravation of hypertension. (iii) Thrombocytopenia or (iv ) Raise of liver enzymes

Superimposed

pre-eclampsia

or eclampsia proteinuria in women with chronic

hypertension (see below)

PRE-ECLAMPSIA

DEFINITION: Pre-eclampsia is a multisystem disorder of unknown etiology characte rized by development of hypertension to

the extent of 140/90 mm Hg or more with proteinuria after the 20th week in a pr eviously normotensive and nonproteinuric

woman. Some amount of edema is common in a normal pregnancy. Edema has b een excluded from the diagnostic criteria unless it is

pathological. The preeclamptic features may appear even before the 20th week as in cases of hydatidiform mole and acute

polyhydramnios.

The term, ‘Pregnancy-induced hypertension (PIH)’ is defined as the hypertension that develops as a direct result of the gravid state. It

includes—(i) gestational hypertension, (ii) pre-eclampsia, and (iii) eclampsia.

DIAGNOSTIC CRITERIA OF PRE-ECLAMPSIA

Hypertension: An absolute rise of blood pressure of at least 140/90 mm Hg, if the previous blood pressure is not known or a rise in

systolic pressure of at least 30 mm Hg, or a rise in diastolic pressure of at least 15 mm Hg over the previously known blood pressure is

called pregnancy induced hypertension.

Calculation based on mean arterial pressure (MAP) as advocated by Page

Systolic pressure + (diastolic pressure × 2)

= MAP3

A rise of 20 mm Hg MAP over the previous reading, or when the MAP is 105 mm Hg or more should be considered as significant.

The rise of blood pressure should be evident at least on two occasions at least 6 hours a part. The level is arbitrary and is based on the

observation, that complications are likely to be more beyond this level. Diastolic blood pr essure is noted at the point of disappearance of

sounds (Korotkoff – V).

Blood pressure is measured on the right arm, with the patient lying on her side at 45° to the horizontal. In the outpatient, sitting posture is

preferred. In either case, the occluded brachial artery should be kept at the level of the heart.

Edema: Demonstration of pitting edema over the ankles after 12 hours bed rest or rapid gain in w eight of more than 1 lb a week or

more than 5 lb a month in the later months of pregnancy may be the earliest evidence o f pre-eclampsia. However, some amount of

edema is common (physiological) in a normal pregnancy.

Proteinuria: Presence of total protein in 24 hours urine of more than 0.3 gm or > 2+ (1.0 gm/L) on at least two random clean-catch urine

samples tested > 4 hours apart in the absence of urinary tract infection is considered significant.

Test for protein in urine by multiple reagent strip (dipstick) as follows: Trace = 0.1 gm/L; 1+ = 0.3 g m/L; 2+ = 1.0 gm/L; 3+ = 3.0

gm/L; 4+ = 10.0 gm/L.

INCIDENCE: The incidence of pre-eclampsia in hospital practice varies widely fro m 5 to 15%. The incidence in primigravidae is

about 10% and in multigravidae 5%. Imperfect documentation and lack of uniformity in the diagnostic criteria are the responsible

factors in variation of its frequency.

RISK FACTORS FOR PRE-ECLAMPSIA

• Primigravida: Young or elderly (first time exposure to chorionic villi)

• Family history: Hypertension, pre-eclampsia

• Placental abnormalities:

– Hyperplacentosis: Excessive exposure to chorionic villi—(molar pregnancy twins, d iabetes)

– Placental ischemia.

• Obesity: BMI >35 kg/M

, Insulin resistance.

• Pre-existing vascular disease (p. 219).

• New paternity.

• Thrombophilias (antiphospholipid syndrome, protein C, S

ETIOPATHOLOGICAL FACTORS FOR PRE-ECLAMPSIA

t Failure of trophoblast invasion (abnormal placentation) p. 32

t Vascular endothelial damage

t Inflammatory mediators (cytokines)

t Immunological intolerance between maternal and fetal tissues (p. 635)

t Coagulation abnormalities (p. 626)

t Increased oxygen free radicals

t Genetic predisposition (polygenic disorder)

t Dietary dieficiency or excess

deficiency, Factor V Leiden p. 275).

