Beischer & MacKay’s Obstetrics, Gynaecology and the Newborn [4th Edition] 9780729583824, 9780729583817, 9780729584050

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Beischer & MacKay’s Obstetrics, Gynaecology and the Newborn [4th Edition]
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Table of contents :
Front Cover......Page 1
Inside Front Cover......Page 2
Half title page......Page 3
Dedication......Page 4
Beischer & Mackay's Obsterics, gynaecology and the newborn......Page 5
Copyright Page......Page 6
Table Of Contents......Page 7
Foreword......Page 12
Preface......Page 13
Acknowledgements......Page 14
List of editors......Page 15
List of contributors......Page 16
List of reviewers......Page 18
1 Anatomy and Physiology......Page 19
Mons pubis......Page 20
Vaginal orifice......Page 21
Vagina......Page 22
Uterus......Page 23
Uterine tubes......Page 24
The bony pelvis......Page 25
The pelvic joints......Page 27
Luteal phase......Page 28
Gametogenesis......Page 29
Postmenopause......Page 31
Fertilisation......Page 32
Ectodermal layer......Page 34
Mesodermal layer......Page 36
Endodermal layer......Page 37
Early trophoblast......Page 38
Further changes in the trophoblast and decidua......Page 39
Tissues separating maternal and fetal circulations......Page 40
Fetomaternal haemorrhage......Page 42
The umbilical cord......Page 43
2 Obstetrics......Page 45
2.1 Normal Pregnancy......Page 46
Maternal age considerations in the timing of pregnancy......Page 47
Optimising treatment for pregnancy......Page 48
Pharmacological advice......Page 49
Diagnosing pregnancy......Page 50
Other means of determining the gestational age......Page 51
Blood group and antibody screen......Page 52
Thyroid function......Page 53
Exercise......Page 54
Infections......Page 55
Further reading......Page 56
Health promotion and preventative medicine......Page 57
Maternal weight......Page 58
Palpation......Page 59
First antenatal visit......Page 60
Blood group antibody screen......Page 61
Group B streptococcus (GBS) screening......Page 62
Further reading......Page 63
Dietary guidelines in pregnancy......Page 64
Iron......Page 65
Weight gain in pregnancy......Page 66
Further reading......Page 68
2.2 Problems of Early Pregnancy......Page 69
Clinical features......Page 70
Further reading......Page 71
Miscarriage......Page 73
Aetiology......Page 74
Assessment......Page 75
Complete miscarriage......Page 76
Missed miscarriage......Page 77
Recurrent miscarriage......Page 78
Tubal rupture......Page 79
Management......Page 80
Medical treatment......Page 81
Localised GTD......Page 82
Choriocarcinoma......Page 83
Initial management......Page 84
Follow-up......Page 85
Further reading......Page 86
2.3 Prenatal Diagnosis......Page 87
Introduction......Page 88
Second trimester maternal serum screening......Page 89
Integrated testing: combining first- and second-trimester screening......Page 91
Diagnostic tests......Page 92
Haemoglobinopathies......Page 93
Prevention of structural abnormalities......Page 94
Abnormalities of the central nervous system......Page 95
Abnormalities of the skeletal system......Page 96
Fetal tumours......Page 97
Management of pregnancies complicated by fetal genetic or structural abnormalities......Page 98
The expected short- and long-term outcomes......Page 99
Post-termination care......Page 100
Further reading......Page 101
2.4 Obstetric Complications......Page 102
Determine aetiology......Page 103
Clinical features......Page 104
Treatment......Page 105
Placental bed ischaemia......Page 106
Who and where?......Page 107
Further reading......Page 108
Fetal growth restriction......Page 109
Investigating for causes of FGR......Page 110
Management......Page 111
Management of labour......Page 112
Assessment of fetal wellbeing......Page 113
Ultrasound assessment of fetal Doppler studies......Page 114
Further reading......Page 115
Epidemiology......Page 116
Examination......Page 117
Calcium channel blockers......Page 118
Significance......Page 119
Conservative management of PPROM......Page 120
Pessary......Page 121
References......Page 123
Incidence......Page 124
Placental insufficiency and consequences......Page 125
Ultrasound and cardiotocography......Page 126
Further reading......Page 127
Incidence and aetiology of twins......Page 129
Determination of chorionicity and amnionicity......Page 130
Management in early pregnancy......Page 131
Fetal growth surveillance......Page 132
Twin–twin transfusion syndrome (TTTS)......Page 133
Death of one twin......Page 134
Labour and delivery of twins......Page 135
High-order multiple pregnancy......Page 136
Further reading......Page 137
Incidence......Page 138
Determine aetiology (look for a cause)......Page 139
Planned vaginal birth versus elective caesarean section......Page 140
Management on admission......Page 141
First stage of labour......Page 142
Delivery of the aftercoming head......Page 143
Breech extraction......Page 144
Diagnosis......Page 145
Further reading......Page 146
2.5 Medical and Surgical Disorders in Pregnancy......Page 147
Classification of hypertension in pregnancy......Page 148
Deficient placentation......Page 149
Neurological......Page 150
Placental......Page 151
Differential diagnosis......Page 152
Management of preeclampsia without severe features......Page 153
Intravascular volume status......Page 154
Prophylaxis......Page 155
Convulsion first aid......Page 156
Further reading......Page 157
17 Thromboembolism, cardiac disorders and respiratory disease......Page 158
Physiological changes in pregnancy......Page 159
Antenatal......Page 160
Peripartum cardiomyopathy......Page 161
Further reading......Page 162
Pathology......Page 163
Management......Page 164
Transplacental (haematogenous) infections......Page 165
Chlamydial infection......Page 166
Mycoplasmal and ureasplasmal infection......Page 167
Tuberculosis......Page 168
Further reading......Page 169
Cytomegalovirus......Page 170
Rubella......Page 173
Diagnosis and management of fetal infection......Page 174
Fetal infection......Page 175
Maternal HIV......Page 176
Management of the infant......Page 177
Malaria......Page 178
Further reading......Page 179
Clinical sequelae......Page 181
Alpha-thalassaemia......Page 182
Haemoglobinopathies......Page 183
Pathogenesis......Page 184
Further readings......Page 185
Acute appendicitis......Page 186
Management......Page 187
Female genital mutilation......Page 188
Motor vehicle accident in pregnancy......Page 189
Ovarian cysts and tumours......Page 190
Physiological changes in pregnancy......Page 191
Pregnancy......Page 192
Further reading......Page 193
Background......Page 194
Clinical features......Page 195
Autoimmune hyperthyroidism (Graves’ disease)......Page 196
Antiphospholipid syndrome......Page 197
Blood transfusion......Page 198
Passive administration of anti-D......Page 199
Determining the partner’s antigen status......Page 200
Management of the moderate- or high-risk immunised pregnancy......Page 201
Neonatal alloimmune neutropenia......Page 202
23 Diabetes mellitus......Page 203
Screening for GDM at 26 to 28 weeks’......Page 204
The effect of diabetes on pregnancy......Page 205
Treatment......Page 206
Intrapartum care......Page 207
Further Readings......Page 208
Multiple sclerosis in pregnancy......Page 209
Postpartum care......Page 210
Cerebral venous thrombosis......Page 211
Further reading......Page 212
Emotional wellbeing in pregnancy......Page 214
Maternity blues......Page 215
Management of mental illness in pregnancy......Page 216
Electroconvulsive therapy......Page 217
References......Page 218
Further reading......Page 219
2.6 Common Clinical Scenarios and Presenting Problems in Pregnancy......Page 220
Management......Page 221
Differential diagnosis......Page 222
Pathophysiology......Page 223
Management......Page 224
Management......Page 225
Pathophysiology......Page 226
Management......Page 227
Assessment......Page 228
Management......Page 229
Further reading......Page 230
2.7 Labour and Birth......Page 231
2.7.1 Normal Labour and Birth......Page 233
The upper and lower uterine segments......Page 234
Biochemical changes in the myometrium, cervix and membranes prior to and in early labour......Page 235
The pain of uterine contractions......Page 237
The stages of labour......Page 238
Descent......Page 239
Trunk delivery......Page 241
Damage to the tissues of the pelvic floor......Page 242
Uterine atony in the third stage of labour......Page 243
28 Management of normal labour......Page 244
Examination......Page 245
The admission cardiotocograph......Page 247
Partner, family and friends......Page 248
Vaginal examination......Page 249
Auscultation of the fetal heart......Page 250
Ambulation and position......Page 251
Management of the normal second stage of labour prior to the actual birth......Page 253
Cord around the neck......Page 254
Clamping of the cord......Page 255
Await uterine contraction, placental separation and descent......Page 256
Controlled cord traction......Page 257
Management of an incomplete placenta......Page 258
Further reading......Page 259
2.7.2 Induction of Labour, Instrumental Delivery and Casearean Section......Page 260
Risks of birth occurring earlier than it would have occurred spontaneously......Page 261
Contraindications to vaginal birth......Page 262
Fetal surveillance following cervical ripening or induction of labour......Page 263
Contraindications to prostaglandin administration......Page 264
Excessive uterine muscular activity......Page 265
References......Page 266
Fetal compromise and/or inadequate progress with the head on the perineum; vaginal breech delivery......Page 267
Midline episiotomy......Page 268
Repair of the vaginal epithelium......Page 270
Prevention......Page 271
Clinical features......Page 272
Vulval or vaginal haematoma......Page 273
Further reading......Page 274
Choice between instruments: forceps or vacuum?......Page 275
Aftercoming head of a vaginal breech delivery......Page 276
Station prior to instrumental birth......Page 277
Obstetric forceps......Page 278
Mid-cavity forceps delivery......Page 279
Failed instrumental birth......Page 282
Shoulder dystocia......Page 283
Further reading......Page 284
Incidence......Page 285
Indications......Page 286
Inadequate progress in labour and/or fetal compromise (Ch 33)......Page 287
Preparation for caesarean section......Page 288
Surgical technique......Page 289
Postoperative care......Page 290
Uterine rupture......Page 291
Likelihood of achieving a vaginal birth if attempted after a previous caesarean section......Page 292
Further reading......Page 293
2.7.3 Intrapartum Clinical Problems......Page 294
Fetal compromise after epidural anaesthesia......Page 295
Umbilical cord......Page 296
Management of acute intrapartum fetal compromise......Page 297
Assess and treat the underlying cause......Page 298
Amniotic fluid quantity and meconium-staining......Page 299
Diagnosis......Page 300
Incidence......Page 301
Further reading......Page 302
The powers......Page 303
Obstructed labour, sepsis, fetal death, genital tract fistula......Page 304
Signs of obstructed labour......Page 305
Rationale......Page 306
Fetal complications......Page 307
Shoulder dystocia (impacted shoulders)......Page 308
Management......Page 309
5. Cleidotomy......Page 310
7. Caesarean section......Page 311
What causes flexion of the fetal head?......Page 312
Aetiology......Page 313
Sequelae of a posterior position at the start of labour......Page 314
Aetiology......Page 315
Clinical sequlae......Page 317
Clinical sequelae......Page 318
Intrapartum......Page 319
Incidence......Page 320
4. Contract the uterus......Page 321
Uterine atony......Page 322
Pathology......Page 323
Management......Page 324
Trauma......Page 325
The retained placenta in the absence of bleeding......Page 326
Further reading......Page 327
Aetiology......Page 328
Aetiology......Page 330
Aetiology......Page 331
Management......Page 332
Pathophysiology of labour pain......Page 333
Therapies that provide effective analgesia of moderate degree in some patients......Page 334
Establishing and maintaining block......Page 335
Anaesthesia for caesarean section......Page 337
General anaesthesia for caesarean section......Page 338
References......Page 339
2.7.4 The Puerperium and Lactation......Page 340
Physiological changes in the puerperium......Page 341
Renal system and urinary tract......Page 342
Physiology of lactation and breastfeeding......Page 343
Further reading......Page 346
0 to 6 hours after birth......Page 347
6 hours to 7 days after birth......Page 349
The first week......Page 351
Further reading......Page 352
Thromboembolism......Page 353
Secondary postpartum haemorrhage......Page 354
Urinary and bowel problems during the puerperium......Page 355
Further reading......Page 356
2.7.5 Global Women's Health and Indigenous Women's Health......Page 357
Introduction......Page 358
Maternal mortality......Page 359
Abortion......Page 360
Cervical cancer......Page 361
References......Page 362
Australian Indigenous women’s health in pregnancy......Page 363
Barriers to accessing healthcare......Page 364
Social and emotional wellbeing......Page 365
Infection......Page 366
References......Page 367
3 Gynaecology......Page 369
3.1 Gynaecological Assessment......Page 370
Surgical history......Page 371
Menstrual history......Page 372
The gynaecological examination......Page 373
Further reading......Page 375
Microbiology......Page 376
Obtaining the cervical sample......Page 378
Pelvic ultrasound......Page 379
Pelvic MRI......Page 382
Instrumentation......Page 384
Vaginoscopic approach......Page 385
Technique......Page 386
Applications of laparoscopy......Page 387
References......Page 388
3.2 Menstrual Disorders......Page 389
Imperforate hymen......Page 390
Hypothalamic–pituitary causes......Page 391
Absence of secondary sexual hair......Page 392
Sexual activity......Page 393
Further reading......Page 394
47 The menstrual cycle and menstrual disorders......Page 395
Menstruation: general description and terms......Page 396
The menstrual process......Page 397
Menstrual hygiene......Page 399
Clinical features......Page 401
Treatment......Page 402
Medical: hormonal......Page 403
Clinical features......Page 404
Medical: non-hormonal......Page 405
Other......Page 407
History and examination......Page 408
Biopsy......Page 409
Medical: hormonal......Page 410
Surgical......Page 413
Aetiology......Page 414
Examination......Page 415
References......Page 416
3.3 Reproductive Endocrinology and Infertility......Page 418
Aetiology......Page 419
Evaluation......Page 420
Management......Page 422
Hypothalamic dysfunction......Page 423
Tubal factors......Page 424
Management of tubal disease......Page 425
Coital factors......Page 426
Intrauterine adhesions (Asherman’s syndrome)......Page 427
Unexplained infertility......Page 428
IVF and intracytoplasmic sperm injection (ICSI)......Page 429
Further reading......Page 430
Definitions......Page 432
Secondary amenorrhoea......Page 433
3. Ovarian failure......Page 434
Hypothalamic: hyperandrogenism including PCOS......Page 436
Assessment......Page 437
Medical treatment......Page 438
Ovulation induction......Page 439
Injectable gonadotrophin therapy......Page 440
Further reading......Page 441
50 Androgen excess, including PCOS, hirsutism and acne......Page 443
Non-classical congenital adrenal hyperplasia......Page 444
Diagnosis and investigations......Page 445
Mild or idiopathic hirsutism......Page 446
Pathogenesis......Page 447
Diagnosis......Page 448
Weight loss......Page 449
References......Page 450
3.4 The Menopause......Page 451
Physiology......Page 452
Assessment......Page 453
Lipid profile and cardiovascular disease......Page 454
Testosterone......Page 455
References......Page 456
Further reading......Page 457
3.5 Sexuality......Page 458
Introduction......Page 459
Sexual orientation......Page 461
Assessment of sexual problems......Page 462
Disparate sexual desire......Page 463
Painful coitus (dyspareunia)......Page 464
Medical care......Page 465
References......Page 466
3.6 Contraception, Sterilisation and Abortion......Page 468
53 Contraception, sterilisation and abortion......Page 469
Pregnancy risk......Page 470
Initiation of contraception......Page 471
Intrauterine contraceptive devices......Page 472
Combined hormonal contraception......Page 473
The vaginal ring......Page 474
The male condom......Page 476
The diaphragm......Page 477
Emergency contraception......Page 478
Calendar methods: rhythm method......Page 479
Vasectomy......Page 480
Medical termination of pregnancy......Page 481
Complications......Page 482
References......Page 483
Vaginal pH......Page 484
History......Page 485
Examination......Page 486
Vulval HSV types 1 and 2......Page 487
Prevention......Page 488
Syphilis......Page 489
Lymphogranuloma venereum......Page 490
Treatment......Page 491
Non-albicans Candida......Page 492
Cervicitis......Page 493
Neisseria gonorrhoea......Page 494
Diagnosis......Page 495
Criteria for the diagnosis of PID......Page 496
Management of PID......Page 497
References......Page 498
3.7 Urogynaecology......Page 500
Level 2: paracolpos......Page 501
Level 3: the perineal body and the levator plate......Page 502
Physical examination......Page 503
POP-Q terminology......Page 504
Evaluation/work-up......Page 505
Manchester repair......Page 506
Conclusions......Page 508
References......Page 509
Anatomy of the lower urinary tract......Page 510
Neurophysiology of the lower urinary tract......Page 511
Classification and aetiology of urinary incontinence......Page 512
Urgency urinary incontinence......Page 513
History......Page 514
Investigations......Page 516
Medication......Page 519
Surgery for stress urinary incontinence......Page 520
References......Page 521
3.8 Pelvic Pain and Endometriosis......Page 522
Nerve pathways......Page 523
Pain characteristics......Page 524
History......Page 525
Investigations......Page 528
Further reading......Page 529
Aetiology......Page 531
Surgical findings......Page 532
Clinical features......Page 533
Medical management......Page 534
Prognosis......Page 535
Further reading......Page 537
3.9 The Breast......Page 538
Breast anatomy, including anomalies......Page 539
Breast anomalies......Page 540
Breast physiology......Page 541
Mammography......Page 542
Fibroadenoma......Page 543
Duct ectasia......Page 544
Breast infection......Page 545
Paget’s disease of the breast or mammary Paget disease......Page 546
Lymph node status......Page 547
Radiotherapy......Page 548
Chemotherapy......Page 549
Locally advanced breast cancer......Page 550
References......Page 551
3.10 Neoplasia and Other Lumps......Page 553
Lichen sclerosus......Page 554
Lichen planus......Page 555
Cicatricial pemphigoid......Page 556
Management......Page 557
Candidiasis......Page 558
Desquamative inflammatory vaginitis......Page 559
Vulvar intraepithelial neoplasia (VIN)......Page 560
Cancer of the Bartholin’s gland......Page 561
Further reading......Page 562
Eversion and nabothian cysts......Page 563
Endocervical polyps......Page 564
Leiomyomas......Page 565
Aetiology and pathogenesis......Page 566
Histology......Page 569
Cervical screening......Page 570
Cytology......Page 571
HPV testing......Page 572
Treatment......Page 573
Adenocarcinoma in situ......Page 574
The diethylstilboestrol (DES) syndrome......Page 575
Stages IB1–IIA1......Page 576
Stages IB-IVA......Page 577
References......Page 579
Pathology......Page 581
Investigations......Page 582
Endometrial polyps......Page 583
Type 1 and type 2 endometrial carcinoma......Page 584
Clinical presentation......Page 585
Differential diagnosis......Page 586
Features of malignancy on ultrasound......Page 587
Further reading......Page 589
History......Page 590
Functional cysts of the ovary......Page 591
Pathology......Page 592
Borderline and malignant ovarian tumours......Page 593
Cystadenomas......Page 594
Borderline ovarian tumours......Page 595
Pathology......Page 596
Sex-cord stromal tumours......Page 597
Germ cell tumours......Page 598
Gonadoblastomas......Page 599
Further reading......Page 600
4 Neonatology......Page 601
Fetus......Page 602
The heart and lungs......Page 603
Introduction......Page 604
The birth of a newborn: the first minutes of life......Page 605
The Apgar score......Page 608
References......Page 609
General care......Page 610
Urine and stools......Page 611
Neonatal heel-prick screening......Page 612
Bonding, family and siblings......Page 613
The physical examination......Page 615
General observation......Page 616
Hands......Page 623
Grasp and Moro reflexes......Page 624
Fontanelles and sutures......Page 625
Encephalocele......Page 626
Mouth......Page 627
Sternomastoid tumour......Page 628
Female external genitalia......Page 630
Dislocation......Page 631
Tone and back......Page 633
References......Page 634
an international perspective......Page 635
Physiology of lactation......Page 636
Management of breastfeeding......Page 637
Breastfeeding difficulties......Page 638
Breast abscess......Page 639
A sleepy or lethargic baby......Page 640
Relactation......Page 641
Volume of feed......Page 642
Vomiting......Page 643
References......Page 644
Normal bilirubin metabolism......Page 646
Investigations......Page 647
Other Considerations......Page 648
Phototherapy......Page 649
ABO haemolytic disease......Page 651
Kernicterus......Page 652
References......Page 653
Developmental events......Page 654
Neonatal encephalopathy......Page 655
Outcome......Page 656
The floppy newborn......Page 657
Nerve palsies......Page 658
Drug withdrawal (neonatal abstinence syndrome)......Page 659
References......Page 660
Lung fluid......Page 661
Causes......Page 662
Management......Page 663
Investigation......Page 664
Respiratory distress syndrome......Page 665
Pneumothorax......Page 666
Diaphragmatic hernia......Page 667
Further reading......Page 668
The small for gestational age newborn......Page 669
The large for gestational age newborn......Page 671
References......Page 672
Antenatally acquired congenital infections: the TORCH infections......Page 673
Herpes simplex......Page 674
Conjunctivitis......Page 675
Systemic infection: neonatal sepsis......Page 676
Specific infections......Page 677
Viral hepatitis......Page 678
References......Page 679
Prevalence......Page 680
Congenital heart disease......Page 681
Hypoplastic left heart......Page 683
Other CNS malformations......Page 684
Hirschsprung’s disease......Page 685
Tracheo-oesophageal fistula......Page 686
Undescended testes......Page 687
Ambiguous genitalia......Page 688
Trisomy 18 (Edwards’ syndrome)......Page 689
Communication with the parents and genetic counselling......Page 691
References......Page 692
Red blood cells......Page 693
Pathological......Page 694
Hydrops fetalis......Page 695
Disseminated intravascular coagulation......Page 696
Blood in the stool......Page 697
Prematurity: definitions......Page 698
Neurological features......Page 699
Jaundice......Page 700
Intraventricular haemorrhage and periventricular leucomalacia......Page 701
Necrotising enterocolitis......Page 703
Patent ductus arteriosus......Page 704
Neurodevelopmental outcome......Page 705
Follow-up and post-discharge care......Page 706
Transport and retrieval......Page 707
References......Page 710
A......Page 711
B......Page 713
C......Page 716
D......Page 720
E......Page 721
F......Page 723
G......Page 724
H......Page 726
I......Page 728
L......Page 730
M......Page 732
N......Page 734
O......Page 736
P......Page 738
R......Page 744
S......Page 745
T......Page 747
U......Page 749
V......Page 750
Z......Page 752

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Beischer & MacKay’s

OBSTETRICS, GYNAECOLOGY AND THE NEWBORN

DEDICATION This book is dedicated to the students who have taught us and our families who have supported us.

Beischer & MacKay’s

OBSTETRICS, GYNAECOLOGY AND THE NEWBORN FOURTH EDITION

Michael Permezel, Susan Walker & Kypros Kyprianou

Elsevier Australia. ACN 001 002 357 (a division of Reed International Books Australia Pty Ltd) Tower 1, 475 Victoria Avenue, Chatswood, NSW 2067 Copyright © 2015 Elsevier Australia. 3rd edition © 1997; 2nd edition © 1986 Elsevier Australia. All rights reserved. No part of this publication may be reproduced or transmitted in any form or by any means, electronic or mechanical, including photocopying, recording, or any information storage and retrieval system, without permission in writing from the publisher. Details on how to seek permission, further information about the Publisher’s permissions policies and our arrangements with organisations such as the Copyright Clearance Center and the Copyright Licensing Agency, can be found at our website: www.elsevier.com/permissions. This book and the individual contributions contained in it are protected under copyright by the Publisher (other than as may be noted herein). Knowledge and best practice in this field are constantly changing. As new research and experience broaden our understanding, changes in research methods, professional practices, or medical treatment may become necessary. Practitioners and researchers must always rely on their own experience and knowledge in evaluating and using any information, methods, compounds, or experiments described herein. In using such information or methods they should be mindful of their own safety and the safety of others, including parties for whom they have a professional responsibility. With respect to any drug or pharmaceutical products identified, readers are advised to check the most current information provided (i) on procedures featured or (ii) by the manufacturer of each product to be administered, to verify the recommended dose or formula, the method and duration of administration, and contraindications. It is the responsibility of practitioners, relying on their own experience and knowledge of their patients, to make diagnoses, to determine dosages and the best treatment for each individual patient, and to take all appropriate safety precautions. To the fullest extent of the law, neither the Publisher nor the authors, contributors, or editors, assume any liability for any injury and/or damage to persons or property as a matter of product liability, negligence or otherwise, or from any use or operation of any methods, products, instructions, or ideas contained in the material herein. National Library of Australia Cataloguing-in-Publication Data Permezel, Michael, author. Beischer & MacKay’s obstetrics, gynaecology and the newborn / Michael Permezel, Susan Walker & Kypros Kyprianou. 9780729540742 (paperback) Obstetrics–Textbooks. Gynecology–Textbooks. Newborn infants–Care–Textbooks. Walker, Susan, author. Kyprianou, Kypros, author. 613.0432 Content Strategist: Larissa Norrie Content Development Specialist: Neli Bryant Project Manager: Devendran Kannan Edited by Leanne Poll Proofread by Julie Ganner Design by Georgette Hall Permissions by Karen Forsythe & Anita Mercy Vethakkan Index by Robert Swanson Typeset by Toppan Best-set Premedia Limited Printed in China by China Translation and Printing Services

CONTENTS Foreword.................................................................................................................................................................................................................... X Preface.........................................................................................................................................................................................................................XI Acknowledgements...............................................................................................................................................................................XII List of Editors............................................................................................................................................................................................... XIII List of Contributors..........................................................................................................................................................................XIV List of Reviewers....................................................................................................................................................................................XVI Section 1  Anatomy and Physiology CHAPTER 1

Reproductive Anatomy and Physiology..............................................................................................................................................2 Peter Wein and Michael Permezel

CHAPTER 2

Anatomy and Physiology of Pregnancy............................................................................................................................................ 14 Michael Permezel and Peter Wein

Section 2  Obstetrics

Section 2.1  Normal Pregnancy CHAPTER 3

The Prepregnancy Consultation...........................................................................................................................................................29 Michael Permezel

CHAPTER 4

The First Antenatal Visit........................................................................................................................................................................32 Michael Permezel

CHAPTER 5

Antenatal Care Beyond the First Antenatal Visit.......................................................................................................................... 39 Michael Permezel

CHAPTER 6

Obesity and Nutrition in Pregnancy................................................................................................................................................. 46 Alexis Shub

Section 2.2  Problems of Early Pregnancy CHAPTER 7

Hyperemesis Gravidarum......................................................................................................................................................................52 Neil Israelsohn

CHAPTER 8

Bleeding in Early Pregnancy.................................................................................................................................................................55 Neil Israelsohn

Section 2.3  Prenatal Diagnosis CHAPTER 9

Screening, Diagnosis and Management of Genetic and Structural Abnormalities in the Fetus.................................... 70 Susan Walker

Section 2.4  Obstetric Complications CHAPTER 10 Antepartum Haemorrhage.................................................................................................................................................................... 85

Neil Israelsohn

v

Contents

CHAPTER 11

Fetal Growth Restriction and Assessment of Fetal Wellbeing................................................................................................... 91 Alexis Shub

CHAPTER 12

Preterm Labour, Including Cervical Insufficiency........................................................................................................................ 98 Alison Fung

CHAPTER 13

The Postdates Pregnancy and Rupture of the Membranes Before Labour at Term......................................................... 106 Michael Permezel and Megan Di Quinzio

CHAPTER 14

Multiple Pregnancy..................................................................................................................................................................................111 Susan Walker

CHAPTER 15

Malpresentation......................................................................................................................................................................................120 Michael Permezel

Section 2.5  Medical and Surgical Disorders in Pregnancy CHAPTER 16

Hypertensive Disorders of Pregnancy Eclampsia ...................................................................................................................... 130 Michael Permezel

CHAPTER 17

Thromboembolism, Cardiac Disorders and Respiratory Disease........................................................................................... 140 Michael Permezel and Lisa Hui

CHAPTER 18

Bacterial Infections in Pregnancy......................................................................................................................................................145 Peter Wein

CHAPTER 19

Viral and Protozoan Infections in Pregnancy............................................................................................................................... 152 Susan Walker

CHAPTER 20 The Blood: Anaemia, Thrombocytopenia and Coagulopathy...................................................................................................163

Lisa Hui and Michael Permezel CHAPTER 21

Gastrointestinal, Hepatobiliary, Gynaecological and Renal Problems....................................................................................168 Michael Permezel

CHAPTER 22 Autoimmune and Isoimmune Disease in Pregnancy.................................................................................................................. 176

Michael Permezel and Gillian Paulsen CHAPTER 23 Diabetes Mellitus....................................................................................................................................................................................185

Peter Wein CHAPTER 24 Neurological Disease...............................................................................................................................................................................191

Susan Walker CHAPTER 25 Mental Health Disorders during the Perinatal Period.................................................................................................................196

Megan Galbally and Martien Snellen

Section 2.6  Common Clinical Scenarios and Presenting Problems in Pregnancy CHAPTER 26 Common Problems in Pregnancy.....................................................................................................................................................203

Michael Permezel and Megan Di Quinzio

Section 2.7  Labour and Birth

Section 2.7.1  Normal Labour and Birth CHAPTER 27 The Physiology of Parturition.............................................................................................................................................................216

Michael Permezel and Megan Di Quinzio CHAPTER 28 Management of Normal Labour....................................................................................................................................................... 226

Michael Permezel

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Contents

Section 2.7.2  Induction of Labour, Instrumental Delivery and Casearean Section CHAPTER 29 Induction of Labour, Including Cervical Ripening.....................................................................................................................243

Michael Permezel and Gillian Paulsen CHAPTER 30 Episiotomy and Vaginal Outlet Tears.............................................................................................................................................. 249

Michael Permezel and Gillian Paulsen CHAPTER 31

Instrumental Delivery.......................................................................................................................................................................... 257 Michael Permezel and Gillian Paulsen

CHAPTER 32 Caesarean Section and Trial of Labour after Caesarean............................................................................................................ 267

Michael Permezel

Section 2.7.3  Intrapartum Clinical Problems CHAPTER 33 Intrapartum Fetal Compromise........................................................................................................................................................ 277

Michael Permezel and Julia Francis CHAPTER 34 Failure to Progress in Labour............................................................................................................................................................ 285

Michael Permezel and Julia Francis CHAPTER 35 Malpresentation and Malposition.................................................................................................................................................... 294

Julia Francis and Michael Permezel CHAPTER 36 Postpartum Haemorrhage...................................................................................................................................................................302

Michael Permezel CHAPTER 37 Maternal Collapse.................................................................................................................................................................................. 310

Michael Permezel CHAPTER 38 Obstetric Analgesia and Anaesthesia...............................................................................................................................................315

Richard Hiscock

Section 2.7.4  The Puerperium and Lactation CHAPTER 39 The Physiology of the Puerperium and Lactation...................................................................................................................... 323

Elizabeth Anne McCarthy CHAPTER 40 Normal Postpartum Care..................................................................................................................................................................... 329

Elizabeth Anne McCarthy CHAPTER 41

Puerperal Disorders...............................................................................................................................................................................335 Elizabeth Anne McCarthy

Section 2.7.5  Global Women’s Health and Indigenous Women’s Health CHAPTER 42 Maternal and Perinatal Mortality and Morbidity and Global Reproductive Health....................................................... 340

Laurel Bennett CHAPTER 43 Australian Indigenous Women’s Health in Pregnancy..............................................................................................................345

Jacqueline Boyle and Marilyn Clarke

Section 3  Gynaecology

Section 3.1  Gynaecological Assessment CHAPTER 44 Gynaecological History and Examination...................................................................................................................................... 353

Emma Readman and Kate McIlwaine

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Contents

CHAPTER 45 Gynaecological Investigations............................................................................................................................................................358

Kate McIlwaine and Emma Readman

Section 3.2  Menstrual Disorders CHAPTER 46 Paediatric and Adolescent Gynaecology......................................................................................................................................... 372

Sonia Grover CHAPTER 47 The Menstrual Cycle and Menstrual Disorders........................................................................................................................... 377

Carol Vance

Section 3.3  Reproductive Endocrinology and Infertility CHAPTER 48 Infertility.................................................................................................................................................................................................. 401

Sameer Jatkar CHAPTER 49 Amenorrhoea, Hyperprolactinaemia and Ovulation Induction...............................................................................................414

Sameer Jatkar CHAPTER 50 Androgen Excess, Including PCOS, Hirsutism and Acne......................................................................................................... 425

Chris Russell

Section 3.4  The Menopause CHAPTER 51

The Menopause, Climacteric and Hormone Replacement Therapy......................................................................................434 Michael Rasmussen, Samantha Mooney and Michael Permezel

Section 3.5  Sexuality CHAPTER 52 Normal Sexuality, Sexual and Relationship Dysfunction, and Sexual Assault...................................................................441

Patricia Moore

Section 3.6  Contraception, Sterilisation and Abortion CHAPTER 53 Contraception, Sterilisation and Abortion......................................................................................................................................451

Patricia Moore CHAPTER 54 Genital Tract Infections.......................................................................................................................................................................466

Kathryn Anne Cook

Section 3.7  Urogynaecology CHAPTER 55 Pelvic Organ Prolapse...........................................................................................................................................................................483

Julio Alvarez and Peter Dwyer CHAPTER 56 Urinary Incontinence........................................................................................................................................................................... 492

Kristina Cvach and Peter Dwyer

Section 3.8  Pelvic Pain and Endometriosis CHAPTER 57 Pelvic Pain................................................................................................................................................................................................505

Lenore Ellett and Peter Maher CHAPTER 58 Endometriosis..........................................................................................................................................................................................513

Peter Maher and Lenore Ellett

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Contents

Section 3.9  The Breast CHAPTER 59 Breast Disorders...................................................................................................................................................................................... 521

Antonia McLaren Jones

Section 3.10  Neoplasia and Other Lumps CHAPTER 60 Benign and Malignant Disorders of the Vulva and Vagina......................................................................................................536

Ross Pagano CHAPTER 61

Benign and Malignant Disorders of the Cervix...........................................................................................................................545 Jeffrey Tan

CHAPTER 62 Benign and Malignant Disorders of the Uterus, and the Pelvic Mass.................................................................................. 563

Michael Quinn and Adam Pendlebury CHAPTER 63 Benign and Malignant Disorders of the Ovary and the Fallopian Tube...............................................................................572

Vivek Arora

Section 4  Neonatology CHAPTER 64 Neonatal Physiology: Adaptation and Resuscitation..................................................................................................................584

Kypros Kyprianou CHAPTER 65 Routine Neonatal Care......................................................................................................................................................................... 592

Kypros Kyprianou CHAPTER 66 Assessment of the Neonate................................................................................................................................................................ 597

Kypros Kyprianou CHAPTER 67 Neonatal Feeding and Nutrition........................................................................................................................................................ 617

Kypros Kyprianou CHAPTER 68 Neonatal Jaundice.................................................................................................................................................................................. 628

Kypros Kyprianou CHAPTER 69 Neonatal Neurological Presentations...............................................................................................................................................636

Kypros Kyprianou CHAPTER 70 Neonatal Respiratory Distress...........................................................................................................................................................643

Kypros Kyprianou CHAPTER 71

The Small for Gestational Age and Large for Gestational Age Neonate...............................................................................651 Kypros Kyprianou

CHAPTER 72 Neonatal Infection................................................................................................................................................................................. 655

Kypros Kyprianou CHAPTER 73 Congenital Malformations.................................................................................................................................................................. 662

Kypros Kyprianou CHAPTER 74 Neonatal Haematology..........................................................................................................................................................................675

Kypros Kyprianou CHAPTER 75 The Preterm Neonate and Perinatal Transport........................................................................................................................... 680

Kypros Kyprianou

Index.............................................................................................................................................................................................................................. 693

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FOREWORD Since the third edition of Obstetrics and the Newborn was published in 1997, there have been enormous changes in the practice of care before, during and after pregnancy, and in gynaecological management of both pre- and postmenopausal women. Routine investigations are more numerous and sophisticated. Caesarean section rates have doubled, but the image of delivery of a healthy infant remains the greatest experience patients will enjoy in their journey through life. Cooperation between carers, midwives, medical officers, and both clinical and laboratory scientists remains an important requirement. Likewise, in gynaecology the number of subspecialties has increased and marvellous new technology and investigative procedures have altered the techniques of surgical procedures. A new range of drugs have given respite from infertility, and improved chemotherapy has significantly advanced the treatment of gynaecological cancers. Unusually, this volume combines the disciplines of obstetrics, neonatal medicine and gynaecology into a single source that facilitates learning for medical students, midwives and postgraduates. This creates harmony, from adolescent gynaecology through to reproductive life and the management of pregnancy, and finally the gynaecological problems of the postmenopausal woman. This volume contains a unique collection of photographs taken many years before restrictions in teaching hospitals, which have now made collecting clinical photographs more difficult. In my view there are no more appealing medical occupations available than the practice of obstetrics, neonatal care and all aspects of gynaecology. It should not be overlooked that in spite of modern changes in practice, the vast majority of women—with conventional methods of support—continue to have a normal labour with spontaneous delivery of a normal, healthy infant. We practitioners should aim to be the custodians of normality. Norman Beischer AO, MD, MGO, FRCS(Ed), FRCOG, FRACS, FRACOG, DMedSci(Hon)

x

PREFACE A love of face-to-face teaching led the authors into their respective academic careers. There are few experiences more exhilarating than seeing not just knowledge but also clinical reasoning being passed to a subsequent generation of students, residents or registrars. Assessment tasks for both undergraduate and postgraduate courses make much of assessing cognitive skills rather than knowledge. However, knowledge is the key ingredient from which the competent clinician conjures the recipe for expert care. Reasoning without a knowledge base is like building with substandard materials: the product may seem good at first, but will not last a lifetime along the clinical journey. This book is for the student who has a genuine interest in women’s health and neonatal paediatrics. While previous editions have been directed largely to the medical undergraduate, this edition will find a place on the bookshelves of the postgraduate preparing for the diploma of obstetrics and gynaecology, the general practitioner with an interest in women’s health, the nurse-midwifery student, and the pre-vocational doctor or new trainee who is preparing for a career in women’s health. This reminds us that if we are to be any good, we will indeed be medical students our whole lives. This book is an evidence-based textbook in obstetrics, gynaecology and neonatal paediatrics. It is more than just lists of referenced facts; sometimes evidence does come from a randomised controlled trial, and the various landmark trials are referenced where appropriate. However, clinical management is often dictated by a thorough understanding of the underlying pathophysiology. It is this deeper knowledge that underpins a lifetime of good clinical care. Our forebears knew it well, spending years on the basic biological sciences before following the clinical sciences and then clinical medicine. This book is about giving an understanding to clinical management. Many of the chapters discuss the non-pathological process of obstetric care and an appreciation of the normal transition to extrauterine life. Modern medicine allows us to better prepare for deviations from this otherwise natural process of pregnancy, gestation and birth. This book aims to clearly differentiate the normal from the pathological. Lastly, from before a newborn enters the world, parental expectations, experiences, dreams and anxieties will shape how families prepare for and adapt to their newborn child. Many of the common issues encountered are variations of normal, and hence this requires recognition by a confident and competent clinician to appropriately reassure families. Similarly, the recognition of the abnormal or pathological process before, during and after birth will allow for the appropriate assessment and management of both mother and baby.

xi

ACKNOWLEDGEMENTS Professor Norman Beischer died on 2 February 2015, as this book came to fruition. Along with his colleague editors of the first three editions of the book, particularly Professor Eric Mackay, he embodied a commitment and passion for teaching students of both obstetrics and midwifery that is—to this day perhaps—unequalled. His example is the inspiration for this latest edition. We have been very fortunate to have parents with a strong commitment to education, unending patience and a determination to give their children every opportunity. Each has had their particular professional, clinical and academic mentors. While we cannot acknowledge all those who guided us, we would particularly like to recognise the absolutely inspiring Sir Lance Townsend, Roger Pepperell, Christopher Targett, Graeme Ratten and all those others who, by their own example, showed us how to practise and teach. Such teachers and mentors cross our paths, often unexpectedly, throughout our journey from student to practicing clinician. These connections are truly priceless; the sharing of wisdom in a spirit of trust, warmth and generosity. These moments of inspiration shape us as doctors: they unite us, keep us grounded, remind us of the humanity of our work, encourage us to teach and allow us to directly contribute to the health and wellbeing of women, their children and their families. Teaching is a privilege and we have had the great fortune to see many of our wonderful students become our residents, then registrars and finally consultant colleagues. Some have authored chapters of this book but all those we have taught have, in truth, also taught us so much. Consultant colleagues—past and present—at the Mercy Hospital for Women and the Royal Women’s Hospital in Melbourne have authored almost all of the women’s health content of this book. Many did so while balancing incredibly demanding clinical schedules. We are extremely grateful to all of them. A textbook of this size is a monumental and time-demanding task. Nothing would be possible without the support and understanding of our families. Yet another evening passes: ‘The book?’ ‘Yes.’ An understanding life partner is priceless.

xii

LIST OF EDITORS Michael Permezel MD, MRCP(UK), MRCOG, FRANZCOG Professor of Obstetrics and Gynaecology, Mercy Hospital for Women and University of Melbourne, Melbourne, Victoria, Australia

Kypros Kyprianou MBBS, FRACP Paediatrician, Royal Children’s Hospital, Werribee Mercy Hospital, Epworth Freemasons Hospital and University of Melbourne, Melbourne, Victoria, Australia

Susan Walker MD, DDU, CMFM, FRANZCOG Professor of Maternal Fetal Medicine, Director of Perinatal Medicine, Mercy Hospital for Women and University of Melbourne, Melbourne, Victoria, Australia

xiii

LIST OF CONTRIBUTORS Julio Alvarez U MD Urogynaecolgy Consultant, Hospital Padre Hurtado, Santiago, Chile; Assistant Professor, Universidad del Desarrollo, Concepción, Chile Vivek Arora MBBS, MD, DNB, FRANZCOG, CGO Consultant Gynaecologic Oncologist, Royal Women’s Hospital and Western Health, Melbourne, Victoria, Australia Laurel Bennett MBBS, FRANZCOG Consultant Visiting Medical Officer, Northeast Health Wangaratta, Wangaratta, Victoria, Australia Jacqueline Boyle MBBS, FRANZCOG, MPH&TM, PhD Senior Staff Specialist, Monash Health, Clayton, Victoria, Australia; Head of Indigenous and Refugee Women’s Health Research, Monash Centre for Health Research and Implementation, Monash University, Clayton, Victoria, Australia Marilyn Clarke MBBS(Class II Hons), GradDipClinEpi, FRANZCOG Staff Specialist, Department of Obstetrics and Gynaecology, Grafton Base Hospital, Grafton, New South Wales, Australia

Alison Fung MBBS, FRANZCOG, CMFM, DDU Specialist in Maternal Fetal Medicine, Mercy Hospital for Women, Melbourne, Victoria, Australia Megan Galbally MBBS, MPM, PhD, FRANZCP Head of Unit and Consultant Psychiatrist, Mercy Hospital for Women, Melbourne, Victoria, Australia Sonia R Grover MBBS, FRANZCOG, MD Clinical Professor, Department of Paediatrics, University of Melbourne, Melbourne, Victoria, Australia; Director, Department of Paediatric and Adolescent Gynaecology, Royal Children’s Hospital, Melbourne, Victoria, Australia; Unit Head, Consultant Gynaecologist, Mercy Hospital for Women, Melbourne, Victoria, Australia; Head of Family Planning Service, Consultant Gynaecologist, Austin Health, Melbourne, Victoria, Australia; Research Fellow, Murdoch Childrens Research Institute, Melbourne, Victoria, Australia Richard Hiscock MBBS, FANZCA Senior Consultant Anaesthetist, Mercy Hospital for Women, Melbourne, Victoria, Australia

Kathryn Anne Cook MBBS, FRANZCOG, FACSHM Obstetrician and Gynaecologist, Mercy Hospital for Women, Melbourne, Victoria, Australia; Sexual Health Physician, Melbourne Sexual Health Centre, Carlton, Victoria, Australia

Lisa Hui MBBS, PhD, GradCertClinEpi, FRANZCOG, CMFM, DDU Specialist in Maternal Fetal Medicine, Mercy Hospital for Women, Melbourne, Victoria, Australia; Senior Clinical Lecturer, Department of Obstetrics and Gynaecology, University of Melbourne, Melbourne, Victoria, Australia

Kristina Cvach MBBS, MPHTM, FRANZCOG, CU Consultant Urogynaecologist, Mercy Hospital for Women, Melbourne, Victoria, Australia

Neil Israelsohn MBBS(Hons), FRANZCOG Consultant Obstetrician and Gynaecologist, Mercy Hospital for Women, Melbourne, Victoria, Australia

Megan KW Di Quinzio MBBS, MD, FRANZCOG Obstetrician Gynaecologist, Mercy Hospital for Women, Melbourne, Victoria, Australia

Sameer Jatkar MBBS(Hons), BA, MSc, MRMed, FRANZCOG Fertility Specialist, Monash IVF, Clayton, Victoria, Australia; Visiting Medical Officer, Monash Health, Clayton, Victoria, Australia

Peter L Dwyer FRANZCOG, FRCOG, CU Head of Urogynaecology Department, Mercy Hospital for Women and University of Melbourne, Melbourne, Victoria, Australia

Antonia McLaren Jones MBBS, BMedSci Fellow in Gynaecological Oncology, Mercy Hospital for Women, Melbourne, Victoria, Australia

Lenore Ellett MBBS(Hons), FRACGP, FRANZCOG Consultant Obststrician and Gynaecologist, Visiting Medical Officer, Mercy Hospital for Women, Melbourne, Victoria, Australia

Peter J Maher MBBS, FRCOG, FRACOG Director, Department of Endosurgery, Mercy Hospital for Women, Melbourne, Victoria, Australia; Clinical Professor, University of Melbourne, Melbourne, Victoria, Australia

Julia Francis MBBS(Hons) Obstetrics and Gynaecology Registrar, Mercy Hospital for Women, Melbourne, Victoria, Australia

xiv

Elizabeth Anne McCarthy MBBS, BMedSc, MD, FRANZCOG, CMFM, GradCertBiostatsEpi, DDU Specialist in Maternal Fetal Medicine, Mercy Hospital for Women, Melbourne, Victoria, Australia; Senior Lecturer, Department of Obstetrics and Gynaecology, University of Melbourne, Melbourne, Victoria, Australia

Michael John Rasmussen MBBS, MRCOG, FRANZCOG Consultant Obststrician and Gynaecologist, Clinical Director of Women’s and Children’s Health, Mercy Public Hospitals Inc., Melbourne, Victoria, Australia; Clinical Director of Gynaecology, Mercy Hospital for Women, Melbourne, Victoria, Australia

Kate McIlwaine MBBS(Hons), FRANZCOG Consultant Gynaecologist, Department of Endosurgery, Mercy Hospital for Women, Melbourne, Victoria, Australia

Emma Readman MBBS, FRANZCOG Consultant Gynaecologist Head of Unit, Mercy Hospital for Women, Melbourne, Victoria, Australia

Samantha Mooney MBBS(Hons), MRepMed, DRANZCOG Registrar, Mercy Hospital for Women, Melbourne, Victoria, Australia

Chris Russell MBBS, FRANZCOG Visiting Medical Specialist, Mercy Hospital for Women, Melbourne, Victoria, Australia

Patricia Moore MBChB, FRANZCOG, BA, PostgradDipBioethics Consultant Gynaecologist, Head of Early Pregnancy Services Unit, Royal Women’s Hospital, Melbourne, Victoria, Australia; Sessional Gynaecologist, Paediatric and Adolescent Gynaecology Unit, Royal Children’s Hospital, Melbourne, Victoria, Australia

Alexis Shub MBBS, FRANZCOG, PhD Specialist in Maternal Fetal Medicine, Mercy Hospital for Women, Melbourne, Victoria, Australia; Senior Lecturer, University of Melbourne, Melbourne, Victoria, Australia

Ross Pagano MBBS, FRCOG, FRANZCOG Consultant Gynaecologist, Head of Vulvar Disorders Clinic, Royal Women’s Hospital, Melbourne, Victoria, Australia Gillian Paulsen MBBS(Hons), MPH, FRANZCOG Consultant Obstetrician, Mercy Hospital for Women and The Northern Hospital, Melbourne, Victoria, Australia; Clinical Lecturer, University of Melbourne, Melbourne, Victoria, Australia Adam Pendlebury MBBS, BMedSci, FRANZCOG Gynaecological Oncology Fellow, King Edward Memorial Hospital, Subiaco, Western Australia, Australia

Martien Snellen MBBS, MPM, FRANZCP Senior Perinatal Psychiatrist, Mercy Hospital for Women, Melbourne, Victoria, Australia Jeffrey Tan MBBS, MRCOG, FRANZCOG Consultant Gynaecologist, Oncology and Dysplasia Unit, Royal Women’s Hospital, Melbourne, Victoria, Australia Carol Vance MBBS, FRANZCOG Obststrician and Gynaecologist, Visiting Medical Officer, Mercy Hospital for Women, Melbourne, Victoria, Australia Peter Wein MBBS, FRANZCOG, GradDipEpidemBiostat Clinical Associate Professor, University of Melbourne, Melbourne, Victoria, Australia; Consultant Obstetrician, Mercy Hospital for Women, Melbourne, Victoria, Australia

Michael A Quinn AM, MBChB, MGO, MRCP, FRCOG, FRANZCOG, CGO Professor of Gynaecological Oncology, Royal Women’s Hospital and University of Melbourne, Melbourne, Victoria, Australia

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LIST OF REVIEWERS Donald Angstetra BSc(Med), MBBS, FRANZCOG Staff Specialist, Gold Coast University Hospital, Southport, Queensland, Australia; Senior Lecturer, Griffith University, Nathan, Queensland, Australia

Elizabeth Hurrion BMedSci, MBChB, MRCPCH, FRACP, GradDipClinEpid Senior Staff Specialist Neonatology, Mater Mothers’ Hospital, Brisbane, Queensland, Australia

Roland Broadbent MBChB, FRACP Associate Professor, Department of Women’s and Children’s Health, University of Otago, Dunedin, New Zealand; Clinical Leader, Neonatal Services, Southern District Health Board, Dunedin, New Zealand

Linda McLaughlin BSc, MBBS, FRACP Neonatology Fellow, Mater Mothers’ Hospital, Brisbane, Queensland, Australia

Michael Carrette MBBS, FRANZCOG Senior Lecturer, Reproductive and Neonatal Health, James Cook University, Cairns, Queensland, Australia Vicki Clifton PhD NHMRC Senior Research Fellow, University of Adelaide, Adelaide, South Australia, Australia; Associate Professor, Conjoint Associate Professor, University of Newcastle, Callaghan, New South Wales, Australia; Editor, Placenta; Director of Clinical Research Development, Lyell McEwin Hospital, Adelaide, South Australia, Australia Girish Deshpande FRACP, MSc Staff Neonatologist, Nepean Hospital, Penrith, New South Wales, Australia Warwick Giles MBBS, FRANZCOG, DDU, PhD, CMFM, OAM Conjoint Professor, Faculty of Medicine, University of Newcastle and University of Sydney, Sydney, New South Wales, Australia

xvi

Roger A McMaster-Fay MBBS, MRCOG, FRANZCOG Clinical Lecturer, Central Clinical School, University of Sydney, Sydney, New South Wales, Australia John Pardey MBBS, FRCOG, FRANZCOG Clinical Director, Women’s Health, Nepean Blue Mountains Local Health District, Penrith, New South Wales, Australia Karen Simmer PhD, FRCAP, FRCPCH Director, NICU, King Edward Memorial Hospital and Princess Margaret Hospitals, Subiaco, Western Australia, Australia; Professor Newborn Medicine, University of Western Australia, Crawley, Western Australia, Australia; Co-Director, NHMRC Centre of Research Excellence for Preterm Infants, Crawley, Western Australia, Australia Mariana S Sousa MD, PhD candidate University of New South Wales, Randwick, New South Wales, Australia

Section 1 ANATOMY AND PHYSIOLOGY Chapter 1

Reproductive anatomy and physiology

Chapter 2

Anatomy and physiology of pregnancy

Chapter 1  REPRODUCTIVE ANATOMY AND PHYSIOLOGY Peter Wein and Michael Permezel

KEY POINTS The anatomy and physiology of the female reproductive system can be understood in terms of its most important function, that of enabling conception, pregnancy and childbirth. The reproductive system plays other important roles in human physiology including sexual function, and through ovarian hormones which affect the tissues of the pelvic floor, bone density, vasomotor symptoms, lipid profile and cardiovascular health. The menstrual cycle should be viewed from four perspectives: hypothalamo-pituitary gonadotrophin secretion; ovarian follicular development and luteinisation; oestrogen and progesterone levels; and the endometrium. The following are the four phases of the menstrual cycle in succession. ■ Follicular phase: rising follicle-stimulating hormone (FSH), follicular development, rising oestrogen, endometrial proliferation. ■ Ovulatory phase: luteinising hormone (LH) surge, ovulation, luteinisation of the follicle, initiation of progesterone production, endometrial transition from proliferative to secretory. ■ Luteal phase: FSH and LH support, corpus luteum development, oestrogen and progesterone production, secretory endometrium. ■ Menstrual phase: declining LH resulting in luteolysis in the absence of a pregnancy, falling progesterone initiating endometrial shedding through ischaemic necrosis. The phases of sexual endocrinology extend from prepuberty (low levels of both gonadotrophins and sex steroids), through puberty (rising gonadotrophin and sex steroid levels), reproductive life (menstrual cycle, pregnancy or lactation), the climacteric (rising gonadotrophins, falling sex steroids) and postmenopause (high gonadotrophins, low sex steroids). For conception to occur, the fertilising spermatozoon and ovum must meet, and this usually occurs in the outer end of the uterine tube mid-cycle. The development of the mature sperm and ovum (spermatogenesis, oogenesis) is the result of a complex series of hormonal interactions between the hypothalamus, pituitary gland and gonad.

REPRODUCTIVE ANATOMY

Mons pubis

EXTERNAL GENITALIA

The mons pubis is a fibrofatty cushion lying anterior and superior to the junction of the two pubic bones (symphysis pubis). It is covered by hair, the distribution of which is gender-specific. In females, usually there is no extension upwards onto the abdominal wall.

The external genitalia are those structures visible on inspection. The different structures are shown in Figure 1.1.

Chapter 1  Reproductive Anatomy and Physiology

Sacrum Fallopian tube

Ureter

Ovary Round ligament

Uterus

Bladder

Posterior fornix

Pubis

Rectovaginal pouch of Douglas

Uterovesical pouch Cervix Urethra

Rectum and anal canal

Vagina

Perineal body Rectovaginal septum

FIGURE 1.1 

Midline view of the pelvic organs. The uterus is in the usual position of anteversion. Source: Courtesy of Prof. Norman Beischer.

Labia majora

Vestibule

The hair-covered, fibrofatty folds that extend from the mons above to the perineum below are the labia majora. They have both sweat and sebaceous glands, and are homologous with the scrotum in the male.

The vestibule comprises the area enclosed by the labia minora. The urethra and vagina open into it, as do the paired Bartholin’s and Skene’s ducts. It represents the lower portion of the embryological urogenital sinus.

Labia minora

Urethral meatus

The labia minora are enclosed by the labia majora and are smaller and more delicate than the labia majora. They are pink in colour and devoid of hair, but contain sebaceous glands and a few sweat glands. They are vascular rich and nerve endings are plentiful. Superiorly, they enclose the clitoris; inferiorly, they merge to form the fourchette, or posterior ring, of the vaginal introitus.

The external urinary orifice is situated 1 to 1.5 cm below the clitoris. It is often covered by the folds of the labia minora, which must be separated to expose it (e.g. for passing a catheter, as shown in Fig 1.2).

Clitoris The clitoris is the homologue of the male penis. It is composed of a vascular plexus (erectile tissue) arranged in a central corpus with two crura which are attached to the inferior rami of the pubis. The clitoris measures 1.5 to 2 cm in length, the terminal 0.5 cm being called the glans. The folds of the labia minora sweep upwards to enclose the clitoris, forming the prepuce above and the frenulum below.

Paraurethral ducts The paraurethral ducts (Skene’s ducts) come from the paraurethral glands (which have a lubricating function). Their tiny openings usually can be seen just below and beside the urethra.

Vaginal orifice The vagina opens onto the lower part of the vestibule. Before puberty, the orifice is closed by the hymenal membrane, which may have one or more small orifices in it. During reproductive life, the hymen is broken down and the interior of the lower vagina is visualised when the 3

Beischer & MacKay’s: Obstetrics, Gynaecology and the Newborn

A

B

FIGURE 1.2 

Technique of catheterisation. A The labia minora are separated to expose the urinary meatus. The vagina often has many folds (rugae) which simulate the urinary orifice. This woman has large thin labia, a relatively large clitoris and a patulous vagina. B A primigravida being catheterised preparatory to caesarean section. Note the sebaceous glands on the perineum, small thick labia minora and hence easy identification of the urinary meatus. Source: Courtesy of Prof. Norman Beischer.

labia are parted. The remnants of the hymen are visible around the vaginal orifice.

Bartholin’s ducts Bartholin’s ducts open onto the vestibule at its posterolateral aspect, just outside the hymen (Fig 1.3). The ducts are 1.5 to 2.0 cm long and run up to the paired Bartholin’s glands, which are situated posterolaterally (5 and 7 o’clock) above the constrictor muscles of the vagina (bulbocavernosus). The glands are pea-sized and are responsible for lubricating the introitus during sexual intercourse. Badly placed episiotomy incisions will either sever the ducts or involve them in the subsequent repair or fibrous scarring.

Perineum The area of the perineum is outlined by the vaginal fourchette anteriorly and the anus posteriorly (Fig 1.1). Deep to it is the perineal body, which lies between the anal canal 4

and the lower third of the posterior vaginal wall (Fig 1.4). It is this area that is incised in an episiotomy, where the introitus is enlarged to facilitate the birth of the baby or where lacerations can occur during the birth process.

INTERNAL GENITALIA Vagina The vagina is a musculomembranous tube which links the uterus to the vestibule. It is 8 to 12 cm in length and, in the resting state, the walls are opposed. It is capable of remarkable distension during the process of childbirth. Anteriorly, the vagina is close to the base of the bladder and the urethra, and posteriorly, to the pouch of Douglas, rectum and anal canal (Fig 1.4). If overdistension of the vagina occurs during childbirth, the fascial supports (vesicovaginal and rectovaginal septa) separating the vagina from the bladder and rectum tear, usually in the midline, allowing prolapse to occur (cystocele, urethrocele, rectocele).

Chapter 1  Reproductive Anatomy and Physiology

Dorsal vein of clitoris Bulbocavernosus muscle External urinary meatus

Perineal Internal pudendal

Veins

Vagina

Bulb of vestibule

Posterior fourchee

Bartholin’s gland and duct

FIGURE 1.3 

The bulbocavernosus muscles form a sphincter around the vagina, enclosing the vascular bulb of the vestibule in which the Bartholin’s gland is embedded posterolaterally. Source: Beischer NA, Mackay EV. Care of the pregnant woman and her baby. Artarmon: W.B. Saunders, 1978.

The lining of the vagina is thrown into folds like a concertina (allowing for expansion during childbirth) and these are known as rugae. The vagina has a stratified squamous epithelial lining, but no glands. Its moisture is provided chiefly by the secretion of the cervical mucous glands and, at the time of coitus, by vaginal transudation. When under the influence of oestrogen (i.e. during the reproductive years and especially during pregnancy), the vaginal squamous cells contain considerable glycogen that allows free growth of lactobacilli, which are normal inhabitants of the vagina. Since these organisms produce lactic acid, the pH of the vagina is acid (4.0 to 5.5) and this minimises the risk of ascending infection by other organisms to the endometrium, uterine tubes or peritoneal cavity. The uterine cervix projects into the upper 1 to 2 cm of the vagina, outlining the four fornices: anterior, posterior and lateral (left and right). The vagina passes through the muscular pelvic diaphragm. The muscles comprising the superficial perineal compartment join behind the vagina to form the perineal body (Fig 1.4).

Uterus The uterus has the critical role of housing and nurturing the embryo and fetus from implantation until birth. It is composed of two functional parts: a lower third that forms the uterine cervix and the upper two-thirds that form the uterine body. The non-pregnant adult uterus measures approximately 7.5 × 5.0 × 2.5 cm with a cavity length of approximately 6 cm. The uterine cervix has both vaginal and supravaginal components. The cervix is a strong pivotal point for

Clitoris 1 Ischiocavernosus

Vagina

2 Superficial transverse perineal

Bulb of vestibule

3 Levator ani pubococcygeus iliococcygeus 4 External anal sphincter 5 Gluteus maximus

Site of Bartholin’s gland Pudendal vessels Ischial tuberosity Perineal body

FIGURE 1.4 

Muscles of the perineum. 5

Beischer & MacKay’s: Obstetrics, Gynaecology and the Newborn

uterine stability, being attached to the pelvic walls by radiating fascial condensations called ligaments: pubocervical anteriorly, uterosacral posteriorly and transverse cervical (‘cardinal’) ligaments laterally. The cervix is delineated inferiorly by the external os and superiorly by the internal os. The shape of the external os is spherical in the nullipara, but usually transverse and more gaping in the multipara. In the latter, the reddish columnar epithelium lining the canal may be seen (perhaps exaggerated by ectropion formation), and also the small orifices of the cervical mucous glands. When the ducts of these glands are blocked by inflammation or scar tissue, small retention cysts form and these are obvious on the surface as nabothian follicles.

Uterine body The uterus is a hollow, muscular organ, the interior being roughly triangular in shape. The upper angles of the triangle are formed by the interstitial portions of the uterine tubes. The uterus is covered externally by the peritoneum, except the lower part anteriorly, where the peritoneum is reflected onto the bladder. It is at this loose attachment that the incision is made in a lower uterine segment caesarean section. The lower uterine segment lies at the junction of the uterus and cervix and while very narrow in the non-pregnant state, it expands during the third trimester of pregnancy and further in labour to some 10 cm in length. The uterus is globular in shape, but flattened in the anteroposterior direction. Normally, it is both anteverted (rotated forwards) and anteflexed (bent forwards on itself). In some 20% of women, the uterus is rotated backwards, lying more in relation to the rectum than the bladder. It is in this group that the rare complication of incarceration of the uterus occurs late in the first trimester of pregnancy, the enlarging uterus being caught in the hollow of the sacrum. The uterus is formed by the fused distal portions of the Müllerian ducts, the former the unfused proximal portions. Occasionally, evidence of this process going awry can be seen in the various duplications and deletions of the uterus which occur. The structure of the uterus is similar to that of most other hollow muscular organs in the body, although each of the three layers is specialised for the function of childbirth. 1. The endometrium or lining is composed of a columnar epithelium which dips into the submucosa in the form of branched, tubular glands. A feature of the endometrium is the typical coiled arteries, which also are under hormonal influence. They enlarge greatly during pregnancy (especially in the region of the placenta), forming the maternal contribution to the blood supply of the placenta. 2. The myometrium is the middle muscular layer and is composed of several interlacing layers of smooth muscle. During pregnancy, great enlargement of the 6

muscle fibres occurs, ready for the task of expelling the fetus in the process of parturition. In contrast to the uterine body, the cervix is fibromuscular with an approximate muscle mass of only 10%. 3. The serosa over the uterine body is continuous with the loose peritoneal covering the lower uterine segment. The cervix is covered by a serosa posteriorly but anteriorly lies in apposition to the posterior wall of the bladder. The blood supply of the uterus is from the uterine arteries on each side (Fig 1.5). These arise from the iliac arteries and pass down to the junction of cervix and uterus, where the cervical and vaginal branches are given off. The vessels then continue upwards at the side of the uterus in a tortuous manner, necessary to accommodate uterine enlargement during pregnancy, linking up with the ovarian arteries in the upper part of the broad ligament.

Uterine tubes The uterine tubes (also known as the fallopian tubes) are approximately 12 cm in length and act as a conduit for sperm to reach the ovum and for the ovum to transit from the ovary to the uterine cavity for implantation. The tube is composed of four parts: the interstitial part, which runs in the outer ‘cornu’ of the uterus; the isthmic part, a narrow portion comprising the inner one-third adjacent to the uterus; the ampullary part, a gradually widening trumpet-shaped outer third, which ends in a series of finger-like projections (the fimbrial part), which wrap themselves around the ovary at the time of ovulation. The Fallopian tube Uterus

Ovarian artery Round ligament Cervix

Uterine artery Anterior division of internal iliac artery

Azygos vaginal artery

FIGURE 1.5 

Vaginal arteries

Arterial blood supply to the internal genitalia. There is free anastomosis between vaginal, uterine and ovarian arteries. Coiling of vessels allows elongation as the uterus enlarges in pregnancy.

Chapter 1  Reproductive Anatomy and Physiology

inner portion of the tube is very narrow, and the epithelium is thrown up into a complex series of branching folds; hence, there is a strong tendency for blockage to occur should the tube become infected. The tubal epithelium is generously supplied with hair-like processes, called cilia, which beat gently in the direction of the uterine cavity to ‘encourage’ the ovum towards the uterus. Partial obstruction of the lumen or impairment of cilial function may result in implantation of the conceptus in the tube rather than in the uterus: a tubal ectopic pregnancy (see Chapter 8). The tubes lie at the top of the broad ligaments, which are composed of peritoneum, folded over the tubes and round ligaments like sheets on a line.

Round ligaments The round ligaments run from adjacent to the uterine cornua to the internal inguinal ring, which is located around the middle section of the inguinal ligament. They provide some anterior support for the uterus, especially during pregnancy when they enlarge markedly. Stretching may cause discomfort or pain (round ligament strain) which can be appreciated readily by gentle palpation at the sides of the uterus late in pregnancy.

Broad ligaments The broad ligaments are folds of peritoneum, lying between the uterus and the lateral pelvic wall. In the upper part lie the round ligaments and uterine tubes and at the base lie the uterine vessels and ureters. The remainder is taken up by delicate areolar tissue, vessels and nerves. Uterine perforation or rupture may occur into the broad ligament and, similarly, tubal ectopic pregnancy may rupture downwards into it.

Infundibulopelvic ligament As the lateral pelvic wall is approached, the blood vessels supplying the ovary sweep upwards out of the pelvic side-wall into the ovary.

Parametrium The tissue adjacent to the uterus in the base of the broad ligaments is called the parametrium, and is important because it represents one of the pathways in the spread of uterine infection, called parametriti, and also lymphatic spread of carcinoma of the cervix. The parametrium contains embryonic remnants related to the vestigial wolffian system of ducts and tubules from the vas deferens in the male but fail to develop in the female. Where remnants are clinically apparent in the female, they are termed Gartner’s duct cysts and usually lie deep within the anterolateral fornices of the vagina.

Ovaries The ovaries are situated on the back of the broad ligaments and are attached by a mesentery (mesovarium). Each ovary is almond-shaped and measures approxi-

mately 3 cm in length. The ovary has two key and related functions: the production of ova during the woman’s reproductive years and the secretion of gonadal steroid hormones. The ovaries have a yellowish-white irregular surface, often characterised by developing Graafian follicles or active or regressing corpora lutea. The ovarian and infundibulopelvic ligaments have already been mentioned, attaching the ovary to the back of the broad ligament and the pelvic side-wall respectively. In structure, the ovary possesses an outer cortex that contains primordial and developing follicles and specialised connective tissue (theca), and an inner medulla that is mainly composed of loose connective tissue and blood vessels. The blood supply of the ovary comes mainly from the ovarian arteries (which arise from the aorta), aided by the anastomosis with the uterine arteries. There are approximately 2 million primary oocytes during fetal life but a process of atresia means that there are only approximately 300 000 primary oocytes (germ cells) in the ovary at puberty. As there is usually only one oocyte released each month, approximately 1000 oocytes fail to reach maturity each month.

SKELETOMUSCULAR SUPPORTS Supporting the external and internal genitalia are the bony and fibromuscular structures which make up the birth canal.

THE BONY PELVIS This is made up of four bones joined together by ligaments. At the sides are the paired innominate (pelvic) bones. These are joined in front at the symphysis pubis. Behind, they articulate with the ala (or wings) of the sacrum forming the sacroiliac joints (Fig 1.6). The fourth bone, the coccyx, is loosely articulated with the lower border of the sacrum. Both the sacrum and the iliac bones are strong and heavy, since it is through them that the weight of the head and trunk is transferred to the legs. The innominate bone is composed of three separate elements: pubis, ischium and ilium. These ossify in early adulthood. The different parts of the bone are shown in Figures 1.7 to 1.9. The sacrum is composed of five fused vertebrae, and a large intervertebral disc separates it from the fifth lumbar vertebra above. The sacrum is directed backwards as well as downwards, and this throws its superior border into prominence as the sacral promontory. The sacrum is concave on its pelvic aspect, providing in part the characteristic curve of the birth canal. Looking into the pelvis from above, one can ascertain two parts: the false pelvis above and the true pelvis below. These are delineated by the iliopectineal line (Fig 1.6). The false pelvis can be appreciated on lateral view (Fig 1.9) as that part of the pelvis above the pelvic inlet. When viewed from the side (Fig 1.9), it can be seen that the birth canal anteriorly is made up only of 7

Beischer & MacKay’s: Obstetrics, Gynaecology and the Newborn

the symphysis pubis and is quite short (about 5 cm). Posteriorly, there is the sweep of the sacrum and coccyx (about 12 cm) which, when added to the fibromuscular perineal body, describes the curve of the birth canal. The dimensions of the true pelvis can be appreciated by studying three arbitrary planes—the pelvic inlet, the midpelvis and the pelvic outlet—the shape and Sacral promontory

Sacroiliac joint and ligament

dimensions of which are shown in Figures 1.8 and 1.9 and in Table 1.1. Four variations in pelvic shape are recognised (as listed in Table 1.2). Although the names are rarely used in clinical practice, it is helpful to know that an individual pelvis may be unusually wide or narrow in a particular dimension and either shallow or deep. The funnelling of the male pelvis with a narrow outlet relative to the inlet is also of clinical importance. Symphysis pubis

Iliopectineal line

Ischial tuberosity

Coccyx

Coccyx

Ischial spine

Sacrospinous and sacrotuberous ligaments

Sacrospinous and sacrotuberous ligaments

FIGURE 1.6 

The pelvic brim. View from above of a large articulated pelvis. The brim is almost round, the pubic arch is generous and there is minimal projection of the sacral promontory.

Sacrum

FIGURE 1.7 

The pelvic outlet. View of articulated pelvis from below. In order to escape injury, the coccyx must fold backwards during delivery of the head. Pelvic Outlet

Pelvic lnlet

Intertuberous diameter (11.5 cm)

Transverse (13.5 cm)

Anteroposterior (true conjugate) (11.5 cm)

FIGURE 1.8 

Anteroposterior diameter (11.5 cm)

The pelvic inlet and the pelvic outlet. The average dimensions of the inlet and outlet illustrated. 8

Chapter 1  Reproductive Anatomy and Physiology

Pelvic cavity This is the region between the pelvic inlet above and the pelvic outlet below, and is bounded by the pubic bones anteriorly, the curve of the sacrum posteriorly, and parts of all three components of the innominate bone laterally. The pelvic inlet is oval-shaped and wider transversely (Figs 1.6 and 1.8). The midpelvic plane (also known as the narrow pelvic plane) is at the level of the ischial spines. The ischial spines are important landmarks, as indicators of the type of pelvis and its size, but also as reference points for designation of the station of the presenting part. Because they are approximately midway down the birth canal (about 5 cm in the central axis), the head is assumed to be engaged when the vertex has reached this L5

S2

S1

S3 Ischial spine

S4 Plane of pelvic brim

S5

Coccyx Midpelvic plane Plane of pelvic outlet Curve of birth canal

FIGURE 1.9 

Sagittal view of the bony pelvis.

point, since the distance from the vertex of the skull to the maximum diameters of the head (biparietal and suboccipitobregmatic) is slightly less than 5 cm in the unmoulded state. The pelvic outlet is outlined by the subpubic arch, the ischial tuberosities, the sacrotuberous ligaments and the coccyx (Figs 1.7 and 1.8).

Pelvic inclination The lateral view of the pelvis indicates that the pelvic brim makes an angle of approximately 50° with the horizontal; this is called the angle of inclination. The inclination lessens as the birth canal is descended, being about 30° in the midpelvis and 10° at the outlet (Fig 1.9).

The pelvic joints The sacroiliac joints are partly cartilaginous, partly fibrous and are very strong. Despite this, pain is often experienced from approximately 20 weeks’ gestation as joint mobility increases with softening of the ligaments. Note that any weight bearing of the upper body on the legs must pass through the sacroiliac joint. The lumbosacral joint lies between the fifth lumbar vertebra and the sacrum. Because of the backward inclination of the sacrum, considerable strain also occurs here during pregnancy. In extreme cases (spondylolisthesis), the fifth lumbar vertebra projects downwards and forwards into the area of the pelvic brim. The two pubic bones are joined anteriorly at the symphysis pubis by fibrous tissue, although a layer of cartilage remains between them. It is through this cartilage that the operation of symphysiotomy is occasionally carried out in resource-poor settings to increase pelvic diameters to allow vaginal birth in cases of obstructed labour or social dystocia. Occasionally, there is abnormal separation of the pubic bones (pubic symphysis diastasis) in late pregnancy or the early puerperium. The condition is usually self-limiting,

TABLE 1.1  PELVIC MEASUREMENTS (AVERAGE). Antero-posterior diameter

cm

Transverse diameter

cm

Pelvic inlet

Upper symphysis to sacral promontory

11.5

Side to side across pelvic inlet

13.5

Midpelvic plane

Mid-symphysis to S2/S3

11.5

Bispinous

10.5

Pelvic outlet

Lower symphysis to coccyx

11.5

Intertuberous

11.5

TABLE 1.2  CLASSIFICATION OF PELVIS SHAPE. Type

Shape

Depth

Inlet versus outlet

Gynaecoid

Round apart from sacral promontory

Normal

Similar

Anthropoid

Anteroposterior wide, transverse narrow

Deep

Similar

Platypelloid

Anteroposterior narrow, transverse wide

Shallow

Similar

Android

Heart shape (very prominent sacrum)

Normal

Funnelling 9

Beischer & MacKay’s: Obstetrics, Gynaecology and the Newborn

spontaneously resolving within weeks of childbirth. The sacrococcygeal joint is less fixed than the other joints, thereby allowing the coccyx to bend backwards as the fetus passes through the birth canal. However, undue displacement may overstretch the ligaments, giving rise to coccydynia (coccygeal pain) during the early puerperium.

Pelvic ligaments These are well developed in the pelvis because of the stresses to which the pelvic bones are subjected. Apart from the ligaments specifically related to the joints mentioned, there are two others of importance: the sacrospinous and sacrotuberous. These run from the sacrum to the ischial spine and ischial tuberosity respectively. Together with the coccyx and lowest part of the sacrum, they form the posterior aspect of the pelvic outlet.

The pelvic soft tissues The bony pelvis is clothed by a number of muscles, the chief of which form the floor of the pelvis and the perineum.

Levator ani The levator ani muscles run on each side from the back of the symphysis pubis and around the lateral pelvic wall on the fascia over the obturator internus muscle to the ischial spine and side of the coccyx, together with the special muscular bundle, the puborectalis. The puborectalis decussates or joins with its opposite number around the vagina and lower rectum. The urethra, vagina and rectum all pass through this muscular diaphragm, which is completed by fascial condensations on its upper and lower surfaces. The muscles of the two sides slope downwards and forwards in the form of a gutter, which assists rotation of the fetal head to occipitoanterior as it strikes against the pelvic floor. The puborectalis is important in helping to maintain closure of the outlet by drawing the different structures passing through it anteriorly towards the shelf of the symphysis pubis.

Urogenital diaphragm The urogenital diaphragm is a triangular-shaped muscular diaphragm through which pass the urethra and vagina. It occupies the space between the inferior borders of the ischiopubic rami (Fig 1.4) and extends posteriorly to the front wall of the rectum. On its deep aspect are two sets of muscles: the constrictors of the urethra and vagina, and the deep transverse perinei. Superficially, there are the ischiocavernosus muscles (passing from the ischiopubic ramus on each side up to the clitoris), the bulbs (erectile tissue) with the associated bulbocavernosus muscles, the superficial perineal muscles and the Bartholin’s glands. Between the vagina and rectum, the superficial and deep perineal muscles, including the anal sphincter, decussate and join to form the strong perineal body. Behind the anal canal, the sphincter muscles decussate to form the anococcygeal raphe. 10

Internal pudendal vessels and the pudendal nerve The internal pudendal vessels and the pudendal nerve pass forwards from the inner aspect of the ischial tuberosity across the fat-filled ischiorectal fossa (which lies between the tuberosity and the rectum) to supply the perineal structures.

REPRODUCTIVE PHYSIOLOGY THE MENSTRUAL CYCLE The menstrual cycle is initiated by the pulsatile secretion of gonadotrophin-releasing hormone (GnRH) from the hypothalamus. This in turn causes the secretion of the two gonadotrophins: follicle-stimulating hormone (FSH) and luteinising hormone (LH) from the anterior lobe of the pituitary gland. FSH and LH act on the ovary to cause follicular growth (especially FSH), ovulation (especially LH) and corpus luteum formation (also LH). They are simultaneously stimulating the secretion of oestrogen from the granulosa cells of the developing follicle (follicular phase of menstrual cycle) and then oestrogen plus progesterone from the lutein cells of the corpus luteum (luteal phase of cycle) (Fig 1.10).

Follicular phase FSH induces secretion of oestrogen by the granulosa cells in the developing follicle. Oestrogen has a growthstimulating effect on the blood vessels, stromal and epithelial cells of the uterine endometrium, producing a proliferative endometrium. There is also a stimulatory effect of oestrogen on the myometrial muscle cells, as well as on the duct tissues of the breast. Oestrogen also causes negative feedback on the hypothalamic–pituitary axis, progressively inhibiting further FSH secretion.

Ovulation Paradoxically. despite the negative feedback of oestrogen on the pituitary, rising oestrogen levels eventually trigger a massive peak of LH (the LH surge), which in turn causes the mature ovarian follicle to release the ovum (ovulation), approximately 30 hours later. Ovulation most commonly occurs on approximately day 14 of a 28-day cycle. The ovum passes into the fimbrial end of the uterine tube to await the potential arrival of ascending spermatozoa.

Luteal phase The space formerly occupied by the ovum is filled with blood and then granulation tissue, and the lining granulosa and theca cells develop under the continued secretion of LH to form the corpus luteum (yellow body). These specialised cells produce the second ovarian hormone, progesterone. Like oestrogen, progesterone has effects on the uterus, breasts and hypothalamic–pituitary system. In the uterus, oestrogen causes proliferation

Chapter 1  Reproductive Anatomy and Physiology

Ovarian cycle

Luteal phase

Follicular phase

Events in the ovary Developing follicle

Corpus luteum Ovulation

80

LH FSH (mU/mL)

LH

Oestradiol

FSH

Progesterone

Inhibin 60

Oestradiol (pg/mL) 40

Progesterone (ng/mL)

1000

10

800

8

600

6

1600

400

4

800

200

2

0

0

Inhibin (ng/mL)

0

20

0

0 Endometrial cycle

2 Menses

4

6

8

10

12

14 Days

Proliferative phase

16

18

20

22

24

26

28–0

Secretory phase

FIGURE 1.10 

Hormonal changes during the menstrual cycle. The menstrual cycle is a cycle of the hypothalamic–pituitary–ovarian axis, as well as a cycle of the targets of the ovarian hormones: the endometrium of the uterus. Therefore, the menstrual cycle consists of both an ovarian cycle (which includes the follicular phase, ovulation and the luteal phase) and an endometrial cycle (which includes the menstrual, proliferative and secretory phases).

Source: Boron WF, Boulpaep EL. Medical physiology updated edition. 2nd edn. Philadelphia: Saunders, 2012. Copyright © 2012 Saunders, An Imprint of Elsevier. Figure 55.9.

whereas progesterone causes increased cellular differentiation and inhibits any further proliferation.

Menstrual phase In the absence of fertilisation, falling gonadotrophin secretion from the pituitary causes corpus luteum degradation (luteolysis) with a consequent fall in oestrogen and progesterone menstruation thus ensues. Menstruation is essentially a normal response to progesterone withdrawal from an ‘oestrogen-primed’ endometrium.

Early pregnancy If fertilisation occurs and successful embedding takes place, the chorionic villi which surround the embryo (Fig 1.11) release human chorionic gonadotrophin (hCG). This hCG prevents regression of the corpus luteum, and

ensures that secretion of oestrogen and progesterone continues, allowing the embryo to develop in its endometrial bed (i.e. menstruation is prevented by sustenance of the corpus luteum).

Gametogenesis Gametogenesis is the process whereby the gametes (mature germ cells) are formed in the female and male gonads. Although only one ovum is produced each month compared with millions of spermatozoa in the male, the fundamental process (oogenesis, spermatogenesis) is the same. Essential to the understanding of the early development of the germ cells are: 1. the chromosome structure of the cells; and 2. the two basic forms of cell division. In both the female and male primary germ cells (and, 11

Beischer & MacKay’s: Obstetrics, Gynaecology and the Newborn

Cerebral cortex

Gonadotrophin-releasing factor Hypothalamus Neurosecretory cells to posterior lobe

Pituitary

Hypophyseal portal system to anterior pituitary lobe

Positive feedback

FSH LH

Negative feedback

Corpus luteum

Ovary

Graafian follicle

Uterus Oestrogen

Oestrogen + progesterone

FIGURE 1.11 

Hypothalamic–pituitary–ovarian–uterine interrelationships in the control of ovulation and menstruation. Source: Beischer NA, Mackay EV. Care of the pregnant woman and her baby. Artarmon: W.B. Saunders, 1978.

indeed, in all cells in the body except those gametes about to be joined in the process of fertilisation) there are 46 chromosomes (pairs of chromosomes 1 to 22 either XX or XY). In order for the number of chromosomes to remain constant when the ovum and sperm finally unite, each must shed half its complement. This special type of reduction division is called meiosis, as opposed to the process which occurs at all other times of cell division which is known as mitosis (Fig 1.12). Thus, there are stem cells in the ovary and testis which have the normal number of 46 chromosomes and these divide by ordinary mitosis to produce daughter cells: the primary oocytes and spermatocytes. When these divide by the process of meiosis to form the secondary oocytes and spermatocytes, there are only 22 autosomal chromosomes and 1 sex chromosome (X or Y) to each cell. Each daughter cell has lost half of its genetic 12

Primary oocyte XX First meiotic division

XX X

X

Primary spermatocyte

XY XY

Second meiotic division

X

Y

(First polar body) X Ovum

X

(Second polar body)

FIGURE 1.12 

X

X

Y

X and Y sperm

In normal gametogenesis, the ova all bear an X chromosome while half the spermatozoa bear X and half Y chromosomes.

Y

Chapter 1  Reproductive Anatomy and Physiology

material, but this will be restored when it unites with its partner at the time of fertilisation. It will be apparent that the oogonia (female germ cell) can only produce a daughter cell with an X chromosome, while the spermatogonia (male germ cell) can produce an X or Y spermatozoa. At conception, if the conjunction is XX, a female will result; if XY, a male.

THE PHASES OF REPRODUCTIVE LIFE FROM A SEX HORMONE PERSPECTIVE Prepuberty The hypothalamic–pituitary axis is hypersensitive to the negative feedback of the very low levels of endogenous sex hormones. As a result, the pituitary gonadotrophins (FSH and LH) remain at very low levels and the ovary is not stimulated to produce oestrogen and progesterone. In the absence of significant sex hormones, internal genitalia, external genitalia, breast development and secondary sexual hair remain in an infantile state.

Puberty The hypothalamic–pituitary axis develops progressively decreasing sensitivity to gonadal steroids and the levels of FSH and LH begin to rise which in turn stimulates the ovary to produce first oestrogen and then progesterone when levels are sufficient to induce ovulation.

Reproductive life Menstrual cycles

Pregnancy During early pregnancy, human chorionic gonadotrophin from the trophoblast cells maintains and stimulates the corpus luteum of pregnancy, which maintains oestrogen and progesterone at levels sufficient to sustain the endometrium and developing pregnancy. With establishment of the pregnancy, oestrogen and progesterone are produced by the placenta and the corpus luteum of pregnancy becomes non-essential from about the 13th week of gestation.

The climacteric The climacteric is the period surrounding the cessation of menses (menopause). Largely as a result of progressive attrition of follicles within the ovary, the ovary is depleted of oocytes and becomes increasingly refractory to stimulation by FSH and LH. As a result, the FSH and LH levels begin to rise as there is less negative feedback from the ovarian oestrogen and progesterone.

Postmenopause The ovary no longer has oocytes with their associated granulosa and lutein cells able to produce oestrogen and progesterone. High levels of pituitary gonadotrophins result. The ovarian stromal cells (which have the same embryological origin as granulosa cells) make small amounts of androstenedione that is converted in adipose tissue to oestrone. The oestrone is small in concentration but clinically important in mitigating the adverse effects of hypo-oestrogenism in the postmenopausal female.

The hypothalamic–pituitary axis stimulates the ovary in a cyclical manner. This results in menstrual cycles, most commonly of 28 days duration.

13

Chapter 2  ANATOMY AND PHYSIOLOGY OF PREGNANCY Michael Permezel and Peter Wein

KEY POINTS Following fertilisation in the outer third of the uterine tube, the conceptus reaches the uterine cavity by day 4 and implants at approximately day 6. The fertilised cell (zygote) divides to produce new cells (blastomeres) which form a cluster (morula). When the cluster develops a cavity, it is termed a blastocyst (Fig 2.1A). The various structures of the fetus are derived from three layers—the outer ectoderm supplying the nervous system and the skin, eye and ear; the middle mesoderm supplying the skeleton, muscles, connective tissue, haematopoietic system and urogenital system; and the inner endoderm supplying the gut, liver, pancreas, lungs, thyroid, parathyroid and thymus. The early trophoblast surrounds the embryo and interacts with the maternal spiral arteries, ultimately creating wide vascular channels that are the maternal blood supply of the placenta. The placenta is derived from the trophoblast as a specialised development of the portion that is closest to the underlying uterine decidua. Key functions include gas exchange, nutrient provision, waste product disposal and hormone production.

FERTILISATION The ovum is released into the peritoneal cavity and ‘captured’ by the fimbrial end of the uterine tube. Fimbrial cilia sweep the ovum towards the tubal ostium. Up to 98% of ova reach the uterine tube, demonstrating the efficiency of fimbrial capture and transmission of the ovum. On average, approximately 200 million sperm are ejaculated into the vagina. Only a few thousand will reach the cervical mucus, uterine body and uterine tube where they may have an opportunity to fertilise an ovum. The cervical mucus assists by nourishing the spermatozoa and acting as a place for temporary storage so that spermatozoa can be progressively released over several days. Spermatozoa can survive for up to 5 days in the cervical mucus but the ova can only survive 24 hours without fertilisation. This means that that pregnancy can occur with sexual intercourse up to 5 days before ovulation but only one day after. Transport of spermatozoa through the uterine body and tubes is aided by uterine and tubal contraction stimulated by prostaglandins in seminal fluid

and oxytocin released from the female posterior pituitary during orgasm. Of the approximately 200 million sperm ejaculated, only approximately 50 spermatozoa reach the distal tube. Figure 2.1A illustrates the development of the conceptus in its transition from ovary to implantation. The ovum remains surrounded by the cumulus oophorus, a ‘cloud’ of cells from the follicle that need to be dissolved by the sperm before it must penetrate a thick glycoprotein shell around the egg—the zona pellucida (Fig 2.1B and C). Hyaluronidase and proteolytic enzymes are released from the acrosomal head of the sperm (acrosomal reaction) and assist with this penetration along with mechanical forces related to sperm motility. Within a few minutes of sperm penetrating the zona, the ovum protects itself against the entry of any further spermatozoa (polyspermy). Chemical changes in the ovum cell membrane prevent sperm from binding and cause any bound sperm to fall off. Changes in the zona pellucida make it even more impenetrable to sperm.

Chapter 2  Anatomy and Physiology of Pregnancy

Zygote Zona pellucida

Morula

Inner cell mass

Blastocyst

A

B

Trophoblast

C

FIGURE 2.1 

The early changes in the fertilised ovum before implantation (which occurs on about day 20 of the menstrual cycle). A Diagram of the early changes. B An oocyte just after ovulation; it is surrounded by a clump of follicular cells in a clear, gelatinous matrix—the cumulus oophorus. C An 8-cell embryo with the spherical cells held in close proximity by the zona pellucida. Cell communication between the blastomeres commences at this stage. A few spermatozoa can be seen still adhering to the zona pellucida. Source: B and C from Beischer NA, Mackay EV. Care of the pregnant woman and her baby. Artarmon: WB Saunders, 1978.

15

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Fusion of the cell membranes of the sperm oocyte results in the formation of a single cell. Completion of meiosis within the oocyte is followed by combination of the genetic material from both ovum and sperm. The previously haploid cells, with 23 chromosomes each, now have formed a single nucleus with 46 chromosomes—the zygote.

PRE-IMPLANTATION DEVELOPMENT After formation of the zygote, rapid cell cleavage takes place by mitosis, with each pair of daughter cells (blastomeres) so formed having the 46 chromosomes of the parent blastomere. The blastomeres adhere to each other, eventually forming a cluster of cells termed the morula. This stage is the beginning of differentiation and the cells lose their totipotency (ability to form a complete individual) if separated away from the other cells. On day 4 after fertilisation, the conceptus passes into the uterus and prepares to embed in the endometrium, where it will differentiate and grow over the ensuing 9 months. At this stage, a fundamental change occurs in the cell mass. A fluid space appears and a division occurs into an inner cell mass, which will form the embryo (embryoblast), and an outer trophoblast, which will form the placenta (aided in part by the underlying maternal endometrium). This is the blastocyst and it is in this form that implantation takes place (Fig 2.1 and Table 2.1). Where the cluster of cells completely divides, monozygotic (identical) twinning results. If this occurs at days 1 to 3, the twins are dichorionic diamniotic; if at days 4 to 8, the twins are monochorionic diamniotic; and if at day 9 or longer, monochorionic monoamniotic.

IMPLANTATION Implantation occurs 6 to 8 days after fertilisation once the blastocyst has hatched from the zona pellucida. The primitive conceptus, after contact with the lining of the uterus, erodes through it and sinks into the deeper layers of the endometrium. The smaller blood vessels and the glands provide early nourishment as they interact with the trophoblastic cells over days 10 to 12. The subsequent development of the two elements—the embryo (later termed fetus) and the placenta—will now be considered separately.

EMBRYONIC AND FETAL DEVELOPMENT Table 2.1 lists the key phrases of development from the conceptus shortly after fertilisation through to term gestation. The inner cell mass flattens to form the embryonic disc at the start of the 2nd week after conception. The inner cell mass soon differentiates into three basic layers 16

(ectoderm, mesoderm and endoderm). From the dorsally placed ectoderm will derive the entire nervous system, the skin and the sensory organs, such as the eyes and ears. The intermediate mesoderm will form the bones, muscles, and connective tissue, as well as the vascular and urogenital systems. The ventrally placed endoderm is responsible for the gastrointestinal tract (including derivative organs such as the liver, gall bladder and pancreas), lungs, thyroid, parathyroid glands and thymus. By the 2nd week, the embryonic disc has become elongated and two cavities develop. The amniotic space appears dorsally, above the ectoderm. This space progressively enlarges over the next 10 weeks so that it covers the entire embryo except at one point—the body stalk— where the embryo is attached to the part of the trophoblast that is to form the placenta (Fig 2.2). By the 14th week of pregnancy, the amniotic sac fills the entire uterine cavity, pressing the non-placental trophoblast against the endometrium of the opposite wall. Ventrally, another space appears—the yolk sac—which is formed from endodermal cells. Unlike the amniotic sac, it never attains a large size although it carries out many essential functions prior to effective placental functioning. The extraembryonic coelom is a fluid-filled cavity which arises in the extraembryonic mesoderm surrounding the embryo. It splits the extraembryonic mesoderm into two layers: the somatic mesoderm, which, together with the trophoblast, forms the chorion; and the splanchnic mesoderm, which, with a fold of ectoderm, forms the amnion. The chorion forms a sac inside which the embryo and its amnion are suspended by the body stalk. As indicated earlier, continued growth of the amniotic cavity eventually obliterates this sac. Anomalies in this process of membrane development may present in the form of amniotic sheets or bands. Usually, amniotic sheets are readily visualised on ultrasonography and are harmless. In contrast, amniotic bands can cause a variety of fetal anomalies by hindering normal development (Fig 2.3). Originally, the extraembryonic coelom communicates with a similar but smaller space in the intraembryonic mesoderm—the intraembryonic coelom. As the embryo grows and folds, the two coelomic cavities become separated in the embryo forming the pleural, pericardial and peritoneal cavities. The body stalk provides the connection between the blood vessels of the fetus and those of the trophoblast (which is specialising to become the placenta). As development progresses, great elongation occurs in the stalk and it becomes the umbilical cord, containing the two arteries and a single vein. From weeks 3 to 8, the three embryonic layers progressively differentiate to provide the definitive organs of the body.

ECTODERMAL LAYER The ectodermal cells thicken in the midline to form the primitive streak that is the forerunner of the nervous

Chapter 2  Anatomy and Physiology of Pregnancy

TABLE 2.1  DEVELOPMENT OF THE CONCEPTUS, EMBRYO AND FETUS. Stage

Age*

I

1

Conceptus

Size

Characteristics Blastomeres form from progressive division of zygote to produce the morula (1–3 days), blastocyst (4–6 days) and trophoblast (7+ days).

(mm) II Embryo (5–10 weeks)

2

Inner cell mass differentiates into bilaminar embryonic disc. Primitive amniotic and yolk sac cavities. Trophoblast erodes maternal blood vessels and forms lacunae. Primitive uteroplacental circulation.

3

Chorionic sac measures 1 cm in diameter; villi around whole surface. Well-defined embryonic disc and body stalk. Somites forming. Fetal vascularisation of villi; intervillous space forming. Major developmental activity in nervous system and heart.

4

4–5

Fetal sac 2–3 cm. Somites forming to provide muscles, bones and nerves of trunk. Heart and pericardium prominent. Arm and leg buds forming. Branchial arches (maxilla, mandible, hyoid); otic pit and lens placode present. Adopting C-shaped curvature.

5

10–12

Amnion enveloping fetus and body stalk. Eyes, ears and nasal organs forming. Heart and circulation formed. Differentiation of thyroid gland and special outgrowths from the gut (liver, pancreas, gall bladder). Digital ridges indicate future fingers.

6

20–25

Head is large compared with the rest of the body. Digits well formed. Intestines enter coelom. Ears and eyes developing. Genital tubercle present. Lungs separating from gullet. Fetus begins to move.

7–8

40

Head rounded; eyes and ears still forming. Neck region delineated. Abdominal protrusion less marked. Definitive kidneys starting to develop; separation of urinary and rectal passages is complete; anal membrane ruptures. Facial clefts have closed. Beginning function of special endocrine glands.

(cm) III Fetus (11–40 weeks)

10

8

Ossification centres in most bones. Appearance of nails on fingers and toes. Functioning of nervous system at a primitive level (reflex responses). Teeth are beginning to form. Blood formation transferring from yolk sac and liver to bone marrow.

14

16

Sexual differentiation definite

18

Stage of organ growth rather than differentiation

22

Development occurring in the brain. Progressive budding, leading to maturation and increase in size in the kidneys, lungs and gastrointestinal tract.

26

36

30

42

34

46

38

50

Progressive appearance of centres of ossification, especially at ends of long bones.

*Weeks after conception

system. A longitudinal groove then develops within the primitive streak. Approximation of the edges of the neural groove convert it into the neural tube, which becomes the future spinal canal and ventricular system of the brain. The spinal column, derived from the mesoderm, develops around the neural tube. The cranial portion of the neural tube enlarges to form the brain.

Neuroblasts differentiate to form the white and grey matter of the brain. Primitive nervous reflex activity is seen as early as 8 weeks’ gestation. Whole body movements occur from 10 weeks’. At 17 to 19 weeks’, fetal movements are sufficiently strong to be first perceived by the mother (‘quickening’). The brain is highly susceptible to teratogenic 17

Beischer & MacKay’s: Obstetrics, Gynaecology and the Newborn

Somatic mesoderm

Chorion

Ectoderm Amniotic cavity Gut Fetus

Splanchnic mesoderm

Amnion

Ectoderm Coelom Yolk sac

Splanchnic mesoderm

Body stalk Allantois Endoderm

Placenta

FIGURE 2.2 

Diagram of 21-day embryo (3 weeks after fertilisation is the same as 5 weeks’ gestation in the language of the clinician).

FIGURE 2.3 

Medial view of the left leg of a 2-day-old female infant, a second twin of birth weight 1320 g born by breech extraction. Note gross oedema of the leg below the deep constriction caused by the amniotic band at the level of which were transverse fractures of the tibia and fibula. The fractures healed and the oedema resolved uneventfully after a relieving incision was made over the constriction. The amniotic band syndrome is rare (approximately 1 in 10 000 births). The band forms when the amnion ruptures and rolls into a cord, the fetus lying within the intact chorion.

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agents, the critical period being from the 10th to the 30th days of embryonic life. Neuronal division occurs from fetal life until approximately 4 years postnatally. The eye develops as an outpouching of the forebrain at the side of the facial cleft. By 6 weeks’ there is a fusing of the optic vesicle and overlying lens placode. The optic vesicle becomes cup-shaped, with the narrow open end forming the pupil. The lens placode differentiates to form the lens. There are two layers: an inner vascularised pigment layer (retina) and an outer fibrous layer (choroid, sclera and cornea). Eyelid folds are fused until the sixth month (Fig 2.4); after the seventh month, the eye will respond to light. At birth, the infant fixes on patterns rather than colours; the optimum focal length is about 30 cm. The eye is highly susceptible to insult between the 18th and 30th days. The ear, like the eye, is a compound development that comes from the first pharyngeal pouch and the otocyst. Development occurs largely over the second half of the embryonic period (4 to 8 weeks’). The ossicles of the middle ear develop from the related mesenchyme, and the central nervous connections are established to the cochlear and vestibular portions. Myelination of auditory fibres occurs from about 24 to 26 weeks’. Sound perception develops slowly over the third trimester; it is geared to the type of noises heard in utero (especially vascular souffles).

MESODERMAL LAYER The mesoderm forms a number of internal structures by processes of proliferation and sculpturing, which are often quite complex. The cardiovascular system is seen initially as a simple network of tubes. In the thorax, the initially straight tube

Chapter 2  Anatomy and Physiology of Pregnancy

FIGURE 2.4 

This 2-day-old infant weighed 270 g at birth at 24.6 weeks’ gestation. She died at 3 days of age. The mother developed preterm premature rupture of the membranes (PROM) at 23 weeks’ gestation after several episodes of threatened preterm labour. Labour occurred 13 days after preterm PROM.

undergoes folding and division. Eventually the heart is formed—with its intricate system of chambers and valves—subserving first the requirements of the fetus where the lungs are by-passed, and later those of the baby, when the pulmonary circulation becomes operational. In the fetus, only 10% of the cardiac output goes to the lungs; of the blood in the descending aorta, 60% goes to the umbilical arteries (and the placenta) and the remaining 40% to the trunk and lower limbs. The heart rate reaches a peak in late embryonic life (approximately 170 bpm) and this slowly decreases to term (approximately 140 bpm). The pressure in the right side of the heart is higher than that in the left side, but this changes rapidly after birth. No nervous tissue is present in the placenta or umbilical cord, so blood flow must be under the control of local autacoids and humoral influences. Active compounds include a number of prostaglandins, angiotensin, bradykinin, serotonin, histamine and acetylcholine. The haematological system first develops in the mesoderm of the yolk sac (weeks 3 to 6), then the liver (weeks 6 to 36), and lastly in the bone marrow (week 20 onwards). Most of the early red blood cells are nucleated (erythroblasts) and contain a different type of haemoglobin. The embryonic haemoglobin gives way to fetal haemoglobin (Hb F) which contains 2 alpha and 2 gamma chains (α2γ2). This is an adaptation to the relative hypoxia of intrauterine life, as is the significantly higher haemoglobin concentrations (approximately 18 g/dL) at birth.

After birth, adult haemoglobin (Hb A), which contains two alpha and two beta chains (α2β2), rapidly increases from approximately 10% of all haemoglobin at birth to approximately 98% during infancy. White blood cells and lymphocytes appear in the peripheral blood late in the first trimester. The white cell count is low early in pregnancy—approximately 1 × 109/L at week 25—but reaches approximately 8 × 109/L at term. Immune globulins are produced after the first trimester, and the presence of an infection in fetal life can be inferred by finding disease-specific immunoglobulin M (IgM) in cord blood. Maternal immunoglobulin G (IgG) traverses the placenta from mother to fetus from about 15 weeks’ gestation and this progressively increases through pregnancy. The urogenital system is derived from swellings on the dorsal body wall. Ridges form and these invaginate to form tubes. The Wolffian is the male accessory duct system and the Müllerian is the female genital system. The gonads are populated by germ cells which have migrated from the primitive yolk sac, and these are juxtaposed to the upper part of the genital ducts. The testis can be distinguished from the ovary by about the 6th week. The luteinising-hormone-like activity of human chorionic gonadotrophin (hCG) is thought to accelerate testicular development, so that by the end of the first trimester fetal testosterone levels are comparable to adult male levels. The kidneys form from metanephric tissue which is invaded by an outpouching of the metanephric duct (the ureteric bud). As with other organs such as the lung and liver, repeated branchings occur until the final units of function are achieved (in this case the nephron, there being 1 million or more in each kidney). At the end of the first trimester, the fetal kidney is able to filter and reabsorb urine, but concentrating ability and acidification is poorly developed until after birth. The bladder forms when the urorectal septum descends and separates the bladder in front from the rectum/anal canal behind. The urethra is formed from grooves which appear on the vulva and close over; the female lacks the penile urethra, the folds remaining open to provide the labia minora. Glomerular filtration and tubular absorption rates are significantly less than in the adult on a surface area basis.

ENDODERMAL LAYER The endoderm becomes enclosed as the embryonic disc folds during the 4th week. The primitive foregut, midgut and hindgut are outlined during the 6th week; the midgut leads to the yolk sac at the umbilicus (Fig 2.2). The gastrointestinal system develops from the elongation and folding of the primitive foregut, midgut and hindgut. The foregut comprises the pharynx, oesophagus, stomach and proximal duodenum. The stomach rotates and its mesenteries form the greater and lesser omentum.



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The midgut extends from the duodenum to the left one-third of the transverse colon. The abdominal bulge seen in the embryo represents the midgut, which is too large to be accommodated in the abdominal cavity and herniates into the umbilical cord from weeks 8 to 12. Occasionally, this persists resulting in an exomphalos. Meckel’s diverticulum indicates the midpoint of the gut. Muscle tissue develops around the endodermal epithelium, and anatomical developments (formation of the appendix and caecum, rotation of the gut) occur in the embryonic period. The fetus swallows amniotic fluid from the end of the first trimester; the amount reaches 50 mL or more per hour in late pregnancy. The hindgut forms the remaining portion of the large bowel. Communication with the allantois ceases at approximately weeks 7 to 8 by the formation of the urorectal septum. Initially there is an occluding membrane or proctodaeum similar to that at the entrance to the foregut (the stomodaeum). This should break down by the end of the 10th week; failure to do so gives rise to the condition of imperforate anus. The respiratory system begins at the 3rd to 4th weeks’ with a tracheobronchial bud from the foregut which grows downwards in relation to the developing heart. There is progressive budding and vascularisation, with air sacs appearing in the terminal branches by about 20 weeks’. There are two types of lining cells: squamous and granular pneumatocytes; the latter, which appear at about the 6th month, produce surfactant that lowers surface tension in the alveolus. Primitive breathing movements can be observed by ultrasound as early as the 12th week of fetal life; they become progressively more frequent, deep and coordinated as gestation advances. The frequency of chest movement is approximately 50 per minute and such activity occupies approximately 50% of any observed time period in late pregnancy. The thyroid, parathyroid and thymus glands are all derived from the pharyngeal pouches over weeks 3 to 5; function usually commences late in the first trimester. The liver bud, which also forms the gall bladder, arises from the first part of the future duodenum. The liver is a comparatively large organ in fetal life, especially during the period of haematopoiesis. Gluconeogenesis occurs from the 10th week and glycogen storage is a feature of late fetal life. Bile formation commences in the fourth month, but many enzyme systems are relatively undeveloped until after birth. The pancreas forms from two buds and the acinar and islet cells develop side by side.



3. disposal of waste products back to the mother 4. hormone production. The placenta therefore functions for the fetus as its lungs, alimentary tract, liver and kidneys. To accomplish this effectively, it must bring the circulations of the fetus and mother into intimate contact but in a manner that minimises exposure of the fetus to undesirable chemicals, microorganisms or immunological attack.

PLACENTAL DEVELOPMENT Blastocyst As indicated previously, the mass of dividing blastomeres (the morula) becomes arranged into two groups: a smaller inner cell mass which develops into the embryo and a larger surrounding mass which forms the trophoblast and ultimately the placenta.

Early trophoblast The trophoblastic cells soon differentiate into an inner cytotrophoblast and an outer syncytiotrophoblast (Fig 2.5). The trophoblast invades the stroma and blood vessels in the decidual layer of the endometrium, a process that is critical to the development of a healthy placenta. The large maternal vascular channels supplying the placenta are derived from trophoblastic invasion of the spiral arterioles in the endometrium. Where this process is defective, maternal blood supply of the placenta is reduced and preeclampsia and/or fetal growth restriction may result. The early trophoblast elaborates human chorionic gonadotrophin (hCG) which sustains the corpus luteum in the ovary, thereby maintaining the levels of oestro­gen and progesterone and preventing menstruation. Progesterone

FIGURE 2.5 

THE PLACENTA The placenta has four critical functions: 1. gas exchange 2. provision of nutrients 20

Recently implanted embryo (aged 10 days) obtained at premenstrual curettage for the investigation of infertility. The primitive trophoblast has opened up sinusoids filled with menstrual blood in the endometrium. The inner cell mass has formed (magnification ×100).

Chapter 2  Anatomy and Physiology of Pregnancy

also encourages uterine relaxation, thereby reducing the likelihood that the rapidly expanding conceptus will be expelled by uterine muscular activity.

Formation of villi and the intervillous space From 12 days after conception, the trophoblastic cells send finger-like processes (villi) into the endometrium. Blood-filled spaces (lacunae) appear between the villi (Fig 2.5). In the mesenchymal core of the villi, fetal blood vessels develop and link through the body stalk with the fetal vascular system. By day 18, the villi have branched several times and both fetal and maternal blood vessels are functioning. The fetal vessels are separated from the intervillous blood lakes by the trophoblastic covering; the

fetal circulation is thus a closed one and does not mix directly with the maternal blood. The heart of the embryo starts to beat from approximately day 22 after fertilisation, creating a functional circulation.

Further changes in the trophoblast and decidua Early trophoblastic growth occurred over the entire circumference of the developing pregnancy (Fig 2.6). With further growth, the villi in contact with the deeper part of decidua (decidua basalis) continue to proliferate to form the chorion frondosum, while those in contact with the superficial part (decidua capsularis) atrophy, forming the chorion laeve (Fig 2.7). Thus, the fetal part of the placenta will be formed by the basal chorion frondosum,

FIGURE 2.6 

Complete miscarriage at 8 weeks’ gestation. Villi are present over the entire surface of the chorion. The limbs, eyes and ears have formed, and the abdomen is protuberant. Source: Reproduced with permission from the Royal Women’s Hospital, Parkville, Victoria.

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Fetal vein and arteries Chorion frondosum Intervillous space

Decidua capsularis

Chorion laeve

Decidua basalis

Amnion

Basal vein Septum Spiral arteriole Chorionic villi

Myometrium

FIGURE 2.8 

Circulation of the maternal blood around the chorionic villi; the latter are pulsating in the intervillous space due to the pumping of the fetal heart.

FIGURE 2.7 

Stage of development of fetus and placenta at 8 to 10 weeks’ gestation. The amnion lines the chorion laeve and fetal surface of the placenta, and becomes continuous with the epithelial covering of the umbilical cord.

and the maternal part by the decidua basalis subjacent to it. The chorion laeve subsequently loses its villi and becomes the outer layer of the membranes, expanded into the cavity of the uterus by the amniotic membrane which becomes the inner amniotic layer. Fusion of these two layers and obliteration of the uterine cavity occurs at approximately 13 weeks’.

Final development of the placenta By 14 weeks’, the placenta has attained its definitive form and, for the remainder of the pregnancy, the only changes are further branching of the villi and an increase in the intervillous space. The increase in size of the placenta is relatively less than that of the fetus so the fetal:placental weight ratio steadily increases through pregnancy, reaching a value of 6:1 at term. That is, a fetus of birth weight 3600 g at term would have (on average) a placenta of weight of approximately 600 g.

PLACENTAL STRUCTURE Anatomical and functional fetal placental units A schematic cross-section of the mature placenta is shown in Figure 2.8. From the basal area, maternal blood enters 22

the cotyledon via the spiral arterioles. There are approximately 100 such major arterioles supplying the placenta. The blood enters in the form of spurts or jets and cascades down over the villi, which are floating in the intervillous space like seaweed in the ocean. Oxygen and nutrients are provided in exchange for carbon dioxide and waste products from the villi. The deoxygenated blood is carried away by large veins, also situated at the basal area. The cotyledon is the unit of the placenta, and is based on the arteriolar vessels supplying it. Each cotyledon is functionally independent, although there is no clear separation of one from another, except by incomplete septa. The intervillous space is thus potentially traversable throughout the entire placenta. The 10 to 35 apparent subdivisions of the maternal surface of the placenta seen on inspection after delivery are also termed ‘cotyledons’, but are more properly termed lobules or lobes (Fig 2.9). These are anatomical rather than functional divisions, each containing a number of the latter. The mature placenta measures approximately 18 to 20 cm in diameter and its thickness ranges from 1 cm at the edge to 4 cm at the centre. The histological unit of the placenta is the villus. The finer fetal vessels (capillaries) form loops in the connective tissue core of the villus (Fig 2.10). As pregnancy progresses, there is an increase in the size and number of capillaries and, towards term, they lie close to the intervillous space, often with no perceptible trophoblastic cover.

Tissues separating maternal and fetal circulations The tissues separating fetal and maternal blood are cytotrophoblast, syncytiotrophoblast, connective tissue and

Chapter 2  Anatomy and Physiology of Pregnancy

A

B FIGURE 2.9 

The placenta at term. A Fetal surface showing how vessels ramify as they disperse from the insertion of the umbilical cord. They are covered by the glistening, transparent amnion. B Maternal surface showing the usual number (20) of fleshy cotyledons (lobules) packed together. There is no retroplacental clot nor macroscopic evidence of infarction or calcification. Source: Courtesy of Prof. Norman Beischer.

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FIGURE 2.10 

Section of a normal term placenta (magnification ×120). Note the rich vascularity of the villi, the thinness of the trophoblastic covering of the villi and the occasional collections (knots) of the syncytial cells. Source: Courtesy of Prof. Norman Beischer.

A FIGURE 2.11 

the endothelium of the fetal blood vessel. This barrier thins near term, creating increased efficiency in exchange of nutrients, waste products, gases and immunoglobulin between mother and fetus. Oxygen and carbon dioxide pass across the villus membrane. The fetal–maternal pressure gradient for carbon dioxide is quite low (0.9 kPa or 7 mmHg) because of a high diffusibility. The transfer of oxygen to the fetus depends partly on the difference in gradient (7.3 kPa or 55 mmHg), but also on the greater binding capacity of fetal haemoglobin relative to adult haemoglobin. The inner cytotrophoblast is mainly responsible for the production of the hCG and decreases in size as gestation advances and hCG levels decline. The outer syncytiotrophoblast produces oestrogen and progesterone and remains prominent until delivery, although it often becomes quite thinned out or gathered into groups of cells at the periphery of the villi (syncytial knots).

Fetomaternal haemorrhage Where there is a breakdown of the ‘barrier’ between fetus and mother, fetal erythrocytes may enter the maternal circulation. This may be responsible for the development of anti-red cell antibodies in the mother where an antigen is expressed by the fetus and not the mother (see Ch 22).

B

Velamentous insertion of the cord. A This cord inserted 10 cm from the nearest placental edge. The membranes are held to demonstrate the vessels and fetal surface of the placenta. B A bipartite (two-lobed) placenta with velamentous insertion of the cord. Source: Courtesy of Prof. Norman Beischer.

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Chapter 2  Anatomy and Physiology of Pregnancy

Large fetomaternal haemorrhages may cause fetal anaemia, fetal hydrops or even fetal death.

Placental calcification Placental calcification increases towards term and is probably a normal physiological process, since it is not more evident when the infant is stillborn. It is excessive in about 5% of placentas, resulting in a gritty maternal surface. Placental calcification has no well-established relationship with either fetal hypoxia or fetal growth restriction.

THE UMBILICAL CORD FIGURE 2.12 

Vasa praevia from a 28-year-old para 1 admitted with irregular contractions and spontaneous rupture of the membranes at 39 weeks’. Twelve hours later she had a sudden painless haemorrhage (200 mL) and the fetal heart became unrecordable; the cervix was 3 cm dilated. Four hours later she delivered a stillborn infant, birth weight 3390 g. Note velamentous cord insertion and torn vessel adjacent to the hole in the membranes. The perinatal mortality rate is high (50 to 80%) with vasa praevia, even if diagnosed quickly when haemorrhage occurs.

The umbilical cord has two umbilical arteries which carry deoxygenated blood from the fetus to the placenta, and a single umbilical vein which carries the oxygenated blood back to the fetus. It normally inserts towards the centre of the placenta, but may insert near the edge (battledore insertion) or even into the membranes (velamentous insertion) (Fig 2.11). This exposes the fetus to great risk if the path of the vessels lies across the cervical opening (vasa praevia) (Figs 10.3 and 2.12). The median length of the cord is 50 cm. True knots are present in approximately 0.75% of births (see Fig 33.8) but approximately 4% of stillbirths.

Source: Courtesy of Prof. Norman Beischer.

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Section 2 OBSTETRICS Section 2.1

Normal pregnancy

Section 2.2

Problems of early pregnancy

Section 2.3

Prenatal diagnosis

Section 2.4

Obstetric complications

Section 2.5

Medical and surgical disorders in pregnancy

Section 2.6

Common clinical scenarios and presenting problems in pregnancy

Section 2.7

Labour and birth

Section 2.7.1 Normal labour and birth Section 2.7.2 Induction of labour, instrumental delivery and casearean section Section 2.7.3 Intrapartum clinical problems Section 2.7.4 The puerperium and lactation Section 2.7.5 Global woman’s health and Indigenous women’s health

Section 2.1 NORMAL PREGNANCY Chapter 3

The prepregnancy consultation

Chapter 4

The first antenatal visit

Chapter 5

Antenatal care beyond the first antenatal visit

Chapter 6

Obesity and nutrition in pregnancy

Chapter 3  THE PREPREGNANCY CONSULTATION Michael Permezel

KEY POINTS The most important aspect of prepregnancy consultation is ensuring that it actually happens. This will be best achieved by measures that work towards avoiding unplanned pregnancies, seizing opportunities as women present for other reasons and educating women about the importance of the prepregnancy consultation. The first objective of a prepregnancy consultation is to ascertain any problems that may be relevant to a future pregnancy. Routine investigations should include an assessment of rubella immunity (if not already performed), varicella immunity (if uncertain) and a cervical smear (if due). If any issues are discovered, they should be thoroughly assessed (including investigations as needed), treatment optimised for pregnancy and the woman counselled with respect to what to expect in pregnancy. Of paramount importance in the advice to be given is the need for preconceptual folic acid. All women who may conceive should have measures in place to ensure that the developing embryo is not exposed to hazards such as alcohol, teratogenic drugs and radiation.

WHEN TO DO A PREPREGNANCY CONSULTATION? ‘Every woman every time.’ Each visit of a woman of reproductive age to a healthcare provider constitutes an opportunity for a prepregnancy consultation. This should be the case regardless of whether the visit is with a general practitioner or a specialist, and also whether for her or an accompanying child, so that each pregnancy is timed according to the woman’s choice and with appropriate periconceptual care as outlined in this chapter. The timetable of early embryogenesis means that critical development has already commenced before the menstrual period is missed and the woman has any idea she is pregnant. By the time of the usual occurrence of the first antenatal visit, many of the most important embryonic developments have taken place.

TIMING OF PREGNANCY The optimum timing of a pregnancy depends on a number of psychological, physical and social factors that will vary from couple to couple. If a pregnancy is not planned at this time, there is an obvious imperative of ensuring effective contraception is in place. Appropriate family planning advice is covered elsewhere in this book.

MATERNAL AGE CONSIDERATIONS IN THE TIMING OF PREGNANCY With advancing maternal age, there is a decline in fertility that can be detected on population studies as early as 32 years of age. This is initially of minimal consequence to most women but a more clinically relevant decline in fertility begins from about the age of 37 years, and then advances more rapidly after 40 years of age. Obstetric complications of advanced maternal age begin with the

Beischer & MacKay’s: Obstetrics, Gynaecology and the Newborn

increased risk of congenital anomalies and miscarriage and a long list of obstetric complications and procedures, including hypertensive disorders, gestational diabetes, placental insufficiency, uterine fibroids and caesarean section.

WHAT TO DO AT A PREPREGNANCY CONSULTATION There are three key tasks for the health practitioner to address when a pregnancy is planned: 1. screening to identify any issues that might impact on pregnancy 2. managing any clinical conditions found 3. giving general advice to all women planning a pregnancy.

SCREENING TO IDENTIFY ISSUES THAT MIGHT IMPACT ON PREGNANCY History and examination A full and detailed medical history will include age, presenting problem (e.g. how long they have already been trying to conceive), medical, surgical, obstetric, gynaecological, family, social, medications and allergy histories. Particular emphasis will be placed on information that could have relevance to early fetal disorders such as family history, environmental factors (e.g. chemicals or ionising radiation at work) and medications. A family history must also be obtained from the partner. The past obstetric history provides an opportunity to ‘debrief’ regarding concerns that might have surfaced since the last pregnancy. Anxieties about pain relief in labour, not getting to the hospital in time, previous obstetric complications and so on can often be alleviated quickly to the great relief of the woman and her partner. The clinical examination will follow the usual pattern beginning with general appearance, height, weight, vital signs, upper limb, head, neck, chest, abdomen and lower limb. Finally, any relevant neurological examination will be followed by a detailed gynaecological assessment. Gynaecological examination will begin with inspection of the external genitalia (e.g. previous female genital mutilation [FGM]), a speculum examination of the vagina and cervix and bimanual palpation of the uterus and adnexa. Particular note should be made of vaginismus in view of the implications for assessments during pregnancy and labour and the birth itself.

Investigations It is axiomatic in clinical medicine that investigations should only be undertaken if they are likely to impact on 30

clinical management. Sometimes extensive investigations are performed prior to pregnancy that have no clinical relevance until the woman is pregnant, and will likely be repeated then anyway. The following are the investigations that must be assessed as there are clinical consequences for the management of the woman prior to pregnancy.

Rubella and varicella immunisation status The obvious consequence of a rubella non-immune status is the need for vaccination prior to pregnancy. Failure to vaccinate prior to pregnancy will mean that the future embryo will be at risk of suffering the potentially devastating congenital rubella syndrome. Rubella vaccine cannot be administered during pregnancy because of perceived small risks from the vaccine itself. The same issues apply to varicella as to rubella but some will omit testing in the presence of a particularly definite clinical history of chickenpox.

Cervical smear Cervical screening should be performed according to recommendations. It is much preferred if cervical neoplasia is diagnosed prior to pregnancy so that treatment can be initiated in a timely manner. If high-grade cervical intraepithelial neoplasia is diagnosed in pregnancy, treatment will be deferred until the puerperium because of concerns that ablative treatment might cause excessive bleeding or precipitate a miscarriage.

MANAGING ANY CLINICAL CONDITIONS FOUND Clinical problems may require further assessment and optimisation of treatment. In rare cases, prognostic advice may lead to serious consideration with respect to whether a pregnancy should be undertaken at this time—or at all.

Diagnostic assessment Many conditions will require further assessment prior to a pregnancy. Some genetic testing of families may take weeks or months to define, especially if samples need to be sent overseas. Any planned imaging with plain X-rays or CT should be performed prepregnancy to minimise radiation exposure during early embryonic development. Prepregnancy diabetes will require knowledge of renal function including microalbumin excretion. A recent ophthalmologic assessment is also advisable.

Optimising treatment for pregnancy There are many medical conditions in which a change in treatment is recommended prior to embarking on a pregnancy. The following is not an all-inclusive list but contains examples that highlight some of the different reasons why therapy might be changed prior to pregnancy. Most anticonvulsant drugs are teratogenic and the need for these should be reviewed at a prepregnancy

Chapter 3  The Prepregnancy Consultation

consultation. In the presence of a prolonged seizurefree interval (say 2 years), consideration might be given to changing from polytherapy to monotherapy, a particularly teratogenic agent (e.g. valproate) to a less teratogenic anticonvulsant drug or even ceasing anticonvulsant medication altogether. In each case where there is a substantive change in therapy, a period of observation (say 6 months) is advised before embarking on a pregnancy. Some of the more common teratogenic medications include warfarin (usually switched to low-molecular-weight heparin for pregnancy) and ACE inhibitors (commonly replaced by antihypertensives with a long history of safety in pregnancy such as methyldopa or labetalol). Methotrexate should be ceased. Medication for asthma should generally be continued. There is good evidence that glucose control during early embryogenesis can limit the occurrence of congenital anomalies in the offspring of women with diabetes mellitus. Prepregnancy therapy should focus on optimum sugar control. This will usually mean switching to insulin if previously on an oral hypoglycaemic regimen. The insulin is commonly administered as a basal-bolus regimen or by continuous subcutaneous infusion for best control. Surgical conditions should, in general, also be managed preconceptually. Treatment of high-grade premalignant conditions of the cervix has already been mentioned but prepregnancy treatment is also advised for ovarian cysts that are unlikely to resolve spontaneously or for symptomatic gallstones. Apart from known contraceptives, not many drugs will actually reduce the likelihood of pregnancy, but sulfasalazine in the male is associated with low sperm counts.

Prognostic advice A few conditions are of such adverse prognosis in pregnancy that the woman must think very carefully if she wishes to proceed with a conception. Examples might include substantive renal impairment (successful pregnancy is very unusual with a serum creatinine of 300  µmol/L or higher and pregnancy probably accelerates progression to end-stage renal failure) and pulmonary hypertension where the maternal mortality approaches 50% in severe cases if the women elects to continue with the pregnancy. A woman with type 1 diabetes complicated by severe proliferative retinopathy and diabetic nephropathy and one healthy child may elect not to increase her family size further in the interests of maintaining her health, particularly eyesight and renal function, for as long as possible. Sometimes it may be a matter of deferring pregnancy pending correction of the underlying problem. The adverse obstetric consequences of morbid obesity are discussed elsewhere and there is an obvious necessity of prepregnancy weight loss, with or without surgical assistance.

GIVING GENERAL ADVICE TO ALL WOMEN PLANNING A PREGNANCY Preconceptual folic acid All women planning a pregnancy are advised to take preconceptual folic acid. The regimen is 0.5 mg daily with a dose of 5 mg recommended for women at risk, including those with a past or family history of neural tube defect, anticonvulsant drugs or with prepregnancy diabetes.

Getting pregnant While it might seem unnecessary to advise a couple on how to conceive, it is quite common for them to have significant misinformation regarding the likelihood of immediate conception and also the optimum timing and frequency of sexual intercourse. The median duration to conception is approximately 4 months and a couple should be also aware that only about 85% are pregnant after one year, with about half of the remainder conceiving in the second year. As far as the frequency of sexual intercourse is concerned, at least every second day leading up to ovulation is advisable to ensure there are spermatozoa present around the time of ovulation. While more frequent intercourse might lower the sperm count, it is most unlikely that this impacts adversely on conception rates. Certainly, having intercourse just once during the cycle on what is guessed to be the optimum day for conception is likely to have lower than normal pregnancy rates.

Smoking, alcohol and illicit drugs All women at risk of pregnancy should be aware of the risk posed to the early embryo by environmental toxins, even before she knows of the pregnancy. Many women would not be aware of the fetal risks of alcohol, and an important stage of fetal development would have passed if corrective action had not taken place before the onset of the next pregnancy. Although moderate alcohol consumption has not been shown to be embryotoxic, the wisest course of action is to for women planning a pregnancy to avoid alcohol altogether. While smoking is not teratogenic, there are increased risks of miscarriage and pregnancy complications including perinatal death. The motivation of an impending pregnancy is an ideal opportunity to tackle this addiction. Structured programs (e.g. ‘Quit’) aided by nicotine replacement are more likely to be successful than advice alone.

Pharmacological advice While it is sensible not to take any unnecessary medication in pregnancy, the woman should be advised that the simple analgesic, paracetamol, is considered safe in early pregnancy. She should make her doctor aware of a possible early pregnancy before she receives other prescribed medication. Diagnostic imaging with CT or X-rays (especially to the pelvic organs) should be strongly discouraged. 31

Chapter 4  THE FIRST ANTENATAL VISIT Michael Permezel

KEY POINTS The diagnosis of pregnancy is often clinical but a blood pregnancy test (serum β-hCG) is extremely accurate if there is any doubt. Gestational age is calculated from the first day of the last normal menstrual period. The most accurate assessment of gestational age will come from an ultrasound in early pregnancy, commonly at 12 weeks’ gestation. Screening for complications that may affect pregnancy should begin with a comprehensive history and examination. Investigations are extensive and include blood tests, imaging and a cervical smear (if due). Any conditions found need to be further assessed (including any additional investigations). Treatment of such conditions needs to be optimised for pregnancy and the woman should be counselled with respect to what to expect in pregnancy. Every pregnant woman requires detailed advice and discussion in early pregnancy. Topics that must be covered include diet, exercise, dietary supplements, medication use, smoking, alcohol, illicit drugs, sexual intercourse and occupational advice. A plan needs to be made for management of the pregnancy and, in particular, a discussion regarding available models of care and places of birth and the appropriateness of these to individual circumstances.