ETIOPATHOGENESIS OF PRE-ECLAMPSIA

HYPERTENSION: The underlying basic pathology is endothelial dysfunction and intense vasospasm, affecting almost all the

vessels, particularly those of uterus, kidney, placental bed and brain. The basic underly ing pathology remains as endothelial

dysfunction and vasospasm. The responsible agent for endothelial dysfunction and v asospasm, still has not been isolated precisely, but

it seems certain to be humoral in origin. The following are the considerations:

• Increased circulating pressor substances (see p. 222).

• Increased sensitivity of the vascular system to normally circulating pressure su bstances (Genetic).

Trophoblast Invasion and Uterine Vascular Changes: Normally, there is invasion of the endovasc ular trophoblasts into the walls of

the the spiral arterioles of the uteroplacental bed. In the first trimester (10–12 weeks) endovascular trophobla sts invades up to decidual

segments and in the second trimester (16–18 weeks) another wave of trophoblasts invades upto the myom etrial segments (Fig. 3.7).

This process replaces the endothelial lining and the muscular arterial wall by fibrin oid formation. The spiral arterioles thereby become

distended, tortuous, and funnel-shaped. This physiological change transforms the spiral arter ioles into a low resistance, low

pressure, high flow system. In pre-eclampsia, there is failure of the second wave of endovascular trophoblast migration and there is

reduction of blood supply to the fetoplacental unit (p. 32).

In normal pregnancy: (1) Angiotensin-II (part of α

globulin) is destroyed by angiotensinase, which is liberated from the placenta.

Thus, the blood pressure is stabilized. (2) The vascular system becomes refractory, selectively to pressor agent angiotensin-II. This is

probably brought out by vascular synthesis of prostaglandin I

and nitric oxide (NO) which have got vasodilator effect. The

interaction between the two systems stabilises the blood pressure in normal pregnancy. Vascular endothelial growth factor (a

mitogenic glycoprotein) — increased VEGF restores the uteroplacental blood flow to norm al level.

In Pre-eclampsia: (1) There is an imbalance in different components of prostaglandins—relative or absolute deficienc y of vasodilator

prostaglandin (PGI

) from vascular endothelium and increased synthesis of thromboxane (TXA

), a potent vasoconstrictor in platelets.

(2) There is increased vascular sensitivity to the pressor agent angiotensin-II . Angiotensinase activity is depressed,

followingproteinuria with elimination of α

globulin (see scheme for pathophysiology). (3) Nitric oxide (NO): It is synth esized in the

vascular endothelium and syncytiotrophoblast from L-arginine. It significantly relaxes vascular smooth muscle, inhibits platelet

aggregation and prevents intervillous thrombosis. Deficiency of nitric oxide contrib utes to the development of hypertension. (4)

Endothelin-1 is synthesized by endothelial cells, and it is a potent vasocons trictor compared to angiotensin-II. Endothelin-1 also

contributes to the cause of hypertension. (5) Inflammatory mediators: Cytokines [tumor necrosis factor (TNFα), interleukins (IL-6) and

others] derived from activated leukocytes cause endothelial injury (6) Abnormal lipid metabolism—results in more oxidative stress.

Lipid peroxides, reactive oxygen species (ROS) and superoxide anion radicals — cause endothelial injury and dysfunction. P latelet and

neutrophil activation, cytokines, superoxide radical production and endothelial damage are in a vicious cycle. (7) Others—mutation of

factor V Leiden increases the risk.

Hence pre-eclampsia is characterized by endothelial dysfunction and vasospasm. Endothelia l dysfunction is due to oxidative stress

and the inflammatory mediators. Vasospasm results from the imbalance of vasodilators (P GI

, NO) and vasoconstrictors (Angiotensin-

II, TXA

, Endothelin-1). Both are in a vicious cycle.