INTRODUCTION The first antenatal visit is a unique opportunity to establish a relationship between the primary carer and the pregnant woman. A motivated patient and a carer receptive to her needs constitute an important relationship over the months ahead. All too often the woman will present with preconceived ideas from friends who have either decided to alarm her with horror stories or, alternatively, mischievously encouraged the woman to adopt a minimalist care approach with the misguided notion that maternity care somehow causes most problems, when in fact the consequences of lacking such care are apparent, not only in the

developing world, but also in the more deprived or more ill-informed sectors of our own society.

DIAGNOSING PREGNANCY As with any medical diagnosis, pregnancy is diagnosed on history, examination and, where necessary, investigations. Common symptoms of early pregnancy include nausea, breast tenderness, nipple soreness and urinary frequency. Most notable is the first missed period— occurring approximately 2 weeks after fertilisation but most often 4 weeks from the first day of the last normal menstrual period.

Chapter 4  The First Antenatal Visit

Clinical examination is mostly unhelpful in the diagnosis of early pregnancy. Some softening of the cervical isthmus (Hegar’s sign) is detectable at 6 weeks’ but obvious uterine enlargement on bimanual palpation is probably not easily discerned until 8 weeks’ gestation. The uterus does not become palpable abdominally in most women until 12 weeks’ gestation, or even later if the uterus is deeply retroverted. Pregnancy tests rely on the detection of the placental hormone hCG which is produced uniquely by the trophoblast.

URINARY PREGNANCY TESTS (UCG) The urinary test may rarely have false positives and false negatives owing to some cross-reactivity with luteinising hormone (LH). Although mostly reliable, the consequences of telling a woman that she is not pregnant when in fact she is—and the reverse—are too serious to allow even rare mistakes.

SERUM β-hCG The blood pregnancy test is considerably more reliable than the UCG. Positive means pregnant, negative means not. Rare exceptions include trophoblast tumours producing hCG. A positive test may, of course, also occur as a result of a failed pregnancy, either within the endometrial cavity or in another ectopic location.

ASSESSMENT OF THE GESTATIONAL AGE—DATING THE PREGNANCY The importance of accurate dating cannot be overestimated, as without it there is a potential for misinterpreted tests and misguided scheduling of an induction of labour or elective caesarean section. The best opportunity for accurate dating will be in the first trimester when menstrual dates are more readily recalled and ultrasound is most accurate in defining gestational age.

FROM WHEN IS A PREGNANCY DATED? A pregnancy is dated from the first day of the last normal menstrual period, approximately 2 weeks before conception takes place. This oddity can be difficult to accept, both for patients and for new carers. A brief explanation that the dating is from when the unfertilised ovum first became responsive to maternal gonadotrophin may help reconcile this longstanding tradition of describing the gestational age of every human pregnancy as 2 weeks longer than it actually is. The most likely date of onset of spontaneous labour is approximately 266 days from ovulation or 280 days from the first day of the last normal menstrual period

(LNMP) if the cycle is regular and of 28 days’ duration. As stated earlier, this date is all-important for management of the pregnancy but unfortunately suffers from inconsistency of nomenclature. It can be variously termed expected date of confinement (EDC), expected date of delivery (EDD) or expected date of birth (EDB). EDD will be used in this book as EDB is used in some centres as an abbreviation for epidural block.

NAEGELE’S RULE The EDD can be calculated from the first day of the LNMP by adding 7 days and 9 months (Naegele’s rule). If the cycle is longer or shorter than 28 days, the EDD should be correspondingly adjusted as the duration of the luteal phase tends to be constant at about 14 days and a longer or shorter cycle will mean a correspondingly longer or shorter follicular phase—and therefore pregnancy. The LNMP cannot be relied on to calculate the EDD if the cycle is irregular or if the last period was that immediately following cessation of the combined oral contraceptive pill (OCP) as ovulation occurs a variable time after ceasing the combined OCP.

ULTRASOUND IN THE ASSESSMENT OF GESTATIONAL AGE Studies repeatedly show that an early ultrasound is more accurate than the LNMP in determining the EDD. Where an ultrasound has been performed before 13 weeks’ gestation, the EDD from that ultrasound would generally be used to determine the EDD. The gestational sac size can be measured early but as soon as a fetal pole is visible, the length of the embryo (crown–rump length [CRL]) gives the most accurate estimate of gestational age. CRL will guide the EDD from approximately 6 weeks’ gestation through to 12 weeks’ gestation and estimates should be within 3 days of the actual EDD. Beyond 12 weeks’, flexion and extension of the embryo mean that the CRL ceases to be of value and the breadth of the fetal head (biparietal diameter [BPD]) is used thereafter to determine the EDD. Prior to 20 weeks’, this should be within 7 days of the true EDD but with advancing gestations beyond 20 weeks’, the BPD becomes progressively less accurate such that it becomes only a very approximate guide in the third trimester of pregnancy.

OTHER MEANS OF DETERMINING THE GESTATIONAL AGE A woman may be very certain regarding the date on which conception occurred. This can be useful where an early ultrasound is not available and the woman is unsure of her menstrual dates. Similarly, where the pregnancy occurred through assisted conception (e.g. in-vitro fertilisation [IVF]), there can be considerable confidence establishing the EDD from the date of embryo transfer. 33

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SCREENING TO IDENTIFY ISSUES THAT MIGHT IMPACT ON THE PREGNANCY HISTORY A complete medical history is required as previously outlined in Chapter 3. Aspects include age, symptoms of pregnancy, medical and surgical history, obstetric and gynaecological history, medications and drug allergies, family history and social history. The latter must include information about smoking, alcohol and illicit drugs, as well as marital status, social supports and occupation. Gynaecological history should include reference to those conditions that might impact on pregnancy such as previous uterine or cervical surgery or genital herpes simplex infection.

EXAMINATION The clinical examination will follow the usual pattern beginning with general appearance, height, weight, vital signs, upper limb, head, neck, chest, abdomen and lower limb. Breast examination is important, as examination for breast lumps becomes increasingly difficult as gestation advances and breast cancer can progress rapidly in pregnancy, so early diagnosis is essential. Finally, any relevant neurological examination will be followed by a detailed gynaecological assessment. Gynaecological examination begins with inspection of the external genitalia (e.g. previous FGM) followed by bimanual palpation of the uterus and adnexa. A speculum examination of the vagina and cervix is performed if a Pap smear

or cervical swabs are indicated. Particular note should be made of vaginismus in view of the implications for assessments during pregnancy, labour and the birth itself.

INVESTIGATIONS—STANDARD RECOMMENDATIONS There are a large number of investigations that are needed in pregnancy because of therapeutic initiatives that will follow an abnormal test. A summary of these tests is provided in Table 4.1, with explanations of the terms used in the text that follows.

FULL BLOOD EXAMINATION (FBE OR FBC) This is necessary to exclude anaemia and acts as a screening test for thalassaemia and thrombocytopenia. Immune thrombocytopenia is one of the most common autoimmune conditions (see Ch 22). Screening for thalassaemia through a low mean corpuscular volume (MCV) is also important given the risk of thalassaemia major in the fetus should the father of the fetus also be a carrier.

BLOOD GROUP AND ANTIBODY SCREEN The blood group will detect the 15% of Caucasian women who are D-negative and require further screening during pregnancy (usually at 28 weeks’ and birth) and also prophylaxis with passive anti-D at prescribed times/events during pregnancy to minimise the risk of immunisation.

TABLE 4.1  INVESTIGATIONS COMMONLY RECOMMENDED AS ROUTINE IN EARLY PREGNANCY. Investigation

Rationale for performing the investigation

FBE (Hb, platelets, MCV)

Anaemia, thalassaemia

Blood group, antibody screen

Diagnose and prevent red cell isoimmunisation

Rubella antibodies, varicella antibodies (if uncertain of history), syphilis serology, Hep B, Hep C, HIV

Treat infection in current pregnancy (syphilis), take steps to reduce vertical transmission (Hep B, Hep C, HIV), vaccinate mother in puerperium (rubella, varicella), warn woman to present for zoster immune globulin if not immune and contact with varicella

MSU mcs

Diagnose and treat asymptomatic bacteriuria (6%)

Pap smear

Assess and monitor (treat in puerperium)

Serum screen for fetal aneuploidy

Screen for fetal anueploidy

12-week scans

Screen for fetal anueploidy (nuchal translucency), diagnose structural anomaly, identify multiple pregnancy

19-week scans

Diagnose structural anomaly, placenta localisation

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Chapter 4  The First Antenatal Visit

It is equally important that all women have an antibody screen at the first antenatal visit. Even women who are D positive may have antibodies against a variety of other red cell antigens such as c, E, K, Fya (see Ch 22).

MICROBIOLOGICAL SEROLOGY Rubella antibodies The obvious consequence of a rubella non-immune status is the need for vaccination early in the puerperium. A seronegative woman should avoid contact with unwell children in the first trimester and be re-screened for seroconversion if there is any possibility of rubella infection in early pregnancy.

Varicella antibodies The same issues apply to varicella as to rubella but some will omit testing in the presence of a particularly definite clinical history of ‘chickenpox’. A woman who is not immune to varicella should also be advised to present for prophylactic zoster immune globulin (ZIG) if she has contact with varicella (either chicken pox or shingles).

Syphilis Treponemal antibody tests are now commonly performed and are very specific. A reagin test such as the venereal disease research laboratory (VDRL) test or rapid plasma reagin (RPR) test may have false positives, including from the antiphospholipid syndrome. Therefore, the patient should be followed up even if a subsequent treponemal antibody test is reassuring.

Hepatitis B, Hepatitis C and HIV RANZCOG recommend screening for each of hepatitis B, hepatitis C and HIV. Despite a low prevalence, important therapeutic initiatives are indicated if the virus is present in order to minimise the risk of vertical transmission. Astonishingly, some other guideline writers do not mandate a recommendation for hepatitis C screening, even though it is by no means rare in the general population and all would take care to minimise invasive testing (e.g. fetal scalp electrode, fetal blood sampling) where the mother is a hepatitis C carrier.

MIDSTREAM URINE FOR MICROSCOPY, CULTURE AND SENSITIVITIES (MSU MCS) Approximately 6% of women will have asymptomatic bacteriuria at the first antenatal visit. Of these, up to onethird will go on and develop pyelonephritis if the bacteriuria is untreated.

CERVICAL SCREENING Cervical screening should be performed according to screening recommendation (listed in Chapter 61). Once the woman is pregnant, treatment of a high-grade cervical

intraepithelial neoplasia will be deferred until the puerperium because of concerns with respect to treatment causing excessive bleeding or precipitating a miscarriage.

SCREENING FOR DOWN SYNDROME See Chapter 9.

INVESTIGATIONS—ADDITIONAL THAT MAY BE CONSIDERED There are other investigations that may be considered in early pregnancy but at the time of writing this chapter they are not part of the routine recommendations of RANZCOG. These are summarised below.

HB ELECTROPHORESIS Hb E and Hb C will commonly not have a low MCV but can produce a transfusion-dependent anaemia if the partner has β-thalassaemia trait. Similarly, sickle cell anaemia needs to be excluded in women of relevant ethnicity.

SERUM FERRITIN Serum ferritin is indicated if there is an increased likelihood of iron deficiency (e.g. vegetarian). In centres of high prevalence of iron deficiency, serum ferritin may be routine in early pregnancy.

CHLAMYDIA SCREENING A cervical swab for chlamydia may be recommended to at-risk women, and is routine in some units for women under the age of 25 years.

VITAMIN D Vitamin D is obligated in those with dark skin and/or reduced sunlight exposure during pregnancy. The significance of low vitamin D for the offspring is awaiting further research, but supplementation is recommended if vitamin D is < 50 nmol/L and some will treat even in the range 50 to 75 nmol/L.

THYROID FUNCTION There is increasing evidence that subclinical hypothyroidism may have consequences for a pregnancy. While a large trial has now established that screening for hypothyroidism is unlikely to have substantive neurocognitive benefits in the offspring, there are still many clinicians who support screening for hypothyroidism in early pregnancy.1 This is to pick up the very small number of cases of severe hypothyroidism and also because there remains some evidence of a possible benefit for the index pregnancy—even if the level of thyroid-stimulating hormone (TSH) is in the subclinical range (i.e. 2.5 to 5.0 mIU/L). 35

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MANAGEMENT OF ANY CLINICAL CONDITIONS FOUND Clinical problems may require further assessment and optimisation of treatment. In rare cases, a very prognostic outlook may lead to a woman to question whether she should continue the pregnancy. Specific management of medical conditions at the first antenatal visit is discussed in the relevant chapters (10 to 27) detailing obstetric, medical and surgical disorders of pregnancy.

FURTHER ASSESSMENT, OPTIMISING TREATMENT AND PROGNOSTIC OUTLOOK Many conditions will need further evaluation, beginning with a detailed, directed clinical assessment (history and examination) and proceeding to relevant investigations. Obviously it is desirable to minimise exposure of a developing fetus to ionising radiation. There are many conditions in which a change in treatment is recommended in a pregnancy. Some of these are discussed in Chapter 3 and also in the chapters devoted to the relevant complications. Only rarely will the outlook be such that the parents give consideration to not proceeding with the pregnancy. If such a decision looks possible, on either maternal or fetal grounds, it is strongly preferred to provide the couple with the necessary detailed information and counselling at an early stage in pregnancy, requiring a degree of urgency from the healthcare providers.

GENERAL ADVICE All women need to be actively informed regarding important health choices that will impact on her pregnancy. The onus is on the health professional at the first ante­ natal visit to cover all the important areas of discussion. That discussion should be tailored to the patient’s needs and considered in the context of her background and a priori knowledge. She should be encouraged to purchase one of the better books that inform and educate around pregnancy and childbirth. At the same time, she should be warned of the hazards of taking too much notice of malicious friends or ramblings on the internet and to seek an early consultation if such has raised extreme levels of anxiety.

NUTRITION Listeria Listerial sepsis is covered elsewhere but may result in a septic miscarriage or lethal chorioamnionitis. Women should be appraised of the most likely sources of food poisoning. The avoidance of soft cheeses is applicable where such is made from unpasteurised milk. Also to be avoided are soft-serve ice-cream, raw fish (e.g. sushi, 36

smoked salmon, oysters), cold meats, salad bars and paté. More important for most women is proper food preparation and handling. Completely thaw before cooking and ensure all meat is cooked thoroughly—most importantly poultry. Take particular care with pre-prepared foods and those made with mayonnaise or crustaceans.

Healthy diet, particularly avoiding nutritional excess The epidemic of our time is obesity. Again, pregnancy is a time where the woman is attending her health practitioner on a regular basis and with added motivation. Reinforcing good dietary habits is an extremely important measure in preventative healthcare. There is good evidence that regular weighing of women at each ante­ natal visit will reduce the incidence of excessive weight gain in overweight patients.

Iron, iodine and calcium Most vegetarians are iron deficient although not necessarily so. Pregnant women who are not vegetarians should be encouraged to eat red meat. Vegetarians should be checked for iron deficiency (serum ferritin) and supplemented with oral iron if ferritin is low. Iodine deficiency is common in non-coastal areas. Salt should be used sparingly but of the iodised variety. Dairy products are a rich source of protein and calcium. Those women who are unable to take dairy may be advised to supplement with calcium tablets.

Multivitamin supplementation It is now common for pregnant women to be taking a proprietary multivitamin preparation suitable for pregnancy. There is clear evidence for periconceptual folic acid supplementation for the prevention of neural defects but the evidence for multivitamin use throughout pregnancy is more circumstantial. Many believe that over the last 50 or so years there has been a marked and progressive decrease in some adverse pregnancy outcomes including severe placental abruption and possibly severe preeclampsia. It has been suggested that better nutrition may be an explanation. A causative rationale has emerged in the form of homocysteine, which is a potential activator of endothelial cells. The levels of homocysteine are increased by mutations of the enzyme methyl tetra hydrofolate reductase but reduced by three key vitamins: folate and vitamins B6 and B12.

EXERCISE A light to moderate level of exercise is generally recommended in pregnancy. This may include continuing exercise programs at the gym or sporting club that preceded pregnancy. Strenuous exertion should probably be avoided as it has been linked to smaller birth weights. The health implications of this are uncertain but it could have adverse consequences in either the short or long term (see Ch 11). Intuitively, maternal hypoxia during exertion

Chapter 4  The First Antenatal Visit

may be detrimental to placental gas exchange and a good working rule is to exercise at a level at which conversation can still be continued.

ALCOHOL, SMOKING AND ILLICIT DRUGS Alcohol The wisest course of action is to avoid alcohol altogether in pregnancy. While the impact of a single episode of alcohol excess is likely to be small, there is no doubt that an alcohol intake of more than two standard drinks per day is associated with significant teratogenesis—fetal alcohol syndrome.

Smoking Smoking is definitely associated with increased risks of miscarriage and perinatal death. All smoking mothers and/or any smoking partners should be offered strategies to assist with complete smoking cessation. This is an example of using the added motivation of pregnancy and protecting the unborn child to achieve an extremely important health outcome for all the family.

Illicit drugs Cannabis, narcotics, cocaine, amphetamines and other illicit drugs all must be strongly discouraged in pregnancy. Each has its specific problems but notably cocaine use may be associated with the long-term consequences of preterm birth, placental insufficiency and placental abruption. Opioids may cause neonatal abstinence syndrome in which the unborn fetus is conditioned to the presence of the narcotic and has a withdrawal reaction in the early neonatal period with irritability, poor feeding and possibly seizures.

MEDICATIONS Women should be appraised of common medications that are almost certainly safe to administer in pregnancy, in their usual doses and in the absence of allergy. Examples would include paracetamol, metoclopramide (for early pregnancy nausea and vomiting) and commonly used penicillins (e.g. amoxycillin). Common asthma medication (e.g. salbutamol and/or corticosteroid inhalers) can and should continue. Mental health medication (see Ch 25) can usually be continued, weighing an uncertain but possible very low risk of fetal sequelae against a known maternal benefit. Some mental health medications (e.g. sodium valproate, lithium) are classified as category D (expected to be harmful to the fetus) yet may still be used in pregnancy occasionally where the benefit outweighs the risks. Constipation is a common pregnancy complication. All maternity healthcare providers should be able to advise on foods that are high in fibre, but women should also be informed that common laxatives are safe in pregnancy. The patient should be aware that all other

medication requires consultation, making sure that the administering doctor is aware that she is pregnant.

SEXUAL INTERCOURSE After such a long list of ‘don’ts’, the patient is often somewhat relieved to hear that there is no evidence to suggest that sexual intercourse is harmful in pregnancy. There is no evidence that preterm birth is increased by sexual activity, but pregnancy duration at term is, on average, a few days shorter in the sexually active woman. Sexual intercourse will generally be avoided within a week of any bleeding in pregnancy and certainly prohibited after rupture of the gestational membranes.

EMPLOYMENT Most women find they are physically fatigued in late pregnancy and a majority will choose to go on maternity leave from about 34 weeks’. However, a small proportion of women elect to work up until the day of the birth. There is evidence that physical work can both raise the blood pressure and increase the risk of preterm birth. If either of these issues are relevant in a particular pregnancy, then employment should probably be ceased.

TRAVEL Travel is seldom a problem in pregnancy until the last months. Long-duration air travel will predispose the patient to an increased risk of venous thromboembolism. Also, any event occurring during a long flight (e.g. antepartum haemorrhage, preterm labour) creates a serious situation in a location that can be many hours remote from any substantive medical care. A working rule might be that flights longer than a couple of hours are undesirable in anyone who is at increased risk of pregnancy complications and probably should be avoided in everyone after about 28 weeks’. Airlines may have various policies in this respect. Consideration should also be given with respect to areas of endemic infectious disease such as malaria or toxoplasmosis. The pregnant woman should carry a summary of relevant sections of her medical record and antenatal progress.

VACCINATIONS Influenza vaccine is safe and particularly important to administer in pregnancy. In general, live vaccines (e.g. rubella, varicella) are contraindicated but killed vaccines are relatively safe (e.g. influenza).

INFECTIONS CMV and toxoplasmosis can both be reduced by sensible handwashing before food preparation and after exposure to risk-prone events such as gardening (toxoplasmosis) or children at childcare (cytomegalovirus). 37

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BOOKING At the end of each first antenatal visit, an initial plan for the pregnancy should be made. Not a plan that cannot be changed, but a plan that sets the initial direction for care.

WHO? The first decision is with respect to the model of care. Who will be looking after the woman and her unborn baby, both during pregnancy and in labour? Nearly always this decision will mean some assessment of complexity and a search for specific complications as described previously. There are just about as many models of care as there are hospitals delivering maternity care, but the following is an overview of the types of care models and which women might be best suited to each.

The maternal fetal medicine (MFM) subspecialist These practitioners are highly skilled in the management of complex pregnancies and have additional training in obstetric ultrasound relative to most specialist obstetricians. While management of very complex pregnancies mostly lies with the specialist obstetrician, some conditions particularly benefit from the additional expertise of the subspecialist. Examples of cases commonly referred to the MFM might be intrauterine transfusion of the anaemic fetus or performing laser surgery of the connecting vessels in twin–twin transfusion syndrome. In most of the larger centres, the MFMs will have a prominent role. However, specialist obstetricians in medium-sized maternity hospitals will manage most of the complex cases themselves, referring only rare cases to an MFM and mostly even then only for advice rather than transferring patient care.

Specialist obstetrician All specialist obstetricians are skilled in the management of complex pregnancies as well as those without identified problems. They may do so within the public or private sector, often in partnership with registrars training to become specialists and always in collaboration with the hospital midwives.

preventative health precedents for the ongoing health of the woman and her family.

Midwife or training obstetrician care Women without additional complexity will commonly be offered care with a midwife or an obstetric resident in training.

Multidisciplinary care Some conditions require input from other specialists. A complex heart disease patient will need to be seen jointly by a specialist obstetrician, an obstetric anaesthetist and a cardiologist. In fact, input for almost every significant medical condition will usually benefit from health communication between the medical specialist and the obstetrician. Where patient numbers can justify it, the establishment of specialised multidisciplinary clinics allows healthy collaboration between different professional groups in the interests of patient care. This is perhaps exemplified by the pregnancy diabetes clinics where the obstetrician, endocrinologist, diabetic educator and sometimes an ophthalmologist or a paediatrician work jointly to achieve the best possible outcomes. Similarly, major disorders of mental health are best managed with a collaboration of treating psychiatrists, obstetricians and midwives.

WHAT PLACE OF BIRTH? Options regarding place of birth should be discussed, allowing an appropriate booking to be made. The major options will be a hospital maternity unit, an ‘alternative’ hospital-based birth centre that may be within a wellequipped hospital or free-standing, the latter without on-site access to operating theatres should unexpected complications develop (e.g. postpartum haemorrhage, acute fetal compromise). In Australia less than 1% of women choose to have a planned home birth. Even with formal arrangements for hospital back-up, most obstetricians believe that, although most home births will result in a favourable outcome, home birth has an unacceptably high risk exposure for both mother and child.

Shared care with a general practitioner obstetrician

REFERENCE 1) Lazarus JH, Bestwick JP, Channon S, et al. Antenatal thyroid screening and childhood cognitive function. N Engl J Med 2012;366(6):493–501.

The shared care general practitioner (GP) often has the great advantage of knowing the woman prior to pregnancy and the ability to meet many of her general health needs and those of her family. Importantly, the GP can enhance the doctor–patient relationship through the repeated visits of antenatal care. At such a time, most women will be more motivated than usual to take advice on important general health issues. These will not only benefit her unborn child but hopefully also will establish

FURTHER READING Joss-Moore LA, Lane RH. The developmental origins of adult disease. Curr Opin Pediatr 2009;21(2):230–4. Wax JR, Lucas FL, Lamont M, et al. Maternal and newborn outcomes in planned home birth vs planned hospital births: a meta-analysis. Am J Obstet Gynecol 2010;203(3):243.e1–8.

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Chapter 5  ANTENATAL CARE BEYOND THE FIRST ANTENATAL VISIT Michael Permezel

KEY POINTS The antenatal period serves as an opportunity for a spectrum of health promotion activities with repeated visits to a health professional at a time when most women are strongly motivated to provide a health environment for the developing baby. Pregnancy complications can be diagnosed early and management instituted. Placental insufficiency and preeclampsia deservedly receive particular focus. Each visit should include a brief history with specific inquiry regarding general wellbeing and fetal movements in pregnancies beyond 20 weeks’ gestation. Physical examination requires a standardised method of blood pressure measurement and fundal height determination as these will be important to compare from week to week, even if the examiner differs. Routine investigations in all women in the latter half of pregnancy include a full blood examination and test of glucose tolerance at 28 weeks’ and a vaginal swab for Group B streptococcus (GBS) at 36 weeks’. Women who are Rh-negative will additionally have their anti-D antibody level assessed at 28 weeks’ and injections of prophylactic anti-D at 28 and 34 weeks’, providing they have not developed endogenous anti-D production.

THE OBJECTIVES OF ANTENATAL CARE There are three key objectives of the routine antenatal visits.

HEALTH PROMOTION AND PREVENTATIVE MEDICINE Pregnancy offers a unique opportunity for health education that has the opportunity to impact not only on the pregnancy, but also the woman herself, her current and future children and her partner. The pregnancy provides very clear motivation. Repeated antenatal visits with a trusted and knowledgeable antenatal care provider

further increases the likelihood that advice will be followed. Issues can be raised, questioned, discussed and then revisited on repeated occasions throughout the pregnancy. Among those matters that may impact on both the pregnancy and future health of her family include dietary behaviours, exercise, weight control, smoking, alcohol and illicit drugs. Medical subjects such as the importance of immunisation and cervical smears can also be raised. Where conditions such as gestational diabetes, hypertension or mental health issues develop in pregnancy, these can be used to further educate in health areas that are likely to be of particular importance to that woman in the future. To not use the antenatal visits for health promotion is to waste one of the great opportunities to impact on the health of the population as a whole.

Beischer & MacKay’s: Obstetrics, Gynaecology and the Newborn

EARLY DIAGNOSIS AND MANAGEMENT OF PREGNANCY COMPLICATIONS Prior to 20 weeks’ but beyond the first antenatal visit, the emphasis is generally on early fetal wellbeing, particularly establishing the genetic and morphological health of the fetus. The approach to this is discussed in other chapters but largely will involve chasing up the results of tests organised at the first antenatal visit and also making sure that the patient attends for a morphology scan (typically organised for approximately 20 weeks’). Beyond 20 weeks’ (and assuming normal morphology), the focus of an otherwise uncomplicated pregnancy shifts towards early diagnosis of the two dominant conditions of late pregnancy: placental insufficiency and preeclampsia. Of course, a myriad of medical and obstetric complications are possible, but very specific attention is directed to both fetal wellbeing and the features of preeclampsia.

MATERNAL SUPPORT AND PREPARATION FOR BIRTH All women will have questions about labour and birth that need to be addressed during the antenatal period. Although information can be obtained from books, videos and antenatal classes, most women find it particularly reassuring to receive pertinent information from the antenatal clinic provider, particularly if that same person is to be also caring for her around the time of labour and birth.

ANTENATAL VISITS BEYOND THE FIRST ONE FREQUENCY OF VISITS There are various regimens recommended for antenatal visit frequency, balancing the costs to the woman and the community of excessive visit frequency against the possible delayed diagnosis of complications and other less tangible benefits of antenatal care, including maternal support and education.

THE TYPICAL ROUTINE ANTENATAL VISIT IN AN UNCOMPLICATED PREGNANCY History

providers should be confident in listening to and advising on management of the common symptoms of pregnancy, including headaches, heartburn, lower abdominal discomfort or round ligament pain, constipation, haemorrhoids, varicose veins (vulval as well as lower limbs), carpal tunnel syndrome oedema, muscle cramps, fainting or light-headedness and general fatigue.

Fetal movements Fetal movements are not commonly felt until approximately 17 weeks’ in a multigravida and 19 weeks’ if it is the first baby. The gestation tends to be later if the placenta is anterior. Where a woman still is not feeling movements beyond 20 weeks’, she may benefit from more frequent antenatal visits as a means of reassurance. Most women will soon perceive fetal movements if advised on what they should be expecting to feel and dedicate some time to concentrate on it. In the third trimester of pregnancy, maternal perception of fetal movements becomes an extremely important parameter in the assessment of fetal wellbeing. Most cases of stillbirth are preceded by many hours or days of no fetal movements. Every provider of antenatal care has an obligation to both inquire of fetal movements at each visit and provide the patient with some clear instruction as to what to expect in terms of fetal movements and what to do if that expectation is not met. Unfortunately, there is no uniform instruction as to how women should check fetal movements. One of three approaches is commonly used but ‘no specific instructions’ is not an option. 1. Check with meals: ‘Check that the baby moves a couple of times with each meal or in the half an hour or so thereafter. If it does, don’t worry until the next meal. If it doesn’t, have a cold, sweet drink and if still not, contact the hospital.’ 2. Count to 10: ‘Count each day until you have 10 movements. If you don’t have 10 movements by 6 pm at night or it is much later than usual, contact the hospital.’ 3. Usual pattern: ‘Get used to the pattern of your baby’s movements and contact the hospital if the baby is much quieter than usual.’ There has not been any significant comparative trial to establish which approach is most effective and because of the low incidence of adverse outcome, a randomised controlled trial is unfeasible. More onerous (e.g. ‘count to 10’) may have the least compliance, whereas less onerous (e.g. ‘usual pattern’ may be less sensitive) and a middle course (e.g. ‘check with meals’) may be best for a majority of women.

General wellbeing and symptomatology

Examination

As a first step, there should be a general inquiry regarding maternal wellbeing. There are many common symptoms that may be very important to the woman, even if of relatively minor medical significance. All antenatal care

After many years of largely ignoring maternal weight during pregnancy, the current obesity epidemic has led to some rethinking in this respect. Good research

40

Maternal weight

Chapter 5  Antenatal Care Beyond the First Antenatal Visit

indicates that self-monitoring maternal weight reduces the incidence of excessive weight gain in overweight and obese women. Although an issue that needs to be handled sensitively, it can be used to focus attention during pregnancy on sensible diet and exercise—extremely important aspects of health promotion for the woman and her family.

Blood pressure Particular care is taken with the accurate recording of blood pressure. This should be taken in standardised fashion with the patient seated, using the right arm at the level of the heart. Diastolic blood pressure (BP) is taken as sound disappearance (Korotkoff phase V) rather than muffling (phase IV).

Abdominal examination The woman should lie comfortably in the supine position, with the arms by the sides and the head well supported by a pillow. The bladder should be empty. The drapes are arranged to give access to the whole abdomen. Because of the occurrence of the supine hypotensive syndrome in some women, particularly in late pregnancy, the mother should be warned to lie on her side if she feels faint. Inspection The normal uterine contour is oval or pear-shaped; this is obliterated if there is an abnormal amount of intrauterine contents (multiple pregnancy and/or polyhydramnios). If the fetus is lying transversely, the fundus will be lower than expected and the transverse diameter will be widened. In the last 4 to 6 weeks, umbilical eversion is common and an umbilical hernia is noted for the first time in 1 to 2% of women. A pigmented line in the midline is common and termed the linea nigra. Palpation The four classical techniques of palpation are sometimes termed Leopold’s manoeuvres or grips (the latter term not accurately describing the procedure adopted). 1. Fundal palpation. The fundal height is estimated by placing the thenar surface of the left index finger at the highest point of the uterus and comparing this with accepted levels for different periods of gestation. This is the same palpation technique as used for a liver or spleen but with the left hand angling down instead of the right hand angling up. Before 20 weeks’, measuring the fundal height is not particularly useful as there is considerable variation from woman to woman. In general, the uterus will commonly be first palpable abdominally at approximately 14 weeks’ and reach the umbilicus at about 20 weeks’. Beyond 20 weeks’, the fundal height should be measured in centimetres from the top of the fundus down to the symphysis pubis and this measurement serendipitously approximates to the gestation in weeks. Because of descent of the head into the pelvis

in late pregnancy, the fundal height may not increase or even decrease as the head descends into the pelvis. Boxes 5.1 and 5.2 list the main reasons for the measured fundal height being greater or less than that expected for the gestational age. 2. Lateral palpation. This is used to ascertain the position of the back in those cases where the lie is longitudinal. The examiner remains in the same position, but the hands are moved down to the level of the umbilicus. With gentle pressure, supplemented with dipping movements, the resistance of the back is sought and its distance from the midline noted. This procedure is made easier if alternate hands are used to steady the trunk and push it towards the opposite examining hand. The fetal limbs will be on the side opposite the back; they are best felt by gliding the hands over the surface of the abdomen, seeking the mobile irregularities by which the limbs are characterised. If the lie is transverse, the characteristic features of the head and breech will be felt in each flank. 3. Pawlik’s grip. Here, the right hand only is used. The fingers are well spread and are placed in the suprapubic skinfold which runs out to each iliac fossa (Fig 5.1). With both this and the next palpation, gentleness must be exercised since the lower segment is more sensitive than the upper segment. Information is mainly derived from the thumb and middle finger, which move in a coordinated scanning fashion to

BOX 5.1  Causes of fundus greater than dates.

Wrong dates Maternal obesity Multiple pregnancy Large fetus Polyhydramnios Ovarian cyst Fibromyoma Hydatidiform mole

BOX 5.2  Causes of fundus less than dates. Wrong dates Small, growth-restricted fetus Oligohydramnios ✚ Placental insufficiency ✚ Rupture of the membranes ✚ Fetal renal insufficiency Transverse lie 41

Beischer & MacKay’s: Obstetrics, Gynaecology and the Newborn

hospitals but a common notation is 5/5, 4/5, 3/5, 2/5, 1/5 or 0/5 corresponding to 10, 8, 6 4, 2 or 0 cm of head being palpable above the pelvic brim. Auscultation The fetal heart becomes audible with the clinical Doppler instrument at about 12 weeks’ gestation. The point of maximal intensity is over the area of abdomen which is related to the left chest wall of the fetus, but is often only determined by trial and error. Generally, the site depends on the period of gestation and the presentation and position of the fetus. For example, in the second trimester, the fetal heart is usually heard best in the midline below the umbilicus; in breech presentations, it is located above (rather than below) the umbilicus; and in posterior positions, it is best heard well out in the flank, unless there is a significant deflexion. Although it is reassuring for the mother and clinician to hear a heartbeat, the greatest clinical importance of routine auscultation may lie in the rare detection of a fetal arrhythmia. Ectopic beats are not uncommon and mostly present no problem to the fetus. Significant bradycardias (e.g. heart block) or tachycardias (e.g. paroxysmal supraventricular tachycardia) may be treatable causes of fetal hydrops and require urgent assessment in a unit experienced in this highly specialised area of fetal medicine.

Urinalysis—proteinuria and glycosuria FIGURE 5.1 

The Pawlik method of palpation identifies the presenting part of the fetus and its station. Source: Courtesy of Prof. Norman Beischer.

determine which pole is presenting (breech or cephalic) and also whether it is mobile above the pelvic brim or fixed within the pelvis. Usually, Pawlik’s method is modified to a combined palpation, where the left hand is placed on the fundus in a mirror image of the right hand. A simultaneous comparison is thus available between what is felt in the upper and lower poles, and the examiner is more likely to be correct as to the presentation. 4. Deep pelvic grip. In this palpation, the examiner turns and faces the woman’s feet. The hands are placed over the sides of the lower uterus in the depression which lies medial to the anterior superior iliac spine and above the inguinal ligaments (Fig 5.2). Initially, the outline and nature of the presenting part is determined. The deep pelvic grip is particularly useful when the head is ‘fixed’ in order to determine how much of the head has entered the pelvis. The station (amount of descent) is determined from the amount of the presenting part (usually the head) which is out of the pelvis. Different notations are in use in different 42

There is a long tradition of testing for protein and glucose at each antenatal visit. With routine glucose tolerance testing as recommended overleaf, the added yield from urine testing of glucose is particularly low. Nevertheless, persistent glycosuria merits an early glucose tolerance test but most will be due to a lowered threshold for renal glycosuria in pregnancy. That is, even with normal blood glucose, sugar may appear in the urine in pregnancy. In contrast, urinalysis for protein at each antenatal visit is an important component of the antenatal visit. Although, most commonly, the hypertension precedes the proteinuria in preeclampsia, there are many cases where the proteinuria precedes the significant hypertension. The detection of ‘more than a trace’ of protein on urinalysis serves to alert the clinician that this may herald developing preeclampsia. If the blood pressure is normal, a urinary tract infection should be excluded and the proteinuria confirmed with a more formal urine collection (e.g. for urinary protein:creatinine ratio). Most importantly, the visit frequency should be increased (e.g. see the following week) so as to ascertain early if the blood pressure begins to rise.

Investigations There are essentially three occasions during pregnancy when investigations are requested.

First antenatal visit The investigations requested at the first antenatal visit are blood tests as specified elsewhere, a cervical smear if indicated, trisomy 21 screening (even though performed

Chapter 5  Antenatal Care Beyond the First Antenatal Visit

FIGURE 5.2 

Deep pelvic palpation.

Source: Courtesy of Prof. Norman Beischer.

approximately 12 weeks’) and the morphology scan (performed approximately 20 weeks’).

At 28 weeks’ gestation

Full blood examinationn There is a normal fall in haemoglobin during pregnancy with a trough at approximately 28 weeks’. For various reasons, particularly iron deficiency, the haemoglobin may fall excessively and therapy may be indicated. A lower limit of 105 g/L would generally be acceptable, with some dietary emphasis with respect to Fe and folate given if the Hb is in the range 105 to 110 g/L. If the patient does have anaemia then investigation is required and appropriate therapy instituted. Most commonly the serum ferritin will be low and oral iron recommended (see Ch 20). Glucose tolerance testing In 2012, the Australasian Diabetes in Pregnancy Society (ADIPS) made screening recommendations for the diagnosis of gestational diabetes mellitus (GDM). These recommendations were derived from the Hyperglycaemia Adverse Pregnancy Outcome (HAPO) study and

developed by the International Association of Diabetes in Pregnancy Societies (IADPSG), and endorsed by the World Health Organisation. ADIPS recommend that, in the absence of risk factors, all women have a fasting 75-g 2-hour oral glucose tolerance test (GTT) at 24 to 28 weeks’. If risk factors are present, screening should also occur in early pregnancy. The criteria for diagnosis are any one of the following:

• • •

fasting venous PG ≥ 5.1 mmol/L one-hour venous PG ≥ 10.0 mmol/L two-hour venous PG ≥ 8.5 mmol/L.

Previous testing regimens for low-risk women had recommended a non-fasting 75-g oral glucose challenge test (GCT) and proceeding to a full GTT only if the GCT 1-hour glucose was ≥ 8.0. This regimen will miss approximately 20% of GDM. Blood group antibody screen A blood group antibody screen tests the maternal plasma against a panel of red cell antigens in order to see if any 43

Beischer & MacKay’s: Obstetrics, Gynaecology and the Newborn

anti-red cell antibodies have developed. All women are screened at the first visit. Some units will screen all women again at 28 weeks’ but most units will only rescreen those women that are Rh(D)-negative simply because the cost-effectiveness of repeat screening is much lower in the Rh(D)-positive population and there is only a very low probability of developing clinically significant antibodies to non-D red cell antigens. For women who are Rh(D)-negative and do not have anti-D antibodies, prophylactic anti-D will be administered at 28 weeks’ and again at 34 weeks’.

At 36 weeks’ gestation As prophylactic anti-D is indicated at 34 weeks’ in the Rh(D)-negative women and Group B streptococcus screening (GBS) screening at 36 weeks’, it is common practice to do both of these at a single hospital visit from 34 to 36 weeks’ in women undertaking shared care with a clinician in the community. Group B streptococcus (GBS) screening Approximately 20% of women will have vaginal carriage of GBS in late pregnancy. In the absence of prophylaxis, about 1 in 200 neonates born to these women will get a

GBS infection of which up to 10% will be fatal, with significant morbidity in the survivors. Intrapartum prophylaxis will greatly reduce the risk of early onset neonatal GBS sepsis. There are essentially two approaches: ‘universal screening’ or a ‘risk-based approach’. Universal screening is recommended by the American College of Obstetrics and Gynaecology and preferred by a majority of Australasian units. In universal screening, all women are screened at approximately 36 weeks’ gestation with a low vaginal and perianal swab to determine whether they are carriers for GBS. GBS carriage is assumed without the need for screening where there has been GBS bacteriuria in pregnancy or there has been a previously affected neonate with early onset GBS disease. In the presence of GBS carriage (on swab or assumed), intrapartum antibiotic prophylaxis is recommended with intravenous penicillin. Where the woman is allergic to penicillin, cephazolin is usually the best choice unless the woman has a history of immediate hypersensitivity to penicillin. If this is the case, antibiotic sensitivities are required as some isolates are resistant to macrolides. If not resistant, clindamycin is the drug of choice; otherwise vancomycin should be used.

TABLE 5.1  FACTORS DETERMINING MODE OF BIRTH. Variable

Rationale

Favouring elective caesarean section

Favouring planned vaginal birth

Maternal tolerance of fetal risk in order to avoid medicalisation of caesarean section

All mothers prioritise fetal welfare but some will be intolerant even of a very small added risk of vaginal birth

Low

High

Likely future parity

Increasing risk of placenta accreta with increasing numbers of caesarean sections

Low

High

Likelihood of achieving a vaginal birth if attempted

Emergency caesarean section increases morbidity relative to the elective procedure

Low

High

Perceived added maternal morbidity of vaginal birth in the index pregnancy

For example, previous third- or fourthdegree tear

High

High

Perceived added maternal morbidity of caesarean section in the index pregnancy

For example, morbid maternal obesity

Low

High

Anticipated added fetal morbidity or mortality of planned vaginal birth

For example, breech presentation, active genital herpes in a mother in labour, previous caesarean section

High

Low

Anticipated added fetal morbidity or mortality of planned caesarean section

Respiratory distress syndrome more common with elective caesarean section, particularly relevant in maternal diabetes mellitus

Low

High

44

Chapter 5  Antenatal Care Beyond the First Antenatal Visit

TIMING AND MODE OF BIRTH TIMING OF BIRTH The median onset of spontaneous labour is 40 weeks’ from the first day of the LNMP, which equates to approximately 38 weeks from fertilisation. However, approximately 1 in 400 women will have a perinatal death or long-term disability for her offspring as a consequence of an event after maturity (38 weeks’). This does not mean that everyone should have their baby at 38 weeks’, but rather emphasises that those women with complications that make the risks of long-term consequences even higher are commonly offered early birth. Some of the more common conditions that mostly would be recommended to be delivered prior to 40.0 weeks’ include hypertensive disorders such as preeclampsia, intrauterine growth restriction, diabetes mellitus and twins. That is not to say that every incidence of these conditions must be delivered before 40 weeks’, but that recommendation would apply to most women. Other factors to consider are: 1. the severity of the condition; 2.

ripeness of the cervix for induction; and 3. priorities of the woman in terms of ‘what level of fetal risk’ is reasonable in order to avoid a medical intervention such as induction of labour.

MODE OF BIRTH While most women would rightly prefer a vaginal birth, there are increasing numbers of women who, having fully informed themselves of the pros and cons of elective caesarean section, choose that mode of birth. Factors that militate in favour of or against an elective caesarean section are given in Table 5.1. FURTHER READING International Association of Diabetes and Pregnancy Study Groups. Recommendations on the diagnosis and classification of hyperglycemia in pregnancy. Diabetes Care 2010;33(3):676–82. Centers for Disease Control and Prevention. Prevention of perinatal Group B streptococcal disease. Revised Guidelines. CDC; 2010.

45

Chapter 6  OBESITY AND NUTRITION IN PREGNANCY Alexis Shub

KEY POINTS

Good nutrition and healthy weight gain can improve maternal and perinatal outcomes. Folate supplementation is recommended prior to pregnancy and during the first trimester. Iodine supplementation is recommended during pregnancy. Iron and vitamin D supplementation may be necessary in at-risk groups. Pregnant women should be given food handling advice to minimise the risk of Listeria infection. Optimal gestational weight gain in pregnancy can optimise pregnancy outcomes. Weight gain targets have been developed for singletons and multiple pregnancies, and across different body mass index (BMI) strata.

INTRODUCTION For many women, pregnancy is a time of extra interest and care in diet and nutrition. Good nutrition and appropriate weight gain can improve pregnancy outcomes. Pregnancy is an ideal time to educate women about healthy lifestyle and to impact both on their own health and that of the next generation. Knowledge in the community of appropriate weight gain targets and nutritional practises in pregnancy is poor and obesity and excess gestational weight gain are common problems in our community. In some groups, additional nutrient supplementation is required. A dietary history and counselling should be part of the first antenatal visit. Topics to be covered include adequate intake of essential nutrients, total energy intake and food safety issues.

DIETARY GUIDELINES IN PREGNANCY Healthcare professionals caring for a pregnant woman have an opportunity to impact on each woman’s

pregnancy and also on her ongoing health and wellbeing and that of her family. A short dietary history should be taken at the first antenatal visit covering amount and variety of food eaten, the intake of fast foods and ‘extra foods’, foods that are higher risk in pregnancy and advice about weight gain. The body mass index (BMI) should be calculated and explained to the woman. Dietary guidelines in pregnancy are similar to those in the non-pregnant population, with an emphasis on consuming a wide range of foods including fruit and vegetables, low-fat dairy products, cereals and proteinrich foods. The additional caloric requirements for pregnancy are surprisingly low. There is no additional requirement in the first trimester. In the second trimester, a further 1.4 MJ (330 calories) per day is needed. Examples of how this can be met are: two serves of fruit, one egg and one carrot, or a low-fat cheese sandwich and one serve of fruit. The additional needs in the third trimester are 1.9 MJ (450 calories) per day, which can be met with the above examples plus an additional half cup of baked beans or one glass of low-fat milk. These additional needs are much lower than the need to ‘eat for two’ that is still widely believed. A typical

Chapter 6  Obesity and Nutrition in Pregnancy

pregnant and non-pregnant diet intake for each day is listed in Table 6.1, demonstrating the small increases required in pregnancy. For some women with more complex nutritional needs, a single visit or ongoing care in conjunction with a dietician may be needed. This includes women: with prepregnancy or gestational diabetes who are significantly underweight or overweight with underlying gastrointestinal pathology such as inflammatory bowel disease with severe or prolonged hyperemesis gravidarum with metabolic disorders such as phenylketonuria who are post-bariatric surgery with eating disorders with fluid restriction due to cardiac or renal disease with restrictive diets (e.g. vegans, restriction of multiple food groups) with very difficult social circumstances such as homelessness.

• • • • • • • • • •

VITAMIN AND MINERAL SUPPLEMENTATION For women with an adequate diet in Australia, good evidence only exists for routine supplementation with iodine and folate. In some subgroups there may be additional need for vitamin D, iron, vitamin B12 or high-dose folate supplementation. For many women, the most practical form of supplementation will be a pregnancy-specific multivitamin containing an adequate amount of folate and iodine. Non-pregnancy multivitamins should be avoided as they may contain excess amounts of vitamin A, which is teratogenic.

FOLATE Maternal intake of adequate folate in the periconceptual period and through the first trimester has been shown to

reduce the risk of fetal neural tube defects (spina bifida and anencephaly) and so is recommended for all women. Bread in Australia, with the exception of organic bread, is made with folate-fortified flour. Folate can also be obtained from fruit, green leafy vegetables and legumes. All women are advised to take folate supplementation of 0.5 mg from the time of planning pregnancy until 12 weeks’ gestation for this purpose. Woman at higher risk of having a baby with a neural tube defect (Box 6.1) are advised to take a higher dose of folate (5 mg). Folate may also have a role in reducing pregnancy complications such as abruption in woman with a poor diet.

IRON In pregnancy, around 4 to 5 mg of iron needs to be absorbed each day in comparison to 1.5 mg in nonpregnant women. The recommended dietary intake (RDI) is 27 mg. Many women will start pregnancy with low iron stores (low ferritin) without having iron deficiency anemia (low haemoglobin). Reference ranges for haemoglobin are lower in pregnancy, and non-pregnant ranges as reported by most laboratories will overdiagnose anaemia in pregnancy. There is variable evidence of the benefits of routine supplementation in women with an adequate diet who are not anaemic, with some suggestion of increased birth weights and less preterm delivery. Women who have iron deficiency anemia will need additional supplementation, with a specific iron supplement, containing at least 60 mg of iron daily. Women

BOX 6.1  Women requiring high-dose folate.

Previous baby with spina bifida or anencephaly Type 1 or 2 diabetes Women taking anticonvulsants Obesity

TABLE 6.1  CORE FOOD GROUP SERVES FOR NON-PREGNANT AND PREGNANT WOMEN. Cereals (breads, rice, pasta and noodles)

Vegetables and legumes

Fruit

Milk, yoghurt, cheese

Lean meat, fish, poultry, nuts and legumes

Extra foodsi

Women aged 19 to 60 (non-pregnant)

4–9

5

2

2

1

0–2.5

Pregnant women (all ages)

4–6

5–6

4

2

1–1.5

0–2.5

i

Foods that do not fit into the five food groups and are not essential to provide the nutrients the body needs. Source: National Health and Medical Research Council. Healthy Eating During your Pregnancy: Advice on Eating for You and Your Baby. Canberra: NHMRC. Online. Available: http://www.nhmrc.gov.au/_files_nhmrc/publications/attachments/n55h_healthy_eating_during_ pregnancy.pdf; 14 Dec 2014. Licensed under Creative Commons Attribution 3.0 Australia License.

47

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with additional iron needs in pregnancy, such as multiple births or decreased dietary iron intake (e.g. vegetarians), should also take iron supplements.

IODINE Overall in the Australian community, there is a mild iodine deficiency but it is difficult to measure an individual’s iodine status. Iodine is found in seafood and seaweed, but in very small amounts in other foods. In Australia it is a requirement that all salt used to make bread (except organic) uses iodised salt and this provides sufficient iodine for most of the population. Because pregnant women and women considering a pregnancy have a greater need for iodine, the National Health and Medical Research Council (NHMRC) recommends supplementation of 150 mcg/day. This is found in some pregnancy multivitamins and should be taken throughout the pregnancy. Further consultation with an endocrinologist should occur in women with underlying thyroid disease.

CALCIUM The total fetal need for calcium throughout the pregnancy is approximately 30 g. The RDI of calcium in pregnancy is 1000 mg/day, which is the same as in the non-pregnant population, as the increased needs of pregnancy are predominantly met by increased maternal absorption of dietary calcium. Calcium is not taken from maternal bone stores in pregnancy. Calcium supplementation may have a role in prevention of preeclampsia in women who are at high risk of preeclampsia and have a low dietary calcium intake.

VITAMIN D Vitamin D deficiency (< 50 mmol/L) and insufficiency (< 75 mmol/L) are common in the Australian obstetric population, especially in the southern states. Adequate vitamin D is very difficult to achieve from diet alone and is primarily obtained from sun exposure. This insufficiency has been linked to reduction in sun exposure due to increased skin cancer awareness and to the changing population demographics with an increase in women who are dark skinned or veiled. There is no current proven association between low maternal vitamin D and poor obstetric outcomes including gestational diabetes mellitus (GDM), intrauterine growth restriction (IUGR) or preeclampsia.1 Low maternal vitamin D is, however, associated with an increased risk of neonatal hypocalcaemia and rickets, and women in high-risk groups should be screened in early pregnancy and treated with 2000 IU vitamin D daily if levels are below 50 mmol/L.

MERCURY Concern has been raised about the mercury content of fish, particularly in larger, longer-lived species, from naturally occurring mercury in the environment. High levels 48

of mercury may impact on fetal neurological development and so a reduced consumption of these is suggested in pregnancy. Pregnant women should eat shark (flake), broadbill, marlin and swordfish no more than once a fortnight and should not eat any other fish during that fortnight. Orange roughy and catfish should be eaten no more than once a week, and no other fish should be eaten during that week. Tinned tuna and salmon are safe to eat two to three times a week, as are other smaller fish not listed above. All these recommendations are based on a serving size of 150 g.

LISTERIA Pregnant women and other immunocompromised groups in the community are at higher risk of foodborne illness such as listeriosis; however, cases of listeria in Australia are uncommon. Listeria is caused by the aerobic and facultatively anaerobic gram-positive bacillus Listeria monocytogenes and is associated with consumption of contaminated food. Listeria in pregnancy is associated with miscarriage, still birth and preterm birth. Listeriosis should be considered in a pregnant women presenting with headache, fever, tiredness, aches and pains. Less common symptoms include diarrhoea, nausea and abdominal cramps. These symptoms may occur weeks after the contaminated food is eaten. Women should be advised to avoid the high risk foods listed in Box 6.2 and use careful safe food-handling practices.

WEIGHT GAIN IN PREGNANCY Optimal weight gain in pregnancy is associated with improved maternal and neonatal outcomes. Excess weight

BOX 6.2  Foods with increased risk of Listeria contamination. Foods to avoid include: cold meats from delicatessen counters and sandwich bars packaged, sliced ready-to-eat meats cold cooked ready-to-eat chicken (whole, portions or diced) pre-prepared or pre-packaged fruit or vegetable salads, including those from buffets and salad bars chilled seafood (such as raw oysters, sashimi and sushi), smoked ready-to-eat seafood and cooked ready-to-eat prawns soft, semi-soft and surface-ripened cheeses such as brie, camembert, ricotta, blue and feta refrigerated pate or meat spreads soft serve ice-cream unpasteurised dairy products.

Chapter 6  Obesity and Nutrition in Pregnancy

gain, even in women who begin pregnancy in the healthy weight range, is associated with increased rates of preeclampsia, macrosomia, babies that are small for gestational age, GDM, failed induction of labour, caesarean section and childhood obesity. Weight gain targets have been defined for each BMI category for singleton and twin pregnancies (Table 6.2). Weight gain targets have not been defined for the extremely obese woman, but many studies show that no weight gain, or even a small weight loss, in these women leads to acceptable outcomes. Overweight and obesity are increasingly common in the Australian community and throughout the world, with approximately 30% of women overweight and 20% of women obese in many centres. Women who are overweight or obese have increased rates of preeclampsia, gestational diabetes, operative delivery and thromboembolic disease.2 Their infants are more likely to be macrosomic, be growth restricted, have higher perinatal mortality and have higher rates of fetal abnormalities. Some of these risks are due to the underlying comorbidities associated with being overweight such as diabetes and hypertension; however, obesity itself appears to increase obstetric risk, which may result from the inflammation and endothelial dysfunction present in obese women. The risks to the mother and the baby increase in proportion to the BMI (Table 6.3). Worryingly, the infants of obese mothers and women with excess gestational weight gain have increased rates of obesity and cardiovascular disease into adult life.3 This probably results both from in utero programming (the epigenetic changes resulting from obesity and concurrent metabolic syndrome) and from lifestyle factors common to the families though infancy and childhood (including breastfeeding, eating habits and patterns of exercise). Outcomes for overweight and obese women in the antenatal and intrapartum period may also be compromised due to the practical implications of increased BMI. These include inadequate ultrasound imaging of fetal anomalies, less accurate clinical and ultrasound assessment of fetal growth, difficulty with intrapartum monitoring of the fetal heart rate and contractions, difficult intravenous access, lower success rate of regional analgesia and increased surgical difficulty for caesarean section.

Many trials have been performed to find the best way to minimise excess gestational weight gain, both in women with healthy weight gain and in the overweight and obese. Studies involving dietary intervention were most effective at minimising excess gestational weight gain, and also reduced preeclampsia and shoulder dystocia, without impacting on other obstetric outcomes. Many women are not aware of the guidelines for gestational weight gain and these should be explicitly discussed as part of routine antenatal care. Regular weighing in the antenatal period was stopped in many hospitals as it is a poor diagnostic or predictive test for preeclampsia or

TABLE 6.3  RISKS OF INCREASED BMI.* Healthy weight range

BMI 30–35

BMI > 40

Hypertension in pregnancy

1

3.2

6.5

Gestational diabetes

1

3.1

6.5

Caesarean section

1

2.0

3.0

Perinatal mortality

1

1.5

2.3

Preterm birth

1

1.2

1.6

Small for gestational age infant

1

1.1

1.6

Large for gestational age infant

1

1.3

1.6

* Adjusted odds ratios for age parity, smoking, ethnicity, insurance status, with healthy weight range as the reference range. Source: McIntyre DH, Gibbons KS, et al. Overweight and obesity in Australian mothers: epidemic or endemic? Med J Aust 2012; 196(3):184–8 © Copyright 2012 The Medical Journal of Australia— adapted with permission. The Medical Journal of Australia does not accept responsibility for any errors in adaptation.

TABLE 6.2  WEIGHT GAIN TARGETS FOR SINGLETON AND TWIN PREGNANCIES. BMI at beginning of pregnancy

Recommended weight gain (kg)

Rate of weight gain/week in 2nd and 3rd trimester

Recommended pregnancy weight gain for twins (kg)

Underweight (< 18.5)

12.5–18.0

500 g

N/A

Normal (18.5–24.9)

11.5–16.0

400 g

17.0–24.5

Overweight (25–29.9)

7.0–11.5

300 g

14.0– 22.5

Obese (≥ 30)

5.0–9.0

200 g

11.0–19.0 49

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IUGR; however, it provides an excellent opportunity for clinicians to discuss weight gain targets and improves gestational weight gain compliance. Many women welcome the opportunity to discuss their weight gain and reduce their risk of postpartum weight retention.

2) McIntyre HD, Gibbons KS, Flenady VJ, et al. Overweight and obesity in Australian mothers: epidemic or endemic? Med J Aust 2012;196:184–8. 3) Morandi A, Meyre D, Lobbens S, et al. Estimation of newborn risk for child or adolescent obesity: lessons from longitudinal birth cohorts. PLoS ONE 2012;7(11).

BARIATRIC SURGERY

FURTHER READING Food Standards Australia. Online. Available: http://www .foodstandards.gov.au Institute of Medicine (US) and National Research Council (US) Committee to Reexamine IOM Pregnancy Weight Guidelines; Rasmussen KM, Yaktine AL, editors. Weight gain during pregnancy: reexamining the guidelines. Washington: National Academies Press; 2009. Thangaratinam S, Rogozińska E, Jolly K, et al. Effects of interventions in pregnancy on maternal weight and obstetric outcomes: meta-analysis of randomised evidence. BMJ 2012;344.

Bariatric surgery is becoming increasingly common in women of reproductive years, and will improve rates of spontaneous conception for many very obese women. Bariatric surgery appears to improve outcomes for the woman, with reduced rates of gestational diabetes and hypertension, but this may be at a cost to the fetus with increased risk of IUGR and perinatal mortality. These results may be more pronounced in women who have malabsorptive surgery rather than restrictive surgery, but restrictive surgery is more common in Australia. Pregnancies after bariatric surgery, especially malabsorptive procedures, require additional dietician input and increased fetal surveillance. REFERENCES 1) Harvey NC, Holroyd C, Ntani G, et al. Vitamin D supplementation in pregnancy: a systematic review. Health Technol Assess 2014 Jul;18(45):1–190.

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Section 2.2 PROBLEMS OF EARLY PREGNANCY Chapter 7

Hyperemesis gravidarum

Chapter 8

Bleeding in early pregnancy

Chapter 7  HYPEREMESIS GRAVIDARUM Neil Israelsohn

KEY POINTS Hyperemesis gravidarum is a specific condition with symptoms and effects over and above the common nausea and vomiting of early pregnancy. Pharmacological therapy is useful for those women who have not responded to the strategies mentioned in this chapter. A stepwise approach to therapy is recommended. Nausea and vomiting with atypical features (e.g. commencing after 12 weeks’ gestation) should not be considered to be hyperemesis gravidarum and needs exclusion of other causes.

DEFINITION Nausea and vomiting in the first trimester is one of the most common symptoms of early pregnancy and will affect the majority of women. Approximately 80% will experience some nausea and 50% will experience vomiting as well. Hyperemesis gravidarum is a specific condition with symptoms and effects over and above the common nausea and vomiting of early pregnancy. It affects approximately 1% of pregnancies. While definitions may vary, a common definition used is: ‘Intractable vomiting associated with weight loss of ≥5% of pre-pregnancy weight, dehydration and electrolyte imbalances which may lead to hospitalisation’.1

AETIOLOGY The exact aetiology of nausea and vomiting of pregnancy is still somewhat debated. It is thought that hormonal factors, specifically rising β-hCG and oestrogen levels, are the most likely primary factor. Other patient factors— gastrointestinal, vestibular, psychological, social and cultural—may mediate the patient’s response to the hormonal changes.

Higher levels of β-hCG (multiple pregnancy, molar pregnancy) are associated with more prevalent and severe nausea and vomiting.

CLINICAL FEATURES The term ‘morning sickness’ is truly a misnomer and women with nausea and vomiting in early pregnancy may experience these symptoms at any time of the day and often throughout the day. Symptoms often begin by 5 weeks’, peak between 11 to 12 weeks’ and resolve usually by 14 weeks’ gestation. Nausea and vomiting may continue into the second or third trimester in up to 20% of women. Symptoms may be aggravated by certain smells, preparing meals and eating particular foods. Fatigue may also increase the severity of symptoms. The psychological impact and effect on relationships and activities of daily living can be profound and warrants appropriate attention and care. Clinical features of severe dehydration, electrolyte disturbance and vitamin deficiency may be present in severe cases. Specifically, thiamine deficiency and the resulting Wernicke’s encephalopathy (ophthalmoplegia, ataxia, confusion) is a very rare, but serious, complication of protracted hyperemesis gravidarum.

Chapter 7  Hyperemesis Gravidarum

MANAGEMENT OF VOMITING IN PREGNANCY ASSESSMENT It is important to exclude other pathological causes of nausea and vomiting before ascribing it to pregnancy. Other causes may include (but are not limited to) gastritis, gastroenteritis, bowel obstruction, biliary colic, cholecystitis, appendicitis, pancreatitis, hepatitis, urinary tract infection and metabolic and neurological conditions. Investigations will depend on the clinical findings but should include: pelvic ultrasound to confirm gestation, exclude multiple pregnancy or molar pregnancy tests for renal function, electrolytes and liver function midstream urine for micro/culture/sensitivity to exclude urinary tract infection urinalysis for urinary ketones. Minor derangements of liver function tests are sometimes seen with hyperemesis gravidarum. Significant abnormalities should raise suspicion of an underlying gastrointestinal cause.

• • • •

TREATMENT FOR NAUSEA AND VOMITING OF PREGNANCY Reassurance regarding the self-limiting nature of the condition is often all that is needed for mild nausea and vomiting in pregnancy. Improving lifestyle factors including dietary changes and rest and avoiding precipitating factors is first-line treatment. Specifically, eating small, frequent meals that are low in fat content is commonly suggested. Ginger may be helpful. Women should drink small volumes often to avoid dehydration and take a multivitamin tablet if tolerated. Other non-pharmacological treatments include acupuncture and acupressure. A Cochrane review did not show a statistically significant effect in reducing the severity or duration of symptoms. Pharmacological therapy is useful for those women who have not responded to the aforementioned strategies. A stepwise approach to therapy is recommended. When oral medication is tolerated, first-line treatment is pyridoxine (vitamin B6). If further therapy is needed, simple antiemetics are prescribed such as doxylamine (Restavit©) or metoclopramide (Maxolon©). Both are classified as pregnancy category A drugs (i.e. taken by a large number of pregnant women without an increase in the frequency of malformation or other harmful effects). For the more refractory cases, ondansetron (Zofran) (pregnancy category B1, i.e. taken by only a limited number of pregnant women without an increase in the frequency of malformation or other harmful effects) would be the common third-line treatment.