EDEMA: The cause of excessive accumulation of fluids in the extracellular tissue sp aces is not clear. Probable explanations are:

Increased oxidative stress → endothelial injury → increased capillary permeability. On this basis, the leaky capillaries and decreased

blood osmotic pressure are the probable explanations.

PROTEINURIA: The probable chain of events is as follows. Spasm of the afferent glo merular arterioles → anoxic change to the

endothelium of the glomerular tuft → glomerular endotheliosis → increased capillary p ermeability → increased leakage of proteins.

Tubular reabsorption is simultaneously depressed. Albumin constitutes 50–60% and alpha globu lin constitutes 10–15% of the total

proteins excreted in the urine.

PATHOPHYSIOLOGY

While the question as to why the syndrome occurs still remains unsolved, the pathologic al changes are well documented, specially in

severe pre-eclampsia or in eclampsia.

Uteroplacental bed: There is increased evidences of premature aging of the placenta. Areas of occasional acute red infarcts and white

infarcts are visible on the maternal surface of the placenta.

Villi: Syncitial degeneration, increased syncitial knots, marked proliferation of cytotrophoblast, thickenin g of the basement layer, and

proliferative endarteritis are evident in varying degrees.

In pre-eclampsia, the normal endovascular invasion of cytotrophoblast into the spir al arteries fails to occur beyond decidua-

myometrial junction (see p. 32). As a result, the musculoelastic media in the myome trial segment remains responsive to vasoconstrictor

stimuli resulting in decreased blood flow (see Fig. 3.7). There is acute atherosis of spira l arteries with obliteration of lumen.

Intervillous circulation: The blood flow is impaired to the extent of about one-third, secondary to the changes in the maternal blood

vessels. This results in placental changes, anatomical and functional, which are responsib le for fetal jeopardy.

Kidney: The changes are conspicuous in the glomerulus which becomes enlarged (glomerular endotheliosis). Endothelial cells swell

up and fibrin like deposits occur in the basement membrane. The lumen may be occlud ed. Interstitial cells in between the capillaries

proliferate. There is associated spasm of the afferent glomerular arterioles. Patchy areas of damage of the tubular epithelium due to

anoxia are evident. The net effects are reduced renal blood flow and glomerular filtration ra te (25%) and impaired tubular reabsorption

or secretory function. Recovery is likely to be complete, following delivery. In severe cases, intense anoxia may produce extensive

arterial thrombosis leading to bilateral renal cortical necrosis.

Blood vessels: There is intense vasospasm. Circulation in the vasa vasorum is im paired leading to damage of the vascular walls,

including the endothelial integrity.

Liver: Periportal hemorrhagic necrosis of the liver occurs due to thr ombosis of the arterioles. The necrosis starts at the periphery of the

lobule. There may be subcapsular hemorrhage. Hepatic insufficiency seldom occurs becau se of the reserve capacity and regenerative

ability of liver cells. Liver function tests are specially abnormal in women with HELLP sy ndrome.

HELLP Syndrome: This is an acronym for Hemolysis (H), Elevated Liver enzym es (EL) and Low Platelet count (LP) (<100,000/mm

This is a rare complication of pre-eclampsia (10–15%). HELLP syndrome may develo p even without maternal hypertension. This

syndrome is manifested by nausea, vomiting, epigastric or right upper quadrant pain, al ong with biochemical, and hematological

changes. Parenchymal necrosis of liver causes elevation in hepatic enzymes (AST and A LT >70 IU/L, LDH >600 IU/L) and bilirubin

(>1.2 mg/dL). There may be subcapsular hematoma formation (which is diagnosed by CT scanning) and abnormal peripheral blood

smear. Eventually liver may rupture to cause sudden hypotension, due to hemoperitone um.