If vomiting continues despite the measures mentioned, corticosteroids (e.g. oral prednisolone) can be effective in some cases, but the dose and duration should both be minimised in view of the maternal side effect profile with high doses or prolonged use.

Adjuvant therapies It is important to manage the coexisting oesophageal acid reflux associated with recurrent vomiting. Ranitidine 150 mg orally twice daily (pregnancy category B1) should be added to improve symptomatic relief.

TREATMENT FOR HYPEREMESIS GRAVIDARUM Patients with hyperemesis gravidarum will require admission for intravenous hydration and control of vomiting and associated biochemical disturbance. Admission may be to a dedicated pregnancy daycare centre, emergency department or inpatient ward depending on facilities available. Fluid replacement usually begins with 0.9% normal saline or Hartmann’s solution 1 L stat in the absence of any significant renal or cardiac condition. Further administration of intravenous fluids will be dictated by level of dehydration. Potassium replacement may be required—if administered intravenously, the rate should not exceed 10 mmol/hr. Oral potassium replacement is preferred if tolerated. Intravenous antiemetics are administered (metoclopramide or ondansetron). A water-soluble vitamin solution can be added to the intravenous hydration. Thiamine 100 mg intravenously/oral daily for 3 days may be required in extreme cases. Once the patient is tolerating light diet and fluids, she may be discharged. Ongoing management through a pregnancy day ward may be necessary (2 to 3 times per week) if the patient is unable to maintain a reasonable oral fluid intake at home. A dietician referral may be made as an inpatient or outpatient. Consideration of parenteral feeding or hyperalimentation may be necessary. REFERENCE 1) Miller F. Nausea and vomiting in pregnancy: the problem of perception—is it really a disease? Am J Obstet Gynecol 2002;186(5 Suppl Understanding): S182–3. FURTHER READING Arsenault MY, Lane CA. The management of nausea and vomiting of pregnancy. Clinical practice guideline 120. Society of Obstetricians and 53

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Gynaecologists of Canada (SOGC). October 2002. J Obstet Gynaecol Can 2002;24(10):817–23. Hiscock R, Palmer G. Nausea and vomiting in pregnancy. In: Gastrointestinal therapeutic guidelines. Version 5. Melbourne: Therapeutic Guidelines; 2011. Marley J, Chamberlain A, Goodman G. Corticosteroids— adverse effects. In: Therapeutic guidelines:

54

dermatology. Version 3. Melbourne: Therapeutic Guidelines; 2009. Matthews A, Dowswell T, Haas DM, et al. Interventions for nausea and vomiting in early pregnancy. Cochrane Database Syst Rev 2010.

Chapter 8  BLEEDING IN EARLY PREGNANCY Neil Israelsohn

KEY POINTS Bleeding in early pregnancy should be considered to be an ectopic pregnancy until proven otherwise. Definitive management of miscarriage and ectopic pregnancy needs to be individualised depending on the patient’s clinical and social circumstances. Young, healthy women may compensate so effectively for significant blood loss as to have no/few signs of haemodynamic instability prior to haemodynamic collapse. Gestational trophoblastic disease should be considered in those with significant, persistent bleeding postpartum.

EARLY PREGNANCY BLEEDING

IS THE PREGNANCY VIABLE?

Early pregnancy assessment clinics (EPAC) are now common in hospitals managing pregnancy. They help to streamline the diagnosis and management of early pregnancy bleeding and provide a point of contact for ongoing medical care and support. Table 8.1 gives a simple differential diagnosis for bleeding in early pregnancy. In assessing the patient with early pregnancy bleeding, two important clinical questions need to be answered. 1. Is the pregnancy intrauterine? 2. Is the pregnancy viable?

Once an intrauterine pregnancy is confirmed, its viability should be determined. Serum β-hCG has little to offer in the management of an intrauterine pregnancy and the presence of fetal heart activity confirms viability. Any one of the following criteria is indicative of a failed pregnancy according to the guidelines of the Australian Society of Ultrasound in Medicine (ASUM): mean gestational sac diameter > 25 mm with no fetal pole fetal pole > 7 mm and no fetal heart activity inadequate growth of the gestational sac or fetal pole over the course of a week (i.e. < 1 mm per day). Poor prognostic features include a bradycardia (< 85 bpm) and significant subchorionic haematoma formation (Fig 8.2).

IS THE PREGNANCY INTRAUTERINE? All patients with bleeding and a non-localised pregnancy should be considered to have an ectopic pregnancy until proven otherwise. Ultrasound (usually transvaginal) and quantitative serum β-hCG form the basis for localising the pregnancy (Fig 8.1). The key component of this algorithm is the use of transvaginal ultrasound irrespective of the serum β-hCG. While intrauterine pregnancy contents are not expected to be visualised if the β-hCG < 1500 IU/L, an ectopic pregnancy with an inappropriate β-hCG for gestation may still be seen.

• • •

MISCARRIAGE A miscarriage is the presence of a non-viable intrauterine pregnancy before 20 weeks’. It is not necessary for there to be an embryo or fetus present. Clinically recognised miscarriage occurs in approximately 15% of pregnancies.

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TABLE 8.1  DIFFERENTIAL DIAGNOSIS OF EARLY PREGNANCY BLEEDING. Diagnosis

Cause

Not pregnant

In rare cases, a woman will have a false positive pregnancy test or for some other reason believe she is pregnant; bleeding may therefore be a menstrual period

Intrauterine pregnancy

Viable intrauterine pregnancy Non-viable (miscarriage, gestational trophoblastic disease)

Ectopic pregnancy

Most commonly tubal but may be ovarian, cervical or abdominal

Incidental cause for bleeding

Cervical polyp/cancer, ectropion, other genitourinary tract cause

Early pregnancy bleeding +/– pain Transvaginal ultrasound

Intrauterine pregnancy

Viable

Non-viable

Extrauterine pregnancy

Unlocalised pregnancy B-hCG < 1500 IU/L

Manage accordingly

B-hCG > 1500 IU/L

?Early intrauterine versus extrauterine pregnancy

Highly suspicious of ectopic pregnancy

Consider admission

Senior obstetric review

Repeat B-hCG in 48 hours Appropriate rise in B-hCG

Inadequate rise in B-hCG

Repeat ultrasound in 1 week

FIGURE 8.1 

Management of bleeding in early pregnancy.

If unrecognised biochemical pregnancies are included, the figure is much higher.

AETIOLOGY The aetiology of miscarriage is as follows. Chromosomal abnormalities. These are the most common cause of miscarriage and are responsible for approximately 50% of spontaneous miscarriages. Most of these abnormalities are non-recurring and include trisomies (e.g. trisomy 13), monosomy X (Turner syndrome) and polyploidies (triploidy and tetraploidy). The incidence of autosomal trisomies increases with advancing age. Endocrine. Poorly controlled endocrine disorders are risk factors for both infertility and miscarriage.





56

Preexisting diabetes, thyroid disease and hyperandrogenism (e.g. polycystic ovary syndrome [PCOS]) are associated with miscarriage. Obesity is also an independent risk factor for miscarriage. Although progesterone is essential for successful implantation and continuation of pregnancy, studies have shown neither a consistent correlation between progesterone levels and risk of subsequent miscarriage nor a benefit in reducing miscarriage with the use of exogenous progesterone. Thrombophilia. Antiphospholipid syndrome is a cause of recurrent miscarriage. The association of other hypercoagulable states and miscarriage is less certain as there are conflicting reports. It may be that thrombophilia has a greater association with late (> 10 weeks’) first trimester miscarriage.



Chapter 8  Bleeding in Early Pregnancy

Bleeding The amount of bleeding with a miscarriage is variable. In complete miscarriage, the loss is variable during the process but thereafter usually ceases entirely. In the majority of women with threatened miscarriage, the pregnancy continues uneventfully. The risk of loss is usually proportional to the amount of bleeding; if the loss continues or recurs or if there is any associated pain, the prognosis is less favourable. First-trimester bleeding predisposes to later pregnancy complications including preterm birth and preterm prelabour rupture of the membranes.

Pain

FIGURE 8.2 

Perigestational haematoma (H). CRL indicates crown–rump length of the fetus equivalent to 7 weeks’ and 6 days’ gestation on this scan.



Uterine abnormalities. Uterine malformations (bicornuate or septate) or fibroids (especially submucous) are implicated in recurrent pregnancy loss. Endometrial scarring (Asherman syndrome) also contributes to miscarriage risk. Chronic maternal disease. Significant maternal medical disease (e.g. cardiac, renal, connective tissue) is another risk factor in miscarriage. Toxins. Heavy tobacco use and heavy alcohol consumption are associated with an increased risk of sporadic miscarriage. Other risk factors are medications (e.g. methotrexate) and environmental toxins (e.g. arsenic, aniline dyes, benzene, ethylene oxide, formaldehyde, pesticides, lead, mercury and cadmium). Trauma. Invasive diagnostic procedures such as chorionic villus sampling (CVS) and amniocentesis are associated with small risks of miscarriage.



Pain is experienced as the uterus contracts or when the cervix is dilating and products of conception are being passed. The pain is felt in the lower abdomen or back, is usually cramp-like and follows the bleeding—in contrast to the sequence in ectopic pregnancy, discussed later in this chapter.

Passage of products of conception The passage of definite tissue defines incomplete or complete miscarriage. A confusing picture is presented when the decidual lining of the uterus is passed in ectopic pregnancy (decidual cast), since this simulates trophoblastic tissue (Fig 8.3). In many women, no fetus is passed at any time, since it is either absent (blighted ovum) or rudimentary and unnoticed.

CLASSIFICATION

Aetiology of recurrent miscarriage

Miscarriages were traditionally classified according to clinical criteria as listed in Table 8.2; that is, whether the cervix is open/closed, whether any products of conception have been passed and the size of the uterus relative to dates. More recently, however, ultrasound has played a more important role in the diagnosis and classification of miscarriage. The far greater availability of firsttrimester ultrasound has led to the diagnosis of significantly more missed miscarriages in asymptomatic women. Note that the term ‘missed miscarriage’ means a ‘non-viable pregnancy that has not yet had any vaginal bleeding’. It does not mean that the diagnosis has not been made.

The causes of recurrent miscarriage are similar to that for non-recurring miscarriage. With regards to chromosomal causes, parental balanced chromosomal translocations is a causative factor in approximately 4% of recurrent miscarriage.

INITIAL MANAGEMENT Assessment





CLINICAL FEATURES Pregnancy symptoms Symptoms and signs of pregnancy are usually present; pregnancy failure may be reflected by a diminution or cessation of typical pregnancy symptoms.

Take the patient’s history to elicit details of the presenting complaint as outlined in the Clinical features section. Clinical examination should include vital signs, abdominal palpation, speculum examination and bimanual palpation. The following investigations are useful: full blood examination (FBE), blood group and save serum, quantitative β-hCG and ultrasound. 57

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Generic treatment Resuscitation The amount of blood loss during miscarriage is highly variable. Fluid resuscitation is often not necessary; however, when the blood loss is heavy and ongoing, the patient will require a crystalloid or colloid infusion while

definitive management is being arranged. If there is evidence of severe haemodynamic compromise, the patient may need O-negative blood pending cross-match.

Passive anti-D for Rh-negative women

25 cm

Anti-D is not necessary for non-immunised, Rh-negative women who have a threatened miscarriage (i.e. bleeding with a viable pregnancy) before 10 weeks’. For other miscarriages, anti-D 250 IU intramuscularly is sufficient due to the small circulating volume of fetal red cells in the first trimester.

Explanation and support Emotional support is important during this time of loss. An explanation of the possible aetiology helps to reassure the woman and her partner that, in the overwhelming majority of cases, no act or omission has either caused the miscarriage or would have helped to prevent it.

FURTHER MANAGEMENT The plan for further management will depend on the type of miscarriage.

Threatened miscarriage 30 cm

Admission is rarely necessary. Reassure the patient regarding the ongoing viability of the pregnancy. Bleeding is seldom sufficient to require transfusion or intravenous fluid.

Complete miscarriage

FIGURE 8.3 

Decidual cast. After withdrawal of hormones due to death of the ectopic chorionic villi, the thickened endometrium is shed, usually in fragments as in menstruation, but sometimes as a single piece or decidual cast of the uterus, which may be mistaken for placental tissue (uterine abortion). Source: Reproduced with permission from the Royal Women’s Hospital, Parkville, Victoria.

There is usually a history of significant bleeding, pain and the passage of products of conception followed by minimal blood loss, a closed cervix and a significant reduction in pain. The uterus is empty on ultrasound. The management is conservative. In the context of an empty uterus on ultrasound, a confident diagnosis of complete miscarriage can only be made if there is pathologic confirmation of products of conception or if the pregnancy has previously been localised as intrauterine. If neither of these criteria are met, one should suspect a possible ectopic pregnancy. In this case, quantitative β-hCG should be performed weekly to document return to non-pregnant levels and the patient

TABLE 8.2  CLASSIFICATION OF MISCARRIAGE. Miscarriage type

Cervix

Products of conception passed

Threatened miscarriage

Closed

No

Viable intrauterine pregnancy

Missed miscarriage

Closed

No

Non-viable intrauterine pregnancy

Inevitable miscarriage

Open

No

Non-viable intrauterine pregnancy; often low in the uterus

Incomplete miscarriage

Open

Yes

Retained products of conception

Complete miscarriage

Closed

Yes

Empty uterus; no extrauterine pregnancy

58

Ultrasound findings

Chapter 8  Bleeding in Early Pregnancy

should be asked to present earlier if she experiences significant pain or bleeding.

Inevitable miscarriage While the patient will go on to pass the products of conception, this may occur after a variable amount of further bleeding and/or pain. Expectant or medical management is most appropriate. Occasionally patients will require a curette if there is sustained heavy bleeding.

Incomplete miscarriage This common presentation causes the most trouble from bleeding and shock; blood transfusion may be required in a few women. Cervical shock may occur if products become trapped within the cervix. This presents as bleeding, significant pain and often vagal/parasympathetic symptoms (bradycardia, hypotension, sweatiness and nausea/vomiting). Speculum visualisation of the cervix and removal of the products with sponge forceps may be necessary (Fig 8.4). It is often necessary to perform a curette to ensure complete removal of products of conception. If there is no

A

evidence of cervical tissue and bleeding is heavy and ongoing, ergometrine 0.5 mg intravenously may be trialled while theatre is arranged for an urgent curette. Usually, the bleeding is much less troublesome, and after the diagnosis has been made, ongoing management options are discussed, as detailed in the next section.

Missed miscarriage Ultrasound criteria for confirming a non-viable pregnancy are described earlier in this chapter. Where there is no suggestion of a septic miscarriage or haemodynamic instability, ongoing management may be expectant, medical or surgical. A Cochrane review has revealed that the rates of infection are similar for each management strategy. While the likelihood of success is a critical factor in determining ongoing management, other issues to consider include the patient’s: tolerance of potential ongoing bleeding and/or pain at home acceptance of having a complete miscarriage in a setting outside of the hospital

• •

B

FIGURE 8.4 

Incomplete miscarriage at 10 weeks’ gestation in a 21-year-old primigravida who presented with heavy vaginal bleeding and abdominal pain. A Placental tissue is seen protruding through the cervical os. Sponge-holding forceps grasp and remove the placental tissue. B Products of conception visible at a partly dilated external os. Source: Courtesy of Prof. Norman Beischer.

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• •

desire to avoid surgery/intervention access to medical services in the case of an emergency.

Expectant management Expectant management of a missed miscarriage is associated with more days of bleeding and unplanned surgical procedures as compared with surgical management. It can take up to 4 weeks for successful spontaneous miscarriage. Success rates are presented in Table 8.3.

Medical management Prostaglandin E1 (misoprostol) is used for medical management of miscarriage due to its low cost, ready availability and benign side effect profile. Side effects may include nausea, vomiting, diarrhoea, flushing and abdominal cramps. One common schedule is 800 mcg misoprostol PV followed by another 800 mcg 12 hours later if pregnancy products have not been passed. Medical management has greater rates of success as compared to expectant management yet still has a longer duration of bleeding and more unplanned procedures as compared with surgical management. Success rates are presented in Table 8.3.

Surgical management Cervical dilation and suction curette provides definitive management in almost all cases of missed or incomplete miscarriage. Minimal bleeding and period-like pain can be expected after the procedure. It is, however, associated with uncommon but potentially serious complications including anaesthetic risks and uterine perforation that may be associated with visceral or vascular damage. Uterine adhesions are very unlikely following a single curette in the absence of infection.

TABLE 8.3  SUCCESS RATES OF EXPECTANT, MEDICAL AND SURGICAL MANAGEMENT OF MISCARRIAGE. Management

Successful spontaneous miscarriage Missed/anembryonic miscarriage (%)

Incomplete miscarriage (%)

Week 1

30

53

Week 2

56

84

Day 3

71

93

Day 8

85

Medical

60

Septic miscarriage may complicate any of the forms of miscarriage but is mostly restricted to those where retained products are neglected. Historically, it was a consequence of criminally induced abortion. These rates have dropped significantly now that abortion is lawful in all Australian states, under certain conditions. In addition to the common symptoms of miscarriage, the patient will commonly have an offensive vaginal discharge, abdominal pain and fever. Common bacteria include anaerobic organisms (streptococci and Bacteroides) and enteric flora (E. coli). Severe infection may lead to septicaemia with ensuing shock, disseminated intravascular coagulation (DIC) and multi-organ failure. In the days of ‘backyard abortion’, Clostridium perfringens (welchii) was the responsible pathogen. Treatment involves broad-spectrum intravenous antibiotics and generally a curette, which is often delayed or performed under ultrasound guidance considering the increased risk of uterine perforation.

PROGNOSIS Most women are worried about both the immediate and long-term implications of bleeding in early pregnancy. Women should be reassured that bleeding in the presence of a viable pregnancy is usually benign and does not result in miscarriage. First-trimester bleeding may also be associated with a small increase in several pregnancyrelated complications: premature rupture of membranes, preterm labour, recurrent antepartum haemorrhage and growth restriction. Although not evidence-based, it may be worth considering cervical surveillance in women with significant and recurrent first-trimester bleeding.

SECOND-TRIMESTER MISCARRIAGE Second-trimester miscarriage affects approximately 1% of pregnancies. For pregnancies greater than 14 weeks’, medical management in a hospital setting is generally utilised in preference to surgical management. Misoprostol is the preferred oxytocic agent. Dilation and evacuation may be preferred in some circumstances by experienced clinicians.

RECURRENT MISCARRIAGE

Expectant

Surgical

Septic miscarriage

90–100

90–100

Recurrent miscarriage is defined as three or more successive miscarriages. It is estimated that recurrent miscarriage affects 1% of couples trying to conceive. Mostly this is idiopathic and no cause will be found in approximately 50% of couples. Investigations that can be undertaken include imaging of the uterus, endocrine profiling (especially thyroid), thrombophilia screening and parental karyotyping. However, even after three successive miscarriages there will be a live birth in approximately 70% women.

Chapter 8  Bleeding in Early Pregnancy

The chances are better in those with idiopathic recurrent miscarriage. If another miscarriage were to occur, the products of conception should be sent for karyotyping.

ECTOPIC PREGNANCY

The classical triad of symptoms is amenorrhoea (75%), lower abdominal pain (95%) and vaginal bleeding (75%). A similar picture may be seen with a miscarriage in progress.

PREDISPOSING FACTORS

An ectopic pregnancy occurs with the implantation of the conceptus outside the uterine cavity, usually in the fallopian tube (Fig 8.5) and rarely in the ovary, abdominal cavity or cervix (Fig 8.6). It occurs in approximately 1% of pregnancies.

The predisposing factors of an ectopic pregnancy are: previous ectopic pregnancy progesterone-only or emergency hormonal contraception intrauterine contraceptive device IVF tubal damage or adhesions. Kinking or narrowing of the tube will prevent the fertilised ovum making its way from the ampulla to the uterine cavity. Apart from the mechanical effect of the narrowing, damage to the cilia of the tubal epithelium will impede transport of the fertilised ovum. Common antecedents are chlamydial or gonococcal salpingitis, postabortal or postpartum salpingitis, and appendicitis. Endometriosis, congenital abnormalities and previous tubal surgery may also impair tubal function.

• • • • •

PATHOLOGY AND CLINICAL FEATURES Tubal pregnancy There are three main outcomes of a tubal ectopic pregnancy.

FIGURE 8.5 

Tubal pregnancy. The tube is grossly distended and has a thickened haemorrhagic wall which accounts for the unusually advanced duration of pregnancy (9 weeks’) before rupture occurred. Source: Courtesy of Prof. Norman Beischer.

Ampulla 55%

Isthmus 18%

Interstitial 4%

Ovary 2% Abdominal cavity 1%

FIGURE 8.6 

Fimbrial 20%

Relative frequency of sites of implantation of ectopic pregnancies.

Tubal abortion The conceptus is extruded out the fimbrial end of the tube. This is accompanied by colicky pain, followed by a more constant pain because of the presence of blood in the peritoneal cavity. The condition may settle spontaneously, but usually pain and bleeding continues and surgery is required.

Tubal rupture If the pregnancy progresses and tubal abortion does not occur, tubal rupture is inevitable (Fig 8.7). Acute rupture is associated with severe intraperitoneal bleeding and acute abdominal pain; often pain is also felt in the shoulder tip (due to irritation of the diaphragm by blood) and on defecation or passing flatus due to blood in the pouch of Douglas between the rectum and the upper vagina. Hypotension is a late sign of significant blood loss in this population and the patient may show few or no signs of haemodynamic instability before deteriorating rapidly in the face of ongoing concealed bleeding. A tachycardia alone should be considered to be highly significant in a patient with known or suspected ectopic pregnancy. The abdomen may exhibit signs of peritonism with generalised and rebound tenderness. Rupture may occur into the broad ligament, forming a broad ligament haematoma (Fig 8.7). Symptoms and 61

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signs of peritonitis are absent, but pelvic pain and tenderness are marked.

Missed tubal abortion



The embryo dies and usually is absorbed. The clinical features are those of early pregnancy, together with a brown or red vaginal loss and perhaps mild, lower abdominal pain. Often no pregnancy is located on ultrasound.

Other sites for ectopic pregnancy The following are other potential sites for an ectopic pregnancy. Cornual/interstitial pregnancy. The pregnancy is implanted in the proximal portion of the tube embedded within the uterine musculature. Because of the thicker muscular coat, such women usually present much later than is the case with the other types and rupture may be sudden and associated with



• • •

catastrophic blood loss. Pregnancy in a rudimentary uterine horn may present similarly. Cervical pregnancy. This is rare, but should be suspected when bleeding is heavy, particularly on vaginal examination. A small, firm uterus can be felt above the expanded cervix; this can be confused with the expansion caused by products of conception in the course of a miscarriage of an intrauterine pregnancy. Ultrasound will help to confirm the diagnosis (Fig 8.8). Uterine scar pregnancy. The pregnancy is located in the scar and is surrounded by myometrium and connective tissue (Fig 8.9). Heterotopic pregnancy. Concomitant intrauterine and extrauterine pregnancy is very uncommon, although it has a higher incidence among IVFconceived pregnancies. Abdominal pregnancy. This is an extremely rare occurrence and may take place due to primary implantation of a fertilised ovum in the peritoneal cavity or secondary implantation after a tubal abortion.

DIAGNOSIS Diagnosis of an ectopic pregnancy with the use of serum β-hCG and transvaginal ultrasound (Fig 8.10) is described earlier in the chapter (see Fig 8.1).

MANAGEMENT A ruptured ectopic pregnancy can present as a medical emergency and maternal collapse. There may be minimal information regarding preceding symptoms. A high level of suspicion should be maintained for any woman of

FIGURE 8.7 

Possible outcomes of tubal pregnancy are rupture into the peritoneal cavity, tubal lumen or broad ligament. Tubal missed abortion without rupture can occur asymptomatically and result in obliteration of the tubal lumen and later sterility. Note that the pregnancy distends the tubal wall, not its lumen; this explains why incision and expression often results in a patent tube. 62

FIGURE 8.8 

Cervical ectopic pregnancy. The body (B) of the uterus is empty. The cervix (C) is distended by the cervical ectopic pregnancy (E). This can often be confused with an inevitable miscarriage.

Chapter 8  Bleeding in Early Pregnancy

FIGURE 8.9 

Uterine scar pregnancy. The fundus (F) is seen with no gestational sac. The ectopic pregnancy (E) is located in the scar, outside of the uterine cavity and above the cervix (C), surrounded by myometrium.

FIGURE 8.10 

Tubal ectopic pregnancy. The adnexal mass (MASS) is seen medial to the left ovary (LO) in the ‘ectopic triangle’ between the ovary and lateral uterine wall.

reproductive age presenting with unexplained severe haemodynamic compromise or collapse. In these cases, it is important to secure intravenous access, take blood for FBE, cross-match 4 to 6 units of blood and perform a coagulation screen. Commence resuscitation with O-negative blood (or intravenous fluid if blood is not immediately available). Anaesthetics should be informed and arrangements made for an emergency laparotomy. In more subacute or asymptomatic presentations, the initial management is similar to that for the woman with suspected miscarriage: essentially intravenous access, blood tests ± intravenous fluid. Treatment of the ectopic pregnancy is generally either medical or surgical. Expectant management may be followed for women with low or declining β-hCG levels and no recognisable ectopic mass on ultrasound.

Medical treatment Methotrexate is a folate antagonist and inhibits DNA synthesis in rapidly dividing cells. The contraindications to medical treatment are listed in Box 8.1. The success rate of medical management in the absence of contraindications is 90%. Side effects of methotrexate are usually mild and include nausea, diarrhoea, stomatitis and gastritis. Less common but severe effects include pneumonitis, abnormal liver function and bone marrow suppression. Renal and liver impairment should be excluded before commencing therapy. There remains a risk of ectopic rupture during medical management. Return of β-hCG levels to normal may take several weeks and a delay of 3 months before conceiving again is generally recommended. It is important that patients are informed of these facts prior to

BOX 8.1  Contraindications to medical treatment. Haemodynamic instability or evidence of tubal rupture β-hCG > 5000 or tubal mass > 3.5 cm Fetal heartbeat Lack of access to timely medical assistance in the event of ectopic rupture Patient not able to comply with post medical treatment follow-up Contraindication to methotrexate (hypersensitivity, renal disease, breastfeeding etc.)

accepting medical treatment. They should be willing, and able, to present weekly for serum β-hCG measurements to ensure resolution of the ectopic pregnancy. Methotrexate may be given as a single injection or as a multi-dose regimen. A single-dose regimen includes the following. Day 1: Quantitative β-hCG. Administer methotrexate, 50 mg/m2 given as a single intramuscular injection. Day 4: Quantitative β-hCG. May rise between days 1 and 4. Day 7: Quantitative β-hCG. Test urea, electrolytes and creatinine; test liver function; and perform FBE. Clinical review. A quantitative β-hCG drop of ≥ 15% between days 4 and 7 is consistent with initial treatment success. Serum β-hCG should continue to be monitored weekly until

• • •

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< 5 IU/L. Patients should present if they experience significant abdominal pain and or bleeding. If the β-hCG level does not drop by 15%, consideration is given to either a second dose of methotrexate or surgical management. The multi-dose regimen has a similar success rate to the single dose for tubal ectopics; however, side effects are more common. It is generally only considered in cases of cornual, scar and cervical ectopic pregnancy.

Other treatment options

Surgical treatment

Live cervical, scar and cornual ectopics may be managed with intra-gestational potassium ± methotrexate injection.

Surgical management is indicated if medical treatment is contraindicated (as outlined earlier in Box 8.1) or if medical treatment fails or is declined by the patient.

Laparoscopy or laparotomy? Laparoscopy is appropriate for almost all ectopic pregnancies (even those with haemoperitoneum) except those with significant haemodynamic compromise. Ultimately the decision depends on the experience and skills of the attending gynaecologist and anaesthetic team.

Salpingectomy or salpingostomy? Laparoscopic salpingectomy (Fig 8.11) is the standard surgical treatment for tubal ectopic pregnancy. Research has shown similar rates of future intrauterine pregnancy and recurrent ectopic rates compared with medical management. Salpingostomy (incision of the affected tube with removal of the products of conception) is occasionally performed with a view to increasing future intrauterine pregnancy rates. Non-randomised studies suggest that

A FIGURE 8.11 

intrauterine pregnancy rates are greater after salpingostomy compared with salpingectomy ONLY in those with contralateral tubal disease. Against salpingostomy, there is increase in both persistent trophoblast requiring treatment and future ectopic pregnancy relative to salpingectomy.

GESTATIONAL TROPHOBLASTIC DISEASE CLASSIFICATION Gestational trophoblastic disease (GTD) encompasses a range of conditions characterised by a proliferative disorder of trophoblastic cells. These disorders can be broadly classified into benign or invasive/malignant (see Box 8.2) and are largely distinguished on histopathology.

Localised GTD Localised molar pregnancies are a result of aberrant fertilisation and as such are primary entities and cannot follow from a clinical pregnancy. Invasive GTD, on the other hand, may follow either a molar or clinical pregnancy including term, preterm, miscarriage or ectopic pregnancy.

B

Laparoscopic salpingectomy. A Shows the left ampullary ectopic pregnancy (E), the left ovary (LO) and the uterus (U). Free peritoneal blood is seen on the visceral and peritoneal surfaces. Evidence of parafimbrial blood clot. B Post-salpingectomy showing the left ovary (LO) and the uterus (U). 64

Chapter 8  Bleeding in Early Pregnancy

BOX 8.2  Classification of gestational trophoblastic disease. Localised (‘benign’) gestational trophoblastic disease (localised GTD) ✚ Partial hydatidiform mole ✚ Complete hydatidiform mole Invasive gestational trophoblastic neoplasia (invasive GTN) ✚ Invasive mole ✚ Choriocarcinoma ✚ Placental site trophoblastic tumour (PSTT)

Invasive GTN In the case of invasive moles, the degree of invasion may be local or may involve metastases, usually to the lungs or vagina. Invasive moles follow approximately 15% of complete moles and 3% of partial moles. The diagnosis is generally made clinically based on persistent β-hCG elevation after molar evacuation. Choriocarcinoma is a malignant disease characterised by abnormal trophoblastic hyperplasia and anaplasia, absence of chorionic villi, haemorrhage and necrosis. This malignant tumour of the trophoblast follows a hydatidiform mole in 50% of cases, normal pregnancy in 25% and miscarriage or ectopic pregnancy in 25% (see Fig 8.12).

PREDISPOSING FACTORS Rates vary significantly based on geographic region, ethnicity and maternal age. The condition is more common in Australasia (1 in 750 pregnancies) than in the United States, the United Kingdom and Europe (1 in 1500), but is most frequent in South-East Asia and Mexico (1 in 500). Choriocarcinoma is more common in older and younger women and there is a 1% recurrence risk if there is a past history of GTD.

HISTOPATHOLOGY AND CYTOGENETICS Complete and incomplete moles differ significantly in certain characteristics (Table 8.4). Complete molar pregnancy occurs as a result of fertilisation of an empty ovum with either two sperm or one that divides. The karyotype is generally 46XX (occasionally 46XY) and all of paternal origin. Partial molar pregnancy results from the fertilisation of an ovum with two sperm or one that divides resulting in triploidy 69XXY, 69XXX or, rarely, 69XYY. There is often a co-existing fetus that is prone to fetal death in utero and growth restriction. Partial moles have a much lower malignant potential.

FIGURE 8.12 

Choriocarcinoma. The woman was aged 17 and presented with a haemoperitoneum. As in 50% of cases, there was no preceding hydatiform mole. Uterine perforation necessitated hysterectomy. There were multiple pulmonary metastases but recovery was complete after hysterectomy. Source: Reproduced with permission from the Royal Women’s Hospital, Parkville, Victoria.

CLINICAL FEATURES AND PATHOLOGY Mole A hydatidiform mole is characterised by oedematous avascular villi with trophoblastic proliferation (Fig 8.13). Typically, a mole is initially diagnosed following an ultrasound performed because of vaginal bleeding (95%) in early pregnancy. Other clinical features may include hyperemesis gravidarum, theca lutein cysts (Fig 8.14), preeclampsia (may be before 20 weeks’ gestation), hyperthyroidism and vaginal passage of hydropic vesicles. Symptoms from metastatic spread of molar tissue may also occur (e.g. haemoptysis and/or pleuritic pain from spread to the lung).

Choriocarcinoma The clinical presentation of choriocarcinoma is varied depending on the antecedent pregnancy. Following a complete molar pregnancy, it may be diagnosed in asymptomatic women with routine β-hCG monitoring. 65

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TABLE 8.4  CHARACTERISTICS OF PARTIAL AND COMPLETE MOLES. Characteristic

Partial mole

Complete mole

Karyotype

69XXY, 69XXX, 69XYY

46XX or 46XY

Embryonic fetal tissue

Present

Absent

Villi

Focal hydropic villi

Diffusely hydropic

Theca lutein cysts

Uncommon

Common

Malignant GTN

3% Almost exclusively invasive mole

15% (invasive mole 90%, choriocarcinoma 10%)

FIGURE 8.13 

Section of a hydatidiform mole showing considerable trophoblastic proliferation. The chorionic villi show the typical enlargement (hydrops) and avascularity. Source: Courtesy of Norman Beischer.

FIGURE 8.14 

Uterus and bilateral theca-lutein cysts seen after hysterectomy at 18 weeks’ gestation in a woman with a hydatidiform mole. Suction curettage is the usual treatment of a hydatidiform mole. Source: Courtesy of Monash Health.

Following a normal pregnancy, persistent vaginal bleeding is the most frequent symptom. Vaginal bleeding after 6 to 8 weeks’ should prompt consideration of GTN along with the other more common conditions such as retained products of conception and endometritis. There may be evidence of metastatic tumour—vaginal metastases are present in 30% cases. These lesions are highly vascular and prone to bleeding. Patients may exhibit respiratory, gastrointestinal or neurological symptoms reflecting sites of distant metastases.

DIAGNOSIS Ultrasound Ultrasound of a complete mole reveals a central heterogeneous mass with numerous discrete anechoic spaces. There is no fetus or amniotic fluid (Fig 8.15)—unless there is a co-existent twin (4 to 6%, Figs 8.16 and 8.17). A partial mole may also have a co-existent fetus. A 66

choriocarcinoma appears as a hypervascular heterogeneous mass.

β-hCG

β-hCG is universally elevated as compared with other intrauterine or ectopic pregnancies. Occasionally, the diagnosis of a partial mole may only be made on histology of curettings from a suspected incomplete abortion.

MANAGEMENT Localised GTD Initial management The initial treatment is similar to that outlined for the woman with suspected miscarriage. Heavy bleeding may complicate this process, so adequate blood must be crossmatched. Suction curette is first-line management for complete and partial molar pregnancy. Hysterectomy

Chapter 8  Bleeding in Early Pregnancy

FIGURE 8.17  FIGURE 8.15 

Complete mole. Enlarged uterus showing hypoechoic vesicles consistent with a molar pregnancy.

Twin molar and normal pregnancy. The mother had severe preeclampsia at 16 weeks’ gestation. The fetus and attached placenta had a normal male karyotype but the separate molar tissue had a female karyotype and was thus a dizygotic twin. Source: Reproduced with permission from the Royal Women’s Hospital, Parkville, Victoria.

molar pregnancy, ongoing follow-up with serial β-hCG measurements for 6 months is important. Contraception should be commenced and if there is a trophoblast registry in the region, the case should be notified. Use of the oral contraceptive pill does not increase rates of invasive disease. The theca lutein cysts are managed conservatively although they may take months to resolve. Surgery may be necessary if torsion ensues.

Invasive GTN Initial management FIGURE 8.16 

Partial mole in association with triploidy 69. The mother had severe preeclampsia and was delivered at 24 weeks’. The single placenta was diffusely molar and the triploidy fetus had multiple abnormalities. Source: Reproduced with permission from the Royal Women’s Hospital, Parkville, Victoria.

would rarely be performed as first line management (Fig. 8.18). Tissue is sent in normal saline (not formalin) for histological analysis and karyotyping if necessary. If the diagnosis of a complete mole is established preoperatively, baseline investigations with a quantitative β-hCG and chest X-ray should be taken.

Follow-up Due to the possibility of persistent GTD (invasive molar pregnancy/choriocarcinoma), especially after complete

The preferred management of invasive GTN is with chemotherapy. Repeat curette is contraindicated due to the significant risk of maternal haemorrhage and uterine perforation. Chemotherapy is the cornerstone of management. ‘Staging’ into low- and high-risk groups takes place to determine the most appropriate chemotherapy. Low-risk women receive single-agent chemotherapy but the high-risk group are prescribed a multi-agent chemotherapeutic regimen (etoposide, methotrexate, actinomycin D, cyclophosphamide and vincristine [EMA/ CO]). Cure rates approach 100% for those treated with single-agent chemotherapy. For high-risk disease necessitating a multi-drug regimen ± adjuvant radiotherapy or surgery, cure rates are approximately 90%.

Follow-up

Once chemotherapy has been completed and β-hCG levels have returned to normal, the β-hCG levels should be monitored at monthly intervals for a further 12 months. The risk of relapse is 3% in the first year and rare after that. Pregnancy should be avoided during the first 12 months 67

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FIGURE 8.18 

Classic hydatidiform mole appearance from a hysterectomy specimen of a 56-year-old woman. Source: Courtesy of Monash Health.

after β-hCG returns to normal in order to facilitate β-hCG surveillance. An effective method of contraception should be used. The combined oral contraceptive pill is considered safe. Due to the risk of recurrence in subsequent pregnancies, women should have an ultrasound in the first trimester, placental histopathology and a serum β-hCG at 6 weeks’.

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FURTHER READING Hajenius PJ, Mol F, Mol BW, et al. Interventions for tubal ectopic pregnancy. Cochrane Database Syst Rev 2007. Luise C, Jermy K, May C, et al. Outcome of expectant management of spontaneous first trimester miscarriage: observational study. BMJ 2002;324(7342):873. Lurain JR. Gestational trophoblastic disease I: epidemiology, pathology, clinical presentation and diagnosis of gestational trophoblastic disease, and management of hydatidiform mole. Am J Obstet Gynecol 2010;203(6):531–9. Lurain JR. Gestational trophoblastic disease II: classification and management of gestational trophoblastic neoplasia. Am J Obstet Gynecol 2011;204(1):11–18. Mol BW, Matthijsse HC, Tinga DJ, et al. Fertility after conservative and radical surgery for tubal pregnancy. Hum Reprod 1998;13(7):1804–9. Neilson JP, Gyte GML, Hickey M, et al. Medical treatments for incomplete miscarriage (less than 24 weeks). Cochrane Database Syst Rev 2010;1. Royal College of Obstetricians and Gynaecologists. The management of early pregnancy loss. Green-top Guideline No. 25. London: RCOG; 2006. Scott F, Meagher S. Media release. Australasian Society for Ultrasound in Medicine (ASUM). Online. Available: ; [24 October 2011]. Soto-Wright V, Bernstein MMHP, Goldstein DP, et al. The changing clinical presentation of complete molar pregnancy. Obstet Gynecol 1995;86:775–9. Van Mello NM, Mol F, Opmeer BC, et al. Salpingotomy or salpingectomy in tubal ectopic pregnancy: what do women prefer? Reprod Biomed Online 2010;21(5):687–93. Zhang J, Gilles JM, Barnhart K, et al. A comparison of medical management with misoprostol and surgical management for early pregnancy failure. N Engl J Med 2005;353(8):761–9.

Section 2.3 PRENATAL DIAGNOSIS Chapter 9

Screening, diagnosis and management of genetic and structural abnormalities in the fetus

Chapter 9  SCREENING, DIAGNOSIS AND MANAGEMENT OF GENETIC AND STRUCTURAL ABNORMALITIES IN THE FETUS Susan Walker

KEY POINTS The incidence of major birth defects is approximately 4%. Congenital defects may be due to genetic, infective or teratogenic influences, but the aetiology in many remains unknown. Screening for birth defects includes screening for Down syndrome and related aneuploidies, and a fetal anatomical survey with ultrasound. Other genetic conditions in high-risk families may be amenable to prenatal screening and diagnosis. Diagnostic tests for genetic abnormalities include amniocentesis and chorionic villus sampling, which have a miscarriage rate of 0.5 and 1% respectively. Cardiovascular and central nervous system abnormalities are the most common major structural abnormalities; however, renal, gastrointestinal, face and skeletal abnormalities may be detected with ultrasound, as may fetal tumours or hydrops. Management of families where a major structural abnormality has been identified is best undertaken by a multidisciplinary team addressing: the underlying cause; implications for the pregnancy, labour and delivery; newborn care and long-term prognosis; risk of recurrence; and options for the pregnancy, including continuation versus termination of the pregnancy.

INTRODUCTION The incidence of major birth defects—those associated with significant medical implications such as abnormalities of the central nervous system, the face or the cardiac, renal, gastrointestinal or skeletal systems—is approximately 4%. Minor birth defects such as skin tags are more common, but usually have no (or only minor) cosmetic implications. Many congenital defects have a genetic origin, whether from chromosomal defects (approximately 10%), single gene disorders (approximately 5%) or where inheritance is multifactorial (approximately 25%). Other defects may be a result of fetal infection, such as toxoplasmosis, rubella, cytomegalovirus and herpes simplex virus (see Ch 19) or exposure to known teratogens. In the majority of cases, the aetiology remains

unknown. Congenital abnormalities may be part of a syndrome, where there is a collection of abnormalities in a characteristic pattern that are genetically linked. Screening for birth defects involves genetic screening for Down syndrome and related chromosomal disorders, and an anatomical survey with ultrasound, usually performed at 18 to 22 weeks’ gestation. Screening for other genetic disorders with important health implications but without a recognisable phenotype on ultrasound may be performed for disorders such as thalassaemia, cystic fibrosis and fragile X syndrome. Management of pregnancies where the fetus is known to have a fetal abnormality or serious medical condition requires the involvement of a multidisciplinary team. Counselling should address the implications of the diagnosis for the remainder of the pregnancy, labour and delivery,

Chapter 9  Screening, Diagnosis and Management of Genetic and Structural Abnormalities in the Fetus

for postnatal care and the long-term implications. Some conditions may be amenable to in utero treatment, while most will involve postnatal surgery, medical treatment or ongoing surveillance. In some conditions, where the outlook is lethal, palliative care may be offered to the newborn. In conditions where a fetus is diagnosed with a serious or life-threatening condition, some families may consider adoption, while many will face the difficult decision of pregnancy termination.

GENETIC CONDITIONS SCREENING FOR ANEUPLOIDY Down syndrome (or trisomy 21) is caused by a complete or partial third copy of chromosome 21 (see Fig 9.1). It is the most common chromosomal abnormality associated with live birth, and the leading cause of intellectual disability associated with a recognisable chromosomal abnormality. Children with Down syndrome have a characteristic phenotype (Fig 9.2) including short stature, flattened nasal bridge, protruding tongue, epicanthic folds, short neck, single transverse palmar crease and hypotonia. Intellectual disability is universal, usually in the mild (IQ 50 to 70) to moderate (IQ 30 to 50) range. Up to 50% of newborns will have congenital heart disease and other structural abnormalities that may be identified prenatally, including duodenal or oesophageal atresia. Medical problems include hypothyroidism, hearing and eye abnor­malities, and an increased risk of

some malignancies. Behavioural and psychiatric problems are more common, as well as autism and early-onset dementia. Down syndrome affects approximately 1:600 to 700 pregnancies, although this depends on the maternal age of the population being studied, since the majority of pregnancies affected by trisomy 21 occur as a result of nondisjunction. Trisomy 21 from nondisjunction occurs when one gamete contributes 24 chromosomes (including two copies of chromosome 21) to the conceptus instead of the usual 23, resulting in 47 chromosomes. The karyotype for a female fetus with Down syndrome is shown in Figure 9.1 (written 47XX + 21). The majority of nondisjunction events are maternal in origin, and are more common with increasing maternal age. This explains the increased risk of miscarriage due to aneuploidy, and of live birth with Down syndrome, observed in older women. Less than 5% of cases of Down syndrome occur as a result of translocation, where the long arm of chromosome 21 is attached to another chromosome, usually chromosome 14. While the translocation is balanced (with a normal and complete complement of genetic material in the carrier parent), this has the potential to become unbalanced at the time of conception. Down syndrome is common. It has important medical implications. While not all families will decide to proceed with genetic screening, screening for Down syndrome, and access to diagnostic testing with amniocentesis or chorionic villus sampling (CVS), is considered an essential component of antenatal care. Historically, maternal age was the only screening test offered for Down syndrome, with all women aged 37 and over at the time of delivery offered invasive testing. However, this results in a screen positive rate of approximately 10% for a Down syndrome detection rate of only 30%. Population-based screening programs using serum screening, ultrasoundbased screening or a combination of both have vastly improved detection rates of Down syndrome, and it is recommended that all women be offered a screening test, regardless of maternal age. The recent arrival of cell-free fetal DNA as an advanced screening test has rapidly changed the landscape of aneuploidy screening, with superior sensitivity and specificity compared to other screening approaches. After Down syndrome, the chromosomal abnormalities most likely to result in live birth are trisomy 13 and trisomy 18, although both are almost inevitably lethal. Figure 9.2 provides a summary of the phenotypic features of trisomy 21, trisomy 18 and trisomy 13.

Screening tests for trisomy 21 Second trimester maternal serum screening FIGURE 9.1 

Trisomy 21 karyotype in a female fetus.

Source: Simpson JL, Elias S. Genetics in Obstetrics and Gynecology. 3rd edn. Philadelphia: WB Saunders, 2003. Figure 10.2.

Maternal serum analytes examined in the second trimester include alpha-fetoprotein, oestriol, β-hCG and inhibin. Gestation-specific reference ranges have been established and so maternal serum screening results are expressed as multiples of the median (MoM). Maternal blood is taken 71

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Epicanthic fold and flat facial profile

Intellectual disability Abundant neck skin

Simian crease

Congenital heart defects Intesinal stenosis

TRISOMY 21: DOWN SYNDROME Incidence: 1 in 700 births Karyotypes: Trisomy 21 type: 47, XX, +21 Translocation type: 46, XX, der(14;21)(q10;q10), +21 Mosaic type: 46, XX/47, XX, +21

Umbilical hernia Predisposition to leukaemia

Prominent occiput

Hypotonia

Intellectual disability Micrognathia

Gap between first and second toe

Low set ears Short neck Overlapping fingers

TRISOMY 18: EDWARDS SYNDROME

Congenital heart defects

Incidence: 1 in 8000 births Karyotypes: Trisomy 18 type: 47, XX, +18 Mosaic type: 46, XX/47, XX, +18

Renal malformations Limited hip abduction

Microphthalmia Polydactyly

Microcephaly and Intellectual disability

Cleft lip and palate

Rocker-bottom feet

Cardiac defects Umbilical hernia

Renal defects

TRISOMY 13: PATAU SYNDROME Incidence: 1 in 15 000 births Karyotypes: Trisomy 13 type: 47, XX, +13 Translocation type: 46, XX, +13, der(13;14)(q10;q10) Mosaic type: 46, XX/47, XX, +13

Rocker-bottom feet

FIGURE 9.2 

Characteristic phenotype and karyotype of fetuses with trisomy 21, trisomy 18 and trisomy 13.

Source: Kumar V, Abbas A, Fausto N, Aster J. Robbins and Cotran Pathologic Basis of Disease, Professional Edition. 8th edn. Philadelphia: Saunders, 2009. Copyright © 2009 Saunders, An Imprint of Elsevier.

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Chapter 9  Screening, Diagnosis and Management of Genetic and Structural Abnormalities in the Fetus

between 14 and 20 weeks’ gestation, with maternal age, weight, gestation and the presence of diabetes or a multiple pregnancy recorded. The pattern of biochemical abnormalities in a pregnancy affected by Down syndrome is a reduced alpha-fetoprotein and oestriol (the fetal contributors) and an elevated inhibin and β-hCG (the ‘placental’ contributors). The likelihood ratio corresponding to the maternal serum MoM is applied to the maternal a priori risk (the risk associated with her age alone) and a new risk is generated. The more maternal serum analytes that are examined, the higher the Down syndrome detection rate. When screening incorporates all four analytes, the detection rate in well-dated pregnancies is approximately 75% using a cut-off of 1:250 or higher and a false-positive rate of 5%. This means that 5% of women will screen positive, having an adjusted individual risk result between 1:2 (highest possible screen-positive risk) and 1:250 (lowest possible screen-positive risk), but almost all of these will turn out to be false-positives (i.e. they will be found to have an unaffected fetus at the time of diagnostic testing). The disadvantage of this test is the later gestation at the time of testing, and that the pregnancy needs to be accurately dated.

Screening with first-trimester nuchal translucency Fetuses with Down syndrome are more likely to have an increased fluid space (the nuchal translucency measurement) in the first trimester (Fig 9.3). This ultrasound is performed when the crown–rump length measures 48 to 84 mm, corresponding to a gestational age of 11 to 13 weeks. The Down syndrome detection rate using nuchal translucency measurement alone is approximately

A

75% using a cutoff of 1:300 or higher and a false-positive rate of 5%. While this test has comparable accuracy to second-trimester maternal serum screening, the advantage is the increased privacy offered by earlier screening; most families and clinicians would favour first-trimester screening and diagnosis. The disadvantage of nuchal translucency measurement is that it is operator dependent. For this reason, the Fetal Medicine Foundation provides only accredited sonographers with access to the software package that generates the customised risk.

Screening with first-trimester combined testing First-trimester combined testing refers to maternal serum screening in the first trimester, using pregnancy-associated plasma protein A (PAPP-A) and hCG combined with the nuchal translucency measurement. With first-trimester combined screening, patients have a blood test performed at 9 to 12 weeks followed by an ultrasound at 11 to 13 weeks (see previous section). The adjusted risk reflects the likelihood ratio generated by both the maternal serum screening and nuchal translucency results applied to the background maternal age risk. Not surprisingly, using the modalities of both ultrasound and maternal serum screening results in an improved sensitivity; the detection rate using first-trimester combined screening is approximately 90% at a cutoff of 1:300 and a false-positive rate of 5%.

Integrated testing: combining first- and secondtrimester screening The Down syndrome detection rate can be further increased (or the false-positive rate minimised) by modifying the first-trimester combined adjusted risk with

B

FIGURE 9.3 

Nuchal translucency measurement. A Normal nuchal translucency, measured with a well-magnified image, separate to the amnion and the neck in a neutral position. B Increased nuchal translucency associated with Down syndrome. Source: Adam, A, Dixon AK, Grainger RG, Allison DJ. Grainger and Allison’s Diagnostic Radiology. 5th edn. Philadelphia: Churchill Livingstone, 2007. Copyright © 2008 Churchill Livingstone, An Imprint of Elsevier. Figure 53.11.

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second-trimester maternal serum screening (the integrated screening test). While not commonly performed, the detection rate using the five maternal serum analytes (PAPP-A in first trimester, plus alpha-fetoprotein, oestriol, inhibin and β-hCG in the second trimester) plus firsttrimester nuchal translucency is 90%, with a false-positive rate of only 2%. This minimises the risk of requiring a diagnostic test, with the attendant procedural loss, while retaining maximal sensitivity. The disadvantage of this test is that the final result is not available until the second trimester, but this may be minimised by the use of sequential or contingent screening. In the former approach, high-risk women on the basis of the firsttrimester results (e.g. > 1:50) are offered diagnostic testing, with the remainder being offered further testing in the second trimester to better quantify their risk. In the latter approach, three levels of risk are identified at the end of first-trimester testing: high-risk women (e.g. > 1:50), who are offered immediate diagnostic testing; lowrisk women (for e.g. < 1:2000) who are offered no further testing, given their extremely low risk; and intermediaterisk women (1:50 to 1:2000) who are then offered secondtrimester maternal serum screening to complete the integrated testing.

characteristic of the Down syndrome phenotype detectable with ultrasound which does not in itself pose any health risk to the fetus. Examples of soft markers include echogenic bowel, a short humerus or femur, clinodactyly of the fifth finger or a ‘sandal gap’ between the first and second toes. Nevertheless, such soft markers are found in approximately 15% of normal pregnancies, and so use of ultrasound alone as a screening test is inadequate. Ultrasound evaluation for structural abnormalities and soft markers may be used in combination with maternal serum screening with detection rates for Down syndrome increasing from approximately 80% to 90% in this setting. A normal second trimester ultrasound is associated with approximately halving the risk generated by maternal serum screening alone.

Abnormal maternal serum screening results: other implications

An exciting new development in the area of prenatal genetic diagnosis is non-invasive prenatal screening (NIPS) using cell-free fetal DNA (cffDNA) from the plasma of pregnant women. Circulating cell-free fetal DNA comprises approximately 10% of total maternal cell-free fetal DNA, and analysis of the fetal fraction of cell-free DNA is associated with detection rates of 99%, 95% and 90% for Trisomy 21, Trisomy 18 and Trisomy 13 respectively, with a false-positive rate of < 0.5%. cffDNA has the highest sensitivity and specificity of any screening test for Down syndrome. While initially only recommended for high-risk women, this technology has rapidly transitioned into clinical practice, and large datasets are confirming excellent test performance characteristics in low-risk women. Although this screening test has predictive characteristics that outperform previous screening tests, with very low false-positive and false-negative rates, it is important to note that it is not a diagnostic test. Confirmation with invasive testing is still necessary for patients with a screen positive result. Given the relatively high cost of this test, appropriate counselling is necessary for patients wishing to consider non-invasive prenatal diagnosis to ensure the limitations of this test, including failed fetal fraction, and the possibility of atypical findings are understood.

Very abnormal maternal serum results may be seen in a range of other pregnancy complications, even if the adjusted aneuploidy risk is low or chromosomal abnormalities have been excluded with diagnostic testing. Further evaluation is recommended in the following cases. First trimester ■ A low PAPP-A (< 0.4 MoM) is associated with a threefold increase in intrauterine growth restriction (IUGR) (positive predictive value 15%), intrapartum fetal distress, preeclampsia and stillbirth. ■ A low β-hCG (< 0.2 MoM) is associated with an increased risk of IUGR, with a positive predictive value of 15%. ■ The finding of a PAPP-A or β-hCG below these thresholds should prompt careful evaluation of fetal growth and wellbeing in late pregnancy, and avoiding post-term pregnancy. Second trimester ■ An elevated maternal serum alpha-fetoprotein in the second trimester (> 2.0 to 2.5 MoM) is associated with a range of structural defects including neural tube defects, exomphalos and gastroschisis. The finding of a maternal serum alpha-fetoprotein in this range should prompt a tertiary-level morphology ultrasound to exclude these and other structural defects. If no abnormality is confirmed, growth surveillance is recommended in late pregnancy. ■ A low oestriol (< 0.2 MoM) is associated with placental sulphatase deficiency, Smith-LemliOpitz syndrome and fetal death. Further evaluation is recommended in these cases.

Second-trimester ultrasound

Diagnostic tests

Approximately 50% of pregnancies affected with Down syndrome will have some clue on their routine morphology scan, such as a structural abnormality (e.g. a cardiac defect or cerebral ventriculomegaly), or a ‘soft marker’ of Down syndrome. A soft marker is a physical

Among women who screen as high risk for aneuploidy, the available diagnostic tests are chorionic villus sampling and amniocentesis. These are ultrasound-guided procedures done as an outpatient and do not require anaesthetic. Anti-D is given to all women who are

Non-invasive prenatal screening using cell-free fetal DNA

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Chapter 9  Screening, Diagnosis and Management of Genetic and Structural Abnormalities in the Fetus

Rh-negative following any invasive procedure, and infective status for blood-borne viral infections should be noted on the referral. Chorionic villus sampling (CVS) is a procedure where a needle is passed into the chorionic (placental) plate and chorionic villi are aspirated (Fig 9.4). The procedure is most commonly performed between 12 to 14 weeks and is often the diagnostic test chosen after abnormal firsttrimester screening. The risk of miscarriage following CVS is approximately 1%. Amniocentesis is performed after 15 weeks’ gestation where approximately 10 to 15 mL of amniotic fluid is aspirated. The advantage of this test is the lower risk of miscarriage (approximately 0.5%), but this needs to be weighed against the problem of later diagnosis. Information that may be obtained from the genetic material taken at diagnostic testing includes fluorescent in-situ hybridisation, banded karyotype, microarray and single gene testing. Fluorescent in-situ hybridisation (FISH). This is a test where fluorescent-labelled probes attach to critical regions on individual chromosomes. The result is available in 48 hours, so FISH is a useful test to promptly exclude the major chromosomal abnormalities (trisomy 21, 18 and 13) and sex chromosome abnormalities (Fig 9.5). A FISH probe can be customised for other critical chromosomal regions to target a specific duplication or deletion (e.g. the 22q microdeletion associated with DiGeorge syndrome). Banded karyotype. Standard karyotyping involves examination of all chromosomes and will diagnose





disorders of chromosome number (aneuploidy) or structure, such as deletions, duplications and translocations. The result from a banded karyotype takes approximately 2 weeks. Microarray (or molecular karyotype). Microarray analysis has successfully transitioned into prenatal clinical care. Microarray analysis enables detection of chromosomal deletions or duplications that are 100 times smaller than those identified on conventional karyotype. These small changes may be associated with significant phenotypic consequences. Nevertheless, microarray analysis carries the potential for findings of uncertain significance, and consultation with a genetic counsellor with attention to pre- and posttest counselling is recommended. Single gene testing. This can be performed on any prenatal sample for autosomal-dominant, recessive or X-linked conditions where the genetic defect is known. This includes conditions such as cystic fibrosis and thalassaemia.





SCREENING FOR OTHER GENETIC CONDITIONS Cystic fibrosis Cystic fibrosis is one of the most common autosomalrecessive disorders, with a carrier frequency among Caucasian populations of approximately 1:25. This means the birth prevalence for cystic fibrosis is 1:2500 (1:25 × 1:25 × 1:4). Cystic fibrosis is a disorder of exocrine gland secretions causing an accumulation of thickened secretions that result in recurrent lung infections, malabsorption, infertility in males and shortened life expectancy. All newborns are screened for cystic fibrosis, but some families wish to know whether they are at risk prior to birth. Antenatal screening involves performing a cheek swab or blood test to check for the most common genes responsible for cystic fibrosis. Approximately 85% of carriers will be identified with this test. Diagnostic testing may be performed where both parents are confirmed to be carriers, where the risk to the fetus is 1:4.

Haemoglobinopathies

FIGURE 9.4

Transabdominal chorionic villus sampling.

Source: Gabbe SG, Niebyl JR, Galan HL, et al. Obstetrics: Normal and Problem Pregnancies. 6th edn. Philadelphia: Saunders, 2012. Copyright © 2012 Saunders, An Imprint of Elsevier. Figure 11.2.

Haemoglobinopathies may be divided into conditions of globin synthesis dysfunction (thalassaemias) or haemoglobin variants (such as sickle cell disease). Thalassaemia may affect either the alpha or beta subunit of the globin chain. Alpha-thalassaemia major (where all four genes coding alpha globin synthesis are missing) is incompatible with life since alpha chain synthesis is necessary for all haemoglobin types. Beta-thalassaemia major is associated with lifelong transfusion-dependent anaemia, a need for chelation therapy and shortened life expectancy. Women may be identified as being at risk (i.e. carriers) because of a personal or family history of thalassaemia. Screening among women without a known history may be based on: 1. assessment of full blood examination 75

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Interphase FISH

21

Y

13

18

X

21 13

18

Normal

Normal male

Trisomy 21

Trisomy 18

FIGURE 9.5

FISH on amniotic fluid cells to screen for aneuploidy.

Source: Lentz GM, Lobo RA, Gershenson DM, Katz, VL. Comprehensive Gynecology. 6th edn. St Louis: Mosby, 2012. Copyright © 2012 Mosby, An Imprint of Elsevier. Figure 2.9.

parameters looking for evidence of an unexplained low mean cell volume (< 80 fl); 2. targeted screening of at-risk ethnic groups (African, South-East Asian and Mediterranean); or 3. universal screening with haemoglobin electrophoresis. Women found to have beta thalassaemia minor should be offered partner screening. If the partner is also found to have thalassaemia minor, they have a 1:4 risk of thalassaemia major in the offspring, and prenatal testing with chorionic villus sampling or amniocentesis should be offered.

reproductive carrier screening for a panel of conditions that are individually rare, but collectively common, is increasing as part of routine antenatal and preconception care. Families need to carefully weigh up the additional information obtained regarding their pregnancy against the financial cost and anxiety generated by unexpected findings. Genetic counsellors are invaluable in assisting with pre- and post-test counselling.

Other genetic conditions

PREVENTION OF STRUCTURAL ABNORMALITIES

Advice should be sought from a prenatal genetic counsellor regarding the place for prepregnancy or antenatal screening of other high-risk groups. Examples include screening of Ashkenazi Jews for Tay Sachs disease, and screening for Fragile X among families with a history of male autism or intellectual disability or those with a known family history of genetic conditions. Prepregnancy identification of high-risk couples enables them to consider assisted reproductive options such as preimplantation genetic diagnosis or use of donor gametes to minimise their risk of an affected child. The use of 76

STRUCTURAL ABNORMALITIES Some women are at higher than average risk for structural abnormalities. This includes women with a positive family history or who have had a previously affected pregnancy. Women with diabetes have an increased risk of malformations, with the risk directly correlated with Hb A1C at the time of conception. Some medications and social exposures are known to be teratogenic, including ACE inhibitors, lithium, warfarin, antiepileptic drugs (AEDs) and alcohol. Obesity is associated with a

Chapter 9  Screening, Diagnosis and Management of Genetic and Structural Abnormalities in the Fetus

small but significantly increased risk of some structural abnormalities. Prevention of structural abnormalities thus includes advice on optimising medications, diabetic control and weight prior to pregnancy. Folic acid should be prescribed to all women contemplating pregnancy, and high-dose folate (5 mg daily) for women at increased risk of neural tube defects. This includes those with a previously affected child, women with diabetes, women receiving AEDs and obese women. Rubella and varicella are both potential teratogens, and vaccination prior to pregnancy is recommended.

DETECTION OF STRUCTURAL ABNORMALITIES The routine second trimester ultrasound is generally performed between 18 and 22 weeks’ gestation. Benefits of the routine second trimester ultrasound include accurate assignment of gestational age, diagnosis of multiple pregnancy, placental localisation and assessment of fetal anatomy. This targeted anatomical survey detects approximately 60% of major anatomical defects, with minor abnormalities more likely to be missed. Many major abnormalities may be detected as early as the first trimester, but even in the second trimester cardiac defects are less likely to be detected than central nervous system (CNS) or genitourinary abnormalities. The detection rate is limited by: the nature of some abnormalities (which may not become apparent until later in pregnancy) the gestation at the time of the ultrasound fetal position and number technical limitations including operator experience, ultrasound machine quality and maternal obesity which can seriously limit visualisation. Women known to be at high risk of structural abnormalities should have their ultrasound performed in a centre dedicated to obstetric ultrasound since detection rates are known to be higher in tertiary centres then in non-tertiary ones. This includes women with risk factors (see above), those who have had an increased nuchal translucency in early pregnancy or those who have suffered a teratogenic insult during pregnancy such as one of the TORCH infections (toxoplasmosis, other, rubella virus, cytomegalovirus and herpes simplex viruses). A brief overview of the most common abnormalities which have important perinatal implications now follows.

• • • •

aorta), abnormalities of venous return or abnormalities of rhythm or function. These lesions vary according to their risk of serious in utero consequences, such as heart failure and fetal hydrops, and important implications for neonatal care, such as cyanotic or ‘duct-dependent’ lesions. Women at increased risk of cardiac structural defects include those with a past or family history of congenital heart disease, women with diabetes or those exposed to teratogens such as AEDs and lithium, women with anti-Ro or anti-La antibodies or those with an increased nuchal translucency measurement in the first trimester. These women should have a detailed fetal echocardiogram performed in the second trimester, as should those with a suspected abnormality on screening examination. Follow-up with a paediatric cardiologist is advised if abnormalities are confirmed.

Abnormalities of the central nervous system Neural tube defects include anencephaly (where the cephalic portion of the neural tube fails to close, resulting in absence of the skull and most of the cerebrum), encephaloceles (where there is a skull defect and brain content herniates through the defect) and spina bifida (where there is a failure of closure of the dorsal aspect of the spine, with subsequent exposure of the meningesmeningocele and spinal cord myelomeningocele; see Fig 9.6). Anencephaly is universally lethal. The outlook for spina bifida depends on the level of the lesion, since the exposed spinal cord is dysplastic and motor and sensory function below the level of the bony defect is affected, resulting in varying degrees of paralysis, sensory dysfunction and disturbance of bowel and bladder function. The development of hydrocephalus will impact on neurodevelopmental outcome. The prognosis will be further affected by the presence of other chromosomal or structural abnormalities. The incidence of neural tube defects has dramatically reduced since the commencement of routine screening

Abnormalities of the cardiovascular system Abnormalities of the cardiovascular system are the most common type of structural abnormality with an incidence of 0.5 to 1%. These include septal defects (atrial, ventricular or atrioventricular septal defects), defects of the outflow tracts (such as tetralogy of Fallot, transposition of the great vessels and coarctation of the

FIGURE 9.6

Neonate with myelomeningocele.

Source: Townsend C, Beauchamp RD, Evers MB, Mattox K. Sabiston Textbook of Surgery. 19th edn. Philadelphia: Saunders, 2012. Figure 68.34.

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and folic acid supplementation. More recently, open fetal surgery has been shown to improve the outcome of children with spina bifida, where the spinal defect is closed via a hysterotomy incision prior to 26 weeks. This specialised surgery is not currently available in Australia and the benefits to the fetus need to be weighed against the maternal morbidity, including preterm birth and the risk of scar rupture in subsequent pregnancies. Nevertheless, this option may be appropriate for well-selected cases. Other CNS abnormalities diagnosed on ultrasound include: ventriculomegaly, which should trigger a series of further investigations looking for developmental, obstructive, chromosomal or infective causes; midline abnormalities, such as holoprosencephaly and agenesis of the corpus callosum; destructive lesions due to infection or haemorrhage; vascular malformations, such as the Vein of Galen malformation; or tumours. Neurosonography by those with experience in ultrasound evaluation of the fetal neural axis should be performed when an abnormality is suspected, and fetal magnetic resonance imaging (MRI) may be recommended, which provides additional useful information.

Abnormalities of the gastrointestinal system The most common abnormalities of the gastrointestinal system are developmental abnormalities of the anterior abdominal wall and, of these, exomphalos and gastroschisis are most common. Exomphalos (also termed omphalocele) is due to failure of return of the midgut to the abdominal cavity, which is usually completed by the end of the first trimester. Ultrasound shows a midline herniation of bowel (with or without liver) into the base of the cord, which is covered by peritoneum and amnion. Exomphalos is strongly associated with aneuploidy and other structural abnormalities. Where isolated, the outlook will depend on the size of the lesion and the ability to achieve successful postnatal surgical closure. Gastroschisis is a full-thickness paramedian abdominal wall defect where the small bowel herniates into the amniotic cavity unprotected by peritoneum (Fig 9.7). Matting of bowel loops and adhesion formation is common, and surgical resection of bowel loops may need to be performed at the time of abdominal wall closure. Gastroschisis is usually an isolated defect, but fetal growth restriction (FGR) in late pregnancy is common and early delivery is often indicated. Fetuses with abdominal wall defects need to be delivered in a facility where advanced neonatal resuscitation is available, and transfer to a surgical ward is usually arranged soon after delivery.

Abnormalities of the genitourinary system The most common abnormality of the genitourinary system is renal pelvis dilation, which may be mild (often resolving in the postnatal period) or severe (due to lower urinary tract obstruction). Bladder outlet 78

FIGURE 9.7

Gastroschisis. Note the protruding loops of small bowel, uncovered by peritoneum.

Source: Gabbe SG, Niebyl JR, Galan HL, et al. Obstetrics: Normal and Problem Pregnancies. 6th edn. Philadelphia: Saunders, 2012. Copyright © 2012 Saunders, An Imprint of Elsevier. E-Figure 21.3.

obstruction, typically due to posterior urethral valves in a male fetus, results in megacystis and severe hydronephrosis with anhydramnios. Amniotic volume assessment is crucial in determining the severity of a renal abnormality, since amniotic fluid is necessary for the fetal lungs to expand and develop normally. Severe renal abnormalities, such as bilateral renal agenesis or complete lower urinary tract obstruction, will be lethal because the subsequent anhydramnios results in lethal pulmonary hypoplasia. Lower grade obstruction, or abnormalities that are unilateral, should be followed up regularly during pregnancy with a plan for postnatal imaging and investigation.

Abnormalities of the face The most common facial abnormalities are cleft lip and/ or cleft palate. Women at risk include those with a family history and those on AEDs. Routine prepregnancy folate supplementation reduces the chance of clefting. Prenatal detection of an orofacial cleft should prompt a search for associated structural abnormalities and an amniocentesis should be offered. Prenatal referral to a paediatric cleft service is recommended to discuss neonatal management, including feeding advice and surgical repair, since surgical repair is associated with excellent cosmetic results (Fig 9.8).

Abnormalities of the skeletal system Skeletal dysplasias are a large group of disorders characterised by abnormal bone growth or development, and may affect only isolated bones or the entire skeleton. Evaluation of a suspected skeletal dysplasia should

Chapter 9  Screening, Diagnosis and Management of Genetic and Structural Abnormalities in the Fetus

A

B

C

D

FIGURE 9.8

Preoperative (A), perioperative (B) and postoperative (C, D) view of unilateral cleft lip.

Source: Townsend C, Beauchamp RD, Evers MB, Mattox K. Sabiston Textbook of Surgery. 19th edn. Philadelphia: Saunders, 2012. Figure 69.4.

involve taking a history for skeletal dysplasias or familial short stature, careful evaluation for other structural abnormalities and FGR, performance of karyotype and referral to a centre with experience in evaluation of skeletal dysplasias. One of the most important assessments is the likelihood of lethality; this is mostly seen in severe skeletal dysplasias with extreme bone shortening and is due to underdevelopment of the fetal chest and resultant pulmonary hypoplasia.

Fetal tumours The most common fetal tumours are sacrococcygeal and cervical teratomas. Sacrococcygeal teratomas (SCT) particularly may undergo rapid growth during pregnancy, and be highly vascular. Accordingly, they may be responsible for high-output cardiac failure and development of fetal hydrops; haemorrhage into the tumour may also result in fetal anaemia. Management of pregnancies with 79

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a known fetal tumour includes frequent assessment of fetal wellbeing, consultation with a paediatric surgeon and possible evaluation with other imaging modalities such as MRI to plan postnatal surgical resection. Delivery may be challenging where tumours are large. Classical caesarean section may be necessary for a large SCT to facilitate delivery and minimise the risk of bleeding and trauma to the tumour at delivery. Where there is a large cervical teratoma, the neonatal airway may be compromised at delivery. In these circumstances, ex utero intrapartum therapy (EXIT) may be considered. The EXIT procedure involves delivering the fetal head by caesarean section under general anaesthetic while maintaining placental circulation until such time as an airway can be established. Such procedures require careful planning and can only be performed in a specialist centre with an experienced anaesthetic, obstetric and paediatric team.

Fetal hydrops Fetal hydrops is the description given to a fetus with fluid accumulation in two or more body cavities (pleural fluid, pericardial fluid, ascites or skin oedema; Fig 9.9). Hydrops may be due to conditions associated with cardiac failure, increased venous pressure or increased interstitial fluid accumulation. While hydrops has a large variety of causes, a useful acronym is CAUSTIC. Cardiac. This covers structural cardiac abnormalities (particularly those associated with high right atrial pressure, such as tricuspid atresia); high-output cardiac failure (e.g. due to fetal thyrotoxicosis or tumours); fetal arrhythmia (e.g. fetal congenital heart block or fetal tachyarrhythmias) and fetal



cardiomyopathy (including those due to infection or metabolic disorders). Anaemia. Fetal anaemia may be due to red blood cell isoimmunisation, feto-maternal haemorrhage, complications of monochorionic twinning or homo­ zygous alpha thalassaemia. Unexplained. A significant group of fetuses may be affected by hydrops due to an unknown underlying diagnosis. Structural. Structural abnormalities associated with hydrops include chest lesions that cause mediastinal compression and impair venous return as well as fetal or placental tumours. Twins. Monochorionic twins may be affected by twin-to-twin transfusion syndrome (TTTS; see Ch 14) which results in high-output cardiac failure in the recipient twin. Infective. Fetal infections such as toxoplasmosis, cytomegalovirus, rubella, syphilis and herpes simplex may result in hydrops due to the combined effects of myocardial inflammation and hepatitis (with decreased protein production) or specific mechanisms such as fetal anaemia due to parvovirus infection. Chromosomal. Chromosomal abnormalities include trisomy 21 or Turner’s syndrome (X0). In pregnancies complicated by fetal hydrops, a thorough evaluation should include establishing an underlying diagnosis. While some conditions such as fetal anaemia or TTTS may be amenable to in utero therapy, most fetuses with hydrops will not have a treatable cause and have a poor prognosis. The excessive placental size due to placental oedema makes the development of maternal preeclampsia (the so-called ‘mirror syndrome’) more likely. Accordingly, pregnancies complicated by fetal hydrops which are continuing require both careful fetal evaluation and close maternal surveillance.

• • • • •



MANAGEMENT OF PREGNANCIES COMPLICATED BY FETAL GENETIC OR STRUCTURAL ABNORMALITIES FIGURE 9.9

Fetal hydrops. Longitudinal view of a fetus with skin oedema, ascites and a hydrothorax.

Source: Adam, A, Dixon AK, Grainger RG, Allison DJ. Grainger and Allison’s Diagnostic Radiology. 5th edn. Philadelphia: Churchill Livingstone, 2007. Copyright © 2008 Churchill Livingstone, An Imprint of Elsevier. Figure 53.17.

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The application of genetic screening and fetal ultrasound in obstetrics has revolutionised the management of pregnancy and its potential complications. While normal findings improve positive feelings about the pregnancy and have been shown to promote earlier bonding, the finding of isolated or multiple serious abnormalities on prenatal ultrasound examination is inevitably stressful. Families require accurate information about the condition as quickly as possible. This is often best achieved with timely review in a multidisciplinary clinic with access to

Chapter 9  Screening, Diagnosis and Management of Genetic and Structural Abnormalities in the Fetus

obstetricians, paediatricians, genetic counsellors, medical geneticists, and ultrasonologists with experience in diagnostic and procedural ultrasound. Discussion within a multidisciplinary team has been shown to improve decision making about management of unborn infants with serious abnormalities. The counselling provided should be unbiased and respectful of the patient’s circumstances, culture, religion and beliefs, and be imparted with empathy and compassion. The information that needs to be provided includes confirmation of the abnormality, the likely aetiology, relevant associations, further investigations required and implications for the remainder of the pregnancy, labour and delivery, as well as the outlook for the patient’s unborn baby as a newborn and beyond, and the choices available to her regarding the future of the pregnancy. Retention of medical information at a time of stress is poor. A follow-up appointment should be planned soon after the disclosure interview, and frequent follow-up will be necessary. The provision of diagrams and written information can be valuable. Many patients will seek additional information on the internet; where possible, the names of recognised and reliable sites for information should be provided.

HISTORY AND EXAMINATION Once a fetal structural abnormality has been identified, a thorough medical, obstetric and family history should be performed. 1. Medical history (and examination where necessary) of both parents should be obtained, considering the possibility of unidentified autosomal-dominant traits (such as 22q11 deletion syndrome, myotonic dystrophy or tuberous sclerosis) that may be variably expressed or have a mild phenotype, escaping detection until adulthood. 2. Obstetric history should identify any potential teratogens, including medications, other drug exposures, infection and radiation. 3. Family history should be detailed, documenting a three-generation pedigree, noting particularly any children born with abnormalities, early deaths or consanguinity between the parents.

IMAGING The detection rate for structural abnormalities is higher in tertiary, compared to non-tertiary units. Because of this, all women with a suspected fetal abnormality should have a tertiary level ultrasound performed to optimise the information obtainable from prenatal ultrasound. This may include the use of 3D ultrasound, since this modality may be particularly useful in the assessment of facial and skeletal abnormalities. Fetal MRI may be of additional use, particularly when assessing brain abnormalities, lung abnormalities, complex abnormalities (particularly those requiring surgical planning) or when oligohydram-

nios is present. Parental imaging may occasionally assist with fetal diagnosis when the abnormality/abnormalities may represent an autosomal-dominant condition, such as polycystic kidney disease, or tuberous sclerosis.

ADDITIONAL TESTING Parental blood tests may be indicated if suspecting an X-linked, autosomal-recessive or autosomal-dominant genetic diagnosis, or where congenital infection may be a possible explanation for the ultrasound findings.

INVASIVE TESTING Fetal karyotype is indicated where the ultrasound findings are associated with an increased risk for aneuploidy. In the setting of structural abnormality, microarray (or molecular karyotyping) is recommended since studies suggest that 1 to 3% of fetuses with a structural abnormality will have an abnormality on microarray that would fail to be detected on conventional karyotype.

COUNSELLING Following confirmation of a fetal abnormality, the following areas should be addressed in counselling.

The likely aetiology and prognosis of the condition There will be cases where prediction of outcome is relatively straightforward and others where it is less so. External referral (e.g. to paediatric surgeon, renal physician) may be necessary to provide more detail on long-term management and the outlook for the baby.

The likely implications for the remainder of the pregnancy Potential obstetric complications may develop during the pregnancy related to the abnormality, such as poly­ hydramnios with anencephaly, preeclampsia with fetal hydrops, or an increased risk of preterm birth or IUGR.

The implications for labour and delivery Depending on the abnormality, delivery may need to be in a tertiary setting and, in some circumstances, timed delivery and/or caesarean section may be indicated.

Care of the newborn Depending on the abnormality, a paediatrician may be required immediately at delivery, or the baby may require admission to neonatal intensive care or transfer to another hospital.

The expected short- and long-term outcomes Parents will require information on the likely prognosis for the abnormality, the potential need for surgery or 81

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long-term medical treatment, the potential complications and how the condition and its treatment will impact on their child’s quality of life.

The risk of recurrence in future pregnancies In conditions with a known genetic diagnosis, the recurrence risk may be certain. In conditions where the underlying diagnosis remains unclear, the risk to a future pregnancy may remain uncertain, but become clearer with postnatal evaluation.

MAKING A DECISION Following this initial period of information gathering, patients will come to a decision regarding the future of the pregnancy.

Ongoing care Most families will elect to continue the pregnancy despite the presence of an abnormality, and the place and timing of ongoing care will depend on the nature of the abnormality, the presence of other maternal or fetal comorbidities, the need for ongoing ultrasound surveillance and the expected needs of the newborn. Most commonly, these women will remain under the care of a multidisciplinary maternal fetal medicine unit.

Lethal abnormalities Where a lethal abnormality has been diagnosed, and the family have decided to continue with the pregnancy, it is essential to consider the implications for the remainder of the pregnancy and the newborn period. This includes determining the place (if any) for monitoring during pregnancy or labour and addressing palliative care of the newborn. The importance of a multidisciplinary team including bereavement care and social work cannot be underestimated to ensure the family’s particular spiritual, cultural and social priorities are fully addressed.

birth registration, and the need for burial or cremation. (See also Ch 53.)

Surgical termination of pregnancy: dilation and curettage (D&C) or dilatation and evacuation (D&E) Access to surgical termination will depend on gestation and the experience of the operator performing this procedure, but is generally not available beyond 20 weeks. Because of the destructive nature of this procedure, the fetus will generally not be intact to see and hold, and postmortem information may be more limited.

Medical termination of pregnancy Medical termination of pregnancy involves induction of labour. It may be offered from 15 weeks’ gestation and is generally recommended after approximately 20 weeks’ gestation. Medical termination of pregnancy means the fetus is delivered intact, which can be preferable for obtaining postmortem information and so that families can see their baby after delivery. Feticide, where an ultrasound-guided injection of intracardiac potassium chloride is administered to the fetus to arrest the heart prior to delivery, may be necessary somewhere around 21 to 23 weeks. Cervical priming with multi-dose misoprostol (synthetic prostaglandin E1) is the preferred method of induction. Mifepristone (RU486) may be administered 48 hours prior to the scheduled induction to improve cervical and myometrial receptivity to prostaglandins. Following delivery, retained placenta occurs in approximately 15% of second trimester deliveries and dilation and curettage (D&C) may be required for retained products of conception. Seeing and holding their baby is an important part of saying goodbye for many families, and they may wish to create memories such as photographs, handprints and footprints, as well as considering an appropriate service or ceremony to farewell their baby.

Postmortem following fetal or neonatal loss in the setting of fetal abnormality

In some circumstances, families will consider they are unable to care for a child facing major health concerns. Adoption will be an option for some of these families. Information regarding adoption should be accessible to patients and the multidisciplinary team should develop an appropriate postnatal care plan to support the woman and her family.

Women and their families should be aware of the value of comprehensive postmortem examination, including imaging and genetic testing, which may help in postnatal counselling regarding the underlying aetiology and the risk of recurrence in future pregnancies. Clinicians should support families and encourage them to consider a complete autopsy, and examination of the placenta, by a perinatal pathologist to provide maximal information on the diagnosis and aetiology of the structural abnormality or abnormalities.

Abortion

Post-termination care

In the face of a serious abnormality, families may request an abortion. Legislative requirements on the upper gestational limit for termination of pregnancy vary from state to state in Australia, as does legislation surrounding

Suppression of lactation is recommended for any woman who delivers a fetus after 18 to 20 weeks. The patient’s general practitioner or referring doctor should be notified of the pregnancy outcome prior to discharge home.

Request for adoption

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Chapter 9  Screening, Diagnosis and Management of Genetic and Structural Abnormalities in the Fetus

Although many women will wish to return home soon after delivery, postnatal bereavement support is essential, and early postnatal review is recommended to assess physical and emotional recovery. Later postnatal review, including the results of investigations such as autopsy, will focus on grief support as well as discussing recurrence risks and plans for future pregnancies. FURTHER READING Gagnon A, Wilson RD, Allen VM, et al. Evaluation of prenatally diagnosed structural congenital anomalies. J Obstet Gynecol Can 2009;31(9):875–81. Noninvasive prenatal testing for fetal aneuploidy. Committee Opinion No. 545. American College of Obstetricians and Gynecologists. Obstet Gynecol 2012;120:1532–24.

Pugash D, Brugger PC, Bettelheim D, et al. Prenatal ultrasound and fetal MRI: the comparative value of each modality in prenatal diagnosis. Eur J Radiol 2008;68:214–26. RANZCOG. Prenatal screening for fetal abnormalities. RANZCOG Statements and Guidelines (C-Obs 35). Online. Available: ; [March 2015]. Savage MS, Mourad MJ, Wapner RJ. Evolving applications of microarray analysis in prenatal diagnosis. Curr Opin Obstet Gynecol 2011;23(2):103–8.

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Section 2.4 OBSTETRIC COMPLICATIONS Chapter 10

Antepartum haemorrhage

Chapter 11

Fetal growth restriction and assessment of fetal wellbeing

Chapter 12

Preterm labour, including cervical insufficiency

Chapter 13

The postdates pregnancy and rupture of the membranes before labour at term

Chapter 14

Multiple pregnancy

Chapter 15

Malpresentation

Chapter 10  ANTEPARTUM HAEMORRHAGE Neil Israelsohn

KEY POINTS Antepartum haemorrhage is defined as vaginal bleeding of ≥ 20 mL after 20 weeks’ gestation. Antepartum haemorrhage (APH) is a serious condition affecting approximately 3% of pregnancies. It accounts for a significant proportion of maternal morbidity and mortality. It is also responsible for up to 50% of very preterm birth and hence neonatal morbidity and mortality. The incidence of APH secondary to placenta praevia is increasing in parallel with the increasing caesarean section rate. Any painless bleeding in the second half of pregnancy must be assumed secondary to placenta praevia until proven otherwise. A vaginal examination should not be performed until placenta praevia is excluded. Placental abruption is a clinical diagnosis. The use of ultrasound and blood tests may be additive but will rarely make or refute the diagnosis.

AETIOLOGY

RESUSCITATION IF NECESSARY

The aetiology of antepartum haemorrhage (APH) is classically described by the site of bleeding, as outlined in Table 10.1. The main focus of attention in both diagnosis and management of APH is aimed at distinguishing between the two most common causes: bleeding from a low-lying placenta (placenta praevia) or from placental abruption. While vasa praevia is rare, it is associated with high neonatal morbidity and mortality and warrants exclusion in anyone presenting with vaginal bleeding. An unknown cause of APH is the most common finding.

Blood loss can be heavy and may be concealed within the uterus. A careful assessment must be made of volume status and correction made as needed. A large bore cannula should be inserted if there is any doubt and bloods should be taken for a haematological profile if moderate or severe abruption is a possibility.

INITIAL MANAGEMENT OF AN APH OF UNKNOWN AETIOLOGY WHERE AND WHO? The woman should be admitted to hospital and carefully assessed by an experienced obstetric team.

ASSESS FETAL WELLBEING Clinically, the mother should report on fetal movements and the fundal height assessed. Ultrasound and cardio­ tocography are both indicated to further evaluate fetal wellbeing.

DETERMINE AETIOLOGY This involves an initial clinical assessment noting the following principles. Placenta praevia is typically recurrent painless small bleeds associated with a non-tender uterus and a high presenting part or malpresentation (because the placenta occupies the lower uterine segment).



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TABLE 10.1  AETIOLOGICAL CLASSIFICATION OF ANTEPARTUM HAEMORRHAGE. Aetiology

Site

Placenta praevia

Placenta: low lying

Placental abruption

Placenta: not low lying (variable location)

Incidental

Cervix and lower genital tract (e.g. cervical polyp)

Uterine rupture

Uterine non-placental

Vasa praevia

Fetal

Unknown cause

Unknown



A placental abruption of moderate or severe degree will be painful and associated with a tense tender uterus. Incidental bleeding commonly follows sexual intercourse or clinical examination. The site is usually apparent on speculum examination (remembering that digital vaginal examination is prohibited until the placental site has been determined and praevia excluded). An ultrasound is indicated to determine placental site and thereby exclude placenta praevia. Management thereafter will be determined by the diagnosis.



PLACENTA PRAEVIA DEFINITION The incidence of placenta praevia is approximately 1 in 250 pregnancies > 20 weeks’ gestation. Placenta praevia is defined as a placenta that inserts wholly, or in part, into the lower uterine segment. It either overlies, or is proximate (≤ 2 cm) to, the internal cervical os. Placenta praevia is often described as mostly anterior or posterior and is then further classified according to ultrasound criteria. Minor: the leading edge of the placenta lies within the lower segment (≤ 2 cm), up to the edge of the cervical internal os. Major: the placenta lies over the internal os. This classification has largely replaced the older classification of Grade 1, 2, 3, 4 placenta praevia shown in Figure 10.1. Several studies have shown that more than 90% of placentas that are considered ‘low lying’ at the 20 week’ scan will no longer be in the region of the cervix at the time of delivery. Apparent ‘placental migration’ was thought to occur during the second and third trimesters owing to the development of the lower uterine segment.

• •

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First (lateral)

Second

Third

Minor

Fourth (central) Major

FIGURE 10.1

Degrees of grades of placenta praevia. The amount of bleeding is proportional to the extent to which the placenta encroaches on the lower uterine segment.

However, it is now believed that the placenta does not move but rather grows towards the better vascularised fundus. Placental tissue in the relatively under-vascularised lower segment/cervix undergoes atrophy. In some cases this atrophy results in placental vessels unsupported by placental tissue (vasa praevia). There is a higher chance of persistence of a low-lying placenta at delivery if: diagnosis is later in pregnancy the placenta is posterior there has been a prior caesarean section if the placenta overlaps the os > 25 mm. Placental bleeding is thought to occur when small changes in the cervix or lower uterine segment cause shearing forces, and partial separation, at the placental attachment site.

• • • •

PREDISPOSING FACTORS The following factors can predispose a woman to placenta praevia: previous caesarean section advanced maternal age increased parity in vitro fertilisation smoking.

• • • • •

CLINICAL FEATURES The classic presentation of placenta praevia is that of painless bleeding in the second and third trimesters. This is not absolute, however, and it should be noted that bleeding from placenta praevia may stimulate some contractions and hence cause some pain. Any painless bleeding in the second half of pregnancy must be assumed

Chapter 10  Antepartum Haemorrhage

secondary to placenta praevia until proven otherwise. A vaginal examination should not be performed until placenta praevia is excluded. Bleeding occurs in 90% of women with placenta praevia. Approximately one-third will bleed prior to 30 weeks’, one-third between 30 and 36 weeks’ and onethird after 36 weeks’ gestation. Most women with a placenta praevia who have had one bleed will likely bleed again. However, the amount and timing is unpredictable. Placenta praevia may also be associated with an unstable lie or malpresentation in late pregnancy. The majority of placenta praevia are asymptomatic and diagnosed at the routine 19- to 20-week ultrasound.

Haemoglobin should be optimised with administration of iron and/or folate supplements as necessary. Ultrasound should be repeated at 32 to 34 weeks’ and include a growth assessment. Advise the woman to avoid sexual intercourse.

DIAGNOSIS

Timing and mode of birth

While clinical suspicion is important in the diagnosis and management of placenta praevia, the definitive diagnosis is generally made with ultrasound. Transvaginal ultrasound is both safe and more accurate than transabdominal imaging in diagnosing placenta praevia. A high index of suspicion is warranted if the clinical scenario suggests a placenta praevia (painless bleeding, mobile presenting part, abnormal lie) irrespective of the previous ultrasound result (Fig 10.2). When discovered at the routine 20-week ultrasound, a follow-up ultrasound should be performed at 32 to 34 weeks’ to confirm persistence of placenta praevia and to exclude vasa praevia and placenta accreta.

Symptomatic placenta praevia (any gestation): vaginal bleeding

MANAGEMENT Asymptomatic placenta praevia: no vaginal bleeding Management of asymptomatic placenta praevia should begin with explaining the diagnosis, including the risk of provoked and unprovoked vaginal bleeding.

Outpatient versus inpatient The woman can usually be an outpatient until 34 weeks’ but then hospitalisation is usually recommended—even in the absence of bleeding for those with a major placenta praevia. Outpatient care requires close proximity to the hospital, mobile communication and preferably the presence of a responsible adult at all times. Delivery should occur at 37 weeks’ if the placenta praevia is major or 38 weeks’ if it is minor. However, delivery will be necessary earlier in the event of heavy continued bleeding. Mode of delivery will be by caesarean section if the placenta is ≤ 2 cm of the internal cervical os. Where a minor placenta praevia has been diagnosed early in the third trimester, a repeat scan at 36 to 37 weeks’ may be warranted—especially if the fetal head is beginning to engage.

If the woman presents with symptomatic placenta praevia with vaginal bleeding, she should be admitted to hospital—for any gestational age.

Resuscitation Obtain intravenous access. Intravenous fluid should be delivered as needed. A blood transfusion may be indicated if there has been substantial blood loss.

Initial investigation Full blood examination, blood group and hold/crossmatch and a coagulation profile (if there is significant vaginal bleeding) comprise the initial blood tests. Fetal wellbeing should be assessed with cardiotocography if > 26 weeks’ gestation.

Treatment

FIGURE 10.2

Anterior placenta praevia.

Corticosteroids (for fetal lung maturity) are indicated if delivery is anticipated prior to 34 weeks’ and is not imminent. Magnesium sulfate (MgSO4) should be considered (for neuroprotection) if delivery is anticipated before 30 weeks’. (Note that delivery should not be delayed if there is ongoing, severe bleeding or fetal compromise.) Tocolysis may be used in selected cases where the bleeding is relatively minor but has initiated labour prior to 34 weeks’. Delivery (by caesarean section) is indicated by: any bleeding at a gestation > 36–37 weeks’ moderate, ongoing blood loss > 34 weeks’

• •

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heavy bleeding with maternal haemodynamic compromise or unremitting bleeding at any gestation.

Outpatient versus inpatient after an episode of bleeding Patients with a major placenta praevia and a moderate to severe bleed will generally remain inpatients until delivery. However, patients may be considered for outpatient management on a case-by-case basis if circumstances allow as mentioned earlier this chapter.

Operative management: caesarean section Where heavy blood loss is anticipated (e.g. suspicion of placenta accreta), a midline skin incision should be employed with general rather than regional anaesthesia. Excessive blood loss from the lower segment at caesarean section is common as the less muscular lower segment does not contract well. In addition to oxytocin and ergometrine, other measures that may be needed to control bleeding include PGF2alpha, suturing the bleeding placental site vessels in the lower uterine segment, uterine artery ligation, balloon tamponade or hysterectomy.

VASA PRAEVIA DEFINITION AND INCIDENCE Fetal vessels traverse within the membranes over the region of the internal os. This condition results from either a velamentous cord insertion or fetal vessels running between two lobes of placenta (Fig 10.3). Incidence is approximately 1 in 2500 pregnancies.

CLINICAL CONSEQUENCES Undiagnosed vasa praevia may be associated with a perinatal mortality of up to 70%. In contrast to the loss of maternal blood with placental abruption or placenta praevia, the bleeding with a vasa praevia is fetal. The vessels are at risk of rupture with either spontaneous rupture of the membranes or amniotomy.

DIAGNOSIS The diagnosis can be made antenatally with ultrasound. Vasa praevia should be actively sought in those with a velamentous cord insertion or succenturiate lobe and on third trimester ultrasound in all women who had a lowlying placenta at 20 weeks’. It may also present as vaginal bleeding after amniotomy or spontaneous rupture of membranes. Severe fetal compromise follows soon afterwards.

FIGURE 10.3

Vasa praevia. The mother reported decreased fetal movements after passing a ‘cupful’ of bright blood vaginally at 37 weeks’ gestation. The infant was stillborn at 3100 g. The arrows show the ends of the torn fetal vessel from which the fetus bled to death. More commonly, bleeding from vasa praevia occurs at the time of membrane rupture during labour.

section is commonly recommended at approximately 36 weeks’ to avoid the possibility of premature, prelabour rupture of membranes and potential fetal exsanguination.

PLACENTA ACCRETA Placenta accreta is a life-threatening condition where there is morbid adherence of the placenta to the myometrium. In this situation, placental separation is difficult and commonly associated with life-threatening haemorrhage, often necessitating hysterectomy. It most commonly occurs where an anterior placenta praevia occurs at the site of one or more previous caesarean sections. Placenta accreta is discussed in detail in Chapter 36.

PLACENTAL ABRUPTION DEFINITION AND INCIDENCE Placental abruption is defined as the partial or total detachment of the placenta from the placental/decidual interface prior to delivery of the fetus. Placental abruption occurs in approximately 1% of pregnancies. The recurrence rate is approximately 10% in subsequent pregnancies.

MANAGEMENT

PREDISPOSING FACTORS Placental bed ischaemia

While there is no definitive agreement on the management of antenatally detected vasa praevia, elective caesarean

The most common mechanism for abruption appears to be ischaemia of vessels in the placenta bed producing necrosis

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Chapter 10  Antepartum Haemorrhage

of anchoring villi and placental separation. Predisposing factors are therefore those of placental insufficiency: hypertensive disorders, including underlying hypertension and preeclampsia; it is important to recognise that placental abruption may be the presenting feature of severe preeclampsia thrombophilia, which remains somewhat controversial; stronger association of poor pregnancy outcome, including abruption, with certain thrombophilias (e.g. antiphospholipid syndrome), antithrombin III deficiency, homozygote genetic thrombophilia or compound heterozygote genetic thrombophilia smoking, cocaine use chorioamnionitis (e.g. following preterm prelabour rupture of the membranes).

• •

• •

Uterine trauma Much less commonly, the anchoring villi are sheared by traumatic injury, most often due to blunt trauma to the abdomen as a result of a motor vehicle accident.

Multiple pregnancy or polyhydramnios The normal cause of placental separation is the shearing force created between the uterine wall and the placental surface as the uterine volume reduces after birth. This same mechanism may lead to an abruption with rupture of the membranes in the presence of polyhydramnios or after birth on one twin prior to delivery of the other.

CLINICAL FEATURES AND CLASSIFICATION Placental abruption is a clinical diagnosis. The classic presentation is that of vaginal bleeding associated with abdominal and/or back pain. The pain is often constant in nature. Contractions will often be present and are usually of a high frequency but low intensity. However, they may also reflect typical labour-like contractions in strength and frequency. As there is often a mixture of concealed and revealed bleeding, the amount of vaginal bleeding is often a poor indicator of the degree of placental separation. As such, vaginal bleeding may be slight and seemingly inconsequential, or severe and life-threatening.

Mild abruption

FIGURE 10.4

Moderate placental abruption covering approximately one-third of the placental surface.

• •

haemodynamic compromise or disseminated intravascular coagulation (DIC) fetal compromise.

Severe abruption Severe abruption leads to fetal death in utero due to a large placental abruption. There is uterine pain and a tense, tender uterus with maternal haemodynamic compromise and DIC.

MANAGEMENT Mild abruption Initial management Generally, the woman should be admitted to hospital even though symptoms and signs are minimal and there is no evidence of maternal or fetal compromise. Careful assessment is needed to ensure that a more severe situation (moderate abruption) is not evolving. If the woman is less than 34 weeks’, corticosteroids will be administered in anticipation of a possible preterm birth.

Further management

In mild abruption, the clinically well patient will have minimal pain or uterine tenderness. There is no fetal compromise and revealed blood loss is less than 200 mL. Presumably, this is due to a marginal placental bleed with minimal separation.

The main concerns are either a repeat abruption of greater severity or evolving placental insufficiency (that may have been causal as well as consequential to the original presentation). Ultrasounds should be performed at least fortnightly for fetal wellbeing and delivery should be expedited at approximately 38 weeks’.

Moderate abruption

Moderate abruption

Moderate placental abruption (Fig 10.4) is diagnosed where any of the following are present and the fetus is alive: tense tender uterus revealed blood loss > 200 mL

Initial management

• •

Who and where? The woman should be admitted to an area where both mother and fetus can be monitored closely. The 89

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anaesthetist and paediatrician should be alerted that early delivery may be needed. Stabilisation Stabilisation involves the following steps. 1. Volume status assessment and replacement as needed. 2. Haematological assessment with correction of anaemia and replacement of platelets and clotting factors as needed. 3. Fetal wellbeing assessment with continuous cardiotocography. 4. Kleihauer on maternal blood to asses fetomaternal haemorrhage. 5. Anti-D administration if mother is Rh-negative. 6. Fetal lung maturity and neuroprotection: if birth is not imminent, corticosteroids if less than 34 weeks’ and MgSO4 if less than 30 weeks’.

Further management Further management involves continued intensive assessment of fetal wellbeing in anticipation of fetal compromise. Delivery should occur if there is: maternal haemodynamic compromise or DIC fetal compromise gestation > 34 weeks’. Prompt caesarean section is indicated if there is fetal compromise but major maternal morbidity or death is a real risk when a caesarean is performed in the presence of coagulopathy. Every effort should be made to stabilise the patient and correct the hypovolaemia and coagulopathy prior to delivery.

• • •

Severe abruption Where the fetus is dead, the mode of delivery is usually vaginal, especially as these patients often labour readily. Caesarean section is occasionally required for the control of severe ongoing bleeding or in the case of contraindicated vaginal birth. All attempts should be made to correct hypovolaemia and haematological disturbances prior to caesarean section. Hysterectomy may occasionally be needed for control of postpartum haemorrhage (Fig 10.5).

BLEEDING FROM THE CERVIX OR LOWER GENITAL TRACT CERVICAL ECTROPION A speculum examination to exclude cancer is especially important in those women with recurrent small bleeds who have not had a recent speculum or Pap smear.

CERVICAL POLYPS Cervical polyps usually do not require removal in pregnancy as this may provoke significant further bleeding. 90

FIGURE 10.5

Hysterectomy specimen of a Couvelaire uterus. The uterus has patches of black from the blood within the subserosal uterine muscle. Complete recovery is usual but there is often associated disseminated intravascular coagulation.

CARCINOMA OF THE CERVIX A speculum examination to exclude cancer is especially important in those women with recurrent small bleeds who have not had a recent speculum or Pap smear. FURTHER READING Ananth CV. Placental abruption in term and preterm gestations. Evidence for heterogeneity in clinical pathways. Obstet Gynecol 2006;107:785–92. Neilson JP. Interventions for treating placental abruption. Cochrane Database Syst Rev 2010. Oyelese Y, Smulian JC. Placenta praevia, placenta accreta, and vasa praevia. Obstet Gynecol 2006;107(4):927–41. Royal College of Obstetricians and Gynaecologists. Placenta praevia, placenta praevia accreta and vasa praevia: diagnosis and management. Green-top Guideline No. 27. London: RCOG; 2011. Royal College of Obstetricians and Gynaecologists. Antepartum haemorrhage. Green-top Guideline No. 63. London: RCOG; 2011. Tikkanen M. Placental abruption: epidemiology, risk factors and consequences. Acta Obstet Gynecol Scand 2011;90(2):140–9.

Chapter 11  FETAL GROWTH RESTRICTION AND ASSESSMENT OF FETAL WELLBEING Alexis Shub

KEY POINTS Fetal growth restriction (FGR), refers to babies who have failed to reach their optimal growth potential. Small for gestational age (SGA) describes babies where the birth weight is less than the 10th percentile for gestation. Low birth weight (< 2500 g) or very low birth weight (< 1500 g) are weight-based descriptions. Such definitions are less useful as they do not differentiate between the preterm baby, the term growth-restricted baby and the preterm growth-restricted baby. Small for gestational age may be due to constitutional influences on growth or FGR. FGR is most commonly due to placental insufficiency, but can also be due to congenital infections or fetal genetic/structural malformations. FGR is the single biggest risk factor for stillbirth and compromise during labour. Risk factors for FGR include hypertension, preeclampsia, diabetes, smoking, obesity and advanced maternal age. Early-onset FGR usually refers to FGR occurring before 32 to 34 weeks’, and is most commonly due to uteroplacental insufficiency, although infection or fetal abnormality should be considered. Late-onset FGR occurs after 32 to 34 weeks’, and is most commonly constitutional or due to uteroplacental insufficiency. Ultrasound is the mainstay in investigation of the small fetus, to assess: ■ fetal size and weight ■ blood flow in the umbilical artery (umbilical artery Doppler assessments) and Doppler assessments of fetal circulation, where indicated ■ parameters of fetal wellbeing (amniotic fluid volume and biophysical profile). FGR at term should be managed with delivery. Management of FGR in the preterm period needs to balance the risks of in utero asphyxia and stillbirth with the risks associated with preterm birth. Multiparameter surveillance, primarily involving ultrasound, is used most commonly to help decide the best time to deliver the severely preterm growth-restricted fetus.

FETAL GROWTH RESTRICTION Detection and management of fetal growth restriction (FGR) is one of the primary aims of antenatal care. Undetected FGR is a leading cause of stillbirth. Growthrestricted babies are more likely to suffer antenatal and

intrapartum stillbirth, suffer neurocognitive deficits and have long-term health problems in childhood and in adult life (Fig 11.1). FGR can be caused by maternal, fetal or placental factors. One of the difficult problems in the antenatal period is differentiating the constitutionally small, but well, baby from the baby with FGR who is at

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risk of antenatal and postnatal complications. Detection of FGR during the antenatal period may enable the cause of abnormal fetal growth to be determined. Detecting FGR also provides intervention opportunities to reduce the risk of intrauterine or intrapartum death.

WHY IS A FETUS SMALLER THAN EXPECTED? Babies may be constitutionally small (the well small baby from the small mother) or pathologically small, and it may not be apparent antenatally which diagnosis applies. Sixty per cent of babies that are small for gestational age (SGA) are constitutionally small and experience no extra complications; these need to be differentiated from babies with FGR who require additional surveillance and intervention. Conversely, identifying the constitutionally small baby prevents unnecessary additional intervention. Babies may have fetal growth restriction but be above the 10th percentile for gestation, having failed to achieve their growth potential. Assessment of the adequacy of fetal growth has to include the optimal birth weight for that baby. Factors that need to be included are primarily the mother’s height and weight, but babies tend to be heavier with increasing parity, and male babies are slightly heavier than females. The use of personalised growth percentiles has been shown to more accurately identify the cause of stillbirth so that many babies that were described as an unknown cause of stillbirth can be defined as FGR

100

175 Morbidity Mortality

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Perinatal morbidity (cumulative)

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60 75

50 40

50

30 20

Perinatal mortality (per 1000)

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10 > 10 10

9

8

7

6

5

4

3

2

1

3800 g) Small fetus (preterm e.g. < 36 weeks’ or growth restricted) Placental insufficiency Fetal head extension (Fig 15.3) Footling breech presentation Evidence of cephalopelvic disproportion (e.g. previous obstructed labour, short stature) 123

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A

B

FIGURE 15.3

Burns-Marshall method of delivering the head. A The baby hangs with back uppermost to flex and promote engagement of the head. B The head is delivered by traction on the feet as they are swung upwards; the head is born by extension as it rotates around the symphysis.

fetal abnormality and head extension) will have been performed and the mother educated with respect to her specific roles in the conduct of the birth. In particular, she will have been informed of the importance of not pushing until the cervix is fully dilated and then the necessity of delivering the breech by expulsive effort from the mother. This is because traction by the accoucheur before the head is deep in the pelvis will cause head extension, with potentially catastrophic outcomes. Where the breech has not been diagnosed antenatally, the above two key aspects of ‘detailed assessment’ and ‘maternal education’ are likely to be deficient and not easily accomplished with a woman in established labour. Continuing with a vaginal breech birth in such 124

circumstances is likely to be associated with increased perinatal risk.

First stage of labour The general care, observations and management are similar to that for a cephalic presentation. As with all births, but even more so for a breech presentation, there should be ready access to immediate caesarean section. A recommendation for continuous electronic fetal monitoring is mandatory. An electrode can be attached to the buttock if necessary, taking care to avoid the genitalia. The passage of meconium is common and not necessarily indicative of fetal compromise. An increased likelihood of emergency anaesthesia should limit oral intake

Chapter 15  Malpresentation

to clear fluids only. Assessment of progress of labour should be vigilant and any delay in progress in the active phase of labour should lead to a recommendation for caesarean section. A vaginal examination should be performed as soon as the membranes rupture to exclude cord prolapse. Epidural anaesthetic for pain relief will have the desirable effect of preventing pushing until full dilatation of the cervix has occurred and the breech is on the perineum. This will be particularly important in the preterm situation where the head is relatively large and the smaller breech may slip through a partially dilated cervix, with subsequent head entrapment by the cervix. However, the downside of an epidural is substantial in that the mother will have reduced expulsive forces in the second stage of labour when, unlike cephalic presentations, there is no option of traction to deliver the body and aftercoming head—at least not until the head is deep within the pelvis and can no longer extend.

Second stage of labour: assisted breech delivery In all cases, an accoucheur skilled in vaginal breech delivery should be in attendance as accoucheur or supervisor. A paediatrician should be in attendance or immediately available.

no stage is there any traction through the atlanto-occipital joint.

Delivery of the shoulders The baby is rotated 90° to deliver the anterior shoulder beneath the pubic symphysis (Fig 15.4). The arm is then delivered by sweeping the humerus across the chest. The baby is then elevated to bring the posterior shoulder into the hollow of the sacrum. The body is then rotated 180° and lowered so that the previously posterior shoulder is also delivered beneath the symphysis pubis and then returned to back uppermost. This is termed Løvset’s manoeuvre. Extended arms are usually a consequence of traction being applied in delivery of the trunk. When this occurs, a hand is introduced into the vagina and each forearm is swept in an arc over the baby’s face (it is usually easier if the posterior arm is delivered first).

Delivery of the aftercoming head After delivery of the shoulders and arms, the baby is allowed to hang downwards while the mother continues to push in order to flex the head and facilitate engagement of the head in the pelvis. When the hair line becomes visible beneath the symphysis, the head is deeply engaged in the pelvis. The final delivery of the

Preparation The woman is placed in the lithotomy position when the breech is visible and the perineum distending. The bladder is emptied by catheter if necessary. If there is no epidural, perineal infiltration with 1% lignocaine and a pudendal nerve block should be performed.

Delivery of the breech and legs The accoucheur is not committed to a vaginal birth until the first (anterior) cheek of the buttock is delivered and the anus is visible. If delivery needs to be expedited in second stage before this point, a caesarean section should be performed. An episiotomy is performed routinely in nulliparas and in multiparas if the perineum is tight. The breech is then born by maternal expulsive effort. If the legs are flexed, they are freed as the breech passes through the introitus. If the legs are extended, they can be delivered by pressure in the popliteal fossa (Pinard’s manoeuvre) to flex them down.

Delivery of the trunk With continued maternal effort, the lower trunk is delivered to the level of the umbilicus. A loop of umbilical cord should be brought down to avoid tension on the cord. A warm cloth is placed over the buttocks and legs, and the baby grasped by the pelvic girdle as excessive abdominal pressure is liable to cause serious injury to such structures as the liver and spleen. The back is rotated uppermost (sacroanterior) to produce the most favourable diameters for the aftercoming head (occipitoanterior). At

FIGURE 15.4

Lövset’s manoeuvre for delivery of the posterior arm by rotation through 180° to the anterior position where it appears beneath the symphysis pubis. The baby is grasped by the pelvic girdle to avoid injury to the abdominal organs. 125

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A

B

FIGURE 15.5

Forceps delivery of the aftercoming head. A The occiput must be anterior (posterior fontanel beneath the symphysis pubis). B When the mouth appears the infant can breathe, although the greatest diameters of the head are still negotiating the narrow pelvic plane and outlet.

aftercoming head can be by forceps (Fig 15.5) or manual traction. With a forceps delivery of the aftercoming head, the assistant elevates the fetus and holds the arms out of the way to enable access of the blades to the sides of the head. Note that the traction force is being applied to the softer parietal bones in this case, rather than the harder base of the skull with a cephalic presentation forceps delivery. With the manual technique (Mauriceau–Smellie– Veit), the fetus is placed on the accoucheur’s arm, straddling it with arms and legs; flexion of the head is maintained by the middle finger placed in the baby’s mouth and the ring and index fingers beside the nose on the alveolar ridge (Fig 15.6). The index finger of the other hand pushes on the region of the occiput to further increase flexion. The head is delivered by drawing the body downwards and then forwards over the mother’s abdomen.

FIGURE 15.6

The Mauriceau–Smellie–Veit technique for delivery of the head is particularly useful when deflexion has caused failure of engagement.

Management of head entrapment Most problems are experienced as a consequence of head extension when traction is applied from below through the atlanto-occipital joint. (In contrast, maternal pressure from above on the vertex will lead to increased head flexion.) Patience is required and the head will usually engage with further maternal effort. If extension is severe, an experienced accoucheur is needed to pass a hand along the hollow of the sacrum up to the head in order to flex it manually. Symphysiotomy may be necessary but requires an accoucheur familiar with this procedure. If the baby is small or the presentation footling, the trunk may slip through a cervix which is not fully dilated. 126

Maternal effort may still achieve delivery of the head but on occasions it will be necessary to incise the cervix, classically at the 2, 6, and 10 o’clock positions (Dührssen’s incision).

Breech extraction Having gone to considerable lengths in the previous section to emphasise that one should never pull on the breech from below for fear of causing both extended arms and head extension, it must be acknowledged that the procedure of breech extraction is sometimes employed

Chapter 15  Malpresentation

for delivery of a second twin. With an epidural in situ, careful pressure by an assistant on the vertex may help maintain flexion of the head along with maternal effort. There are two reasons why some traction is allowable for a second twin. First, the traction force on the atlantooccipital joint is considerably less as the soft tissues have already been distended by the first twin birth. Second, a twin is usually small relative to the pelvis, and a minor degree of head extension should still result in diameters that are able to pass through the pelvis. If the second twin is known to be large, breech extraction should not be attempted and a caesarean section will be needed if delivery of the second twin must be expedited before an instrumental delivery is possible.

PROGNOSIS The perinatal mortality and long-term morbidity are increased in breech presentations both by virtue of the reason for the breech presentation and also consequences of the breech delivery itself. Fetal structural, abnormalities, neurological deficits and tight nuchal cords are all more common in breech presentations. Cord prolapse and head entrapment will be the two most common complications of the birth itself, causing long-term sequelae.

TRANSVERSE/OBLIQUE LIE: SHOULDER PRESENTATION If labour begins when the lie is transverse or oblique, the shoulder is the part that presents; that is, the part first felt on vaginal examination. There is no mechanism for

A

B

delivery in such cases and either the lie must be corrected or a caesarean section performed. The incidence at term (37 weeks’) is approximately 1 in 200 pregnancies.

PREDISPOSING FACTORS Predisposing factors are as for breech presentation, but there is a particular preponderance for high parity. The grand multipara has little tone in the uterus or anterior abdominal wall and therefore little form to the uterine cavity to drive the fetus to a cephalic presentation. However, as gestation advances in late pregnancy, there is still considerable fetal growth and less and less room for the fetus to lie transverse or obliquely. The majority of these transverse or oblique lies therefore correct spontaneously in late pregnancy. Placenta location remains an important predisposing factor for transverse lie (Fig. 15.7).

DIAGNOSIS Unless obscuring features are present (such as multiple pregnancy or obesity), transverse and oblique lies are relatively easy to diagnose. The general appearance of the abdomen often gives the first clue to transverse lie, because of lateral expansion. Furthermore, there is no fetal pole palpable in the fundus or lower uterus. The rounded, hard, ballottable fetal head will then be palpated in one flank or the other, with the softer breech on the opposite side. Confirmation by ultrasonography in the antenatal clinic or labour ward is very straightforward and within the skill range of all care providers.

C

FIGURE 15.7

Transverse lie. A Fundal placenta with fetus facing upwards. B The central (type 4) placenta praevia would prevent either fetal pole entering the pelvis. C Neglected transverse lie with prolapsed arm in labour. Uterine rupture would be imminent. 127

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MANAGEMENT Determine aetiology (look for a cause) Only a very small number of pregnancies will be found to have a transverse or oblique lie at 36 weeks’ or beyond. The history and examination should be reviewed. In the absence of an obvious cause (e.g. grand multiparity, placenta praevia), ultrasonography is indicated to exclude important predisposing factors such as fetal abnormality or a previously undiagnosed placenta praevia.

External cephalic version ECV is usually relatively easy with an oblique or transverse lie, but a high proportion revert almost immediately to their original position. It is obviously pointless to do repeated ECVs when the procedure is having no lasting impact on the malpresentation.

Admission to hospital If the abnormal lie persists to 38 weeks’, the safest course may be for the woman to be admitted to hospital until the lie corrects or a caesarean section is performed. The principal concern in late pregnancy is prolapse of the cord at the time of labour or prelabour rupture of the membranes. In hospital there is an opportunity for an immediate vaginal examination and prompt caesarean section if the cord is palpable. Cord prolapse at home carries a high mortality rate, and having the patient remain at home should be considered only if she lives adjacent to the hospital and there is someone with her all the time to take her immediately to the hospital should labour begin or the membranes rupture.

What happens in hospital? If the condition is due mainly to laxity of the uterus in a woman of high parity, it is likely that as full term approaches, the lie will stabilise longitudinally. The woman is reviewed daily to see if this has occurred and is discharged from hospital only if the lie has been stable longitudinally for 48 hours. Correction to longitudinal before labour becomes progressively less likely at or beyond the due date, and most will resort to caesarean section at this time. A common situation is an older woman of high parity who is more likely to have complications like hypertension or diabetes mellitus that would lead to a recommendation for birth at about 39 weeks’.

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If labour commences with the lie oblique or transverse, external cephalic version may be performed and the membranes ruptured in the hope that a longitudinal lie will establish. This course of action carries a significant risk of cord prolapse and should be contemplated only if immediate recourse to caesarean section is available.

Caesarean section for a transverse or oblique lie This can be a difficult procedure as the lower uterine segment may be poorly formed and a limb will be difficult to grasp if the back is down. If there is adequate liquor, internal version to either cephalic or breech is accomplished relatively easily during the caesarean birth. With no liquor and the back down, particularly if the lower segment is poorly formed, the wisest course of action may be to perform a vertical incision in the lower uterine segment that can be extended into the upper segment (classical caesarean section) if delivery proves difficult. FURTHER READING American College of Obstetricians and Gynecologists. External cephalic version. ACOG Practice Bulletin No. 13. Obstet Gynecol 2000, reaffirmed 2009;95(2):1–7. Hannah ME, Hannah WJ, Hewson SA, et al. Planned caesarean section versus planned vaginal birth for breech presentation at term: a randomised multicentre trial. Lancet 2000;356:1375–85. Hofmeyr GJ, Kulier R. External cephalic version for breech presentation at term. Cochrane Database Syst Rev 2000;(2):CD000083. RANZCOG. Management of breech presentation at term. RANZCOG Statements and Guidelines (C-Obs 11). Online. Available: ; [March 2015]. Rietberg CT, Elferink-Stinkens PM, Visser GHA. The effect of the Term Breech Trial on medical intervention behaviour and neonatal outcome in the Netherlands: an analysis of 35 453 breech infants. BJOG 2005;112(2):205–9. Silver RM, Landon MB, Rouse DJ, et al. Maternal morbidity associated with multiple repeat caesarean deliveries. Obstet Gynecol 2006;107:1226–32.

Section 2.5 MEDICAL AND SURGICAL DISORDERS IN PREGNANCY Chapter 16

Hypertensive disorders of pregnancy eclampsia

Chapter 17

Thromboembolism, cardiac disorders and respiratory disease

Chapter 18

Bacterial infections in pregnancy

Chapter 19

Viral and protozoan infections in pregnancy

Chapter 20

The blood: anaemia; thrombocytopenia and coagulopathy

Chapter 21

Gastrointestinal, hepatobiliary, gynaecological and renal problems

Chapter 22

Autoimmune and isoimmune disease in pregnancy 

Chapter 23

Diabetes mellitus

Chapter 24

Neurological disease

Chapter 25

Mental health disorders during the perinatal period

Chapter 16  HYPERTENSIVE DISORDERS OF PREGNANCY ECLAMPSIA  Michael Permezel

KEY POINTS Gestational hypertension is hypertension developing in pregnancy but without systemic effects, and affects approximately 10% of pregnancies. Preeclampsia is a major cause of both maternal and perinatal morbidity and mortality. Preeclampsia is unique to pregnancy, appearing after 20 weeks’ gestation and disappearing within days of delivery, and is characterised by generalised vasospasm, platelet aggregation, increased capillary permeability and widespread tissue ischaemia. Primary causes of preeclampsia include immunological issues, vascular disease and conditions associated with a large placenta (hyperplacentosis). Mild preeclampsia requires close surveillance of both fetal condition and progress of the disease, with a possible role for antihypertensive drugs. Delivery should occur at 38 weeks’ or earlier if indicated by fetal condition or disease progression. Severe preeclampsia requires intensive nursing care, stabilisation and delivery. Stabilisation includes: prophylaxis of eclampsia, control of blood pressure, management of intravascular volume status, attention to platelets and clotting factors, renal and liver function, and close fetal surveillance with corticosteroids for fetal lung maturity if less than 34 weeks’. Eclampsia occurs with almost equal frequency in the antenatal period and the puerperium. Most cases of eclampsia have not previously been diagnosed with preeclampsia at the time they present. Eclampsia requires acute management of the generalised tonic clonic convulsion, stabilisation as for severe preeclampsia and prompt delivery.

CLASSIFICATION OF HYPERTENSION IN PREGNANCY Hypertension in pregnancy can be defined as either a systolic blood pressure (SBP) ≥ 140 mmHg and/or a dia­ stolic blood pressure (DBP) ≥ 90 mmHg (Korotkoff phase 5), elevated recordings being made on at least two occa­ sions, some hours apart. Severe hypertension is defined as an SBP ≥ 160 mmHg and/or DBP ≥ 110 mmHg. Classification suffers from lack of uniformity in defi­ nition. A simple approach is as follows.

1. Preexisting or chronic hypertension: hypertension in pregnancy that is present before 20 weeks’. 2. Gestational hypertension: hypertension in pregnancy after 20 weeks’ gestation in a previously normo­ tensive woman without evidence of systemic involvement. 3. Preeclampsia: hypertension in pregnancy after 20 weeks’ gestation in a previously normotensive woman with evidence of systemic involvement including the one or more of the following. ■ Renal: significant proteinuria, renal insufficiency (serum creatinine > 90 µmol/L), oliguria.

Chapter 16  Hypertensive Disorders of Pregnancy Eclampsia 

Haematological: thrombocytopenia, haemolysis, disseminated intravascular coagulation. ■ Hepatic: serum transaminases raised, epigastric or right upper quadrant pain. ■ Neurological: convulsions, hyperreflexia with sus­ tained clonus, severe headache, persistent visual disturbance, stroke. ■ Pulmonary: oedema. ■ Placental: abruption, fetal growth restriction. 4. Chronic hypertension with superimposed preeclampsia. 5. Other related disorders (eclampsia, HELLP syndrome: a manifestation of severe preeclampsia with haemol­ ysis, elevated liver enzymes and low platelets).

aggregation and microthrombus formation. There is hypersensitivity to circulating vasoconstrictors such as angiotensin II and reduced response to vasodilators such as nitric oxide. The fundamental issue in preeclampsia is that the widespread endothelial dysfunction is secondary to a factor liberated from an ischaemic placenta. The conse­ quent generalised tissue ischaemia also affects the pla­ centa, thereby exacerbating the process in an escalating cycle of positive feedback, culminating in severe pre­ eclampsia and possibly eclampsia. Teleologically, it makes sense that the ischaemic placenta will initially drive the blood pressure higher to aid placental perfusion. In pre­ eclampsia, the process has escalated to the extent that the ischaemia also affects the placental circulation, making perfusion worse rather than better.

CHRONIC HYPERTENSION

What is ‘factor X’?

The incidence ranges from 1 to 2%. Essential hyperten­ sion is responsible for over 90% of cases (other causes include renal disease, endocrine disorders and collagen vascular disease). Under careful supervision, patients should be taken off antihypertensive medications with adverse side effects such as ACE inhibitors and diuretics. If antihypertensive treatment is necessary, suitable first-line agents include methyldopa, labetalol and nifedipine. Maternal risks include exacerbation of hypertension, superimposed preeclampsia and placental abruption. Fetal risks are directly related to the degree of hyperten­ sion, and are increased in pregnancies where antihyper­ tensive treatment is necessary. Careful surveillance of maternal and fetal wellbeing during pregnancy is necessary. In cases where antihyper­ tensive treatment is administered, delivery at 38 to 40 weeks’ is indicated.

Much research has been directed to a possible agent that is liberated by an ischaemic placenta that has widespread effects on endothelial function, resulting in systemic vasospasm and platelet aggregation. There are many putative candidates and, at the time of writing, there are probably multiple factors that contribute to the endothe­ lial ‘activation’. Pre-eminent candidates at this time include an increase in antiangiogenic factors sFlt-1 and soluble endoglin and a reduction in circulating VEGF and placental growth factor. Probably all contribute, perhaps to different degrees in contrasting patients and their clinical scenarios. This research will hopefully point to new initiatives for early diagnosis, prevention and man­ agement of this common but potentially devastating disease.



GESTATIONAL HYPERTENSION There is a wide geographical variation but the average incidence is about 10%. Predisposing factors are similar to those of preeclampsia, with obesity being prevalent among women with gestational hypertension. Management is largely directed to careful surveil­ lance on an outpatient basis, looking for evidence of sys­ temic involvement that would indicate the development of preeclampsia. Clinical surveillance should be increased through more frequent outpatient visits supplemented by regular investigation of renal and liver function, plate­ lets, urinalysis and assessments of fetal wellbeing. Deliv­ ery is indicated at 38 to 40 weeks’ gestation depending on the severity.

PREECLAMPSIA PATHOPHYSIOLOGY The widespread endothelial dysfunction results in vasospasm, increased capillary permeability, platelet

PREDISPOSING FACTORS There are three classical pathways to initiate placental ischaemia as the trigger for the positive feedback process (Fig 16.1). Among the more common predisposing factors are a new partner, cohabitation of less than 6 months, essential hypertension and obesity. Overriding this is a genetic predisposition to the disease, which is reflected in the incidence being three to four times greater if a first-degree relative suffered from preeclampsia. That is, not all women will develop pre­ eclampsia with the same aetiological impetus.

Deficient placentation There is a fundamental requirement in mammalian evolution for maternal immunological tolerance of trophoblastic antigens of paternal origin. Failure of this mechanism results in an abnormal interaction between invading trophoblast cells and the decidua, with defective invasion of the muscular layer of the spiral arteries in the decidua and myometrium by the cytotrophoblast early in placentation. Failure to convert the spiral arteries to lowresistance vascular channels leads to a diminished utero­ placental blood supply (Fig 16.2). 131

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Deficient placentation

Maternal vascular disease

Excessive placental size

Failure of immunological tolerance

Hypertension, renal disease, SLE

Twins, diabetes, hydatidiform mole placental hydrops

Placental ischaemia sFlt-1, soluble endoglin Endothelial dysfunction: vasospasm, capillary permeability platelet aggregation, microthrombus formation

Cardiovascular

,

Neurological Renal

Haematological Hepatic

FIGURE 16.1 

Pathogenic pathways of preeclampsia.

Maternal vascular disease

Renal

Women with vascular diseases are also more likely to develop preeclampsia. This includes hypertension (essen­ tial or secondary), renal disease, diabetes mellitus and diseases of the connective tissues. The incidence is also increased in women with obesity. Both the hereditary and acquired thrombophilias appear to increase the risk of preeclampsia in case control studies.

The serum uric acid level becomes elevated relatively early in the progress of the disease. It reflects increased distal tubular reabsorption in the presence of reduced renal perfusion and correlates with the risk of placental insufficiency. Urinary protein is increased in normal pregnancy, but is abnormal if it is greater than 300 mg/ 24 hours or 30 mg/mmol on a spot urinary protein : cre­ atinine ratio. Oliguria and renal insufficiency (serum cre­ atinine > 0.09 mmol/L) are later changes.