Management: Principles of management are same as that of pre-eclampsia and eclamps ia (see p. 227). Antiseizure prophylaxis with

magnesium sulphate (see p. 230) is started. Careful assessment of maternal and fetal stat us followed by delivery is done. Administration

of corticosteroids (see p. 315) improves perinatal (↑ pulmonary maturity, ↓ IVH and ↓ necrotizing enterocolitis) and maternal (↑

thrombocyte count, ↑ urinary output) outcome. Cesarean section is the common mod e of delivery. Epidural anesthesia can be used safely

if the platelet count is >1,00,000/mm

). Platelet transfusion should be given if the count is <50,000/mm

. Patient should be managed in

an ICU until there is improvement in platelet count, urine output, BP and liver enzymes. Recurrence risk of HELLP syndrome is 3–19%.

Expectant management has been carried out selectively when pregnancy is < 34 weeks, w ith bed rest, plasma volume expansion

(infusion of 5–25% albumin), antithrombotic agents (dipyridamole), immunosuppressiv e agents (steroids) and others (fresh frozen

plasma). In HELLP syndrome perinatal mortality ranges between 5 and 60% and mater nal mortality may be up to 25%. Complications:

Maternal: Abruptio placenta, DIC, acute renal failure, severe ascites, pulmon ary edema, pleural effusions, cerebral edema, laryngeal

edema, retinal detachment, subcapsular liver hematoma, ARDS, sepsis, and de ath. Perinatal: Morbidity and mortality are significantly

increased. This is due to preterm delivery, prematurity, RDS and sepsis (see p. 605).

Brain: Neuroimaging (CT, MI) studies revealed: hypodense areas in the cortex, cerebral edema , capillary thrombosis, infarction,

intraventricular and parenchymal hemorrhages, and necrosis. Clinical manifestations of headache, scotomata, blindness, convulsions are

due to posterior reversible encephalopathy syndrome involving the parietal and occipital lobes.

Heart : Subendothelial hemorrhages may occur. Focal necrosis and hemorrhage in th e myocardium may affect the conducting system

leading to heart failure.

Lungs: There is evidence of edema or hemorrhagic bronchopneumonia. This is due to low oncotic pressure and leaky capillaries. Other

organs: Adrenal glands show hemorrhage and necrosis. Stomach shows feature of hemorr hagic gastritis.

Water and electrolyte balance: There is lot of controversy and confusion about the ch anges in water and electrolyte balance in pre-

eclampsia. The consensus of opinion is varying degree of salt retention. The precise me chanism is not clear. It is not due to increase in

aldosterone which, in fact, is diminished in pre-eclampsia. The retention is likely due to r enal vasoconstriction leading to reduction of

GFR. The salt retention increases extracellular fluid volume; increases sensitivity to angio tensin-II and may increase peripheral

resistance by causing arteriolar endothelial swelling. The net effect is intravasc ular dehydration and extravascular overhydration.

Thus, there is hemoconcentration and rise in hematocrit value.

Immediately following delivery, there is rapid mobilization of sodium and water from the ex travascular compartment into the

intravascular space. If this mechanism fails, the patient may develop shock (Post partum vascular collapse).

Hematological changes: Blood volume — The extent of increase in blood volume in normal pre gnancy is not evident in severe pre-

eclampsia. Due to vasospastic state, the intravascular fluid is forced out into the extravas cular space. Thus, there is hemoconcentration

with increased hematocrit values. After delivery, the plasma volume increases with decreas e in hemoglobin and hematocrit values.

Erythrocyte destruction — There is evidence of increased erythrocyte destruction following ecla mpsia with resultant hemoglobinaemia

and hemoglobinuria.

Coagulation — There is evidence of disseminated intravascular coagulopathy (DIC) a ffecting widespread organs of the body as opposed

to selective DIC only at the placental site in normal pregnancy. The process appears to b e initiated by the release of thromboplastin into

the circulation. It may arise from the blood platelets as in Shwartzman reaction or from r elease of trophoblastic fragments into the uterine

circulation. There is reduction of platelets, fibrinogen, antithrombin-III, and plasminog en level in the blood. The microthrombi

affect the arterioles of all the vital organs apart from the placenta to produce s pecific pathological changes. Degree of thrombocytopenia

reflects the severity of pathology. Fibronectin, D-dimer and thrombin levels are elevated.