Excessive placental size A large placenta (hyperplacentosis) is seen in multiple pregnancy, diabetes mellitus, hydatidiform mole and hydrops fetalis, all of which predispose to the develop­ ment of preeclampsia.

CLINICAL FEATURES Typically, the patient with preeclampsia is asymp­ tomatic.

Cardiovascular Increased capillary permeability causes generalised oedema affecting in particular the feet, hands and face. Hypertension is a direct consequence of the generalised vasospasm and it therefore, to some extent, represents a marker of the severe tissue hypoxia seen in the disease. Unchecked severe hypertension (> 170/110) can result in fatal maternal intracranial haemorrhage; placental abrup­ tion is more likely, particularly in early-onset disease. Pulmonary oedema may occur as a consequence of leaky pulmonary capillaries, making overenthusiastic volume replacement unwise. 132

Haematological Thrombocytopenia reflects increased platelet turnover, and the platelet count is a further parameter that may be used to monitor progress of the disease. Disseminated intravascular coagulation usually occurs later but is par­ ticularly hazardous and mandates delivery.

Hepatic Small haemorrhages and hypoxic swelling of the liver results in epigastric pain, tenderness at the right costal margin and elevation of transaminases and/or bilirubin. Rarely, rupture of the liver capsule may occur with poten­ tially difficult-to-control haemorrhage that may be fatal (Fig 16.3). Pancreatitis has even been reported, although this too is rare.

Neurological Other features of particularly serious cases include effects on the eye, brain, liver and lungs. The woman may experi­ ence visual blurring as a consequence of retinal arterial

Chapter 16  Hypertensive Disorders of Pregnancy Eclampsia 

NORMAL Placenta Cytotrophoblast stem cells

Anchoring villus cytotrophoblast column

Decidua

Myometrium

Tunica media smooth muscle

Cytotrophoblast Syncytiotrophoblast

Maternal blood

Bloo d flow

Spiral artery

Floating villus Cytotrophoblast

Maternal endothelial cells

Endovascular cytotrophoblast

PREECLAMPSIA Placenta Cytotrophoblast stem cells

Anchoring villus cytotrophoblast column

Decidua

Maternal endothelial cells

Cytotrophoblast Syncytiotrophoblast

Myometrium

Maternal blood

Less bloo d flow

Fetal blood vessel Floating villus

Tunica media vascular smooth muscle layer

Spiral artery

Cytotrophoblast

FIGURE 16.2 

Abnormal placentation in preeclampsia. In normal placental development, invasive cytotrophoblasts of fetal origin invade the maternal spiral arteries, transforming them from small-calibre resistance vessels to high-calibre low-resistance vessels capable of high blood flow. In preeclampsia, cytotrophoblasts fail to adopt an invasive endothelial phenotype. Invasion of the spiral arteries is shallow and they remain small-calibre high-resistance vessels, resulting in later placental ischaemia. Source: Mount DB, Pollak MR. Molecular and Genetic Basis of Renal Disease. Philadelphia: Saunders, 2007. Copyright © 2007 Saunders, An Imprint of Elsevier. Figure 25.1.

ischaemia. Inspection of the optic fundi may reveal arterial spasm or even exudates/haemorrhage. Similar changes in cerebral arterioles may result in headaches, hyperreflexia and convulsions (eclampsia). Typically, ischaemic stroke involves the occipital lobes (Fig 16.4).

Placental Fetal compromise results from placental insufficiency with intrauterine growth restriction (Fig 16.5), fetal

hypoxia and even fetal death. Forewarning may be obtained by assessment of fetal wellbeing using ultra­ sound and CTG in addition to clinical parameters. Placen­ tal abruption may result in rapid fetal demise and represents a considerable danger for the mother as well. The course of the disease is variable but may be very rapidly progressive. Borderline or labile blood pressure elevation may advance to a life-threatening crisis in the space of a week or less. In other cases, the early course 133

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is benign—only to develop rapidly at a later gestation. Although preeclampsia is more common in nulliparas, it is important to remember that the disease can be severe and of sudden onset in multiparas. The signs of pre­ eclampsia (or eclampsia) may first be observed during labour or after delivery.

Site of liver laceration with sutures in situ

Unruptured subcapsular hematoma

FIGURE 16.3 

Subcapsular hematoma of the liver in a fatal case of eclampsia.

Source: Management of Acute Obstetric Emergencies. Barton, John R., M.D.; Sibai, Baha M., M.D.. Published January 2, 2011. Pages 125–135. © 2011.

DIFFERENTIAL DIAGNOSIS Apart from gestational hypertension, the other most common cause of raised blood pressure in pregnancy is chronic hypertension. The most useful distinguishing feature is the gestation at onset. Apart from the uncom­ mon instance of a hydatidiform mole, preeclampsia almost always begins after 20 weeks’ gestation. Retro­ spective diagnosis of chronic hypertension may be made when the disease is persistent after delivery. Proteinuria may be a consequence of underlying renal disease. Differentiation from severe preeclampsia can be extremely difficult as there is often hypertension and oedema as well. The dilemma is often to what extent the clinical picture is explained by underlying renal disease versus an element of superimposed preeclampsia. The latter has more sinister implications for the fetus and rapid deterioration in maternal health. Intensive surveil­ lance of fetal and maternal wellbeing is imperative in such a situation. In unusual cases, phaeochromocytoma

At onset

FLAIR

DWI

FIGURE 16.4 

Occipital lobe lesions in a woman with eclampsia. A 23-year-old primigravida woman at 30.5 weeks’ gestation awoke with a headache, nausea and vomiting, followed by a generalised tonic–clonic seizure. On presentation to the hospital, her blood pressure was 160/100. She was obtunded with mild right arm and leg weakness, hyperreflexia, and a right Babinski’s sign. Axial fluid-attenuated inversion recovery (FLAIR) images done on presentation show the high-intensity lesions involving the white and gray matter of both occipital lobes. Source: Schapira AHV. Neurology and Clinical Neuroscience. St Louis: Mosby, 2006. Copyright © 2008 Mosby, An Imprint of Elsevier. Figure 112.3A.

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Chapter 16  Hypertensive Disorders of Pregnancy Eclampsia 

BOX 16.1  Features of severe preeclampsia. Severe hypertension not controlled with medication Renal insufficiency; heavy proteinuria (> 5 g/24 hours) Hepatocellular enzymes markedly elevated; jaundice Severe thrombocytopenia; disseminated intravascular coagulation Neurological sequelae including stroke and convulsions (eclampsia) Pulmonary oedema

management by predetermined hospital protocols and that delivery is indicated in most cases within 24 to 48 hours of the diagnosis. The specific serious complica­ tions denoted in Box 16.1 are absolute indications for deliv­ ery on maternal grounds, regardless of gestational age.

MANAGEMENT FIGURE 16.5 

Severe intrauterine growth restriction in preeclampsia at 36 weeks’ compared to a normally grown term fetus. The growth-restricted fetus weighed 1930 g at 36 weeks’ from a mother with severe preeclampsia. Source: Courtesy of Prof. Norman Beischer.

or antiphospholipid antibody syndrome should be excluded as a possible underlying cause. Dependent oedema of the legs is common in preg­ nancy and may be exaggerated by prolonged standing, multiple pregnancy or individual variations in lymphatic drainage. Some swelling of the fingers (tightness of the rings) may occur in normal pregnancy, but significant generalised oedema should always alert the clinician to the possibility that preeclampsia may be developing. Rare differential diagnoses that may be considered include lupus nephritis, haemolytic-uraemic syndrome (HUS), thrombotic thrombocyopenic purpura (TTP) and acute fattly liver of pregnancy.

CLASSIFICATION OF PREECLAMPSIA There is no consensus as to how preeclampsia should be classified according to severity. Differentiating mild and moderate disease separately is not necessarily of critical importance as there are no major differences in manage­ ment through this spectrum of the disease. Close monitor­ ing is required and delivery should take place with fetal maturity. In contrast, the diagnosis of ‘severe preeclamp­ sia’ denotes that the disease requires intensive inpatient

The aim of therapy is to manage the major sequelae of the disease, recognising that there will be little impact on the underlying disease process until delivery, which must be effected at the most appropriate time for both mother and fetus. Management therefore depends on the severity of the preeclampsia, the gestational age and fetal wellbeing. Little is to be gained in continuing pregnancy when the fetus is mature but with severe disease at very immature gestations, delivery is sometimes temporarily deferred with intensive surveillance and possibly treat­ ment. Where an absolute maternal indication for delivery is present, delivery must be effected regardless of gesta­ tional age or fetal considerations.

Management of preeclampsia without severe features Mild preeclampsia is somewhat of a misnomer since it is never a condition to be taken lightly. Initial assessment is required of both disease severity and fetal condition. Disease severity will be determined by symptoms (oedema, epigastric pain, visual disturbance, headache), clinical signs (blood pressure monitoring, hyperreflexia) and investigations. Investigations in the woman with pre­ eclampsia should include FBE, urinary protein : creatinine ratio, serum uric acid, platelet count and hepatic trans­ aminases. Fetal surveillance should include clinical parameters such as maternal perception of fetal move­ ment and clinical assessment of fundal height, along with CTG and ultrasonography with estimated fetal weight, amniotic fluid volume, fetal activity and Doppler mea­ surement of umbilical vessel blood flow. 135

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The disease progression is unpredictable. Women with mild preeclampsia should be managed in hospital or with recurrent pregnancy day assessment admissions where the patient is assessed once or twice weekly for symptoms, clinical features (especially blood pressure) and the above investigations. Antihypertensive drugs are indicated with a SBP ≥ 160 mmHg or DBP ≥ 100 mmHg. With SBP 140 to 160 mmHg or DBP 90 to 100 mmHg, there is a trend towards benefit, but larger randomised controlled trials are underway to more definitively determine an overall net gain. Magee et al. suggest tighter control of blood pressure results in fewer episodes of severe hyperten­ sion.1 Methyldopa has a long history of safe use in preg­ nancy but has side effects of lethargy and depression and may increase the risk of deep vein thrombosis (DVT). It is increasingly being replaced by drugs with better side effect profiles such as labetalol and nifedipine. Delivery is indicated at fetal maturity (38.0 weeks’) or earlier if there is evidence of significant fetal compromise or there is rapid disease progression towards severe preeclampsia.

Management of severe preeclampsia The presence of severe preeclampsia marks a quantum change in management. Intensive observation and treat­ ment must be instituted and termination of the preg­ nancy is required, almost regardless of the period of gestation. At very premature gestations, control of severe hypertension with drugs and/or lesser degrees of protein­ uria may permit delivery to be deferred temporarily, although frequently the presence of fetal compromise makes delivery indicated anyway. Poorly controlled blood pressure or evidence of other organ damage (renal, hepatic, neurological, haematological, pulmonary) are absolute indications for delivery at any gestational age (Box 16.1).

Where and who manages the patient? After establishing the diagnosis of severe preeclampsia, the woman should be admitted to an appropriate area of the hospital equipped for intensive nursing. The anaes­ thetic service should be informed and an obstetric physi­ cian may be consulted, but the primary responsibility for care must remain with the obstetric team. The paediatric team should be informed if the patient is preterm.

Stabilisation prior to delivery A number of principles of management for stabilisation of the disease prior to delivery need to be followed accord­ ing to an established hospital protocol for the condition. These principles are (in order): 1. convulsion prophylaxis 2. blood pressure monitoring and treatment 3. intravascular volume assessment and volume replace­ ment as required 136

4. haematological profile, liver and renal function tests, with appropriate treatment if deranged 5. fetal surveillance.

Convulsion prophylaxis Convulsions are potentially life-threatening to both mother and fetus. Prophylaxis is certainly indicated in the presence of hyperreflexia and some units will use prophylaxis in all cases of severe preeclampsia. Therapy should precede antihypertensive therapy, as magnesium sulfate will have a vasodilatory effect of its own and will also offer some protection against convulsions that may be precipitated by too rapid lowering of the blood pres­ sure. The best choice for convulsion prophylaxis is mag­ nesium sulfate. Anticonvulsant therapy should be continued until at least 12 to 24 hours after delivery. Magnesium sulfate has had a long history of use, and apart from decreasing central nervous system excitability, the vasodilatation induced appears to get at the cause of the problem (focal cerebral ischaemia). A loading dose of magnesium sulfate (4 g = 8 mL of a 50% solution given intravenously over 15 minutes) is followed by a continu­ ous infusion (1 to 2 g per hour = 2 to 4 mL of a 50% solution). Blood levels should be checked 8-hourly (thera­ peutic range 2 to 4 mmol/L). Overdosage may result in serious respiratory depression and can be reversed with intravenous calcium gluconate (10 mL of a 10% solution).

Blood pressure control Control of severe hypertension is necessary to prevent complications such as cerebral haemorrhage and placental abruption. Severe hypertension in pregnancy (SBP ≥ 160 or DBP ≥ 110) should be regarded as a medical emergency. Nevertheless, rapid and excessive lowering of blood pres­ sure may aggravate ischaemia in areas of persistent vaso­ spasm in the brain or placenta. A DBP of 90 to 100 mmHg is therefore desirable. Hydralazine and labetalol are alter­ natives for intravenous bolus administration to lower blood pressure and can be followed by an infusion.

Intravascular volume status The intravascular compartment is much reduced in severe preeclampsia as a consequence of chronic veno­ constriction. However, central venous pressure and venous return are maintained for the same reason. Prob­ lems can occur with the administration of venous compartment dilators (magnesium sulfate and anti­ hypertensives), which may result in a significant fall in central venous pressure and consequently cardiac output, further compromising tissue perfusion. Practically, the jugular venous pressure and hourly urine output act as barometers of central venous pressure. If these are reduced, then an intravascular fluid bolus is indicated. Failure of a urine input to increase with fluid is an indica­ tion for expert management with a possible need for a central venous pressure (CVP) line. If fluid replacement

Chapter 16  Hypertensive Disorders of Pregnancy Eclampsia 

is necessary, colloidal or crystalloid solutions can be used. There are pros and cons of both approaches. Excessive infusion can be fatal with the development of lifethreatening pulmonary oedema in the presence of ‘leaky’ pulmonary capillaries. For this reason, most units will insist on a CVP line before intravascular volume is expanded substantially.

lift-out forceps or vacuum extraction should take place. Ergometrine is contraindicated for the third stage and oxytocin (5 units intravenously) should be used instead.

The puerperium

Transfusion of platelets and/or fresh frozen plasma/ plasma concentrates may be required as judged by hae­ matological studies. If the platelet level is < 30 × 109/L, 6 units of platelets should be administered and the level should be > 50 × 109/L for delivery. Clotting factors should be replaced with fresh frozen plasma if the pro­ thrombin time or partial thromboplastin time is pro­ longed. Seriously impaired renal function or jaundice require expert medical assistance and are extremely adverse developments.

After delivery, the pathophysiological abnormalities are reversed fairly rapidly; for example, the low renal perfusion/output and depressed platelet levels usually return to normal in 3 to 4 days. If the disorder is severe and has occurred in the second or early third trimester, recurrence is likely in the succeeding pregnancy. The woman should be investigated in the puerperium for any residual hypertension and for an underlying disorder such as renal disease, systemic lupus erythematosus (SLE) or the antiphospholipid syndrome. The patient should be followed up at 6 weeks. In addition to a clinical review, FBE, urea and electrolytes, LFT uric acid and urinary protein should be assessed to ensure all have normalised.

Fetal surveillance and therapy

Future treatments

Haematology, liver and renal function

Fetal surveillance usually consists of continuous cardioto­ cographic monitoring up until the time of delivery. If delivery is to be deferred, ultrasound for fetal growth, amniotic fluid volume and Doppler studies along with daily CTG are essential. Corticosteroids are indicated if delivery is likely before 34 weeks’. Magnesium sulfate administered for convulsion prophylaxis will have a dual purpose with fetal neuroprotection indicated at gesta­ tions less than 30 weeks’.

Delivery An absolute rule is that the woman is assessed (and stabi­ lised where possible) with respect to anticonvulsant pro­ phylaxis, blood pressure control, blood volume status, haematology, renal function and liver function before embarking upon delivery. Epidural analgesia is useful in reducing pain, stress and the level of blood pressure but is contraindicated if there is severe thrombocytopenia or dis­ seminated intravascular coagulation. A decision regarding the timing and route of delivery is made on the basis of careful monitoring of the maternal and fetal condition.

Mode of delivery It is an axiom in obstetrics that women with severe pre­ eclampsia labour well after amniotomy and are often found to have an unexpectedly favourable cervix despite a very premature gestation. In some women with severe preeclampsia, caesarean section will be required because of fetal distress, a markedly unfavourable cervix, breech presentation or antepartum haemorrhage; however, severe preeclampsia of itself is not an indication for cae­ sarean section. There will be occasional exceptions to this rule when the condition of the mother is serious or dete­ riorating rapidly. The neonatal paediatrician and anaes­ thetist should be warned in advance so that appropriate arrangements can be organised. Prolonged pushing is contraindicated if the blood pressure is high, and a

Currently there are no medical therapies to treat the underlying pathophysiology of preeclampsia. Consider­ able research is being performed in an attempt to identify treatments that might reduce sFlt-1 and soluble endoglin and stabilise the disease process. Statins are cholesterollowering drugs with vasoprotective properties and have been shown to reduce sFlt-1 in preeclamptic mice models. The StAmP trial is currently investigating whether pravas­ tatin can reduce sFlt-1 secretion in preterm preeclamptic patients. Extracorporeal removal of sFlt-1 or the adminis­ tration of VEGF are other proposed treatments currently being explored.

Prophylaxis Prevention of preeclampsia necessitates an appreciation of the predisposing factors. Specific therapy of aetiologi­ cal conditions may reduce the risk of preeclampsia; for example, control of SLE with anti-inflammatory drugs, control of essential hypertension with antihypertensives or low-molecular-weight heparin for antiphospholipid syndrome. There is a generally accepted benefit of low-dose aspirin in preventing preeclampsia among those at increased risk. This needs to be commenced early in preg­ nancy to be effective and should be 100 mg daily. Calcium supplementation has also been demonstrated to reduce the risk of preeclampsia and so should be recommended, particularly in high-risk women and those with low dietary calcium intake. Folic acid supplementation in a multivitamin preparation may also contribute to a lower­ ing of preeclampsia risk (possibly through a reduction in homocystine levels) but vitamin C and vitamin E have been shown to be ineffective. Closely allied with prevention of preeclampsia is timely diagnosis. Antenatal care is obviously important in every pregnancy but closer clinical monitoring is nec­ essary in the presence of a predisposing factor for 137

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preeclampsia. The search continues for a reliable test to identify those women destined to develop preeclampsia. Raised blood pressure in the second trimester appears as reliable as any other test and as yet there is no reliable early pregnancy laboratory or ultrasound marker of future preeclampsia. The search continues.

HELLP SYNDROME HELLP syndrome (haemolysis, elevated liver enzymes, low platelets) is a special variant of severe preeclampsia. It is important to distinguish it from similar conditions of acute endothelial cell damage such as haemolytic uraemic syndrome and thrombotic thrombocytopenic purpura. Management is the same as severe preeclamp­ sia, with added attention to the haematological and bio­ chemical disturbances.

ECLAMPSIA Eclampsia is a generalised tonic-clonic seizure as a con­ sequence of pregnancy-related cerebral hypoxia. Eclamp­ sia is a very serious complication because of the high risk to the life of the mother and baby. Early diagnosis and active treatment of preeclampsia will enable the avoid­ ance of eclamptic fits in the majority of cases.

PATHOGENESIS The basic disorder is cerebral hypoxia, brought about by intense vasospasm and contributed to by cerebral oedema. Eclampsia may be more likely in women with a lower inherent threshold for convulsions. Imaging will demonstrate cerebral haemorrhage or thrombosis in a small number of these women.

INCIDENCE Eclampsia occurs in approximately 1 in 1500 deliveries. It is obviously considerably less common than preeclamp­ sia (1 in 50 pregnancies). There is, however, a wide geo­ graphical variation due partly to differing standards of antenatal care and partly to poorly understood factors such as diet and climate.

CLINICAL FEATURES In approximately 50% of women, eclampsia precedes the onset of labour; a small number first present in labour but most of the remaining 50% present in the early puerperium. Severe headache, visual disturbance, drowsiness, irri­ tability, restlessness, and twitching or jitteriness may precede the convulsion, as may other systemic features of severe preeclampsia. The convulsion is typical of a generalised tonic-clonic seizure. Usually there is a preictal stage or aura and the 138

woman is dissociated from her surroundings. This is fol­ lowed by a tonic stage, lasting approximately 30 seconds, when the skeletal muscles are in a generalised spasm: because of the virtual cessation of respiration, the woman becomes cyanosed. This stage gives way to the clonic stage of alternate muscular spasm and relaxation, which lasts up to 2 to 3 minutes. In this stage, the woman is at considerable risk of self-injury (tongue biting, striking herself against unyielding surroundings, or falling out of bed). Finally, there is the postictal stage of reduced level of consciousness, which lasts for a variable period, some­ times hours, depending on the number of fits, degree of vasospasm and cerebral hypoxia.

DIAGNOSIS Eclampsia should not present a diagnostic dilemma if preceded by severe preeclampsia. In the absence of obvious preeclampsia, other causes of convulsions need to be considered. Such conditions include maternal hypotension (‘fainting fit’), idiopathic epilepsy, intra­ cranial neoplasia, cerebrovascular accident, local anaesthetic toxicity (inadvertent intravenous injection), alcohol withdrawal and metabolic disturbances (e.g. hyponatraemia, hypoglycaemia).

PROPHYLAXIS OF ECLAMPSIA Prevention of eclampsia is largely via early diagnosis and prompt treatment of severe preeclampsia. This implies that the obstetric team is vigilant during the antenatal, intrapartum and postnatal periods to the symptoms and signs of preeclampsia and in no way underestimates the potentially catastrophic sequelae of the condition.

MANAGEMENT OF ECLAMPSIA The aims are to provide initial first aid for the convulsion, then stabilisation as for severe preeclampsia, and finally termination of the pregnancy as soon as practicable.

Convulsion first aid First aid for convulsion should be as follows. 1. Prevention of injury. The woman should positioned so as to protect her from physical injury. 2. Airway and oxygen. A rubber airway placed in her mouth will inhibit tongue-biting and protect the airway. Oxygen should be provided by means of a mask or nasal catheter. Artificial ventilation with bag and mask may be necessary in the early postictal phase, particularly if large amounts of diazepam were required. 3. Posture. The woman should be nursed in the semi­ prone position to facilitate drainage of the airway and to minimise pulmonary aspiration. 4. Anticonvulsant. Diazepam or clonazepam intrave­ nously remains the most effective means of stopping

Chapter 16  Hypertensive Disorders of Pregnancy Eclampsia 

a convulsion. Loading with 4 g magnesium sulfate should occur as soon as feasible. 5. Transport. If the woman is to be transferred to hos­ pital, it is desirable that a doctor or nurse accompany her in the ambulance.

STABILISATION PRIOR TO DELIVERY As for severe preeclampsia, the woman should be admit­ ted to an area of the hospital that is equipped for inten­ sive nursing care. If there is an impaired conscious state, neurological observations should be performed and the woman nursed in a semiprone position. Further fits should be anticipated with the availability of oxygen, bag and mask, rubber airway, reliable intravenous access and diazepam. Management is then similar to that discussed under severe preeclampsia: 1. prevention of further fits (magnesium sulfate, phe­ nytoin or diazepam) 2. blood pressure monitoring and control 3. intravascular volume assessment 4. haematology 5. renal and liver function 6. fetal surveillance.

EXCLUDE INTRACRANIAL PATHOLOGY Intracranial imaging is needed at some stage to exclude intracranial pathology, but stabilisation as above is the first priority.

DELIVERY Delivery should be expedited as soon as the woman is stabilised. In most circumstances this will be by cae­ sarean section, but some women will be able to give birth vaginally if the fits are controlled on magnesium sulfate infusion and the cervix is very favourable.

PROGNOSIS Maternal death may occur in relation to eclampsia. This is most commonly due to cerebral haemorrhage, with

renal or cardiac failure being less common. Other serious complications include pulmonary oedema, disseminated intravascular coagulation, psychosis and cortical blind­ ness. In surviving women, there is usually complete recovery of function. Perinatal death occurs in 10 to 15% and is due mainly to hypoxia and prematurity. REFERENCE 1) Magee L, Von Dadelszen P, Rey E, et al. Less tight versus tight control of hypertension in pregnancy. NEJM 2015;372(5):407–17. FURTHER READING Altman D, Carroli G, Duley L, Magpie Trial Collaboration Group, et al. Do women with pre-eclampsia, and their babies, benefit from magnesium sulphate? The Magpie Trial: a randomised placebo-controlled trial. Lancet 2002;359(9321):1877–90. American College of Obstetricians and Gynecologists; Task Force on Hypertension in Pregnancy. Hypertension in pregnancy. Report of the American College of Obstetricians and Gynecologists’ Task Force on Hypertension in Pregnancy. Obstet Gynecol 2013;122(5):1122–31. Koopmans CM, Bijlenga D, Groen H, HYPITAT study group, et al. Induction of labour versus expectant monitoring for gestational hypertension or mild pre-eclampsia after 36 weeks’ gestation (HYPITAT): a multicentre, open-label randomised controlled trial. Lancet 2009;374(9694):979–88. Lowe SA, Bowyer L, Lust K, et al. The SOMANZ guidelines for the management of hypertensive disorders of pregnancy 2014. Aust NZ J Obstet Gynaecol 2015;55(1):11–16. Roberts JM, Bodnar LM, Lain KY, et al. Uric acid is as important as proteinuria in identifying fetal risk in women with gestational hypertension. Hypertension 2005;46(6):1263–9. Wen SW, Chen XK, Rodger M, et al. Folic acid supplementation in early second trimester and the risk of preeclampsia. Am J Obstet Gynecol 2008;198:45, e1–7.

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Chapter 17  THROMBOEMBOLISM, CARDIAC DISORDERS AND RESPIRATORY DISEASE Michael Permezel and Lisa Hui

KEY POINTS Thromboembolism ■ The hypercoagulation of pregnancy increases the risk of thromboembolism and is one of the more common direct causes of maternal death. A high index of clinical suspicion is required in the symptomatic patient followed by definitive investigation and treatment with low-molecular-weight (LMW) heparin if the diagnosis is confirmed. ■ In women with predisposing factors for thromboembolism, daily self-administered LMW heparin is indicated, ceasing with labour and recommencing 6 hours postpartum. Cardiac disease ■ Substantial changes occur in cardiovascular physiology during pregnancy, most notably a 40% increase in cardiac output with diminished cardiac reserve. ■ Some of the more common symptoms (e.g. oedema, dyspnoea) and signs (e.g. systolic flow murmur) of normal pregnancy need to be carefully assessed to exclude underlying cardiorespiratory disease. ■ More women with severe forms of congenital heart disease are surviving to reproductive age, leading to a particularly challenging obstetric population. Pulmonary hypertension (of any cause) has a particularly poor prognosis in pregnancy, as does Marfan’s syndrome with aortic involvement and any heart disease with severe compromise. ■ Management of the cardiac patient requires a multidisciplinary approach, ideally with prepregnancy assessment and counselling. Optimisation of medication for pregnancy includes a consideration of whether there is a need for thromboembolism or infectious endocarditis prophylaxis. ■ Cardiovascular disease, particularly pulmonary hypertension, may exacerbate in the puerperium. ■ In peripartum cardiomyopathy, the physiological events around labour, birth and the early postpartum period culminate to produce life-threatening cardiac insufficiency in a woman with no prior history of cardiac disease but a presumed inherent sensitivity to these changes. Respiratory disease ■ An increase in ventilation by about 40% is associated with decreased respiratory reserve in pregnancy. ■ Asthma is the most common preexisting respiratory condition in women of childbearing age. Deterioration of lung function during pregnancy may occur with moderate or severe disease, and adherence to medication is essential. Short-acting beta-sympathomimetics and corticosteroids are regarded as safe to continue in pregnancy.

Chapter 17  Thromboembolism, Cardiac Disorders and Respiratory Disease

THROMBOEMBOLISM

PREVENTION

Pregnancy, and particularly the puerperium, is associated with an increase in clotting factors to help meet the haemostatic challenge of delivery. Venous stasis and blood vessel injury also contribute to the prothrombotic state of pregnancy. Deep vein thrombosis occurs in about 0.1% of women during pregnancy or the puerperium and about 50% of these are asymptomatic. Pulmonary thromboembolism occurs in about 10% of women with a deep vein thrombosis, and 1 in 50 000 pregnant women die as a result of this complication. With preeclampsia and haemorrhage, this is one of the three major causes of maternal mortality. The most important risk factor for venous thromboembolism in a pregnant woman is a prior history of deep venous thrombosis or pulmonary embolism. Other predisposing factors are given in Table 17.1.

Steps to prevent thromboembolism are imperative and include: 1. early mobilisation after delivery or surgery; and 2. prophylactic anticoagulant therapy with lowmolecular-weight (LMW) heparin for women at increased risk. It is important that this is continued into the early puerperium when the risk is greatest.

CLINICAL FEATURES AND DIAGNOSIS Deep vein thrombosis The woman may report pain or swelling of the leg. Clinical examination reveals the leg to be tender in the calf or thigh, oedematous and warm. The diagnosis can be confirmed by colour flow imaging with ultrasound of the lower limb deep veins.

Pulmonary embolism Clinical features vary considerably according to the size of the embolus. At one extreme there may be complete occlusion of the major arteries to the lung with maternal hypotensive collapse, while in contrast a small embolus can often be totally asymptomatic. Between these extremes, obstruction to a small- or medium-sized vessel may result in shortness of breath, chest pain or haemoptysis. Diagnosis is confirmed by CT pulmonary angiography.

TABLE 17.1  PREDISPOSING FACTORS FOR THROMBOEMBOLISM. Congenital thrombophilia

Acquired

Hyperhomocysteinaemia

Obesity

Factor V Leiden mutation

Smoking

Prothrombin gene mutation

Prolonged bed rest

Protein S deficiency

Surgery, infection

Protein C deficiency

Antiphospholipid syndrome, thrombocytosis

Antithrombin III deficiency

Cardiac disease, hypoproteinaemia

TREATMENT Treatment is with LMW heparin, initially at full anti­ coagulant dose levels, but it may be reduced to prophylactic dose for the remainder of pregnancy and the puerperium. The LMW heparin is discontinued when spontaneous labour occurs or 12 hours before planned delivery and recommenced 6 hours postpartum. If longterm anticoagulation is needed, warfarin can be commenced in the early postpartum period as it does not pass into breastmilk. Side effects of long-term LMW heparin include haemorrhage and thrombocytopenia. Warfarin (unlike heparin) crosses the placenta, and may produce chondrodystrophy, optic atrophy and haemorrhagic problems in the fetus. Insertion of an inferior vena cava filter is reserved for those women with repeated emboli despite anticoagulation, or women with a contraindication to anticoagulation. Surgical thrombectomy would be considered as a life saving measure if there has been a massive pulmonary embolism.

CARDIAC DISORDERS PHYSIOLOGICAL CHANGES IN PREGNANCY The cardiac output increases by about 40% in pregnancy but may double with maternal effort in the second stage of labour. This physiological adaptation is not only in response to the increased demands of the uteroplacental circulation but also other organs (e.g. renal). Both stroke volume and heart rate increase. The cardiac work increase is partly offset by reductions in both peripheral resistance (afterload) and blood viscosity with the physiological anaemia of pregnancy. The cardiac work rises through pregnancy and plateaus early in the third trimester. The hyperdynamic circulation commonly results in a soft ejection systolic murmur along the left sternal edge. It should be distinguishable from pathological murmurs by being quieter (grade 1 or 2), having an absence of other abnormalities, and the normal splitting of the second heart sound (widening with inspiration and closing with expiration). The normal ECG in pregnancy may show some left-axis deviation. Suspicious cardiovascular symptoms that suggest a pathological cause include severe dyspnoea, paroxysmal nocturnal dyspnoea, syncope with exertion, haemoptysis or chest pain with exertion. 141

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AETIOLOGY Congenital anomalies are the most common maternal cardiac problems in pregnancy. Problems may occur in combination (e.g. tetralogy of Fallot). Of particular sinister prognosis is Eisenmenger’s syndrome, where there is a left-to-right shunt through a septal defect or patent ductus in childhood, characterised by severe longstanding pulmonary hypertension and eventually a rightto-left shunt resulting in cyanosis. Rheumatic heart disease is still a major problem globally. Other causes of cardiac insufficiency in pregnancy include tachyarrhythmias, viral myocarditis, idiopathic cardiomyopathy, ischaemic heart disease and pulmonary hypertension of any aetiology.

CLASSIFICATION BY SEVERITY The New York Heart Association classification is as follows: grade 1, normal exercise tolerance; grade 2, breathless on moderate exertion (heavy household work); grade 3, breathless on less-than-moderate exertion (light household work); grade 4, breathless without significant activity.

CLASSIFICATION BY PATHOPHYSIOLOGY It is useful to have a concept of how the heart is com­ promised in order to predict performance during pregnancy or response to stresses such as general or regional anaesthesia. 1. Pump failure is a defective myocardial performance and may be due to ischaemia, idiopathic cardiomyopathy or viral myocarditis. 2. Volume load (preload) includes valvular regurgitation and high-output states (anaemia, thyrotoxicosis, peripheral shunting). Pregnancy has a similar effect on the heart. 3. Pressure load (afterload) may be intrinsic (aortic or pulmonary stenosis) or extrinsic (systemic or pulmonary hypertension). 4. Tachyarrhythmias may increase in frequency in pregnancy, particularly paroxysmal supraventricular tachycardia. 5. Reduced ventricular filling may be due to mitral/ tricuspid stenosis or reduced venous return.

CLINICAL FEATURES OF HEART DISEASE IN PREGNANCY The demands of the antenatal period will be a stress on the already limited cardiac reserve, further exacerbated during labour. Cardiac failure ensues when the cardiac reserve cannot meet the demand. In women at risk of endocarditis, pregnancy and its interventions increase 142

the risk of this complication. The hypercoagulable state of pregnancy may combine with a sluggish circulation to cause thrombosis and/or embolism. If the circulation is particularly poor, there is a risk of placental insufficiency with intrauterine growth restriction.

PROGNOSTIC FACTORS The conditions that have a particularly poor prognosis in pregnancy are pulmonary hypertension, Marfan’s syndrome with aortic involvement or grade 4 heart disease of any cause. In these circumstances, pregnancy should be advised against and termination considered if pregnancy occurs. Myocardial infarction is very rare in pregnancy unless the woman has multiple risk factors, such as a strong family history, hypertension, diabetes and a history of smoking. This condition is very serious, however, and carries a significant mortality.

MANAGEMENT Prepregnancy It is essential that a woman with cardiac disease be assessed before pregnancy with respect to both the nature of the lesion and the severity of diminished cardiac reserve. Assessment may include electrocardiogram, echocardiography and cardiac stress test. Treatment should be optimised in anticipation of a pregnancy, bearing in mind the relative benefits and disadvantages of maintenance therapy such as anticoagulants, vasodilators and antiarrhythmics. Corrective surgery, if necessary, should take place before conception as cardiopulmonary bypass may not provide adequate uteroplacental perfusion. If maternal prognosis is poor, appropriate contraceptive advice is required. Anticoagulation with warfarin is usually contraindicated because of the risk of teratogenic sequelae in the fetus including saddle nose, basophilic stippling of bones, microphthalmia, optic atrophy and intellectual disability. LMW heparin is usually substituted for warfarin as soon as a pregnancy is confirmed. In the case of a mechanical prosthetic heart valve, LMW heparin may be combined with aspirin. Angiotensin-converting enzyme (ACE) inhibitors are contraindicated in pregnancy because of an impact on fetal renal function, and beta-blockers have been associated with intrauterine growth restriction and should be used with caution. Appropriate immunisations should be performed prior to pregnancy (e.g. influenza, pneumococcal, tetanus, rubella). Genetic counselling regarding the risk of congenital heart disease in the baby should also be offered.

Antenatal Where medication is inappropriate for pregnancy, this should be adjusted as above. If the maternal prognosis

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during pregnancy is very poor, termination should be offered. The woman needs to be booked under spe­ cialist care with frequent obstetric and cardiologist review. In pregnancy, early diagnosis and prompt treatment of any deterioration in cardiac condition is imperative. Minimisation of aggravating factors is also important. Anaemia is obviously a potential aggravating factor, as is excessive weight gain. Prophylaxis against thromboembolism should be considered if the cardiac defect specifically predisposes to this complication (e.g. pulmonary hypertension) or prolonged bed rest is necessary. Additional fetal surveillance should include ultrasonography in the third trimester to detect intrauterine growth retardation.

Timing and mode of delivery Spontaneous labour is usually preferred to an induction as it should be more efficient and therefore place less demand on cardiac reserve, particularly if the cervix is unripe. In most conditions, vaginal delivery is preferable to elective caesarean section. There may be some possible exceptions (e.g. pulmonary hypertension, coarctation of the aorta) that benefit from elective caesarean section rather than vaginal delivery, but such decisions should be made only after consultation between obstetrician, anaesthetist and cardiologist. If caesarean section is undertaken, a discussion regarding tubal ligation at the time of surgery may be appropriate.

Intrapartum management: first stage Where there is a lesion at risk of bacterial endocarditis, an intravenous line is required for the infusion of prophylactic antibiotics. Amoxycillin (or vancomycin if the patient has a penicillin allergy) and gentamicin are suitable agents. Care must be taken not to infuse excessive intravenous fluid that may precipitate cardiac failure. The woman must be observed closely in the labour ward. In addition to the routine observations, regular checks of jugular venous pressure and lung bases for crepitations should be performed. The patient’s oxygen saturation should be monitored with pulse oximetry. If the woman is not anticoagulated, epidural analgesia may be administered with careful control of intravascular volume to avoid hypotension, but this is contraindicated in aortic stenosis and hypertrophic obstructive cardiomyopathy, and may also be hazardous in mitral stenosis or pulmonary hypertension. In these women, the epidural administration of opioid drugs alone can provide safe analgesia.

Second stage of labour The woman’s head and shoulders should be elevated during labour and delivery, with the legs dependent.

Specifically, the lithotomy position should be avoided because of the risk of acute pulmonary oedema. Forceps or vacuum extraction should be used to avoid prolonged pushing in the second stage.

Third stage of labour These women withstand blood loss poorly and prophylaxis against postpartum haemorrhage is necessary, even though ergometrine is contraindicated. Oxytocin 10 units by slow intravenous injection should be administered after completion of the second stage. In the event of a postpartum haemorrhage, intravenous ergometrine should be given, as the two reasons for avoiding it initially (excessive preload and afterload) are no longer present and hypovolaemia in these women can have catastrophic sequelae.

Puerperium Rapid haemodynamic alterations occur at this time that may precipitate right or left heart failure. This includes a physiological ‘autotransfusion’ of blood volume into the circulation from the contracted uterus and mobilisation of extracellular fluid. Women with mitral stenosis are particularly at risk of pulmonary edema during this period due to restricted left vetnricular filling. Pulmonary hypertension commonly deteriorates in the early puer­ perium, possibly as a consequence of progesterone withdrawal. Attention is given to the prevention of thromboembolism by early mobilisation and prophylactic LMW heparin. Contraception is important, as unwanted pregnancies may unnecessarily risk deterioration in maternal cardiac condition. The combined oral contraceptive pill is undesirable because of the thromboembolic risk, but progestogen-only contraception is safe. An intrauterine contraceptive device may risk endocarditis. Laparoscopy may be relatively contraindicated in these women (cardiac embarrassment from pneumoperitoneum), as is general anaesthesia (risk of thromboembolism). Vasectomy of the partner or tubal ligation at the time of cesarean section are suitable options if permanent contraception is desired.

PERIPARTUM CARDIOMYOPATHY This is a rare condition (about 1 in 2000 pregnancies) where a cardiomyopathy develops for the first time in the peripartum period. It often presents with sudden maternal decompensation at the time of a peripartum event such as a preeclampsia or postpartum haemorrhage. Cause is likely to be a preexisting sensitivity to peripartum events such as the withdrawal of oestrogen, a known positive inotrope. Treatment is along the usual lines for a dilated cardiomyopathy. Even when recovery appears complete, there is a high recurrence rate in any subsequent pregnancy. 143

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RESPIRATORY DISEASE PHYSIOLOGICAL CHANGES IN PREGNANCY Ventilation is increased in pregnancy by about 40%. There is no significant change in the respiratory rate so the increase in minute volume is largely met by an increase in tidal volume due to a direct effect of progesterone on the central respiratory centre. The increased ventilation causes a reduction in maternal carbon dioxide tension in maternal blood, which facilitates gas exchange across the placenta. Oxygen exchange is aided by the differing oxygen dissociation curves for fetal and adult haemoglobin. In the third trimester, there is a considerable fall in expiratory reserve volume and residual volume due to upward pressure by the uterine fundus on the diaphragm. Episodic mild shortness of breath sometimes occurs mid-pregnancy as an awareness of the increased respiratory work. It is not exercise related and not nocturnal. It requires careful clinical assessment to identify any underlying cardiorespiratory disease before attributing the symptom to physiological reasons.

ASTHMA This is the most common disease affecting the lungs in pregnancy. There is no uniform pattern of the disease in pregnancy. Mild asthma has little effect on pregnancy but with moderate or severe asthma there is an increased risk of intrauterine growth restriction, preterm birth and preeclampsia. Most drugs used for asthma are relatively safe in pregnancy, including the beta-sympathomimetics and corticosteroids. As in non-pregnant women, potential adverse effects will be lessened with inhaled rather than oral medication. Caution should be exercised with the administration of prostaglandins for cervical ripening, induction of labour or postpartum haemorrhage.

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Prostaglandin F2-alpha is particularly prone to cause bronchoconstriction. Anti-inflammatory drugs postpartum may exacerbate asthma. Management of asthma in pregnancy is similar to that in the non-pregnant state. Adherence to medication is even more important than usual in the interests of both the mother and the offspring. It is important that the carer educates the mother with respect to the risk–benefit equation, strongly favouring any needed medication. Peak expiratory flow should be checked regularly as a guide to therapy. The basic aim of drug therapy is to pro­ vide bronchodilator and anti-inflammatory activity. For mild intermittent asthma, inhaled beta-sympathomimetic (e.g. salbutamol or terbutaline) for occasional symptom relief may be all that is needed. If attacks are more frequent, prophylaxis with an inhaled corticosteroid (e.g. beclomethasone, budesonide) should be instituted to reduce beta-agonist dependence. Antibiotics should be used if there is associated infective bronchitis. Short courses of oral corticosteroids may be needed for exacerbations and hospitalisation may be necessary for severe attacks. FURTHER READING Lewis G, editor. The Confidential Enquiry into Maternal and Child Health (CEMACH). Saving mothers’ lives: reviewing maternal deaths to make motherhood safer—2003–2005. The Seventh Report on Confidential Enquiries into Maternal Deaths in the United Kingdom. London: CEMACH; 2007. McLintock C, Brighton T, Chunilal S, et al. Recommendations for the prevention of pregnancyassociated venous thromboembolism. ANZJOG 2012;52:3–13. Murphy VE, Schatz M. Asthma in pregnancy: a hit for two. Eur Respir Rev 2014;23(131):64–8. Royal College of Obstetricians and Gynaecologists. Cardiac disease and Pregnancy. Good Practice Guideline No. 13. London: RCOG; 2011 June. Online. Available: ; [16 Dec 2014].

Chapter 18  BACTERIAL INFECTIONS IN PREGNANCY Peter Wein

KEY POINTS Bacterial infection in pregnancy remains a challenge due to increasing antibiotic resistance, changing common organisms and patterns of infection. Normal physiological changes of pregnancy and lactation put the pregnant woman at increased risk of infection. Preterm premature rupture of the membranes and prolonged labour are prime causes of ascending infection and chorioamnionitis. The human immunodeficiency virus (HIV) has seen the return of infections thought to be conquered, such as syphilis and tuberculosis. Infection is often ‘silent’ in terms of clinical features. A high index of suspicion is thus necessary if the wellbeing of the mother, fetus and neonate is to be maintained.

INFECTIONS BY SITE The mother is predisposed to infection in four classical sites: the uterus, urinary tract, breast and (depending on the mode of birth) either the perineal or abdominal wound. Infection is particularly common in pregnancy owing to the relative immune suppression, together with physiological changes such as urinary tract dilatation and stasis. Even a normal confinement leaves every woman with a large healing placental site, tantamount to a surgical wound in a potentially contaminated area; many also have an episiotomy or sutured laceration in close proximity to bowel bacteria. The neonate with immature defence mechanisms is at particular risk of bacterial infections. This will be more pronounced in the premature neonate or, less commonly, a neonate compromised by specific immune deficiencies (e.g. neonatal alloimmune neutropenia). A variety of organisms may be involved, both aerobic and anaerobic, reflecting the microflora of the lower birth canal. The fetus is also at risk from microorganisms acquired transplacentally, originating in the mother’s bloodstream.

Infection of the mother during pregnancy usually affects the fetus directly, but indirect manifestations such as fever and endotoxin liberation (e.g. from vaginal or urinary tract infection) may precipitate premature rupture of the membranes and/or premature labour. When treating infection in the pregnant or puerperal woman, the possible effects on the fetus or newborn of drugs given to the mother should be remembered. Antibiotics should never be given indiscriminately; most of the treatable infections have relatively specific drug regimens.

REPRODUCTIVE TRACT INFECTION CHORIOAMNIONITIS Pathology Infection of the fetus, secundines (placenta and membranes) and amniotic fluid is secondary to infection

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or colonisation of the mother by pathogenic microorganisms. When the infection arises in the vagina, the membranes and amniotic fluid are involved primarily; the baby and placenta are involved secondarily. The organisms reflect the normal vaginal flora—mixed aerobic and anaerobic bacteria—or intercurrent disease. Bacteria can gain access to the fetus via the nasopharynx during normal ‘breathing’ movements in utero.

Predisposing factors The usual situation is preterm premature rupture of the membranes (PPROM), with ascent of pathogens from the cervix/vagina. The presence of a cervical suture increases the risk of infection and, if present, should usually be removed if the membranes rupture irrespective of the gestation. Chorioamnionitis can occur with intact membranes and prolonged labour, the latter causing a breakdown of the normally effective barrier. Transplacental infections can occur during pregnancy in the absence of premature rupture of the membranes or labour. There may be an unnoticed or mild illness in the mother (e.g. listeriosis). The primary damage is seen in the placenta or in the fetal liver.

Diagnosis Early signs are often absent or minimal; with a more established infection, there may be maternal and/or fetal tachycardia, maternal fever, uterine tenderness and odour. Full blood examination will show an increased white blood cell count, with a neutrophilia and left shift. Acute phase reactants such as C-reactive protein (CRP) levels are usually elevated, although the rise in CRP may not occur until after clinical chorioamnionitis and a need for expedited delivery is apparent. The cardiotocography commonly shows a fetal tachycardia. If the diagnosis is in doubt, amniocentesis is very occasionally performed, enabling amniotic fluid microscopy and culture and a definitive diagnosis. This may be difficult where there is oligohydramnios as a consequence of PPROM.

Management Established chorioamnionitis requires delivery, and failure to expedite birth may result in a maternal death. The major issues are the mode of birth and the most appropriate antibiotics. In women with PPROM, there is good evidence that prophylactic treatment with erythromycin reduces the incidence of chorioamnionitis. In established chorioamnionitis, the usual combination of antibiotics while awaiting identification of a specific organism is as follows: amoxycillin/ampicillin 2 g intravenously 6-hourly plus gentamicin 5 to 6 mg intravenously 24-hourly for three doses (if normal renal function) plus metronidazole 500 mg 8-hourly. Gentamicin should only be used as empiric therapy for 72 hours. If there is an organism isolated that is only

• • •

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sensitive to gentamicin, further dosing should be guided by serum levels.

POSTPARTUM ENDOMETRITIS Pathology The ‘childbed fever’ that was the great scourge of the 19th century was due to Streptococcus pyogenes (Group A strep) and led to one of the greatest ever simple advances in medicine—handwashing before attending a birth. This was instigated by Ignaz Semmelweiss in 1852. The common organisms now are those colonising the vagina and perineum including Group B streptococci (GBS), coliforms and anaerobes. The placental site is usually infected first, after which spread occurs to the surrounding tissues, resulting in parametritis and pelvic peritonitis but rarely general peritonitis or septicaemia (see Ch 41).

Predisposing factors Predisposing factors include prolonged labour greater than 12 hours, multiple vaginal examinations, operative delivery (both vaginal and caesarean birth) and retention of products of conception. Infection complicates caesarean section in 5 to 10% of elective and 10 to 30% of emergency cases. Prophylactic antibiotics (usually a firstgeneration cephalosporin) significantly decrease post­ operative infection.

Management Management includes resuscitation as necessary, identification of the organism if possible (although the infection is often polymicrobial) and broad-spectrum antibiotics until the organism is identified.

POSTABORTAL ENDOMETRITIS Predisposing factors Predisposing factors include preexisting infection (e.g. Chlamydia) and retained products of conception.

Pathology The usual organisms are lower genital tract flora. Illegal (‘backyard’) abortion was historically associated with Clostridium perfringens and commonly fatal.

Diagnosis The patient presents with a combination of increased bleeding, pelvic pain, fever and offensive discharge. Examination may show fever, lower abdominal tenderness, cervical motion and forniceal tenderness on pelvic examination, and the presence of a vaginal discharge. Cervical swabs should be taken for Gram stain and culture and polymerase chain reaction (PCR) testing for Chlamydia.

Management For mild to moderate disease, oral treatment with amoxycillin and clavulanate and a single dose of azithromycin

Chapter 18  Bacterial Infections in Pregnancy

(repeated after 7 days) is appropriate. Severe disease is treated with intravenous amoxycillin, gentamicin and metronidazole as for chorioamnionitis. Ultrasound examination may be required to determine if there are significant retained products of conception. If there are, curettage may be necessary to remove the nidus of infection.

URINARY TRACT INFECTION PATHOGENESIS Microorganisms grow more readily in the urine of pregnant women, possibly due to differences in pH and the greater amounts of sugar and amino acids that escape reabsorption in the renal tubules. In addition, there is some obstruction to urine flow in the ureters, and decreased smooth muscle tone due to progesterone. The risk of urinary tract infection (UTI) in pregnancy is thus increased and is further aggravated by catheterisation and trauma to the urethra and bladder during delivery. In the great majority of women with urinary infection, a coliform or other gram-negative organism is cultured. In about 6% of women in early pregnancy, significant bacteriuria (> 108 colony-forming units/L) will be found in a midstream specimen of urine (MSU). If untreated, approximately one-third of these women will develop acute pyelonephritis, with increased rates of prematurity and perinatal mortality. Universal screening for asymptomatic bacteriuria is therefore recommended at the first antenatal visit. As the infection is only diagnosed by the results of urine culture, the organism and sensitivity are known and so the most appropriate antibiotic can be used. Depending on sensitivities, the usual antibiotics are amoxicillin, cephalexin, amoxycillin with clavulanate or nitrofurantoin. The infection should be treated for 5 days and the urine retested 1 week after treatment finishes. If it persists or recurs, the infection is retreated. If the infection recurs again, suppressive treatment with a low dose of antibiotic (nitrofurantoin 100 mg at night) can be used for the duration of pregnancy. UTIs that persistently recur may indicate an abnormality of the upper urinary tract (stone or congenital malformation), and renal ultrasound examination may be helpful.

ACUTE PYELONEPHRITIS Acute pyelonephritis is suspected when there are symptoms of urinary tract infection together with fever and loin pain. Bacteraemia (in about 20% of patients) and severe sepsis can occur, so it should be treated aggressively. Initial investigation is with MSU, blood cultures, full blood examination and renal function tests. Empiric treatment should be commenced with ampicillin 2 g intravenously 6-hourly plus gentamicin 5 to 6 mg intravenously 24-hourly for three doses (if normal renal function). Once the patient is

symptomatically improved and afebrile for 48 hours, she can be switched to the appropriate oral antibiotics for a total of 10 days. A ‘proof of cure’ urine culture should be performed at least 48 hours after the end of the course. As there is a significant risk of recurrence, prophylactic nitrofurantoin 100 mg at night should be used for the remainder of the pregnancy.

BREAST INFECTION PATHOGENESIS The chief predisposing causes of puerperal mastitis are stagnation of milk in poorly drained lactiferous sinuses and trauma from suckling. It is probable that the invading bacteria (almost always Staphylococcus aureus) come from the baby rather than the mother. The baby is colonised from the hospital environment and therefore these organisms are usually penicillin-resistant.

DIAGNOSIS The mother will present with pain and redness in the breast, often localised to one quadrant. With more severe infection, very high fevers (40°C), rigors and generalised symptoms may occur.

MANAGEMENT Mastitis should be treated promptly with a broadspectrum antibiotic to prevent a breast abscess. Women who are clinically well can be treated with oral dicloxacillin (or clindamycin if allergic to penicillin). However, some women develop a marked pyrexia, and may need treatment with intravenous flucloxacillin. Symptomatic treatment with non-steroidal anti-inflammatory drugs (NSAIDS) and cold compresses will relieve the symptoms. It is vital to ensure the breast is emptied. The best way to do this is to continue breastfeeding. If a breast abscess is suspected, it can be confirmed with ultrasound examination. In most cases, the abscess can also be drained using ultrasound guidance to aspirate the pus. If this fails, occasionally formal incision and drainage is necessary (Fig 18.1). Candida albicans is also often diagnosed as a cause of shooting breast and nipple pain. (See Chs 39 and 41 for more details.) It is not clear whether Candida really causes these symptoms or whether treatment with antifungal drugs helps.

SPECIFIC ORGANISMS TRANSPLACENTAL (HAEMATOGENOUS) INFECTIONS Full details of Chlamydia and gonorrhoea infections can be found in Chapter 54. This section will deal with special features of these infections relating to pregnancy. 147

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[Treponema pallidum haemagglutination]). There are a number of causes of false-positive reagin tests, including the anticardiolipin syndrome.

Management A

B

FIGURE 18.1 

Breast abscess is an avoidable complication of breastfeeding if an antibiotic is given at the onset of localised redness and tenderness with or without pyrexia. A There is a painful fluctuant lump often deep within the breast without involvement of overlying skin. B Treatment is a wide incision in a radial direction from the nipple into the depth of the abscess cavity over the most dependent area with adequate drainage.

Syphilis Epidemiology This ancient disease is caused by the spirochaete, Treponema pallidum. It has largely been controlled in areas where antenatal care is adequate because of routine serological testing of all women at the first antenatal visit. However, syphilis is still relatively common in rural and regional Indigenous populations and in less-developed countries. It is estimated that there are 500 000 perinatal deaths in the world every year due to maternal syphilis, with a similar number of babies born with congenital syphilis. Detection and treatment is highly cost-effective, with an estimated cost of about $10 per life saved.

Sequelae The spirochaete crosses the placenta and causes congenital syphilis. This is associated with significant perinatal mortality, as well as osteochondritis, rash of palms and soles, nasal discharge, hepatosplenomegaly, anaemia, IUGR, fetal hydrops, microcephaly, pneumonitis, nephrosis, thrombocytopenia, petechial rash, uveitis, chorioretinitis, leukaemoid reaction and the typical ‘saddle nose’.

Diagnosis Although syphilis is rare, the consequences of untreated maternal syphilis are serious. There is an inexpensive, reliable test and a very effective low-cost treatment, so universal screening at the first antenatal visit remains cost-effective. High-risk populations, where syphilis may be contracted during pregnancy, should be retested at 28 weeks’ gestation. If the serology is positive on screening (usually RPR [rapid plasma reagin] or Venereal Disease Research Laboratory [VDRL]), a more detailed study is made to confirm the presence of the disease by specific anti-treponemal testing (FTA [fluorescent Treponema antibody] and TPHA 148

Treatment requires an adequate course of penicillin: benzathine penicillin 1.8 g intramuscularly for early syphilis (< 12 months) or benzathine penicillin 1.8 g intramuscularly for three doses at weekly intervals if the duration of the disease is more than 12 months or unknown. Because the alternatives to penicillin have not been shown to prevent congenital syphilis, patients who are allergic to penicillin should be desensitised then treated with penicillin. In addition, the woman’s partner should be tested and treated if serology is positive. It is also important that the disease be notified and sexual contacts examined. The baby should be carefully examined and investigated with syphilis serology, which should be less than four times the mother’s titre. If both are negative, the baby should receive a single dose of benzathine penicillin 37.5 mg/kg intramuscularly.

Listeriosis Listeria monocytogenes is a ubiquitous environmental gram-positive organism. Although uncommon, infection of the mother with Listeria monocytogenes may have serious consequences for the infant. The organism is ingested with poorly cooked meat or seafood, pates and smallgoods, contaminated soft cheese, soft-serve ice cream or vegetables that have not been adequately washed. It can grow in refrigerated products, so pregnant women should not eat at-risk foods that have been stored for more than 24 hours. Typically, the mother has a non-specific, flu-like febrile illness; back pain and rigors may also be present. It can lead to premature labour, fetal death or a severe disseminated fetal infection (lung, liver, central nervous system) resulting from transplacental transmission. Meconium staining of the amniotic fluid is common even in the late second trimester. Unless the diagnosis is thought of and energetic treatment given, the baby has a high risk (25 to 50%) of dying. If the diagnosis is clinically suspected, blood cultures and genital tract cultures should be performed. There may a place for amniocentesis and culture of amniotic fluid. Treatment of suspected or documented infection is with intravenous ampicillin 2 g 6-hourly.

Chlamydial infection Untreated genital Chlamydia trachomatis infection in pregnancy increases the risk of PPROM, preterm labour and preterm birth. The baby has about a 30% risk of conjunctival infection and a 15% risk of pneumonia. These outcomes can be prevented by simple treatment of pregnant women with genital chlamydial infection. However, it is unclear whether screening all or some pregnant women for Chlamydia is an effective policy. The Centers for Disease Control and Prevention (United

Chapter 18  Bacterial Infections in Pregnancy

States) recommends screening of all pregnant women. The Royal Australasian College of Obstetricians and Gynaecologists recommends that ‘selective testing for Chlamydia should be considered for those who may be at increased risk (e.g. less than 25 years)’ and the National Institute for Clinical Excellence (NICE) in the United Kingdom suggests that Chlamydia screening should not be offered as part of routine antenatal care. Testing should definitely be performed in women with symptoms, or those who are at high risk. Testing can be performed by nucleic acid amplification tests of vaginal swabs or urine. The recommended treatment is a single 1-g dose of oral azithromycin. The patient should be tested for gonorrhoea. Sexual contacts should be followed up and treated. A test of cure should be performed in not less than 3 weeks.

prolonged induction-delivery interval after artificial rupture of the membranes.

Gonorrhoea

Prevention

Neisseria gonorrhoea infection in pregnancy is very rare in Australia. If untreated, it is associated with an increased risk of preterm delivery. The baby is at risk of a severe gonococcal conjunctivitis, ophthalmia neonatorum, which can lead to blindness if not treated. In the United States, routine prophylaxis for this condition with topical erythromycin is still mandated in many states. Women with symptoms of cervicitis, those with chlamydial infections and those who have had sexual contact with men who have had gonorrhoea should be tested as described above. The appropriate treatment is ceftriaxone 250 mg intramuscularly and azithromycin 1 g orally, both as a single dose. Again, contact tracing and test of cure are vital.

Awareness of the condition and the introduction of prophylaxis have led to a marked decline in the incidence of the early-onset disease. The most effective method used to reduce early-onset disease is the culture-based approach; all pregnant women are tested at 35 to 37 weeks’ gestation by a vaginal and anorectal swab cultured in selective medium. Women who test positive and other women with risk factors receive intrapartum antibiotics prophylaxis. The indications for treatment are listed in Box 18.1. The prophylaxis of choice is benzyl penicillin where GBS is the principle concern. If chorioamnionitis is suspected, broad-spectrum antibiotic therapy that includes an agent known to be active against GBS should replace GBS prophylaxis. It is important at the first antenatal visit to characterise accurately ‘penicillin allergy’. Women who state that they are allergic to penicillin but do not give a history of immediate-type hypersensitivity to penicillin (anaphylaxis, angioedema, respiratory distress or urticaria) should receive intrapartum prophylaxis with cefazolin. Those who have immediate-type hypersensitivity to penicillin or any other beta-lactam should receive an alternative antibiotic guided by the antenatally determined antibiotic sensitivity of the GBS. If this is not available, clindamycin is a common alternative, but up to 20% of GBS have resistance to clindamycin. The recommended approach to antibiotic choice is shown in Figure 18.2.

GROUP B β-HAEMOLYTIC STREPTOCOCCUS Epidemiology This gram-positive coccus is present in the vagina at some time during pregnancy in approximately 20% of women; it often can also be isolated from the rectum in such women. About 50% of the babies born to colonised women are themselves colonised; of these, about 1% develop serious early-onset Group B streptococcal disease, so that the overall prevalence of this condition in untreated populations is about 1/1000 (20% × 50% × 1%). Prior to treatment of women at risk of having a baby with early-onset disease, this was the most common micro­ organism causing serious infection in the newborn.

Clinical features Group B streptococcus can cause asymptomatic bacteriuria (see above); these women are at a particularly high risk of having an affected baby. Premature labour and premature rupture of the membranes are more common. Approximately 1.5 to 2.0% of women will experience puerperal infection (uterine), chiefly as a complication of

Neonatal sequelae There are two main syndromes. The first is an early-onset septicaemia, sometimes with meningitis or pneumonia, often presenting as an idiopathic respiratory distress syndrome/cardiovascular collapse. While prematurity is a risk factor, most cases occur in term babies because there are more of them. There is a significant associated mortality of at least 5% even if treated promptly, with a 20% risk of severe morbidity in the survivors. The second main syndrome is the late-onset form. This is seen usually after the first week of life, the baby being lethargic, anorexic and jaundiced; meningitis is a common complication.

MYCOPLASMAL AND UREASPLASMAL INFECTION The female genital tract of sexually active women is often colonised by mycoplasmal organisms (Mycoplasma hominis, Ureaplasma urealyticum, Ureaplasma parvum). There is an association between these organisms and chorioamnionitis, premature labour, puerperal and neona­ tal infection. However, it is not clear whether asymptomatic woman colonised with these organisms benefit from 149

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Patient allergic to penicillin? Yes

No

Patient with a history of any of the following aer receiving penicillin or a cephalosporin?¡¡ • Anaphylaxis • Angioedema • Respiratory distress • Urticaria

Penicillin G, 5 million units IV initial dose, then 2.5—3.0 million units¡ every 4 hrs until delivery or Ampicillin, 2 g IV initial dose, then 1 g IV every 4 hrs until delivery

Yes

No

Isolate susceptible to clindamycin¡¡¡ and erythromyciniv ?

Cefazolin, 2 g IV initial dose, then 1 g IV every 8 hrs until delivery No

Yes

Vancomycin, 1 g IV every 12 hrs until delivery

Clindamycin, 900 mg IV every 8 hrs until delivery

¡

Doses ranging from 2.5 to 3.0 million units are acceptable for the doses administered every 4 hours following the initial dose. The choice of dose within that range should be guided by which formulations of penicillin G are readily available to reduce the need for pharmacies to specially prepare doses. ¡¡ Penicillin-allergic patients with a history of anaphylaxis, angioedema, respiratory distress or urticaria following administration of penicillin or a cephalosporin are considered to be at high risk for anaphylaxis and should not receive penicillin, ampicillin or cefazolin for GBS intrapartum prophylaxis. For penicillin-allergic patients who do not have a history of those reactions, cefazolin is the preferred agent because pharmacological data suggests it achieves effective intra-amniotic concentrations. Vancomycin and clindamycin should be reserved for penicillin-allergic women at high risk for anaphylaxis. ¡¡¡ If laboratory facilities are adequate, clindamycin and erythromycin susceptibility testing (box 3) should be performed on prenatal GBS isolates from penicillin-allergic women at high risk for anaphylaxis. If no susceptibility testing is performed, or the results are not available at the time of labour, vancomycin is the preferred agent for GBS intrapartum prophylaxis for penicillin-allergic women at high risk for anaphylaxis. ¡v Resistance to erythromycin is oen, but not always, associated with clindamycin resistance. If an isolate is resistant to erythromycin, it might have inducible resistance to clindamycin, even if it appears susceptible to clindamycin. If a GBS isolate is susceptible to clindamycin, resistant to erythromycin, and testing for inducible clindamycin resistance has been performed and is negative (no inducible resistance), then clindamycin can be used for GBS intrapartum prophylaxis instead of vancomycin.

FIGURE 18.2 

Recommended regimens for intrapartum antibiotic prophylaxis for prevention of early-onset Group B streptococcal (GBS) disease.i Broader spectrum agents, including an agent active against GBS, might be necessary for treatmeant of chorioamnionitis. Abbreviation: IV = intravenously. Source: Centers for Disease Control and Prevention. Morbidity and Mortality Weekly Report. Online. Available at http://www.cdc.gov/mmwr; 19 November 2010;59(RR-10).

treatment. Many clinicians would only treat colonisation with these organisms in the presence of PPROM or cervical insufficiency. If a Mycoplasma hominis infection is to be treated, the best drug in pregnancy is clindamycin. M. hominis is resistant to macrolides (e.g. erythromycin), and the best drug, doxycycline, is contraindicated in the second and third trimesters. Ureaplasmas are sensitive to macrolides, 150

but more to the newer agent clarithromycin than erythromycin. They are not sensitive to clindamycin.

TUBERCULOSIS Tuberculosis is not specifically affected by pregnancy, nor does it have any specific adverse effects on pregnancy

Chapter 18  Bacterial Infections in Pregnancy

BOX 18.1  Indications and non-indications for intrapartum antibiotic prophylaxis to prevent early-onset Group B streptococcal (GBS) disease.i Intrapartum GBS prophylaxis indicated Previous infant with invasive GBS disease GBS bacteriuria during any trimester of the current pregnancyii Positive GBS vaginal-rectal screening culture in late gestationiii during current pregnancyii

Unknown GBS status at the onset of labour (culture not done, incomplete or results unknown) and any of the following: ✚ delivery at < 37 weeks’ gestation ✚ amniotic membrane rupture ≥ 18 hours ✚ intrapartum temperature ≥ 38.0°C ✚ intrapartum nucleic acid amplification tests (NAAT)i positive for GBS

Intrapartum GBS prophylaxis not indicated Colonisation with GBS during a previous pregnancy (unless an indication for GBS prophylaxis is present for current pregnancy) GBS bacteriuria during previous pregnancy (unless an indication for GBS prophylaxis is present for current pregnancy) Negative vaginal and rectal GBS screening culture in late gestationiii during the current pregnancy, regardless of intrapartum risk factors Caesarean delivery performed before onset of labour on a woman with intact amniotic membranes, regardless of GBS colonisation status or gestational age

i

Adapted from Centers for Disease Control and Prevention. Prevention of Perinatal Group B Streptococcal Disease: Revised Guidelines from CDC, 2010. MMWR 2010 Nov 19;59(No. RR10). Online. Available: http://www.cdc.gov/mmwr/pdf/rr/rr5910.pdf; 16 Dec 2014. ii Intrapartum antibiotic prophylaxis is not indicated in this circumstance if a caesarean delivery is performed before onset of labour on a woman with intact amniotic membranes. iii Optimal timing for prenatal GBS screening is at 35 to 37 weeks’ gestation.

apart from its effects on the mother. It often becomes known in pregnancy because that may be the first time a woman who has recently emigrated from a high-risk area seeks medical care. The investigation, diagnosis and treatment of tuberculosis are the same in pregnancy as in non-pregnant women. Chest X-rays can be performed with adequate shielding of the fetus. If active tuberculosis is diagnosed, it should be initially treated with isoniazid, rifampicin, ethambutol and pyrazinamide. FURTHER READING Capoccia R, Greub G, Baud D. Ureaplasma urealyticum, Mycoplasma hominis and adverse pregnancy outcomes. Curr Opin Infect Dis 2013;26(3):231–40.

Centers for Disease Control and Prevention. Prevention of perinatal Group B streptococcal disease. Revised guidelines from CDC, 2010. Recommendations and Reports 2010;59(RR10):1–32. Online. Available: . Semmelweiss IP. Die Ätiologie, der Begriff und die Prophylaxis des Kindbettfiebers (‘The etiology, concept and prophylaxis of childbed fever’) 1861. CA Hartleben’s Verlags-Expedition, Pest. Online. Available: ; [30 Nov 2014]. Therapeutic Guidelines. Antibiotic. Version 15. Melbourne: Therapeutic Guidelines Limited; 2014.

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Chapter 19  VIRAL AND PROTOZOAN INFECTIONS IN PREGNANCY Susan Walker

KEY POINTS Infections during pregnancy can be considered as predominantly harmful to the mother (where she may be susceptible to more severe complications such as with varicella pneumonia), the fetus only (e.g. rubella, which may have only minor or subclinical manifestations in the mother but devastating effects on the fetus) or to both. Infection in pregnancy may be detected: ■ during routine antenatal screening (e.g. rubella, syphilis, hepatitis B, hepatitis C and HIV) ■ by screening for seroconversion following suspected contact (e.g. parvovirus or varicella) ■ following suspicion of clinical illness (e.g. herpes simplex) ■ following prenatal diagnosis of suspected fetal malformation associated with congenital infection (e.g. toxoplasmosis, cytomegalovirus). A summary of management of viral and protozoal infections in pregnancy is provided in Table 19.1. Simple hygiene measures can reduce the risk of congenital infection and should be provided to all pregnant women (Boxes 19.1 and 19.2). Prevention of serious maternal and perinatal morbidity can be achieved with prepregnancy rubella and varicella vaccination. Prevention of serious maternal and infant morbidity is possible with influenza vaccination during pregnancy. Prevention of serious infant morbidity due to pertussis may be achieved either with cocooning (vaccination of close contacts) or vaccination of women in late pregnancy to provide passive protection to the newborn.

INTRODUCTION Viral and protozoal infections may have serious consequences for the mother, fetus and neonate. A summary of the maternal, perinatal and fetal risks together with prevention and treatment strategies is found in Table 19.1.

CYTOMEGALOVIRUS Congenital cytomegalovirus (CMV) is the most common form of infective neurological handicap in the developed world. Approximately 50% of Australian women are seronegative and 1% will seroconvert (primary infection)

during pregnancy. Women at increased risk of seroconversion include daycare workers (8% seroconversion/ year) and parents of children shedding CMV (24% seroconversion/year). The majority of maternal infections will be silent since CMV infection in immunocompetent adults is generally asymptomatic. While congenital CMV can be the result of non-primary infection, the risk of fetal transmission and infant sequelae is highest with primary infection. The risk of fetal transmission with maternal primary infection is approximately 40%. Among infected fetuses, 10 to 15% will be symptomatic at birth, with symptoms such as jaundice, hepatosplenomegaly, hydrops, thrombocytopenia, anaemia, microcephaly, seizures and chorioretinitis (Fig 19.1).

Maternal sequelae

Nil; seroconversion in pregnancy = 1%

Mild maternal illness

Mild maternal illness

Maternal varicella may be complicated by severe pneumonia

Maternal infection may be more severe in pregnancy

Primary infection more likely to disseminate in pregnancy

Infection

Congenital cytomegalovirus (CMV)

Rubella

Parvovirus

Varicella

Measles

Herpes simplex virus (HSV)

Infection within 1 week of delivery may result in severe neonatal infection Neonatal infection more likely with primary infection and lesions at delivery

Fetal sequelae only with primary infection

Suppressive aciclovir from 36 weeks’ in women with recurrent attacks; caesarean within 6 hours of rupture of membranes or labour onset if active lesions at time of delivery

Prepregnancy vaccination; post-exposure prophylaxis with immunoglobulin

Continued

Observation, isolation, swabs and/or treatment of newborn if significant exposure

Neonatal surveillance

Aciclovir for maternal or neonatal disease Prepregnancy vaccination; zoster immunoglobulin (ZIG) within 96 hours of contact if mother nonimmune

Risk of severe neonatal varicella if maternal infection within 2 weeks of maternal infection

Up to 2% risk of congenital varicella syndrome; infection may be confirmed with amniocentesis No congenital syndrome

Middle cerebral artery peak systolic velocity (MCA PSV) surveillance for fetal anaemia for 12 weeks post maternal exposure and follow with intrauterine transfusion (IUT) if necessary

Hygiene advice; avoid contacts

In infected fetuses, fetal loss risk = 10%; fetal hydrops with infection risk 15% < 20 weeks’

Consider abortion if confirmed infection early pregnancy

Surveillance for fetal defects; consider administration of CMV hyperimmunoglobulin (HIG)

Risk of fetal infection = 50%

Prepregnancy vaccination

Hygiene advice (see Box 19.1)

Management

Cardiac abnormalities, eye abnormalities, deafness, neurodevelopmental delay

Infants symptomatic at birth = 10%; symptomatic later = 10%

Fetal infection risk = 40%; confirmed with amniocentesis

Prevention strategy

High-risk multiple abnormalities in first trimester; uncommon sequelae after 20 weeks’

Perinatal sequelae

Fetal infection

TABLE 19.1  SUMMARY OF VIRAL AND PROTOZOAL INFECTIONS IN PREGNANCY.

Chapter 19  Viral and Protozoan Infections in Pregnancy

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154

Maternal sequelae

No impact on disease course

No impact on maternal disease course

No impact on disease course

Mild mononucleosislike illness

Maternal illness worse in pregnancy; severity related to degree of partial immunity

Pregnancy significant risk factor for major respiratory morbidity with influenza infection

Infection

Human immunodeficiency virus (HIV)

Hepatitis B

Hepatitis C

Toxoplasmosis

Malaria

Influenza

FGR; neonatal death

Infant sequelae due to preterm birth and consequences of maternal infection

Miscarriage; preterm birth; stillbirth

No congenital syndrome but increased stillbirth risk

Infant sequelae highest with early pregnancy infection

Overall fetal infection = 50%; transmission increases with gestation; confirmed with amniocentesis

Treatment dictated by disease severity and local resistance patterns Oseltamivir, symptomatic/ supportive treatment; isolation; vaccination of healthcare workers Vaccination during pregnancy to reduce risk of maternal and infant serious respiratory morbidity

Spiramycin from time of maternal infection; pyrimethamine-sulfadiazine combination with folinic acid if confirmed fetal infection > 18 weeks’

Maternal follow-up plus follow-up of infant and family members

Antivirals to reduce viral load in late pregnancy in women with high viral load; maternal follow-up plus follow-up of infant and family members

Neonatal ART; surveillance to confirm no infant infection

Management

Avoid travel to endemic areas; avoid mosquito contact and take chemoprophylaxis

Hygiene and food advice (see Box 19.1)

Minimise invasive procedures; avoid breastfeeding if nipples cracked or bleeding

Transmission risk = 5%; almost exclusively in RNA-positive women

No congenital syndrome

Antiretroviral therapy (ART) during pregnancy and delivery; caesarean if detectable viral load; avoid breastfeeding

Prevention strategy

Hepatitis B immune globulin and vaccine at birth; minimise antenatal and intrapartum invasive procedures

Perinatal transmission approximately 25% in the absence of interventions

Perinatal sequelae

Peripartum transmission results in perinatal infection in 1% with low viral load; up to 10% with high viral load

No congenital syndrome

No congenital syndrome

Fetal infection

TABLE 19.1  SUMMARY OF VIRAL AND PROTOZOAL INFECTIONS IN PREGNANCY—cont’d.

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Chapter 19  Viral and Protozoan Infections in Pregnancy

BOX 19.1  Advice for CMV seronegative women in order to minimise the risk of seroconversion during pregnancy. Wash hands with soap and water for 15 to 20 seconds after handling body fluids, dirty laundry or children’s toys, changing nappies, bathing or feeding young children. Do not share food, drinks or eating utensils with young children. Do not put a dummy in your mouth or share a toothbrush with a young child. Avoid contact with saliva when kissing a child. Clean toys, countertops and so on that come into contact with children’s urine or saliva.

FIGURE 19.1

CMV disease in a 2-day-old infant causing jaundice, hepatosplenomegaly and pneumonia requiring intubation and ventilator support. Source: Courtesy of Prof. Norman Beischer.

Of these infants, approximately 10% will die and 50% will be left with permanent sequelae. Among infants with congenital CMV who are asymptomatic at birth, 10 to 15% will become symptomatic later, most commonly with sensorineural hearing loss. While no country has yet implemented universal screening for CMV, this position may change if trials currently underway demonstrate that fetal CMV infection can be reliably prevented, or its sequelae minimised, by antenatal interventions.

MANAGEMENT OF THE SERONEGATIVE MOTHER Women known to be seronegative should be given advice on how to minimise primary infection in pregnancy (Box 19.1). These interventions have been shown to reduce the risk of seroconversion in pregnancy.

MANAGEMENT FOLLOWING SEROCONVERSION Following the diagnosis of maternal primary CMV, fetal infection can be confirmed with amniocentesis, performed after 21 weeks’ gestation and 7 weeks after mater-

nal infection. The presence of CMV polymerase chain reaction (PCR) in the amniotic fluid confirms fetal infection. Trials underway are examining the role of CMV hyperimmune globulin (CMV HIG) to reduce the chance of fetal transmission among women with primary infection in pregnancy.

MANAGEMENT OF THE INFECTED FETUS In fetuses with confirmed infection, discussion with parents needs to include: 1. surveillance for evidence of fetal sequelae, using serial ultrasound and, possibly, fetal MRI; 2. the potential for in utero therapy with CMV HIG or antivirals, such as valaciclovir; and 3. their options if they elect to terminate the pregnancy. Among fetuses with evidence of damage on antenatal imaging, sequelae at birth are almost inevitable. Although normal imaging provides some reassurance, serious sequelae may still occur despite normal antenatal imaging, particularly sensorineural hearing loss. Accordingly, all newborns where the mother has had primary infection in pregnancy should be carefully followed up after delivery.

RUBELLA Due to widespread vaccination programmes, congenital rubella syndrome has now been almost eliminated in developed countries. However, when maternal infection occurs, particularly during the first trimester, the effects on the fetus can be profound. Although the majority of pregnant women are immune, it is recommended that routine testing for rubella antibodies be carried out at the first antenatal visit. If she is immune, she can be reassured; if not, she should be immunised in the puerperium. If the vaccine is inadvertently given in early 155

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pregnancy, there is no indication for abortion; to date, there have been no cases of congenital rubella syndrome in fetuses born to women inadvertently exposed to the vaccine during pregnancy. Other advice to seronegative women includes contact avoidance, and the importance of presenting for serological testing in the event of suspected exposure (see below).

MATERNAL INFECTION The infection is usually spread by droplets and after an incubation period of 2 to 3 weeks, a fine rash appears which lasts for 1 to 5 days. The rash is not characteristic, but lymphadenopathy (usually suboccipital, postauricular and cervical), together with joint pain and swelling (particularly of the wrists and fingers), are suspicious. The infected patient is highly infectious for 1 week before and 2 weeks after the appearance of the rash. Unfortunately, there is no rash in 50% of rubella infections, and 50% of rubella-like rashes are due to other conditions. If a woman presents after suspected contact, she should have her rubella antibodies checked. If she has IgG antibodies prior to the onset of the rash, then the antibodies represent prior infection. If the titre is low or negative, a further test 2 to 3 weeks later should be carried out. Acute rubella is diagnosed in the presence of: 1. a fourfold rise in rubella IgG titre between the acute and convalescent serum specimens; and 2. the appearance of rubella-specific IgM. Rubella IgM antibodies appear 1 week after the onset of infection and persist for approximately 1 month. Post-exposure prophylaxis with human

A FIGURE 19.2

immunoglobulin has not been shown to be effective in preventing the risk of infection in non-immune contacts.

FETAL INFECTION The fetus is infected by transplacental passage of the virus during the stage of maternal viraemia. The risk of transmission causing sequelae are highest in the first trimester. Congenital rubella infection can cause fetal growth restriction (FGR), fetal death in utero, congenital malformations and neurodevelopmental delay. The most common malformations include cataracts, deafness and cardiac abnormalities (Fig 19.2). The effect on the fetus is largely related to gestational age, with cardiac and eye abnormalities more likely with infection in the first trimester and hearing loss with maternal infections up to 18 weeks’ gestation. The incidence of defects is 80 to 85% in the first trimester, whereas congenital defects are uncommon with infection after 18 to 20 weeks’ gestation and FGR is the only consequence of late-pregnancy infection.

DIAGNOSIS AND MANAGEMENT OF FETAL INFECTION Faced with the high likelihood of multiple, severe abnormalities, most families will elect for abortion following confirmed rubella infection in early pregnancy. Confirmation of fetal infection may be difficult but, if requested, PCR on chorionic villus appears the most useful. The

B

A Congenital rubella syndrome (purpuric rash, hepatosplenomegaly, bilateral cataracts, pulmonary stenosis, placental insufficiency) in a 1-day-old small for gestational age infant, birth weight 2110 g at 38.2 weeks’ gestation. B Cataract in the left eye displayed when the infant shown in A was aged 7 days. Source: Courtesy of Prof. Norman Beischer.

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place of intravenous immunoglobulin (IVIG) is controversial, but may prolong the incubation period and provide some fetal protection. Human immunoglobulin is only recommended for women with confirmed rubella infection who do not wish to terminate the pregnancy.

DIAGNOSIS IN THE NEWBORN Diagnosis in the newborn relies on demonstration of a rubella-specific IgM antibody or infant IgG rubella antibody level that persists at a higher level than the maternal antibody (remembering that maternal IgG crosses the placenta). Rubella can also be cultured from neonatal fluid such as a throat swab, urine, cerebrospinal fluid (CSF) or blood. In addition, nucleic acid testing is available in many centres for the detection of rubella virus. Infants with congenital rubella may continue to excrete the virus for over a year.

PARVOVIRUS B19 Parvovirus B19 (or ‘slapped cheek’ infection) can occur in both a sporadic and endemic form, and is transmitted by droplet spread. Sixty per cent of women are seropositive; of the remaining 40%, the risk of seroconversion during pregnancy depends on the nature of exposure. If they are a teacher in a daycare centre or school and exposed, 20 to 30% of susceptible women will seroconvert while 50% will seroconvert if there is a positive household contact.

MATERNAL INFECTION While the facial rash sparing the mouth, nose and eyes (‘slapped cheek’), followed by a truncal rash, is characteristic in young children, many adults will be asymptomatic. The most common symptom in adults is a transient symmetrical polyarthropathy, lasting weeks to months. Most women will thus only be diagnosed following seroconversion after a known contact. Parvovirus IgM-specific antibody is usually detectable by the third day after symptoms and usually disappears within 30 to 60 days, but may persist for up to 120 days. Parvovirus IgG antibody is detectable by day 7 of the illness and usually persists for life. Paired sera, 2 to 4 weeks apart, should be performed to detect seroconversion.

FETAL INFECTION Fetal transmission occurs in 50% of cases, and parvovirus may be associated with fetal loss and the development of fetal hydrops, but is not associated with congenital malformation. Transient isolated pleural or pericardial effusions may also be seen and are presumed to be due to pleural or myocardial inflammation. Generalised hydrops is usually due to severe fetal anaemia because parvovirus replicates in rapidly proliferating cells such as red blood cell precursors. The risk of fetal loss following maternal

parvovirus infection is estimated at approximately 10% prior to 20 weeks’ and < 1% after 20 weeks’. The risk of hydrops is approximately 15% with infection prior to 20 weeks’ (when circulating fetal red cells have the shortest half-life), compared to less than 5% after 20 weeks’. Accordingly, weekly ultrasound surveillance is recommended to look for evidence of fetal hydrops or fetal anaemia by measuring the middle cerebral artery peak systolic velocity (MCA PSV). Surveillance is recommended for 12 weeks after maternal exposure; 85% of cases requiring transfusion are diagnosed within 10 weeks’ of maternal infection. In fetuses with signs of severe anaemia, intrauterine transfusion (IUT) is indicated.

VARICELLA (CHICKENPOX) MATERNAL INFECTION The varicella zoster virus (VZV) is highly contagious and because of this, many children contract varicella before reaching adolescence. In addition, many children receive varicella vaccination and so susceptible pregnant women are uncommon. The incubation period for varicella zoster virus is 10 to 21 days. If a non-immune woman is exposed to varicella zoster, she should be offered zoster immunoglobulin (ZIG) if the exposure was within the past 96 hours. The purpose of ZIG is to reduce the occurrence of maternal disease, but it is not 100% effective and a woman who has received ZIG may still develop chickenpox, albeit with milder manifestations. Maternal varicella may be severe, including pneumonia, which develops in 10 to 20% of patients. If maternal varicella occurs, then a woman should be considered for antiviral therapy (aciclovir) if she presents within 24 hours of rash onset to reduce the severity of maternal disease. Antivirals may also be considered after 24 hours in the setting of progressive symptoms or in an immunocompromised host.

FETAL INFECTION ZIG is not known to reduce the risk of fetal sequelae from maternal varicella infection. The risk of congenital varicella syndrome depends on the trimester that the mother is infected. The risk with maternal infection prior to 12 weeks’ is 0.4%, rising to 2% between 12 and 20 weeks’ gestation. Fetal infection can be confirmed with varicella PCR on amniotic fluid, although a negative PCR does not exclude the diagnosis. The fetal anomalies that can result from congenital varicella syndrome include FGR, limb hypoplasia, eye damage, skin lesions and brain atrophy, so review with detailed ultrasound is recommended at least 5 weeks following maternal infection, as is consideration of repeat imaging if the amniocentesis is positive. Neonatal follow-up is indicated whenever a mother has varicella during pregnancy. 157

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INFECTION OF THE NEWBORN Neonatal varicella may occur when VZV transmission occurs just prior to delivery; it has a mortality of up to 30%. Infants of mothers with varicella within 2 weeks of delivery are at risk, but neonates born to mothers who have clinical varicella within 5 days prior to 2 days after delivery are at the greatest risk, as they acquire the infection without the protection of passive transfer of maternal IgG. Isolation, post-exposure prophylaxis and treatment needs to be considered in these cases.

MEASLES This infection is caused by a paramyxovirus. The incubation period is 10 to 14 days. It is rare in pregnant women because of lasting immunity from childhood infection or immunisation. Approximately 10 days after exposure, clinical symptoms comprising of fever, coryza conjunctivitis and cough develop. During the next 2 to 3 days, Koplik’s spots may appear (tiny, granular, slightly raised white lesions) followed by a generalised maculopapular skin rash. The rash starts on the head and neck then spreads to the trunk and upper extremities. The lower extremities are usually involved by day 3 of the rash. The clinical course may be altered by receipt of immunoglobulin, and may be given to non-immune pregnant women up to 7 days following contact with measles. In pregnancy, measles is associated with an increased risk of preterm labour and pregnancy loss but there is no congenital syndrome. However, severe disease in the mother can result in pneumonia, encephalitis, myocarditis and hepatitis. If infection is acquired within a week of delivery, there is a significant risk of neonatal mortality, especially in the premature baby. In such cases, immunoglobulin may be given to the mother and baby.

HERPES SIMPLEX VIRUS The seroprevalence of herpes simplex virus (HSV) 1 is approximately 70% and HSV 2 approximately 15%. While historically HSV 1 was considered to be mostly associated with non-genital infections (lips, mouth, eyes) and HSV 2 with genital infections, HSV 1 has increased in prevalence and is now considered the infective agent in approximately 40% of genital infections. The major concern with herpes infection in pregnancy is perinatal transmission and neonatal disease.

MATERNAL INFECTION The immunosuppression accompanying pregnancy means that gingivostomatitis and vulvovaginitis of pri­ mary infection is more likely to disseminate in pregnancy. Women with primary infection should be treated with oral aciclovir for 7 to 14 days. Recurrent attacks are 158

usually short and self-limiting, not usually requiring treatment during pregnancy, although suppressive ther­ apy may be considered from 36 weeks’ gestation (see below) or in the setting of frequent recurrences.

INFANT INFECTION Infection of the neonate is far more likely with primary HSV than during recurrent episodes or asymptomatic shedding (30% versus < 2%). Symptoms in the infant usually appear after an incubation period of 3 to 6 days. The spectrum of clinical disorder is wide and is often considered in three broad groups: skin and/or mucosal disease, encephalitis and disseminated HSV with severe multi-organ dysfunction. The mortality rate of encephalitis and disseminated HSV is high; local HSV has a low mortality rate, but a high risk of dissemination if untreated.

MANAGEMENT IN PREGNANCY Women with first-episode HSV in pregnancy should be treated with 7 to 14 days of oral aciclovir. Women with recurrent herpes who have active lesions or prodromal symptoms at the time of labour or rupture of membranes should be delivered by caesarean section, ideally within 6 hours of membrane rupture. In women with recurrent herpes, routine surveillance with vaginal or cervical swabs in late pregnancy are not recommended because of their poor predictive value. Prophylactic aciclovir from 36 weeks’ until delivery has been shown to reduce the rate of clinical recurrence at the time of delivery, to reduce asymptomatic shedding and to reduce the rate of caesarean section.

HUMAN IMMUNODEFICIENCY VIRUS (HIV) With the introduction of combination antiretroviral therapy the life expectancy of people living with human immunodeficiency virus (HIV) has increased and HIVrelated mortality has significantly reduced. Therefore, many women infected with HIV are choosing to have children. In addition, universal screening for HIV in pregnant women is now recommended in most countries around the world resulting in women often being diagnosed with HIV for the first time during pregnancy. Optimal management of HIV and pregnancy is essential to maximise the mother’s health, minimise transmission to partners and to prevent HIV transmission to the newborn.

MATERNAL HIV In the absence of interventions, vertical transmission from mother to infant occurs in 15 to 25% of cases. In resource-rich settings, the reported rate of transmission

Chapter 19  Viral and Protozoan Infections in Pregnancy

(with interventions including maternal and neonatal antiretroviral therapy [ART], avoidance of breastfeeding and consideration of caesarean section) is reduced to between 0.1 and 1%. ART should be offered to all women with HIV to reduce the risk of mother-to-child transmission. ART is usually a three-drug combination with the aim of viral suppression. The time to commence ART needs to be individualised according to maternal and perinatal indications. ART should be continued during the intrapartum period, whether during labour and delivery or caesarean section. While caesarean section is generally recommended to minimise transmission in women with a detectable HIV viral load in their blood, current data does not confirm an additional benefit of caesarean section over vaginal birth in women with an extremely low viral load.

DIAGNOSIS OF HIV IN THE INFANT While the diagnosis of HIV infection in adults is readily established by the detection of HIV antibodies, the situation is more complex in babies born to HIV-positive women. During the pregnancy, the fetus passively acquires maternal HIV antibodies across the placenta. Therefore, all babies born to HIV positive women will test positive to HIV antibodies for at least the first 6 months of life. It may take up to 18 months for a baby to clear these maternal antibodies. For this reason, a sensitive technique based on nucleic acid (the polymerase chain reaction [PCR]) is used to detect the presence of HIV in babies. Multiple negative tests up until the age of 3 months are required to confirm an uninfected status in exposed infants. In uninfected babies, it is recommended that the child have an HIV antibody test at 12 to 18 months to confirm the baby has cleared all the passively acquired HIV antibodies. If a PCR is positive, the test is always repeated as soon as possible (on a new sample) before it is confirmed that the baby is infected.

HEPATITIS B Transmission with hepatitis B may be either horizontal through sexual contact and blood products or vertical, from mother to child. The likelihood of chronic carriage depends on the timing of infection, with infection during infancy associated with a 90% rate of chronic carriage, compared with only 10% if infected during adulthood. In Australia, the prevalence of chronic hepatitis B is just under 1% with high-risk groups including immigrants from countries where hepatitis B is endemic, people engaging in high-risk sexual activity and injecting drug users.

MANAGEMENT OF THE PREGNANT WOMAN WITH CHRONIC HEPATITIS B Acute hepatitis B in pregnancy has a similar course as outside pregnancy, with often an initial flu-like upset

(malaise, anorexia, fatigue) giving way to nausea, fever, liver tenderness and jaundice; the urine is dark and the stools are pale. There is a 10% perinatal transmission rate with acute hepatitis B. Screening for chronic hepatitis B is recommended for all pregnant women since studies confirm that approximately 50% of chronically infected adults are unaware that they are infected until screened. The standard test available is the hepatitis B antigen (HBsAg) enzyme immunoassay (EIA or ELISA). All HBsAg-positive pregnant women should be tested for HBeAg and should have HBV DNA measured, since the risk of vertical transmission depends on the maternal viral load. The higher the viral load, the greater the risk of transmission despite interventions such as hepatitis B immunoglobulin and birth dose hepatitis B vaccination. Liver function tests should be performed each trimester for assessment of liver inflammation. Chronic hepatitis B is associated with potential long-term sequelae in the mother such as cirrhosis of the liver and hepatocellular carcinoma, and women identified in pregnancy should be referred to a specialist clinic for ongoing surveillance and management. If the mother has been found to be a carrier on routine testing, her partner and any previous children should be tested and all counselled regarding current and future management. Women requiring invasive prenatal testing should be counselled about the potential for perinatal trans­ mission, particularly if the viral load is high. Amniocentesis is preferred to chorionic villus sampling and transplacental passage of the needle should be avoided if possible.

MANAGEMENT OF THE INFANT Reducing the risk of exposure includes minimising invasive procedures in labour. Post-exposure prophylaxis includes administration of hepatitis B immunoglobulin within 12 hours of delivery together with intramuscular hepatitis B vaccine, followed by similar doses of vaccine at 1 and 6 months of age or 2, 4 and 6 months of age depending on the local immunisation schedule. Infants of women with a high viral load are at a higher risk of failed post-exposure prophylaxis and becoming infected. The risk of the infant being infected following post-exposure prophylaxis is estimated at 1% among antigen-negative mothers, rising to nearly 10% in the setting of high viral load. Recent trials have confirmed that giving antiviral treatment (such as tenofovir) to women in the third trimester who have a high viral load can significantly reduce the viral load (and hence, risk of transmission) by the time of delivery. Hepatitis B has been found in colostrum and breastmilk but as long as the baby receives immunoglobulin and birth dose vaccine, there is no evidence that there is an increased risk of transmission via breastfeeding. 159

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HEPATITIS C Hepatitis C is transmitted by blood so risk factors for infection include injecting drug use, receipt of blood products (particularly prior to routine blood product screening), tattoos and residence in endemic countries. The risk of transmission to the infant is approximately 5%, with the risk almost exclusively confined to women with detectable hepatitis C RNA in the blood. The risk of transmission is also higher among women co-infected with HIV. Women found to be hepatitis C positive during pregnancy should have an assessment of viraemic status performed and liver function tests checked. They should be referred to a viral hepatitis clinic and counselled regarding partner and family contacts, similar to hepatitis B. Caesarean section is not recommended for women who are hepatitis C positive, although invasive procedures during pregnancy and in labour should be minimised. There is no evidence that infants who are breastfed are at a higher risk of infection with hepatitis C, but direct infant contact should be minimised if the nipples are cracked or bleeding.

PROTOZOAL INFECTIONS TOXOPLASMOSIS Toxoplasma gondii is an obligate intracellular parasite. Cats are the definitive host, and oocytes are shed into cat faeces. Humans and other animals become intermediate hosts through ingestion of contaminated food or water. Women may become infected in pregnancy directly through ingestion of cysts or by eating undercooked meat, where bradyzoites may live dormant in cysts in animal muscle indefinitely. Advice for women on minimising the risk of toxoplasmosis in pregnancy can be found in Box 19.2.

Maternal infection Sixty per cent of adults are seronegative and susceptible to primary infection. Infection in immunocompetent adults is usually asymptomatic, but may present as a mononucleosis-like illness. Primary infection is diagnosed with the appearance of toxoplasmosis-specific IgM or IgG seroconversion.

Fetal infection The risk of transmission is 50% overall with an increase from approximately 15% in the first trimester to 45% in the second trimester and 70% in the third trimester. Fetal infection can be confirmed with amniocentesis performed approximately 1 month after maternal infection. The risk of infant sequelae is highest in the first trimester, and includes ventriculomegaly, microcephaly, chorioretinitis, FGR and fetal loss. Ultrasound surveillance is recommended for fetuses known to be infected. 160

BOX 19.2  Advice for women in order to minimise the risk of toxoplasmosis infection in pregnancy. Avoid ingesting soil by carefully washing fruit and vegetables before eating and washing hands carefully after gardening. Avoid raw or undercooked meats by washing food-preparation surfaces carefully, cooking meat to 66°C or higher or freezing meat for at least 24 hours at −12°C. Avoid travel to underdeveloped countries (particularly South America) where more virulent strains predominate. Avoid drinking contaminated water. Oocytes are only infective if matured outside the cat for 2 to 3 days, so avoid contact with old cat faeces (e.g. in the garden) and changing the cat litter tray.

Treatment in pregnancy Treatment of toxoplasmosis in pregnancy is associated with a lower risk of fetal transmission and sequelae. Treatment with spiramycin, which concentrates (but does not cross) the placenta, is recommended from the time of maternal seroconversion to reduce fetal trans­ mission. If fetal infection is subsequently confirmed with amniocentesis, then spiramycin should be changed to pyrimethamine-sulfadiazine combination with folinic acid. Paediatric follow-up of infected infants after delivery is necessary.

MALARIA Malaria is a preventable and treatable parasitic infection caused by five species of plasmodia. It is transmitted by mosquitoes and associated with significant maternal and perinatal morbidity and mortality. Pregnancy is associated with an increased risk of parasitaemia and severe disease; the WHO estimates that 10 000 maternal deaths each year are as a result of malaria in pregnancy. The severity of malarial infection is inversely related to disease prevalence. In areas of low immunity, pregnant women are more likely to experience severe symptoms such as hypoglycaemia, cerebral malaria, severe anaemia, acute pulmonary oedema and death. Malarial parasites reside and multiply in the placenta, contributing to spontaneous abortion, preterm birth, stillbirth and neonatal death; malaria is estimated to be responsible for 200 000 infant deaths worldwide each year. Individuals living in endemic areas develop partial immunity and malarial infection is more likely to be mild, associated with maternal anaemia and impaired fetal growth. Malaria should be suspected in women returning from a malaria-endemic area with a febrile illness.

Chapter 19  Viral and Protozoan Infections in Pregnancy

Diagnosis should be made by peripheral blood smears and rapid diagnostic tests. Treatment needs to be individualised, taking into account gestation, disease severity and the likelihood of drug resistance. Women should be advised not to travel to malaria-endemic areas while pregnant. If unavoidable, they should consider chemoprophylaxis with hydrxoychloroquin or mefloquine, and avoiding contact with mosquitoes by covering exposed skin, staying indoors between dusk and dawn, applying insect­ icide containing diethyltoluamide (DEET) and using insecticide-impregnated nets.

VACCINATIONS RUBELLA Women planning pregnancy should have an assessment of their rubella immunity performed, given the potential for serious sequelae of congenital rubella syndrome (see the section on rubella earlier in this chapter). Women coming from resource-poor settings are those most likely to be non-immune. Those found to be non-immune should have the measles, mumps, rubella (MMR) vaccination prior to pregnancy and be advised to avoid conception for 28 days following vaccination. The vaccine can be safely administered while breastfeeding.

VARICELLA Women planning pregnancy should also have an assessment of their varicella immunity status, given the potential for serious maternal and fetal sequelae of primary infection in pregnancy (see the section on varicella earlier in this chapter). Women found to be non-immune should be vaccinated prior to pregnancy and advised to avoid conception for 28 days.

INFLUENZA Influenza vaccination during pregnancy is an essential part of antenatal care. Pregnancy is associated with an increased risk of severe morbidity and mortality from influenza, likely due to a combination of the cardiorespiratory changes and immunomodulation associated with pregnancy. Women suspected of having influenza should be treated with antivirals (oseltamivir 75 mg twice daily for 5 days) and antipyretics, provided with appropriate supportive care and receive treatment for secondary bacterial infections. Healthcare workers in contact with pregnant women should be vaccinated every year. The most effective means of reducing the risk of influenza in pregnancy is with administration of the influenza vaccine. The influenza vaccine has also been shown to reduce the risk of infant respiratory morbidity. This is because of the ‘triple benefit’ of maternal vaccination: 1. transplacental passage of maternal IgG; 2. passage of secretory IgA in breastmilk; and 3. cocooning (i.e. those most likely to infect the newborn are close contacts,

so vaccination of the parents indirectly protects the infant). It is estimated that only five vaccination doses are necessary to prevent one case of serious maternal or infant respiratory illness. Influenza vaccination safety is well established. No study to date has shown an adverse consequence of inactivated influenza vaccine in pregnant women or their offspring. Influenza vaccination is recommended for all pregnant women regardless of gestation, and is usually available from February each year in the Southern Hemisphere. Unvaccinated pregnant women should be immunised at any time during influenza season as long as the vaccine supply lasts.

TETANUS, DIPHTHERIA AND PERTUSSIS (DTPA) Prevention of pertussis in the newborn is important because of the high morbidity and mortality in this condition among infants less than 3 months of age. To reduce the risk of infant pertussis, vaccination of the mother and other household contacts (cocooning) is one means of protecting them; the other is to administer dTpa to women after 20 weeks’ during each pregnancy to provide transplacental passive protection for the infant in the first vulnerable months. This latter approach is currently recommended by the Centers for Disease Control and Prevention in the United States and by the Department of Health in the United Kingdom, although Australian guidelines are yet to endorse these recommendations.

OTHER VACCINATIONS Advice on other vaccinations that may be relevant to pregnant women (e.g. those with special health needs or planning travel) can be found in the Australian Immunisation Handbook. FURTHER READING Arshad M, El-Kamary SS, Jhaveri R. Hepatitis C virus infection during pregnancy and the newborn period—are they opportunities for treatment? J Viral Hepat 2011;18(4):229–36. Australian Technical Advisory Group on Immunisation. The Australian immunisation handbook. 10th edn. Canberra: Australian Government Department of Health; 2013. Centers for Disease Control and Prevention. CDC guidelines for vaccinating pregnant women. Online. Available: ; [30 Nov 2014]. Dijkmans AC, de Jong EP, Dijkmans BA, et al. Parvovirus B19 in pregnancy: prenatal diagnosis and management of fetal complications. Curr Opin Obstet Gynecol 2012;24(2):95–101. Giles ML, Visvanathan K, Lewin SR, et al. Chronic hepatitis B infection and pregnancy. Obstet Gynecol Surv 2012;67(1):37–44. 161

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Giles ML. HIV and pregnancy—how to manage conflicting recommendations from evidence-based guidelines. AIDS 2013;27(6):857–62. Hui L, Wood G. Perinatal outcome after primary maternal cytomegalovirus infection in the first trimester: a practical update and counseling aid. Prenat Diagn Jan 2015;35(1):1–7. Hutchinson BJ, Palma-Dias R, Walker SP. Universal cytomegalovirus screening: time for reappraisal? Fetal Matern Med Rev May 2014;25(2):117–33. Kaye A. Toxoplasmosis: diagnosis, treatment, and prevention in congenitally exposed infants. J Pediatr Health Care 2011;25(6):355–64. Knight M, Lim B. Immunisation against influenza during pregnancy. The benefits outweigh the risks. BMJ 2012;344:e3091.

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Lazzarotto T, Guerra B, Gabrielli L, et al. Update on the prevention, diagnosis and management of cytomegalovirus infection during pregnancy. Clin Microbiol Infect 2011;17(9):1285–93. Palasanthiran P, Starr M, Jones C, et al., editors. Management of Perinatal Infections. Sydney: Australasian Society for Infectious Diseases; 2014. Women’s Health Committee. RANZCOG College statement: influenza vaccination during pregnancy (C-Obs 45); Nov 2013. Online. Available: ; [30 Nov 2014].

Chapter 20  THE BLOOD: ANAEMIA, THROMBOCYTOPENIA AND COAGULOPATHY Lisa Hui and Michael Permezel

KEY POINTS The expansion of blood volume in pregnancy results in a ‘physiological haemodilution anaemia’ with a haemoglobin threshold of 10.5 g/dL for the diagnosis of anaemia in late pregnancy. The major cause of anaemia in pregnancy is iron deficiency. Folic acid deficiency and the haemoglobinopathies are the other two common causes. All women should have a full blood examination and red cell indices at the first antenatal visit and then a haemoglobin check again at 28 weeks’. Abnormalities should be investigated and corrected. Couples at risk for hemoglobinopathies should be offered testing to determine the risk of a severely affected child. The most common cause of thrombocytopenia in pregnancy is the relatively benign condition of gestational thrombocytopenia. Other causes included preeclampsia, immune or thrombotic thrombocytopenic purpura, disseminated intravascular coagulation, systemic lupus erythematosus (SLE), drugs, infection and bone marrow neoplasia. Disseminated intravascular coagulation is a serious condition characterised by intravascular activation of the clotting pathway. Obstetric causes include placental abruption, postpartum haemorrhage, prolonged fetal death, severe preeclampsia, amniotic fluid embolism, septicaemia and sustained hypotension. There is a secondary consumption of clotting factors and platelets, which produces a haemorrhagic diathesis. Treatment is by replacement of deficient blood factors and correction of the basic disorder.

ANAEMIA

DEFINITION

PHYSIOLOGY

Anaemia can be defined by a haemoglobin value < 11.5 g/dL in the first trimester, or < 10.5 g/dL in later pregnancy.

The blood volume increases 35% in pregnancy. As the plasma volume increases more than the red cell volume, there is a resulting 10% fall in the Hb level known as the ‘physiological anaemia of pregnancy’. Adult red blood cells predominantly contain Hb A (composed of two alpha and two beta globin chains), with a small amount of Hb A2 (two alpha and two delta chains). Fetal red cells, however, contain predominantly Hb F (two alpha and two gamma chains), which has a different oxygen dissociation curve to adult haemoglobin. The oxygen affinity of Hb F is higher at lower partial pressures, which facilitates transfer of oxygen across the placenta.

CLINICAL SEQUELAE Non-specific tiredness and fatigue are common pregnancy symptoms but will be exacerbated by anaemia. Anaemia is associated with an increased risk of intrauterine growth retardation, preterm labour and puerperal sepsis. The impact of a relatively moderate postpartum haemorrhage may be catastrophic. Inheritance of a severe fetal anaemia must be considered where both parents have a haemoglobinopathy.

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PRINCIPAL CAUSES OF ANAEMIA IN PREGNANCY Anaemia during pregnancy is most commonly caused by: 1. iron deficiency; 2.folic acid (or B12) deficiency; and/or 3. haemoglobinopathy.

Iron deficiency

Vitamin B12 deficiency Vitamin B12 deficiency is rare in pregnancy. It may be due to autoimmune pernicious anaemia, dietary deficiency (e.g. vegan diet), or disease of the terminal ileum (e.g. Crohn’s disease). Serum B12 levels may be spuriously low in pregnancy and serum holotranscobalamin is required for a more confident diagnosis.

Physiology

Haemoglobinopathies

Approximately 4 mg of elemental iron is needed daily during pregnancy and lactation. Usually only about 10% of dietary iron is absorbed but this increases to about 20% in pregnancy and lactation. The total amount of iron stored in the body (excluding red cells) may be up to 1200 mg, but many women have iron stores depleted by a poor diet, menorrhagia or previous pregnancies.

Classification

Incidence and predisposing factors Iron deficiency accounts for about 90% of anaemia in pregnancy, except in communities where the haemoglobinopathies are prevalent. Iron deficiency anaemia is more common where iron stores have been depleted by: 1. dietary deficiency 2. malabsorption syndromes 3. excessive loss (grand multiparity, menorrhagia, antepartum haemorrhage, hookworm infestation).

Diagnosis The diagnosis is suggested by a hypochromic microcytic anaemia on full blood examination (FBE) and confirmed by a low-serum ferritin. It is critical to exclude co-existent thalassaemia as this can have major implications for family planning and prenatal diagnosis.

Folate deficiency Predisposing factors Folate deficiency may occur through the following. 1. Dietary deficiency. Folate is present in leafy green vegetables, legumes and some fruits, and is readily destroyed by excessive cooking. 2. Increased demand such as any haemolytic anaemia (e.g. haemoglobinopathy), multiple pregnancy, anticonvulsant drug therapy (especially phenytoin).

Clinical sequelae Apart from anaemia, folate deficiency is associated with an increased risk of neural tube defects and may elevate homocystine levels with possible thrombophilic sequelae.

Prevention All women are recommended to have at least 3 months’ preconceptual supplementation with folic acid 0.5 mg daily as prophylaxis against neural tube defects. Where there is a predisposing factor (e.g. haemoglobinopathy, multiple pregnancy, anticonvulsant drug therapy), 5 mg/ day is recommended. 164

Haemoglobinopathies are inherited anomalies of haemoglobin synthesis. Definitive diagnosis usually involves a combination of haemoglobin electrophoresis and DNA testing. 1. Thalassaemias are quantitative defects in haemoglobin production affecting either the alpha or beta globin chains. 2. Haemoglobin variants are qualitative defects of haemoglobin synthesis, in which an abnormal form of haemoglobin is being produced (e.g. Hb S [sickle cell disease]).

Beta-thalassaemia This is a single gene condition predominantly seen in people of Mediterranean, Middle Eastern, Indian subcontinent and South-East Asian backgrounds. A person with a single gene mutation (‘beta thalassaemia minor’) is called a carrier and is usually asymptomatic. Beta thalassaemia carriers are usually healthy, but have a mild haemolytic anaemia with Hb levels typically 8 to 10 g/dL in the third trimester. The principal relevance to pregnancy, however, is the one in four risk of betathalassaemia major in the child if the partner is also affected with beta-thalassaemia minor. Beta-thalassaemia major is a severe transfusion-dependent anaemia that manifests in early childhood, and prenatal diagnosis should be offered to couples at risk.

Alpha-thalassaemia Alpha thalassaemia genes are most common in people of Asian origin, but are also found in people of African, Middle Eastern and Mediterrean background. The genetics are more complex than beta thalassaemia as there are four (rather than two) gene loci coding for the alphachain. Between one and four of these genes may be affected. A single gene deletion does not usually affect the haemoglobin level; two gene deletions produce a mild anaemia. Three gene deletions produce a more severe anaemia (Hb H disease) that may be transfusion dependent and four gene deletions are incompatible with postnatal survival and result in hydropic fetal death (Barts hydrops). Haemoglobin electrophoresis is normal for one and two gene deletions but Hb H (beta4-tetramer) may be present on haemoglobin electrophoresis when three genes are absent. The mean corpuscular volume (MCV)

Chapter 20  The Blood: Anaemia, Thrombocytopenia and Coagulopathy

is normal with a single gene deletion but usually reduced with two and three gene deletions. Diagnosis is with DNA analysis. Barts hydrops is only possible if both parents have at least a two-gene deletion in a heterozygous pattern (−/−, +/+) rather than (+/−, +/−), and prenatal diagnosis should be offered to these couples.

Sickle cell haemoglobin (Hb S) Sickle cell disease is an autosomal recessive disorder caused by a beta globin gene mutation that leads to the production of an abnormal form of haemoglobin (Hb S). The homozygous form (sickle cell disease) is characterised by hemolysis and vaso-occlusive complications. Sickle cell trait is the heterozygous form of the disease. It does not cause serious morbidity in pregnancy, but is associated with increased risk of urinary tract infections. The genes for sickle cell disease are most common in people of African, Middle Eastern, Southern European, Indian, Pakistani and Caribbean origin. The importance for the pregnancy is the risk of sickle cell disease in the offspring if the partner is also affected. Again, prenatal diagnosis is offered if both parents are affected. Women with sickle cell disease are at increased risk of complications during pregnancy. The incidence of sickle cell crises is probably increased by pregnancy. Complications include pneumonia, pyelonephritis, miscarriage, preeclampsia and prematurity.

Other haemoglobinopathies Combinations of haemoglobin variants, thalassaemia or other haemoglobin variants may produce a severe anaemia, and antenatal diagnosis should be considered where such a combination in the fetus is genetically possible. For example, the combination of sickle cell trait and beta-thalassaemia minor may have a clinical condition similar to sickle cell disease. Haemoglobin E/beta-thalassaemia is a severe transfusion-dependant anaemia.

PREVENTION OF NUTRITIONAL ANAEMIAS Folic acid supplementation is indicated in all women at prepregnancy counselling to reduce the risk of neural tube defect. Iron supplementation is not routinely recommended but those at risk should be screened with serum ferritin.

Screening for anaemia in pregnancy The haemoglobin level is checked at the first visit and again at about 28 weeks’. If there is excessive loss at birth, a further check should be made postpartum. Red cell indices are performed at the first antenatal visit to detect haemoglobinopathies; although these will not all have anaemia, the majority will have a reduced MCV. Haemoglobin electrophoresis should be performed routinely at the first antenatal visit in ethnic groups at increased risk of haemoglobinopathy.

MANAGEMENT OF ANAEMIA IN PREGNANCY Determine aetiology of anaemia A clinical history may reveal dietary deficiency, gastro­ intestinal disorders, menorrhagia or other blood loss. Physical examination should note hepatosplenomegaly or lymph node enlargement. FBE with red cell indices will enable categorisation as follows. Hypochromic microcytic anaemia may be iron deficiency and/or a haemoglobinopathy. Serum ferritin will screen for iron deficiency. Haemoglobin electrophoresis and DNA analysis will detect the haemoglobinopathies. Normocytic or macrocytic anaemia require a reticulocyte count, renal function, serum folate and B12. If B12 is low, serum holotranscobalamin should be used to confirm. Bone marrow examination is indicated if there are any suspicious features or the anaemia is inexplicably refractory to treatment.

• •

Iron deficiency anaemia Assessment Iron deficiency anaemia in pregnancy does not usually require further investigation, as gastrointestinal pathology is not commonly present. Nevertheless, appropriate tests should be performed if the clinical assessment is suggestive of chronic gastrointestinal blood loss.

Treatment Oral iron supplementation is the first-line treatment in early pregnancy. Unless the woman is not taking, tolerating or absorbing the oral iron, the haemoglobin level should rise by about 1 g/week. If oral iron is not tolerated, if response is poor or if more rapid haemoglobin elevation is needed, an intravenous iron infusion can be administered.

Folate or vitamin B12 deficiency All women should be treated with 0.5 mg daily of preconceptual folic acid as prophylaxis against neural tube defects. Folate deficiency is treated with folic acid (5 mg daily). The cause (dietary, increased demand, malabsorption) is usually apparent clinically. Vitamin B12 deficiency is rare in pregnancy. The aetiology should be determined (e.g. strict vegan, autoimmune, Crohn’s disease) and appropriate intramuscular replacement instituted.

Haemoglobinopathies Assessment of the genetic implications of these inherited disorders (e.g. thalassaemia, sickle cell) is imperative due to their increased red blood cell turnover. Central to the determination of fetal risk is full assessment of the male partner with FBE, Hb electrophoresis and DNA analysis. Thalassaemia carriers should take folic acid 165

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supplementation and ferritin levels should be checked to exclude co-existent iron deficiency due to their increased requirements. Sickle cell disease requires specialised treatment to minimise the risk of sickle cell crises.

THROMBOCYTOPENIA The normal platelet count is 150 to 400 × 109/L. Surgical bleeding or postpartum haemorrhage may occur if platelets are < 50 × 109/L. Spontaneous bleeding may occur with platelets < 30 × 109/L. Box 20.1 lists the causes of thrombocytopenia in pregnancy.

GESTATIONAL THROMBOCYTOPENIA This is defined as thrombocytopenia of mild or moderate degree (75 − 150 × 109/L) and detected for the first time during late pregnancy, with the platelet count returning to normal within 7 days of delivery. It occurs in about 5% of all pregnancies and is responsible for about 65% of all cases of thrombocytopenia in pregnancy. The cause is most probably an increase in physiological platelet turnover. Gestational thrombocytopenia is very rarely (< 1% of affected pregnancies) associated with severe fetal thrombocytopenia.

PREECLAMPSIA Thrombocytopenia is a relatively common occurrence in preeclampsia and particularly the special variant of preeclampsia known as HELLP syndrome (haemolysis, elevated liver enzymes, low platelets). Treatment is by appropriately timed delivery.

IMMUNE THROMBOCYTOPENIC PURPURA In immune thrombocytopenic purpura (ITP) there is normal or increased production of platelets, but these are destroyed by antiplatelet antibodies. Treatment should be instituted if the platelet count falls below 75 × 109/L.

BOX 20.1  Causes of thrombocytopenia in pregnancy. 166

Gestational thrombocytopenia Preeclampsia Immune thrombocytopenic purpura (ITP) Disseminated intravascular coagulation Thrombotic thrombocytopenic purpura (TTP) Drugs (e.g. heparin, quinine) Infections SLE Haematological malignancies

Prednisolone and/or immunoglobulin infusions are the principle modalities of therapy. In severe cases, intrapartum platelet transfusions may be required to facilitate safe birth and anaesthesia.

Newborn sequelae Since the antiplatelet antibodies cross the placenta, the newborn may also have thrombocytopenia. The period of highest risk for newborn bleeding complications is around days 2 to 5 of life, when the platelet count is at a nadir. Maternal platelet and circulating antibody levels do not reliably predict the severity of thrombocytopenia. The strongest predictor of newborn thrombocytopenia is a past history of an affected newborn. However, in most situations this history is not present and the mode of delivery is determined by the usual obstetric indications. Where there are concerns regarding severe fetal thrombocytopenia, avoiding a traumatic instrumental birth is desirable. However, just as importantly, a scar on the uterus will predispose to a future placenta accreta in a woman with compromised platelets.

THROMBOTIC THROMBOCYTOPENIC PURPURA Thrombotic thrombocytopenic purpura (TTP) is a rare medical emergency characterised by widespread microthrombi as a consequence of vascular endothelial cell damage. Multiple organs may be affected, including the central nervous system, liver, kidney and placenta. It may be very difficult or impossible to distinguish TTP from HELLP syndrome, and TTP probably has a very similar pathogenesis. It usually requires plasmapheresis and replacement with fresh frozen plasma. In contrast to preeclampsia, the course of the disease is not dramatically improved by delivery.

COAGULATION DISORDERS DISSEMINATED INTRAVASCULAR COAGULATION Pathogenesis Tissue thromboplastins are the normal activators of the extrinsic coagulation pathway in response to local tissue damage. Rich sources of thromboplastins include the placenta and amniotic fluid. When there is systemic release of thromboplastins into the bloodstream, disseminated intravascular coagulation (DIC, ‘microvascular clotting’) occurs with consumption of platelets and clotting factors (especially fibrinogen factors V, VII, VIII ) and tissue ischaemia, which may result in secondary damage to the kidneys, liver, lung and brain. Red blood cells encountering fibrin strands in the small blood vessels may become fragmented (microangiopathic haemolytic anaemia).

Chapter 20  The Blood: Anaemia, Thrombocytopenia and Coagulopathy

Aetiology The causes of DIC in pregnancy are as follows: 1. placental abruption, but this is uncommon unless the abruption is severe enough to cause fetal death 2. postpartum haemorrhage 3. sepsis, particularly involving the genital tract (septic abortion, chorioamnionitis) or haemolysis (e.g. Cl. perfringens, E. coli) 4. amniotic fluid embolism 5. severe preeclampsia 6. sustained hypotension which causes widespread endothelial damage with resulting intravascular coagulation. 7. fetal death in utero, but generally only if the fetus is at least 20 weeks’ size and period of death is greater than 4 weeks.

Clinical features DIC presents almost invariably with a haemostatic problem, either as genital tract bleeding from the placental site or persistent bleeding from the wounds (vaginal tears, caesarean section, venepuncture sites).

Investigations The following investigations are indicated. 1. Blood film and platelet count. Evidence of microangiopathic haemolysis with fragmentation of red cells may be present. Platelet count is reduced. 2. Coagulation profile. Activated partial thromboplastin time (APTT) and prothrombin time will be prolonged. 3. Fibrinogen. This may be depleted (normal range in pregnancy 4 to 6 g/L; coagulation fails at levels < 1 g/L).

Treatment The basic treatment principles are removal of the precipitating cause if possible, correction of aggravating factors and replacement of missing coagulation factors and platelets. Correction of aggravating factors such as shock, hypothermia and hypoxia is important. This includes blood transfusion if necessary and oxygen administration. Replacement of clotting factors is most effectively done with fresh frozen plasma. Clotting factor concentrates such as fibrinogen concentrate or cryoprecipitate may be required. Platelets should be maintained > 50 × 109/L in the presence of active bleeding by the administration of fresh packs of group-compatible platelets. Any aetiological condition should be treated promptly, often by

delivery of the fetus. Anticoagulants (e.g. heparin, streptokinase) do not have a role in obstetric DIC complicated by bleeding. Similarly, antifibrinolytic drugs (epsilonaminocaproic acid, aprotinin) are not helpful.

INHERITED ANOMALIES OF COAGULATION FACTORS Von Willebrand’s disease There is typically a history of epistaxis, heavy menstrual loss, easy bruising and operative/postoperative haemorrhage. The basic defect is in the factor VIII-related antigen (von Willebrand’s factor) leading to a relative deficiency of factor VIII and a platelet function disorder. Diagnosis is made on the basis of a prolonged bleeding time and an assay of von Willebrand’s factor. The main effect in pregnancy is a tendency to postpartum haemorrhage. The likelihood of this is best gauged by the woman’s past history and an estimation of factor VIII level in late pregnancy. If lower than about 40% of normal, fresh frozen plasma, cryoprecipitate or desmopressin acetate (except in type IIB disease) is indicated. The anti-fibrinolytic agent tranexamic acid may also be used in the peripartum period to reduce the risk of postpartum haemorrhage. Since this is an autosomaldominant inherited disorder, there is a possibility of a haemorrhagic diathesis in the neonate.

OTHER COAGULATION FACTOR DISORDERS The most common congenital disorder, haemophilia, is an X-linked recessive disorder and therefore affects almost exclusively males. It has been observed that some 10% of carrier females will exhibit a tendency to excessive bleeding, and fresh frozen plasma may be required at the time of delivery. In a female carrier with a male offspring, there will be a 50% probability of an affected baby with implications for prenatal diagnosis and mode of birth. FURTHER READINGS RANZCOG. RANZCOG College statement: routine antenatal assessment in the absence of pregnancy complications (C-Obs 03b); March 2013. Online. Available: ; [30 Nov 2014]. RCOG. Management of sickle cell disease in pregnancy. Green-top Guideline No. 61. July 2011. Online. Available: ; [16 Dec 2014].

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KEY POINTS Appendicitis in pregnancy can be difficult to diagnose because of the expanded differential diagnosis and the altered anatomy, as the appendix is both lifted and partially obscured by the expanding uterus. Cholestasis of pregnancy is associated with an increase of stillbirth, but both symptoms and liver function can be largely normalised with ursodeoxycholic acid treatment. Acute fatty liver of pregnancy (AFLP) has many features in common with preeclampsia and is characterised by hepatic functional impairment (jaundice, coagulopathy, hypoglycaemia) that is usually out of proportion to the abnormalities in hepatic enzyme levels. Incarceration of a retroverted pregnant uterus may occur at approximately 14 weeks’ gestation and results in acute urinary retention. Resolution is usually effected with urinary catheterisation; surgical correction is rarely necessary. Fibromyomas are common in obstetric patients. Fundal height measurements may no longer reflect fetal growth. Complications include red degeneration of the fibroid and malpresentation. Ovarian cysts may be of any type but luteal cysts are particularly common in early pregnancy. Complications include torsion as the uterus expands. Surgical removal is best performed early in the second trimester and would commonly be recommended for cysts of 6 cm or more diameter. Urinary tract infections complicate approximately 6% of pregnancies. They are often asymptomatic but approximately one-third will progress to pyelonephritis if left untreated. Minor degrees of renal functional impairment predispose to preeclampsia and preterm birth. More severe degrees (e.g. serum creatinine > 0.3 mmol/L) are rarely associated with a successful outcome. Prospects are much better post-transplantation.

THE GASTROINTESTINAL AND HEPATOBILIARY SYSTEMS ACUTE APPENDICITIS Appendicitis complicates about 1 in 1000 pregnancies. Miscarriage or preterm labour can be precipitated by the intraperitoneal infection. The diagnosis is more difficult because of the upward displacement of the appendix

(Fig 21.1) and confusion with pregnancy complications. The differential diagnosis of abdominal pain in pregnancy includes round ligament strain, ovarian cyst complication (e.g. torsion), red degeneration of a fibromyoma, gastroenteritis and pyelonephritis. Treatment is appendicectomy, which can be more difficult with the uterine enlargement. Laparoscopy is difficult once the uterine size has attained 16 weeks or so. In late pregnancy, caesarean section may be performed at the same time to enable better access to the appendix.

Chapter 21  Gastrointestinal, Hepatobiliary, Gynaecological and Renal Problems

BOX 21.1  Causes of jaundice in pregnancy.

9 months’ 6 months’ 3 months’

McBurney point

Haemolytic ✚ Septicaemia (e.g. Clostridium, E. coli) Hepatocellular ✚ Viral hepatitis ✚ Severe preeclampsia, HELLP syndrome ✚ Acute fatty liver of pregnancy ✚ Medications ✚ Autoimmune chronic active hepatitis Obstructive ✚ Cholestasis of pregnancy ✚ Cholelithiasis ✚ Drug-induced ✚ Primary biliary cirrhosis ✚ Pancreatic carcinoma

hepatocellular enzymes as well as elevated bile salts. Rarely, vitamin K malabsorption may lead to a bleeding tendency. Premature labour is relatively common and there is a marked increase in the risk of stillbirth.

Management FIGURE 21.1

The increasingly elevated position of the appendix in pregnancy as gestation advances.

JAUNDICE Jaundice is traditionally classified into three categories: haemolytic, hepatocellular and obstruction (Box 21.1). Causes may be either consequential to, or independent of, the pregnancy. Clinical features suggesting cholestasis include pruritus, dark urine and pale stools. Biochemical tests will also help differentiate between hepatocellular damage and obstruction. Hepatocellular damage is associated with an increase of predominantly unconjugated bilirubin and hepatocellular enzymes. Caution must be exercised in interpreting alkaline phosphatase levels due to the placental production. An ultrasound examination is helpful in demonstrating dilatation of the biliary tree in cases of extrahepatic obstruction.