Hormones: There is a conflict regarding the hormonal status in pre-eclampsia. Estrogen and pr ogesterone levels are lowered, whereas

chorionic gonadotropin level may be increased. The serum level of HPL is decreased.

Biochemical values: Nonprotein nitrogen and urea levels of normal pregnancy of 25 mg/dL an d 20 mg/dL respectively are maintained in

mild pre-eclampsia. In severe pre-eclampsia, however, both the levels are increased. B lood uric acid level is raised beyond the normal

level of 4 mg/dL. Uric acid is secreted by the distal tubules. Raised serum uric acid level indicates renal involvement (increased tubular

reabsorption, decreased tubular secretion and/or diminished renal blood flow). High le vel of serum uric acid is found to correlate with the

severity of pre-eclampsia, volume contraction and fetal jeopardy. Serum creatinine is elevated in severe pre-eclampsia. Blood chlorides

are increased due to delay in the excretion of sodium. Serum protein level is lowered, particularly the albumin fraction. Oxidative stress

(p. 221): Hyperhomocysteinemia found in pre-eclampsia causes oxidative stress and endot helial damage.

CLINICAL TYPES

The clinical classification of pre-eclampsia is arbitrary and is principally dependent on th e level of blood pressure for management

purpose. But proteinuria is more significant than blood pressure to predict fetal outcome .

• Mild: This includes cases of sustained rise of blood pressure of more than 140/90 mm Hg but less than 160 mm Hg systolic or 110 mm

Hg diastolic without significant proteinuria.

• Severe: (1) A persistent systolic blood pressure of >160 mm Hg or diastolic pressure of >110 mm Hg. (2) Protein excretion of >5

gm/24 hr. (3) Oliguria (<400 ml/24 hr). (4) Platelet count < 100,000/mm

. (5) HELLP syndrome. (6) Cerebral or visual disturbances. (7)

Persistent severe epigastric pain. (8) Retinal hemorrhages, exudates or papilledema. (9) I ntrauterine growth restriction of the fetus. (10)

Pulmonary edema.

From the prognostic point of view , a diastolic rise of blood pressure is more important tha n the systolic rise. Moreover,

convulsions may occur even with moderate rise of blood pressure; conversely, even w ith alarming high rise of pressure, the pregnancy

may have an uneventful outcome. This calls for a strict vigilance whenever the blood pressur e is raised to the pre-eclamptic level or even

before that.

CLINICAL FEATURES

Pre-eclampsia frequently occurs in primigravidae (70%). It is more often associated wi th obstetrical–medical complications such as

multiple pregnancy, polyhydramnios, pre-existing hypertension, diabetes etc. The clinic al manifestations appear usually after the 20th

week.

ONSET: The onset is usually insidious and the syndrome runs a slow course. On rare occasion, however, the onset becomes acute and

follows a rapid course.

SYMPTOMS: Pre-eclampsia is principally a syndrome of signs and when sym ptoms appear, it is usually late. Mild symptoms:

Slight swelling over the ankles which persists on rising from the bed in the morning or tightness of the ring on the finger is the early

manifestation of pre-eclampsia edema. Gradually, the swelling may extend to the face, abdomin al wall, vulva and even the whole body

(see Fig. 17.1A & B).

Alarming symptoms : The following are the ominous symptoms, which may be evident either singly or in combination. These are

usually associated with acute onset of the syndrome. (1) Headache — either located over the occipital or frontal region (2) Disturbed

sleep, (3) Diminished urinary output—Urinary output of less than 400 ml in 24 hours is ver y ominous, (4) Epigastric pain—acute

pain in the epigastric region associated with vomiting, at times coffee color, is due to hem orrhagic gastritis or due to subcapsular

hemorrhage in the liver, (5) Eye symptoms—there may be blurring, scotomata, dimness of v ision or at times complete blindness. Vision

is usually regained within 4–6 weeks following delivery. The eye symptoms are due to spasm of retinal vessels (retinal infarction),

occipital lobe damage (vasogenic edema) or retinal detachment. Reattachment of the reti na occurs following subsidence of edema and