Cholestasis of pregnancy Pathogenesis Cholestasis of pregnancy is due to an oestrogen-sensitivity effect and exhibits a familial tendency. It may be frequently recurrent in successive pregnancies and may even occur with the combined oral contraceptive pill.

Clinical features Pruritus, particularly of the palms and soles, is characteristic. Liver function tests usually show some elevation of

Other causes of obstructive jaundice should be excluded. Increased surveillance of fetal wellbeing is indicated (e.g. ultrasound, cardiotocography). Ursodeoxycholic acid is usually effective in controlling symptoms and normalising liver function tests. Induction of labour is indicated at 37 to 38 weeks or earlier if liver function deteriorates on ursodeoxycholic acid. The condition resolves rapidly after pregnancy.

Acute fatty liver of pregnancy Pathogenesis Like severe preeclampsia, acute fatty liver is unique to pregnancy, more common in primigravidas and extremely uncommon before the late second trimester. Interestingly, about 25% of cases are due to an autosomal recessive condition (LCHAD deficiency) in the fetus that impacts on the mother by the transplacental passage of hepatotoxic fetal-derived fatty acids.

Clinical features This potentially fatal syndrome comprises malaise, fatigue, epigastric discomfort and vomiting. Jaundice soon follows. There is a significant leucocytosis, abnormal transaminases, hyperbilirubinaemia, hypoglycaemia and often coagulopathy.

Management The woman should be placed in an intensive care unit: intravenous fluids are administered, together with albumin, dextrose and clotting factor replacement with fresh frozen plasma. The pregnancy should be terminated, usually by urgent caesarean section. 169

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Cholelithiasis and acute cholecystitis

Clinical features

Cholelithiasis is another disease in women of childbearing age. Gallstones are present in approximately 3% of women in pregnancy. Biliary colic is usually caused by a stone in the cystic duct or common bile duct. The pain is severe, tends to be constant and usually lasts for 12 to 15 hours. Acute cholecystitis is rare in pregnancy. The condition is treated conservatively with antibiotics and analgesia. Surgery is rarely necessary during pregnancy and usually can be deferred until the puerperium.

Mid-trimester miscarriage, preterm labour and preterm premature rupture of the membranes are possible consequences. Malpresentation may result from the altered shape of the uterine cavity. Uterine abnormalities are frequently detected as an incidental finding at the time of the obstetric ultrasound, laparoscopy, curettage or caesarean section (Fig 21.2).

THE REPRODUCTIVE SYSTEM CONGENITAL DISORDERS OF THE MÜLLERIAN SYSTEM Types of anomaly Approximately 1% of women have one of the following anomalies. 1. Faulty midline fusion. The anomaly may involve the uterus, cervix, vagina or a combination of these. The extreme form is represented as a completely separate system on each side (uterus didelphys). 2. Faulty development of one duct gives rise to incomplete, non-canalised or absent structures on that side (e.g. unicornuate uterus). There are often anomalies of the renal tract on the same side.

Management Obstetric management is usually expectant, but the caesarean section rate is increased, usually as a result of malpresentation. A vaginal septum can be stretched markedly during labour and can be incised between clamps and ligated.

FEMALE GENITAL MUTILATION Female genital mutilation (FGM) is an important obstetric issue and needs a clear understanding of not only the physical considerations but also the psychological, social and legal considerations. In order to birth vaginally, surgical enlargement of the introitus is usually necessary and most often best accomplished by division of adherent labia in the anterior section of the perineum, sometimes termed an anterior episiotomy. This can be performed antenatally or in labour. In most jurisdictions it is illegal to recreate the anatomy of the FGM postpartum by suturing the labia back together.

FIGURE 21.2

Uterus didelphys found at caesarean section. The non-pregnant half of the duplicated system is also hypertrophied by the hormones of pregnancy. Source: Reproduced with permission from the Royal Women’s Hospital, Parkville, Victoria.

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INCARCERATION OF THE UTERUS The uterus lies in a retroverted position in around 20% of women. Although spontaneous correction occurs late in the first trimester in the great majority, the growing uterus occasionally becomes incarcerated in the hollow of the sacrum. With continued growth, there is pressure on the bladder neck and the woman experiences increasing difficulty in voiding, leading to complete urinary retention (Fig 21.3). The condition is relieved by the insertion of a Foley catheter, which is left to drain. The uterus can then be pushed gently out of the pelvis with the woman in the knee/chest position if spontaneous correction does not occur.

UTEROVAGINAL PROLAPSE IN PREGNANCY

Management usually involves replacement with a ring pessary and periods of recumbency. Vaginal birth can be undertaken. Although there is considerable improvement in the puerperium, surgery is eventually likely to be needed.

MOTOR VEHICLE ACCIDENT IN PREGNANCY The woman may suffer uterine rupture, placental abruption and/or pelvic fracture as a result of motor vehicle injury. Seat belts should be worn as they minimise the risk of fatal injury. Following a significant traumatic injury to the abdomen, prolonged fetal cardiotocographic monitoring (e.g. 4 hours) should be undertaken in view of the possibility of placental abruption or even traumatic uterine rupture (Fig 21.5).

This becomes more likely with increasing parity. The condition improves after the fourth month as the uterus becomes abdominal in position, but may recur late in pregnancy because of the weight of the uterus (Fig 21.4).

FIGURE 21.3

Incarceration of a retroverted gravid uterus may occur at about 12 to 14 weeks’ when it fills the pelvis. The cervix is displaced upwards and anteriorly, causing the urethra to become elongated, and may obstruct, causing urinary retention.

FIGURE 21.4

Cervical hypertrophy and prolapse at 39 weeks. The cervix pulled up in labour and the woman had a normal vaginal birth. Source: Reproduced with permission from the Royal Women’s Hospital, Parkville, Victoria.

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FIGURE 21.5

Uterine rupture following a motor vehicle accident at 36 weeks’. The uterine rupture was discovered 2 hours after the car accident at caesarean section because of a poor cardiotocograph. Source: Courtesy of Prof. Norman Beischer.

UTERINE FIBROMYOMAS Clinical features About 1% of pregnancies are complicated by fibromyomas, particularly in older women. While most commonly asymptomatic, fibromyomas do increase in size during pregnancy and may cause malpresentation, obstructed labour (cervical fibroid) or postpartum haemorrhage (bleeding submucous fibroid). About 10% of these women will experience red degeneration (infarction), which causes severe abdominal pain and needs to be considered in the differential diagnosis of an acute abdomen in pregnancy. Torsion or bleeding from a subserous fibroid are rarer complications. The diagnosis of uterine fibromyomas can usually be confirmed by ultrasonography. 172

Management Myomectomy is virtually never indicated other than for torsion of a pedunculated subserous fibroid. Pain in association with red degeneration may be treated with analgesics. If a caesarean section is needed, care with the uterine incision should be taken to avoid transection of a fibromyoma and any temptation to perform a myomectomy should be resisted.

OVARIAN CYSTS AND TUMOURS Ovarian tumours are potentially serious because of their liability to develop complications in pregnancy. Twothirds of the tumours are cystic: originating in the corpus luteum (luteal cyst), covering epithelium (serous or mucinous cystadenoma), germinal elements (cystic teratoma,

Chapter 21  Gastrointestinal, Hepatobiliary, Gynaecological and Renal Problems

dermoid) or vestigial remnants (parovarian cyst). Solid tumours are usually fibromas.

Clinical features Diagnosis is usually incidental at the time of an obstetric ultrasound. Clinical problems may arise when the tumour itself complicates (torsion, haemorrhage, incarceration, necrosis, rupture, infection, malignancy) or the tumour impacts on the pregnancy (obstructed labour from a cyst deep in the pelvis, malpresentation).

Management Small cysts (< 6 cm) with a simple internal structure on ultrasonography can be followed conservatively, as they are likely to be functional in nature (corpus luteum cyst) and resolve spontaneously. Women should be advised of the symptoms of torsion and the importance of prompt presentation. Endometriotic cysts are also best managed conservatively. Larger cysts, or those with ultrasound features of neoplasia, are best treated surgically early in the second trimester. Surgery in the first trimester is more likely to cause an interruption to the pregnancy, and is reserved for women with complications such as torsion. Where a cyst is discovered late in pregnancy, removal is deferred until early in the puerperium, or at caesarean section if this is the mode of birth for other reasons.

therapy or a combination of both is usual. Occasionally a microinvasive lesion may be treated more conservatively with cone biopsy where preservation of childbearing is a high priority. The major factors influencing treatment are the stage of the disease, the gestational age at diagnosis and the parity/desire for children. On occasions, a difficult decision must be made with respect to whether a delay in therapy can be justified to enable fetal viability at the risk of maternal progression of disease.

THE URINARY SYSTEM PHYSIOLOGICAL CHANGES IN PREGNANCY The smooth muscle relaxant properties of progesterone combine with some ureteric compression to produce considerable dilatation of the renal pelvis and ureters, so-called physiological hydronephrosis (Fig 21.6). Renal blood flow and glomerular filtration rate increase by about 40% in pregnancy. There may be glycosuria in the presence of a relatively normal blood glucose (lowered renal threshold for glucose). Normal values for proteinuria are < 150 mg/24 hours in the normal adult but increase to < 300 mg/24 hours in preg-

CERVICAL INTRAEPITHELIAL NEOPLASIA Clinical features With routine cervical cytology, features suggestive of cervical intraepithelial neoplasia (CIN) may be found in about 0.5% of pregnant women. The lesion is asymptomatic unless it progresses to invasive carcinoma. Such an outcome appears to be exceedingly uncommon during pregnancy, with few cases reported in the literature.

Management High-grade abnormal cervical cytology in pregnancy should be assessed with colposcopy, repeat cytology and target biopsy if needed. Cone biopsy is performed only if microinvasion is suspected colposcopically or on target biopsy. As progression of CIN to invasive cancer is exceedingly rare during pregnancy and treatment may compromise the pregnancy, management of appropriately assessed CIN is conservative (colposcopic reviews) until after the pregnancy. Between 6 and 12 weeks postpartum, the lesion should be re-evaluated and if high-grade CIN is present, it can be removed.

CERVICAL CARCINOMA

FIGURE 21.6

Invasive cervical carcinoma is exceedingly rare in pregnancy. There may be watery or blood-stained discharge or frank bleeding. Radical treatment by surgery, radio-

Source: Reproduced with permission from the Royal Women’s Hospital, Parkville, Victoria.

Physiological hydronephrosis of pregnancy.

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nancy. The frequency of micturition increases consequent on an increase in total urine produced and the pressure effects exerted by the enlarging uterus on the bladder.

LOWER URINARY TRACT INFECTION The predominant organism in urinary tract infection (UTI) is Escherichia coli, which is responsible for about 80% of infections. Enterococcus faecalis, Aerobacter aerogenes, Klebsiella, Proteus and β-haemolytic streptococci are less common urinary tract pathogens and more suggestive of underlying renal pathology.

Clinical features Asymptomatic bacteriuria is found in about 6% of women when screened at the first antenatal visit. Clinical pyelonephritis will develop in about one-third of these women while being very uncommon in those without bacteriuria on initial screening. These women are also at increased risk of obstetric complications, particularly preterm labour. Symptomatic UTIs may occur at any time but are more common in pregnant than non-pregnant women.

Management

CHRONIC RENAL INSUFFICIENCY Aetiology Causes include chronic pyelonephritis, chronic glomerulonephritis and polycystic kidney disease. Glomerulonephritis may be classified according to aetiology (e.g. idiopathic, familial, lupus, diabetic), histology (e.g. diffuse or focal, membranous or proliferative) or clinical picture (e.g. nephritic, nephrotic, benign haematuria). The incidence appears to be decreasing with the reduced prevalence of streptococcal infections.

Clinical features Anaemia, preeclampsia, premature labour, fetal growth retardation/placental insufficiency and perinatal mortality are all increased in the presence of renal disease. Severe impairment of renal function (serum creatinine > 0.2 mmol/L) has a poor prognosis and successful pregnancy is rarely seen with serum creatinine > 0.3 mmol/L or with a woman requiring dialysis. Progression of glomerulonephritis may occur with superimposed preeclampsia, and recurrent urinary tract infection may aggravate the course of chronic pyelonephritis.

Diagnosis is confirmed with a properly collected midstream urine microscopy, culture and sensitivities. Appropriate antibiotic therapy is commenced, often amoxicillin unless antibiotic sensitivities indicate otherwise. A further urine specimen should be tested after completion of the course and at intervals of 2 to 3 months during the pregnancy. If bacteriuria recurs, nocturnal antibiotic prophylaxis is usually recommended (e.g. nitrofurantoin 100 mg at night).

Management

ACUTE PYELONEPHRITIS Clinical features

Pregnancy

In the absence of screening for asymptomatic bacteriuria, 2% of women will develop acute pyelonephritis. The woman complains of dysuria and frequency of micturition, pain in the flank radiating to the loin, fever and chills; anorexia and vomiting are often associated. Loin tenderness, fever and tachycardia are usually present. Rarely, serious infections may be associated with septicaemic shock.

Management Diagnosis is confirmed on urine microscopy. Antibiotic therapy should be instituted on clinical grounds before the urine culture result is available, and the parenteral route may be chosen for a more rapid response or because of vomiting. Analgesics are often needed, and fever should be treated with tepid sponging and antipyretic medication. An adequate fluid intake is essential and an intravenous infusion is necessary if there is nausea or vomiting. Follow-up in the puerperium should look for an underlying cause (e.g. calculi). 174

Prepregnancy Full assessment of the severity, nature and aetiology of the renal disease should take place. If the prognosis is poor, effective contraception is required. A woman needing renal transplantation in the near future should have this performed before pregnancy. Where the cause is treatable (e.g. lupoid nephritis), the disease should be controlled before commencing a pregnancy. An accurate assessment of gestational age is essential. An early ultrasound should be performed if there is discordance among clinical findings. Routine screening for other problems (clinical and investigations) must not be omitted. If the renal disease has not been recently assessed, this needs to be done with respect to cause and severity. Treatment of the renal disease should be optimised for pregnancy. If immunosuppressants are being used, some modification may be required. Occasionally, an extremely poor prognosis for mother and fetus leads to a recommendation of pregnancy termination. The woman should be booked into a suitably equipped hospital with specialist obstetric and renal physician care. Subsequent antenatal care should be directed towards the potential complications in pregnancy. The renal disease itself requires close surveillance as a serious deterioration in renal function mandates delivery. Anaemia should be anticipated and iron/folate supplement should be given. Preeclampsia is particularly prevalent and care should be initially directed at prevention (rest, blood pressure control, low-dose aspirin, calcium supplementation) and early diagnosis through more frequent antenatal

Chapter 21  Gastrointestinal, Hepatobiliary, Gynaecological and Renal Problems

visits. The latter can be difficult as the features of preeclampsia mimic those of chronic renal disease. The timing of delivery will be very much dependent on fetal growth and maternal progress. With significant renal impairment, it is unlikely that the pregnancy would be allowed to proceed beyond 38 weeks’ gestation.

Pregnancy after a renal transplant Pregnancy is not contraindicated by a prior renal transplant, but the woman’s condition should be stable, with minimal hypertension, proteinuria or evidence of graft rejection. Immunosuppressant drugs can be used cautiously, even in the first trimester. The incidence of spontaneous abortion, premature labour, preeclampsia and urinary tract infection are all increased. If a caesarean section is performed, care must be exercised to avoid the pelvic kidney.

ACUTE URINARY RETENTION Incarceration of a retroverted pregnant uterus Late in the first trimester, a retroverted uterus may become ‘incarcerated’ between the hollow of the sacrum and the rear of the pubic symphysis. Pressure is exerted on the bladder neck and proximal urethra as the uterus expands forwards. The retention may be masked by incontinence, which is due to overflow. The condition is usually cured by catheterisation, with the catheter indwelling for 24 to 48 hours, sometimes aided by the prone position and manual anteversion of the uterus.

Intrapartum urinary retention The fetal presenting part may cause occlusion at the level of the bladder neck. The resulting bladder fullness is discomforting to the woman, encourages infection and

inhibits uterine contractions. If neglected, serious damage to the base of the bladder may result, even to the extent of fistula formation. The other cause of intrapartum urinary retention is epidural analgesia since the woman is often unable to void.

Postpartum urinary retention Bruising at the bladder base or perineal discomfort from an episiotomy or lacerations may reflexly inhibit bladder function, making micturition difficult. It should be remembered that the bladder has a poor tone after delivery and considerable distension may occur without the usual discomfort or urgent desire to micturate. If voiding has not occurred by about 12 hours, a urinary catheter should be passed. A full bladder may give a false idea of the height of the uterine fundus.

STRESS INCONTINENCE Statistics indicate that about 5% of women have this problem prior to pregnancy, about 30% during and about 10% after delivery. Deterioration of urinary control is more likely with a large infant and a prolonged second stage, and less likely after caesarean section. FURTHER READING Bacq Y, Sentilhes L, Reyes HB, et al. Efficacy of ursodeoxycholic acid in treating intrahepatic cholestasis of pregnancy: a meta-analysis. Gastroenterology 2012;143(6):1492–501. Phelan ST. Renal disease in pregnancy ambulatory issues. Clin Obstet Gynecol 2012;55(3):829–37. Wei Q, Zhang L, Liu X. Clinical diagnosis and treatment of acute fatty liver of pregnancy: a literature review and 11 new cases. J Obstet Gynaecol Res 2010;36:751–6.

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Chapter 22  AUTOIMMUNE AND ISOIMMUNE DISEASE IN PREGNANCY Michael Permezel and Gillian Paulsen

KEY POINTS Antibodies may cross the placenta and impact on the fetus. The antibody transfer progressively increases through pregnancy, from very little before, say, 16 weeks’ and then only gradually increasing until an exponential increase at term. In the case of autoantibodies, the fetus usually has a similar condition to that of the mother; for example, immune thrombocytopenia (ITP) produces thrombocytopenia in the fetus and autoimmune hyperthyroidism can produce hyperthyroidism in the fetus. These and other examples are discussed in this chapter. An unusual exception is that autoimmune salivary and lacrimal gland disease (Sjögren’s) can produce heart block in the fetus due to differing antigenic expression. Isoantibodies (also known as alloantibodies) do not impact at all on the mother but can have lethal consequences for the fetus. Most important are the anti-red blood cell isoantibodies, but there are also less common conditions where isoantibodies are directed against white cells or platelets. Disease severity of anti-red blood cell antibodies is largely reflected by the level (titre) of the antibody and ranges from mild jaundice at one extreme through severe anaemia to hydropic fetal death at the other. All women are screened for anti-red blood cell antibodies at the first antenatal visit and those that are Rh-negative are re-screened at 28 weeks’. Prophylaxis against immunisation from fetomaternal haemorrhage is only available for the D antigen through administration of passive anti-D at times of bleeding, trauma, birth and also prophylactically at 28 and 34 weeks’ gestation.

BACKGROUND The conceptus is antigenically foreign and therefore immunologically ‘privileged’ in not being rejected. This immunological tolerance is a product of both specific features of the conceptus that limit the presentation of antigens to the mother and changes in the maternal immune response—both specific to the fetal antigens as well as a degree of general immune suppression. Placental insufficiency and preeclampsia may sometimes be the result of insufficient immunological tolerance. The immune system of the fetus becomes progressively more competent as the pregnancy advances. The

immune competence of the fetus and subsequent neonate is further enhanced by progressively increasing transfer of maternal antibody across the placenta as the pregnancy advances. The obvious downside of this antibody transfer is the potential for antibodies directed against fetal tissues to cross the placenta and have adverse effects on the fetus. Where an antibody crosses the placenta and is directed against an antigen that the fetus possesses but not the mother, it is termed an isoantibody and the condition is called isoimmunisation. The problem is most common with red cell antigens but may also occur with the various platelet or leucocyte antigens.

Chapter 22  Autoimmune and Isoimmune Disease in Pregnancy

The fetus may also be involved, indirectly, by the transfer of harmful maternal autoantibodies, usually producing a variation of the problems seen in the mother. The antibodies may be organ specific, examples of which include myasthenia gravis, autoimmune thyroid disease and immune thrombocytopenic purpura. Alternatively, antibodies may be against more widespread antigens such as the antinuclear factors (ANF or ANA) in systemic lupus erythematosus (SLE). Antiphospholipid antibodies are particularly harmful to the conceptus in that they are associated with an increased risk of spontaneous abortion and widespread intravascular thrombosis, including the placenta. In these conditions, the adverse affect on the pregnancy may be mediated more by the impact of the disorder on the maternal vascular perfusion of the placenta rather than the binding of the antibody to tissues within the fetus.

AUTOIMMUNE DISEASE IN PREGNANCY Early in fetal life when the immune system is immature, it accepts as normal all the developing tissues around it; they are recognised as ‘self’. As the system matures, it is able to differentiate between self and non-self. Occasionally, there is a breakdown in the system and the immune system starts to attack its own tissues by production of an autoantibody. These antibodies can be directed against many different tissues and cause problems in the mother as the antibody binds to the maternal antigen against which it is directed. In pregnancy, these harmful antibodies may cross the placenta and cause clinical problems for the fetus that may continue into early neonatal life. Table 22.1 summarises the features of some of the autoimmune diseases

which may complicate pregnancy and which are not covered in other chapters. The following facts should be remembered. 1. Antibodies of the IgG type pass freely across the placenta and affect the fetus. In contrast, IgM does not cross the placenta. 2. The clinical manifestation in the fetus is usually similar to the mother but differences in antigenic expression may lead to entirely different consequences; for example, anti-Ro or anti-La antibodies producing Sjögren’s syndrome in the mother (dry mouth and dry eyes due to binding of the antibody to the salivary and lacrimal glands respectively) but heart block in the fetus due to binding of the antibody to the conducting system within the heart. 3. The fetus (and newborn) may be affected in the absence of maternal features (the fetal tissues are more susceptible to the antibodies), or after the mother has been treated (e.g. by thyroidectomy in the case of Graves’ disease or splenectomy in the case of immune thrombocytopenic purpura). 4. The fetal disorder is usually self-limited (2 to 3 months), but permanent damage may occur (e.g. heart block in the case of antibodies to the cardiac conducting system). The following conditions are examples of maternal autoimmune disease that may impact on the fetus.

IMMUNE THROMBOCYTOPENIC PURPURA Clinical features In immune thrombocytopenic purpura (ITP), an antiplatelet autoantibody causes thrombocytopenia in the

TABLE 22.1  AUTOIMMUNE DISEASES THAT MAY IMPACT ON THE FETUS. Disorder

Antibody

Maternal clinical features

Pregnancy effects

Systemic lupus erythematosus (SLE)

Anti-dsDNA

Renal disease, skin lesions, polyarthritis

Miscarriage, IUGR, preeclampsia, preterm labour

Antiphospholipid syndrome

Anticardiolipin

Thrombosis

Miscarriage, IUGR, preeclampsia

Sjögren’s syndrome

Anti-Ro, anti-La

Dry mouth, dry eyes

Congenital heart block

Immune thrombocytopenia

Antiplatelet

Thrombocytopenia

Thrombocytopenia

Autoimmune hypothyroidism

Anti-thyroperoxidase (anti-TPO), antimicrosomal

Hypothyroidism

Hypothyroidism

Autoimmune hyperthyroidism

Anti-TSH receptor

Hyperthyroidism, goitre, exophthalmos

Hyperthyroidism including CCF, IUGR goitre

Myasthenia gravis

Anti-acetylcholine receptor

Maternal muscle weakness

Fetal muscle weakness, rarely arthrogryposis 177

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mother. The condition may have presented with a bleeding tendency but in pregnancy it is most likely to be diagnosed in the course of a routine full blood examination at the first antenatal visit. Most concern in pregnancy will be around the risk of postpartum haemorrhage for the mother, but the fetus may also be thrombocytopenic and at particular risk of traumatic haemorrhage at birth. It is, however, very uncommon for the fetus to be severely affected and in general the thrombocytopenia is less severe than that seen with neonatal alloimmune thrombocytopenia (NAIT) discussed later in this chapter. Predicting the fetal platelet count is difficult and maternal antiplatelet antibody levels are not helpful. The maternal platelet count is a guide and the fetus may be at particular risk where the maternal platelet count is low in spite of a past maternal splenectomy, being indicative of severe disease.

Management ITP is variously treated with corticosteroids (e.g. oral prednisolone) with or without the addition of immunoglobulin therapy (usually by weekly infusion). The intention is usually to maintain the platelets at a level of more than 50 × 109/L during pregnancy and at a level where the anaesthetist would be comfortable inserting regional analgesia if necessary, mostly around 80 × 109/L.

A

B

AUTOIMMUNE HYPERTHYROIDISM (GRAVES’ DISEASE) A thyroid-stimulating autoantibody (TSaab) (more commonly termed TSH-R autoantibody) binds to and stimulates the thyroid-stimulating hormone (TSH) receptor, producing hyperthyroidism in both mother and fetus. Usually the disease has been diagnosed before the pregnancy. If not, astute observation is needed since there is considerable overlap in symptoms and signs with the changes of normal pregnancy. Goitre and tachycardia (particularly if persisting during rest or the Valsalva manoeuvre) are very suspicious; weight loss (this may be obscured by the normal increase in pregnancy), exophthalmos, pretibial oedema, vomiting, diarrhoea and hand tremor are other signs which should lead to laboratory investigation. Preeclampsia, congestive cardiac failure and fetal morbidity are more likely in the untreated mother. In the baby, hyperthyroidism is rare but may arise from transplacental passage of the thyroid-stimulating autoantibody. Usually, the effect of the TSaab is counteracted by concomitant antithyroid drugs, which also cross the placenta. Neonatal thyrotoxicosis may be seen where the mother has no requirement for antithyroid drugs, despite high levels of circulating TSaab (e.g. previous I131 or thyroidectomy) (Fig 22.1).

C

FIGURE 22.1

Graves’ disease in pregnancy. A Hypothyroid 21-year-old mother who experienced Graves’ disease at age 7 years and was treated by subtotal thyroidectomy. She was given maintenance therapy with daily thyroxine throughout pregnancy. B Her infant girl was born at term with severe Graves’ disease, goitre and exophthalmos that persisted for 6 months. C The child was healthy at 20 months old.

Source: Gleason CA, Devaskar, SU, eds. Avery’s Diseases of the Newborn. 9th edn. Philadelphia: Saunders, 2011. Copyright © 2011 Saunders, An Imprint of Elsevier. Figure 9.6.

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The diagnosis is confirmed by an elevated free T4 value (normal range 10 to 19 pmol/L) and a very low TSH level (< 0.5 mU/L). The woman should be screened for thyroid antibodies (stimulatory or inhibitory), which may cross the placenta and affect the fetus. Fetal surveillance is indicated with fetal heart rate assessment at each antenatal visit and serial ultrasounds to detect evidence of IUGR or evolving CCF. Most women are now treated with antithyroid drugs such as carbimazole or propylthiouracil, which block the uptake of iodine by the gland and hence the formation of the thyroid hormone. Another action of propylthiouracil is to block the peripheral conversion of T3 to T4 (the more active tissue hormone). Propylthiouracil is the preferred drug for the breastfeeding mother because of a lower concentration in milk. It is usually possible to reduce the dose progressively during the second half of pregnancy, the free T4 being kept near the upper limit of normal. During the course of pregnancy, the free T4 and TSH should be checked every month. An exacerbation is often observed postpartum and an increase in drug dose may be necessary. Maternal side effects of antithyroid drugs include rash, pruritus, nausea, fever and leukopenia. In Graves’ disease, the fetal sequelae of antithyroid drugs are counterbalanced by the transplacental passage of TSaab. Fetal hypothyroidism may occur where the antithyroid drugs are required in the absence of TSaab. Such a clinical situation may arise with an active thyroid adenoma. A selective beta-adrenergic blocking drug may be useful early in treatment to control quickly the sympathetic effects of the disease. Subtotal thyroidectomy is rarely necessary during pregnancy as good control can usually be achieved medically. The neonate should be examined for evidence of goitre, hypothyroidism or hyperthyroidism and cord blood should be sent for measurement of free T4 and TSH. The presence of a thyroid nodule will require referral and usually fine needle biopsy.

AUTOIMMUNE HYPOTHYROIDISM (HASHIMOTO’S DISEASE) Antithyroid peroxidase or ‘non-stimulatory’ anti-TSHreceptor antibodies may cause thyroid dysfunction in both mother and fetus. The classical features of hypothyroidism are a general slowing of body functions (tiredness, constipation, bradycardia, puffy/dry skin, cold sensitivity, decreased mental alertness, impaired memory and depression/irritability). On investigation, T4 levels are low and TSH is elevated. In the untreated condition, pregnancy is unlikely to occur; if it does, there is an increased incidence of miscarriage, preeclampsia, cardiac dysfunction and postpartum haemorrhage. The puerperium may be complicated by lactation difficulty or a puerperal mental illness, especially depression. The fetus may be affected by transplacental passage of an antithyroid antibody which

may result in congenital hypothyroidism (cretinism). In general, the fetus should be protected during pregnancy by adequate treatment of the mother but may need supplementation through early infancy. If the mother has established hypothyroidism, replacement with thyroxine will be necessary, the usual dose ranging from 100 to 200 mcg/day. The dose should be titrated to the serum free thyroxine level and the serum TSH. Thyroxine levels should be maintained in the upper normal range (and low for TSH) as the fetus may be dependent on transplacental passage of thyroxine if its own thyroid has been adversely affected by the antibody. An increase in thyroxine dose is usually required in pregnancy.

MYASTHENIA GRAVIS In myasthenia gravis, there is an autoantibody against a protein in the neuromuscular junction, causing muscle weakness in the mother. Like other autoimmune conditions, the antibody crosses the placenta and can cause the neonate to have transient muscle weakness, sometimes of clinical significance. Rarely, the impact on fetal muscular function is profound and there may be lethal contractures in relation to an absence of muscular function (arthrogryposis).

SYSTEMIC LUPUS ERYTHEMATOSUS Systemic lupus erythematosus (SLE) is a clinical definition but is characterised by the presence of antidsDNA antibodies in approximately 90% of cases. Other antinuclear antibodies such as anti-Ro and anti-La or antiphospholipid antibodies may co-exist. The anti­ bodies cross the placenta but the impact on the pregnancy may be more a reflection of the maternal vascular disease than the direct impact of the antibody on the fetus. Like autoimmune thyroid disease, SLE is particularly prevalent in women of childbearing age, affecting approximately 1/1000 women in pregnancy. The likelihood of adverse outcomes increase with renal involvement, hypertension and periconceptual disease activity. Pregnancy complications include miscarriage and stillbirth, preeclampsia, preterm birth and placental insufficiency. Management should be multidisciplinary, with obstetrician and physician working together to minimise complications. Disease flares are usually managed with corticosteroids but other drugs such as hydroxychloroquine are sometimes used, although hydroxychloroquine is relatively contraindicated in early pregnancy (category D). Where anti-Ro/La or anti-phospholipid antibodies are co-existent, these may have the dominant effect on the pregnancy outcome.

ANTIPHOSPHOLIPID SYNDROME This is an important autoimmune condition because of a particular tendency to impact adversely on pregnancy. 179

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There may be some overlap of this condition with SLE as some women have both antinuclear and antiphospholipid autoantibodies, but it is best viewed as a distinct entity. Clinical features in the mother are largely a consequence of both arterial and venous thromboses throughout the body, with a predilection for the placental bed. Recurrent miscarriage is the most common presentation but the syndrome may also be associated with intrauterine fetal death, severe growth restriction or preeclampsia. Diagnosis can be made by demonstration of the autoantibody or the ‘lupus’ anticoagulant. The latter is a real misnomer since it is associated with thrombosis rather than a bleeding tendency and is a feature of the antiphospholipid syndrome rather than SLE. In management of the antiphospholipid syndrome, anticoagulant therapy is of prime importance and this may be combined with antiplatelet drugs or even immunosuppression in extreme cases. Even moderate levels of antiphospholipid antibodies would often not be treated in the absence of a history of clinical sequelae.

ANTI-RO AND ANTI-LA SYNDROMES These are antibodies directed against cytoplasmic ribonucleoproteins Ro and La. In the mother, these antibodies characteristically cause Sjögren’s syndrome (dry mouth and dry eyes), a photosensitive rash or even an SLE-like syndrome. Potential clinical features in the fetus include the photosensitive rash (5%) and complete heart block (2%). The risk is greater if there is a previously affected child (16%) or two previously affected children (50%). The heart block is permanent and may be fatal. Onset may be as early as 18 weeks’ and may be associated with a myocarditis of variable severity, from antibody binding to the fetal cardiac muscle as well as the cardiac conducting system. Detection of fetal arrhythmias is the key objective of auscultation of the fetal heart at each antenatal visit—in all pregnancies, not just those with anti-Ro or anti-La. Where there is a high risk of heart block (e.g. previously affected pregnancy), the P-R interval of the fetal cardiac cycle may be measured to anticipate impending heart block. Salbutamol can be beneficial if bradycardia is causing heart failure, but treatment may be limited by maternal side effects. Dexamethasone (sometimes supplemented by plasmapheresis) may benefit any myocarditis but will not reverse the heart block. These may be instituted prophylactically if there have been poor outcomes in previous pregnancies. Early neonatal therapy will depend on the degree of heart failure but a pacemaker may be necessary. If the fetus survives the neonatal period, the outlook is generally good but a small number will have irreversible myocardial damage that leads to neonatal death or ongoing myocardial insufficiency. 180

RED CELL ISOIMMUNE DISEASE IN PREGNANCY PATHOPHYSIOLOGY In red cell isoimmunisation, the fetus has red cell antigens that the mother does not possess. The mother is able to make an anti-red blood cell antibody that does not affect her but can cause haemolysis in the fetus.

WHICH ANTIGENS? The most common red cell antigen that is responsible is the D antigen at the rhesus locus. Approximately 85% of all red cell immunisation is related to the D antigen. Some of the other, more common antigens that may be responsible are listed in Table 22.2. Antibodies against other antigens may not cause clinical problems for the fetus because either they are predominately IgM (e.g. anti-A, anti-B, anti-P) or the fetal red cell does not express that antigen (anti-Le). The rhesus or Rh factor or D antigen is present in approximately 85% of Caucasians, 95% of African Americans and 99% of Asians and is so named because it is present in the rhesus monkey. In the preprophylaxis era, it was responsible for 98% of all cases of red cell isoimmunisation affecting pregnancy but now as many of 15% are caused by other anti-red blood cell isoantibodies, particularly anti-c, Kell, E and Duffy.

How did the mother acquire the anti-red blood cell isoantibody? Blood transfusion Although all blood administered is ABO and Rh group compatible, there is generally no matching for all the other red cell antigens capable of initiating an immune

TABLE 22.2  RED CELL ANTIGENS AND HAEMOLYTIC DISEASE OF THE NEWBORN. Red cell antigens associated with haemolytic disease of the newborn

Red cell antigens not associated with haemolytic disease of the newborn (or only mild disease)

Rhesus antigens: D, c, E, C

Rhesus antigen: e

Kell (K), Kidd (Jka and Jkb), Duffy (Fya and Fyb)

ABO antigens: A and B

M, N, S, s

Lewis (Le) P, P1

Chapter 22  Autoimmune and Isoimmune Disease in Pregnancy

response. The mother will not have a ‘transfusion reaction’ as such when she is first exposed to that antigen; however, this will serve as a primary immune stimulus and antibody production will be initiated that might impact on a current or future pregnancy.

Fetomaternal haemorrhage The fetus will usually inherit one or more major blood group factors from the father which are absent in the mother. When fetal red cells leak across the placenta into the mother’s circulation, she may react to these ‘foreign’ red cell antigens by forming isoantibodies. As little as 0.1 mL of fetal blood may lead to a maternal primary immune response.

Consequences of anti-red blood cell isoantibodies If anti-red blood cell isoantibodies are IgG in type, these will pass across the placenta from the mother to the fetus and cause agglutination and destruction of red blood cells. Transfer of antibody across the placenta increases as gestation advances and is minimal before about 16 weeks’ gestation. In late pregnancy, there is a surge of antibody transfer to equip the neonate with antibodies to fight infection. The breakdown of fetal erythrocytes has two consequences. First, bilirubin is a breakdown product of haemoglobin and while not a problem in utero (as the mother will clear the bilirubin from the fetus), accumulation of unconjugated bilirubin in the neonatal period can have serious consequences for the neonate, with the possible development of ‘kernicterus’ (see Ch 68). Where the amount of haemolysis is great, the accelerated erythropoiesis will not be able to keep up with the rate of haemolysis and anaemia will occur. Where anaemia is severe, the fetus will develop congestive cardiac failure with widespread accumulation of fluid subcutaneously and in the peritoneal, pleural and pericardial cavities—fetal hydrops. Further haemolysis will produce fetal death. Maternal white cell

ABO incompatibility ABO incompatibility is numerically three to four times more common than rhesus incompatibility. It is very rarely (if ever) responsible for fetal deaths or even severe anaemia; the usual clinical problem is early jaundice which may require phototherapy or possibly exchange transfusion. This condition is further characterised by fetal involvement in first pregnancies and unpredictable severity in future pregnancies.

PREVENTION OF RED CELL ISOIMMUNISATION Blood transfusion compatibility When a woman needs a blood transfusion, it is impractical to transfuse only blood that is antigenically fully compatible with the woman for all possible red-cell antigens. In practice, no D-negative person should receive D-positive blood. Kell-positive blood is generally only given to males or women beyond childbearing age. No specific efforts are generally made to avoid blood transfusion causing a primary immune response to other antigens (e.g. c, E, Duffy, M).

Passive administration of anti-D To prevent the development of anti-D antibodies, passive administration of anti-D was introduced in the late 1960s. As illustrated in Figure 22.2, passively administered anti-D binds to the D antigen on the fetal red cell and prevents recognition by the maternal immune system, therefore preventing primary immunisation as a consequence of fetomaternal haemorrhage. It should be noted that there is no similar process for preventing anti-c, anti-Kell or any other red cell isoimmunisation. This is simply because the high frequency of anti-D isoimmunisation makes the passive anti-D program cost-effective, whereas a program to prevent immunisation to other antigens would not be costeffective. Note that the passive administration of anti-D

Maternal red cells

anti-D

Fetal red cell

Passive antibody

FIGURE 22.2

Mechanism of action of passive anti-D. Administration of passive anti-D blocks the D-antigenic sites on the fetal red cells and prevents the primary immune response. 181

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is only effective to prevent primary immunisation and has no impact in preventing a fetomaternal haemorrhageinduced titre increase in a woman who is already immunised with anti-D.

When to administer anti-D Anti-D is generally administered at times of likely fetomaternal haemorrhage. There are broadly four such occasions: 1. bleeding in pregnancy (miscarriage, abortion, ectopic pregnancy, antepartum haemorrhage); 2. trauma (amniocentesis, chorionic villus sampling (CVS), external cephalic version, major fall or motor vehicle accident); 3. third-trimester administration (at 28 and 34 weeks’); and 4. following birth. In the latter circumstance, there is the opportunity to test the neonate to determine if the neonate is D-positive. In the event that the neonate is D-negative, unnecessary wastage of anti-D can be avoided by withholding passive anti-D.

Testing the partner This issue is obviously complex; in a small number of cases, there will be paternal uncertainty or even a desire to obscure the identity of the father of the child. Practically, it is best to assume that any fetus might be positive until it can be tested at birth. One possible exception is where the mother, without prompting, volunteers that her partner is also D-negative. Some clinicians are content to take this as evidence of undoubted paternity and withhold anti-D during pregnancy to a D-negative woman. The same would obviously not apply if the woman was asked to determine the D-status of her partner. It also needs to be noted at this point that in cases of immunisation being present (i.e. the presence of circulating maternal antibodies), the partner is tested. This is because invasive testing is likely during the pregnancy which could not be justified if the partner was negative, so asking for detailed grouping of the father of the child is therefore justifiable.

Amount of passive anti-D There are a number of different formulations of anti-D currently available. For sensitising events prior to 12 weeks’, 250 IU would commonly be administered. After 12 weeks’, prophylaxis occurs with 625 IU of anti-D. In some countries, a single dose of 1500 IU of anti-D will be given at 28 weeks’ instead of two doses of 625 IU at 28 and 34 weeks’. Kleihauer testing of maternal blood is able to detect the presence and amount of fetal erythrocytes and permits a more scientific approach to prophylaxis. A Kleihauer should be performed in the presence of a sensitising event in late pregnancy to see if more than one ampoule of anti-D is required to neutralise the amount of fetally derived D-antigen in maternal blood. In the case of a massive fetomaternal haemorrhage, a large amount of passive anti-D will be needed.

anti-D from approximately 10% of pregnancies to only 1% of pregnancies with a D-positive fetus and D-negative mother. With passive anti-D also being administered prophylactically at 28 and 34 weeks’ gestation, the number developing anti-D antibodies may drop to as low as 0.1%. These persisting cases may result from spontaneous fetomaternal haemorrhage before the prophylactic anti-D is administered at 28 weeks’, an unusually large fetomaternal haemorrhage that has not been administered sufficient anti-D or failure to appropriately administer anti-D globulin (due to blood group error, oversight, refusal by the woman). Some will question whether the passively administered anti-D can cause problems in the fetus. In fact, the anti-D does cross the placenta and bind to fetal red cells but the amount of anti-D is very small and the amount of haemolysis occurring clinically insignificant.

DETECTION OF ANTI-RED BLOOD CELL ANTIBODIES Apart from seeing that anti-D prophylaxis is appropriately carried out in D-negative women, the other major task of the obstetric attendant is to ensure that maternal antibodies, if present, are detected by routine antenatal testing. All women are screened at the first antenatal visit for the presence of anti-red blood cell antibodies. If no antibodies are present at the first visit, further checks are made in D-negative women at 28 weeks’, prior to the administration of passive anti-D. Some units will do repeat screening on all women at 28 weeks’ but the costeffectiveness is less in those women that are D-positive as the proportion that become immunised during pregnancy (e.g. with ‘c’, ‘E’ or Kell) will be less than that of D-negative women with ‘D’. If antibodies are present at any time, the woman must be referred to a specialist or special centre dealing with this problem. A number of complex decisions and therapeutic measures will be required if moderate or severe haemolysis is occurring in the fetus (next section).

MANAGEMENT OF A PREGNANCY WITH ANTI-RED BLOOD CELL ANTIBODIES Allocation of risk at the first antenatal visit Approximately 1% of women will be found to have anti-red blood cell antibodies at the first antenatal visit. They have become immunised as a consequence of a previous pregnancy or blood transfusion. As a first step, it is then necessary to determine the likely risk of this antibody to the fetus.

Effectiveness of passive anti-D

Determining the partner’s antigen status

The introduction of anti-D in the late 1960s reduced the incidence of the mother becoming immunised with

The partner’s genotype needs to be determined with respect to the offending antigen. He may be homozygous

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positive (e.g. DD, all children will be affected), heterozygous (e.g. Dd, 50% of offspring will be affected) or homozygous negative (e.g. dd, no children affected). For Fya/ Fyb C/c, K/k, E/e and so on, zygosity may be determined precisely. It is very important to realise that if the partner is negative for the relevant antigen, the fetus will have no problem whatsoever and any concerns of the parents or healthcare provider can be dismissed very early in the pregnancy.

Quantifying the amount of antibody in maternal plasma The likelihood of significant problems for the fetus can be estimated from the antibody level in the maternal plasma (Table 22.3).

Does the specific antigen affect risk? The management of an affected pregnancy is largely dependent on the amount of antibody, rather than which particular antibody is present. The exception is anti-Kell, which may be more serious than others at the same antibody level because the Kell antigen is particularly expressed on the erythroblast.

Management of the low-risk immunised pregnancy Maternal isoantibody levels should be estimated every 4 weeks until 28 weeks’ and fortnightly thereafter until birth. While the antibody level remains in the low-risk range, antenatal management can generally remain with the chosen model of care. If the titre were to rise, the woman should be managed as for moderate or high risk and referred appropriately. If the antibody is anti-D, there is no value in administering prophylactic passive anti-D; however, anti-D would still be administered to Rh-negative women with another isoantibody. At birth, the cord blood should be sent for grouping, bilirubin and haemoglobin determination. The baby should be managed by a doctor with experience in the management of immunised neonates. Early severe jaundice is possible and may follow a quite different course from that of physiological jaundice.

Management of the moderate- or high-risk immunised pregnancy Women with antibody levels in the moderate or high range (Table 22.3) should be referred to a unit with experience in the management of isoimmunised pregnancies. In most situations, this will be under the direction of a fetomaternal medicine subspecialist. Where the partner is heterozygous, it is pertinent to know whether the fetus inherited the relevant antigen. CVS should be avoided as this may provoke fetomaternal haemorrhage and an increase in antibody level. Amniocentesis is less likely to produce a rise in titre but it is increasingly possible to isolate free fetal DNA from the maternal bloodstream and type the fetus on the basis of that DNA. Fetal anaemia can be anticipated on the basis of peak systolic velocity (PSV) in the middle cerebral artery (MCA) of the fetus. In severe cases, this may be commenced as early as 17 weeks’ gestation and would commonly be performed weekly. It may be less reliable after 34 weeks’ gestation and would then be complemented by weekly or twice-weekly cardiotocography. Cardiotocography may be initially non-reactive in fetal anaemia, with a sinusoidal pattern only developing as a late sign (Fig 22.3). If anaemia is thought probable on the basis of the MCA PSV, fetal blood sampling may be performed under ultrasound control into either the umbilical cord or the ductus venosus. Fetal anaemia can be corrected with the infusion of donor blood into the fetal vessel. The blood infused will be negative for whichever antigen the maternal antibody is directed against. Fetal transfusions are commonly needed frequently at first (e.g. twice weekly) but with reducing frequency (e.g. even four-weekly) as the fetal blood type ‘changes’ to that of the donor blood and is no longer being destroyed by the maternal antibody. Delivery will be indicated when the risks of fetal transfusion exceed the risks of prematurity. It would be uncommon to continue to transfuse after 35 weeks’ gestation. The neonate needs to be carefully watched for both severe jaundice and anaemia. If transfusions have

TABLE 22.3  FETAL RISK AND MATERNAL ANTIBODY LEVEL. Risk level

Likelihood of fetal anaemia if titre remains unchanged

Likelihood of clinically significant neonatal jaundice

Titre level

Quantified antibody level

Low

Negligible

Moderate

≤ 16

< 4 IU/L

Moderate

Low

High

32–256

4–10 IU/L

High

High

Very high

≥ 512

> 10 IU/L 183

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FIGURE 22.3

Sinusoidal cardiotocograph due to severe fetal anaemia.

Source: Martin R, Fanaroff AA, Walsh MC. Fanaroff and Martin’s Neonatal-Perinatal Medicine. 9th edn. St Louis, Mosby, 2010. Copyright © 2010 Mosby, An Imprint of Elsevier.

not occurred, severe jaundice should be anticipated. In contrast, the fetus that has had many transfusions may not have jaundice at all but may suffer from later anaemia as the transfusions have suppressed fetal erythropoiesis, which needs to re-establish in the neonatal period.

WHITE CELL AND PLATELET ISOIMMUNE DISEASE IN PREGNANCY NEONATAL ALLOIMMUNE THROMBOCYTOPENIA Pathophysiology In neonatal alloimmune thrombocytopenia (NAIT), the isoantibody is directed against an antigen on the fetal platelets that the mother does not possess. This is most commonly anti-HPA-1a. Approximately 2% of mothers are HPA-1a negative and therefore capable of developing anti-HPA-1a antibodies, but clinically significant NAIT occurs only in about 1 in 2000 pregnancies.

Clinical sequelae NAIT is inappropriately named as the antibody crosses the placenta and may produce a profound fetal thrombocytopenia (i.e. not just neonatal). Spontaneous fetal haemorrhage may occur as early as 18 weeks’ gestation, particularly intracranial or gastrointestinal. The former

184

may present clinically with a porencephalic cyst or asymmetric enlargement of the cerebral ventricles. Gastrointestinal haemorrhage may be evidenced by increased intestinal opacity on ultrasound. Other cases will not present until birth with extensive petechiae or bruising that may be wrongly attributed to a traumatic delivery.

Management NAIT is a rare condition and all suspected cases should be referred to a major centre. In general, most cases will be managed with weekly immunoglobulin infusion from early pregnancy. However, severe cases may require more aggressive therapy, including such modalities as corticosteroids, plasmapheresis or even fetal platelet transfusion prior to birth of a persistently severely thrombocytopenic fetus.

NEONATAL ALLOIMMUNE NEUTROPENIA In this condition, the isoantibody is directed against an antigen on the fetal neutrophil that the mother does not possess. As a result, the fetus and neonate are severely neutropenic. This is generally not a problem in utero but the neonate is at risk of overwhelming bacterial sepsis and requires immunoglobulin infusion and antibiotic prophylaxis. Recovery may take weeks as the antibody affects the bone marrow production of white cells and not just the circulating neutrophils.

Chapter 23  DIABETES MELLITUS Peter Wein

KEY POINTS Diabetes mellitus is relatively common in pregnancy and, if not diagnosed and managed skilfully, has the potential for serious complications to both mother and baby. Pregnancy represents a stress on islet-cell function because of the effect of pregnancy hormones on carbohydrate metabolism. This leads to an increase in insulin requirement in prepregnancy diabetics or may lead to the onset of a diabetic condition in pregnancy (gestational diabetes). Although it usually resolves after delivery, recognition of gestational diabetes is important in alerting the attendant to the possibilities of fetal macrosomia and, for the mother, the risk of subsequent development of permanent diabetes (approximately 30% develop diabetes mellitus over the following 15 years; 95% of these will have type 2 diabetes). There is a twofold increase in the risk of congenital malformations in women with prepregnancy diabetes. This risk can be significantly reduced by periconceptional close control of blood glucose values. The risk of fetal malformation is not increased in gestational diabetes since hyperglycaemia and associated metabolic derangements are not present at the time of organogenesis. Both prepregnancy and gestational diabetes may be complicated by a number of other important clinical sequelae including fetal macrosomia, intrauterine death, placental insufficiency, polyhydramnios and prematurity. In the neonate, hypoglycaemia and respiratory distress syndrome are more common. The latter may even occur in large infants born near full term. Perinatal mortality is increased to about 2% in prepregnancy diabetes. Screening for the development of gestational diabetes in pregnancy is necessary to enable appropriate surveillance and treatment. This is achieved by the performance of a glucose tolerance test in the late second trimester in all women. Recent trends emphasise the need for early diagnosis, preconceptional counselling and stabilisation, team management, close blood sugar monitoring, precise insulin dose regimen, careful fetal monitoring, optimal timing of delivery and good neonatal intensive care facilities. Reduced perinatal mortality related to the above has highlighted the residual problem of severe fetal malformation. Improvement in this area has been achieved with preconceptional counselling and better glycaemic control in the first 6 to 8 weeks of pregnancy. The increased risk of intrauterine death in late pregnancy in prepregnancy diabetes and the mechanical problems caused by macrosomia lead to a recommendation for delivery at 38 to 39 weeks’ gestation, depending on the glucose control and the degree of macrosomia. Close monitoring of fetal wellbeing is mandatory.

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PHYSIOLOGY In early pregnancy, glucose tolerance is largely unchanged or may even improve through consumption of glucose by the developing pregnancy. From the early second trimester, there is a progressive increase in insulin demand. This is largely due to the effect of the placental hormone human placental lactogen (hPL). This hormone structurally resembles growth hormone and shares the common property of promoting insulin resistance. Increased levels of corticosteroids may also contribute to the diabetogenic effect of pregnancy.

CLASSIFICATION OF DIABETES IN PREGNANCY BY AETIOLOGY Gestational diabetes mellitus (GDM) is defined as carbohydrate intolerance of varying severity with onset or first recognition during pregnancy. The definition applies irrespective of whether or not insulin is used for treatment or if the condition persists after pregnancy. Prepregnancy diabetes may be type 1, type 2 or other. Type 1 diabetes is characterised by insulin dependence, the presence of circulating islet cell antibodies, an onset usually before the age of 35 years and a tendency to ketoacidosis. There is low or absent endogenous insulin production. Type 2 diabetes typically has non-insulin dependence, absence of islet cell antibodies, onset after the age of 35 years and obesity; ketoacidosis is uncommon. There is a tendency to high endogenous insulin production and insulin resistance. Other diabetes may occur as a consequence of pancreatic disease, pancreatectomy, contra-insulin hormonal

disturbances (acromegaly, Cushing syndrome), drugs and some rare genetic syndromes.

INCIDENCE Gestational diabetes occurs in about 10% of pregnancies. Prepregnancy diabetes is present in about 0.5% of the obstetric population but the incidence of type 2 diabetes is increasing due to the obesity epidemic.

DIAGNOSIS PREPREGNANCY DIABETES Where prepregnancy diabetes (of any type) is present, further confirmation during pregnancy is unnecessary. A glucose tolerance test (GTT) is usually necessary for the diagnosis of gestational diabetes, but if the condition is clinically florid (polyuria, polydipsia, weight loss, ketonuria), a single high random plasma glucose (≥ 11 mmol/L) is sufficient for the diagnosis.

SCREENING FOR GDM IN EARLY PREGNANCY The type of screening required for GDM in early pregnancy depends on the presence or absence of the risk factors shown in Table 23.1.

SCREENING FOR GDM AT 26 TO 28 WEEKS’ All women not known to have GDM should have a 75-g glucose tolerance test (GTT) at 26 to 28 weeks’ gestation. Two-step testing with an oral glucose challenge test and

TABLE 23.1  EARLY PREGNANCY SCREENING FOR GDM. Risk level

Risk factors

Screening test

Low

Nil

Random blood glucose in early pregnancy

Moderate

• • • •

High

186

• • • • • • •

Ethnicity: Asian, Aboriginal, Torres Strait Islander, Pacific Islander, Māori, Middle Eastern, non-white African BMI of 25 to 35 kg/m2 Family history of diabetes (first-degree relative with type 2 diabetes) Previous macrosomia (baby with birth weight > 4500 g or > 90th percentile)

Fasting blood glucose in early pregnancy

Abnormal random or fasting blood glucose Multiple ‘moderate’ risk factors Previous GDM Maternal age ≥ 40 years BMI > 35 kg/m2 Polycystic ovarian syndrome Medications: corticosteroids, antipsychotics

GTT in early pregnancy

Chapter 23  Diabetes Mellitus

50

55

proceeding to a POGTT if abnormal is no longer recommended as it misses approximately 30% of GDM and delays diagnosis in many other women.

45

DIAGNOSTIC CRITERIA

Congenital malformations are twice as common in women with prepregnancy diabetes compared with the normal population. The most common malformations are of the central nervous system (particularly neural tube defects) but cardiovascular (transposition of the great vessels, ventricular septal defects, coarctation of the aorta), genitourinary and gastrointestinal malformations may also occur. The caudal regression syndrome (sacral agenesis) is very rare but it is almost pathognomonic of the infant of a diabetic mother. Congenital malformations appear to be related to glycaemic control around the time of organogenesis. They are therefore not increased in women with gestational diabetes. Spontaneous abortion is increased if there is poorly controlled disease. Problems that may occur later in pregnancy include: 1. preeclampsia; 2. polyhydramnios; 3. preterm labour; 4. placental insufficiency; 5. unexplained intrauterine death; 6. infections (e.g. urinary tract, vaginal candidiasis); and 7. macrosomia (large-for-dates fetus) (Figs 23.1 and 23.2). Macrosomia may result in cephalopelvic disproportion, prolonged or obstructed labour, and impacted shoulders during delivery. There is a tendency for the newborn to suffer from hypoglycaemia and respiratory distress in addition to the increased risk of congenital malformations, birth injury (from macrosomia) and prematurity. Perinatal mortality is considerably increased in the presence of poor glycaemic control, complications of longstanding diabetes (nephropathy, hypertension) and specific complications of pregnancy (congenital malformations, preeclampsia, prematurity, polyhydramnios, placental insufficiency, macrosomia). Unexplained intrauterine death is more common with macrosomia and poor glucose control. It is not a

35 30 25 20 15 10 5 cm

THE EFFECT OF DIABETES ON PREGNANCY

40

After a fasting plasma glucose sample has been taken, a glucose load of 75 g is given orally and the plasma glucose repeated at 1 and 2 hours after the glucose load. The woman must be fasted overnight. The definition of gestational diabetes, based on the Hyperglycaemia and Adverse Pregnancy Outcome (HAPO) study and recommended by the International Association of Diabetes in Pregnancy Study Groups (IADPSG) and endorsed by the World Health Organisation (WHO), the Australasian Diabetes in Pregnancy Society (ADIPS) and RANZCOG, requires either a fasting glucose value of ≥ 5.1 mmol/L or a 1-hour value of ≥ 10 mmol/L or a 2-hour value of ≥ 8.5 mmol/L after a 75-g oral glucose load.

FIGURE 23.1

This fetus from a diabetic mother weighed 6420 g when stillborn at 35 weeks’ gestation.

Source: Reproduced with permission from the Royal Women’s Hospital, Parkville, Victoria.

FIGURE 23.2

The 6700-g infant of a diabetic mother delivered by caesarean section after a failed attempt at forceps delivery. Source: Courtesy of Prof. Norman Beischer.

feature of women with well-controlled gestational diabetes and no macrosomia. Findings at autopsy in these babies are usually indicative of hypoxia, but the precise pathogenesis is uncertain. The effect of diabetes on pregnancy depends largely on its severity. For example, early diabetes is characterised 187

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by effects of the elevated maternal blood sugar resulting in macrosomia, polyhydramnios and preeclampsia. With increasing instability, there is a greater likelihood of congenital malformations and perinatal morbidity/mortality. Finally, at the stage of maternal vascular disease, the predominant effect on the fetus is one of growth restriction and fetal death due to uteroplacental insufficiency.

THE EFFECT OF PREGNANCY ON DIABETES In the first trimester of pregnancy, there is an improvement in glucose tolerance partly as a result of fetal demands and partly because of diminished appetite. Insulin requirements may therefore slightly decrease during early pregnancy. Hyperemesis gravidarum may affect carbohydrate intake and require careful insulin adjustment to avoid hypoglycaemia. In the second half of pregnancy, the above tendency is counteracted by the anti-insulin effect of placental hormones (particularly hPL) and to a lesser extent an increase in glucocorticoids, resulting in higher insulin requirements. After delivery, the situation is reversed and the insulin requirement is rapidly reduced, usually to that existing before the pregnancy began. If glycaemic control is poor, there may be more rapid progression of microangiopathy (retinopathy and nephropathy). With changing insulin requirements and often superimposed illness, hypoglycaemic attacks and ketoacidosis are more common than in the non-pregnant diabetic woman.

MANAGEMENT PREPREGNANCY Preconceptional advice is important in women with known diabetes. One of the most useful measures is the minimisation of spontaneous miscarriage and birth defects by ensuring optimum control during the period of fetal organogenesis. As with any prepregnancy counselling visit, a general assessment should be made with a complete history, physical examination, rubella and varicella status and cervical cytology. As there is some crossover with other autoimmune diseases, these women should be screened for hypothyroidism and coeliac disease. Preconceptual folic acid is recommended at a dose of 5 mg daily. The diabetes needs to be fully assessed with respect to glucose control (home blood glucose monitoring, Hb A1c), renal function and retinopathy. Appropriate treatment should be instituted, aiming for tight control of the blood sugar using dietary manipulation and insulin. Advice should be given regarding anticipated problems in pregnancy, particularly if there is evidence of micro­ angiopathy or a history of previous perinatal death. The danger of smoking should be emphasised, since there is a compounding ill-effect on blood flow in smaller blood vessels. 188

FIRST ANTENATAL VISIT As with any high-risk pregnancy, accurate assessment of gestational age is important. An early ultrasound is recommended. A full screening assessment for coincident problems should not be overlooked. The usual first visit management for all women must not be forgotten, and screening for hypothyroidism and coeliac disease should be performed if not already done.

DIABETIC MANAGEMENT Surveillance Assessment of diabetes should be instituted with home blood glucose monitoring. This is a vital part of glucose control throughout the pregnancy. Blood glucose measurements should be performed fasting and 2 hours after every meal. The aim should be to maintain fasting blood glucose levels in the range 4.5 to 5.5 mmol/L, with 2-hour postprandial levels 6.0 to 7.0 mmol/L. More information about very short-term and overnight fluctuations in glucose levels can be obtained using continuous monitoring of interstitial fluid glucose levels (CBGM). A sudden drop in insulin requirements should raise the suspicion of fetal compromise and should be reported promptly. A general idea of blood sugar control over the preceding weeks is obtained by measurement of glycosylated haemoglobin (Hb A1c). A satisfactory value is < 8%, optimally near 6%. Renal function and eye disease should be reassessed.

Treatment Diet and exercise are important components of diabetes management, whether insulin is being taken or not. The keynotes are regular and more frequent meals, 130 kJ/kg/ day for non-obese women, with an extra 120 kJ/kg/day for each kilogram of weight gain in pregnancy with 50% of this as carbohydrate (mostly complex). In type 1 diabetes, the woman is often not overweight and quality rather than quantity of food is important. In type 2 diabetes, an attempt should be made to achieve ideal weight for height (by calorie reduction); with the decrease in obesity, insulin sensitivity usually improves. In both conditions, the aim is to maintain blood glucose levels in the normal range, prevent ketonuria and allow for a normal weight gain through the pregnancy. Obese women need only 105 kJ/kg/day. The following are suggested daily intakes at the beginning of pregnancy for the ‘standard’ 58-kg woman: protein 70 g, carbohydrate 270 g and fat 50 g; this should make up 7500 kJ per day. Complex carbohydrates or starches (low glycaemic index [GI]) are much preferred to concentrated sucrose-type sweets (high GI). Brown and/or basmati rice is preferred to white jasmine rice, and wholemeal bread should be recommended rather than white bread. Insulin regimens differ from centre to centre. There is increasing evidence from diabetes outside pregnancy that tight glycaemic control has benefits in terms of

Chapter 23  Diabetes Mellitus

reduction in the long-term complications of diabetes (nephropathy, retinopathy, vascular disease). Many women will therefore enter pregnancy using the ‘basalbolus’ insulin regimen, and many centres are advising all pregnant women with insulin-dependent diabetes to use this regimen. It involves using a small dose of medium- or long-acting (isophane, detemir or glargine) insulin in the evening to provide constant basal insulin levels, and bolus doses of short-acting insulin analogue (lispro, aspart or glulisine) before each meal in an attempt to mimic physiological patterns of insulin secretion.

Planning care for the pregnancy The pregnant woman with diabetes should be managed jointly by a team with a special interest in this problem: obstetrician and internist/endocrinologist, consulting with diabetic educator, dietician and, later, a neonatal paediatrician.

SUBSEQUENT ANTENATAL CARE Diabetic management Home blood sugar monitoring, repeat Hb A1c (e.g. 4-weekly), diet, exercise and insulin form the fundamentals of care. Regular ophthalmological examination should be carried out to assess retinal vascular changes. An important distinction should be made between starvation ketosis (normoglycaemia) and diabetic ketosis (hyperglycaemia); the former requires glucose, the latter insulin. Women with gestational diabetes should perform home blood glucose monitoring four times per day as for women with prepregnancy diabetes. The targets are fasting glucose < 5.1 mmol/L and 2-hour postprandial glucose levels < 6.7 mmol/L. If these targets are persistently exceeded despite dietary modification and exercise, insulin should be used. Control can sometimes be achieved with once- or twice-daily injection of isophane insulin, but some women require basal-bolus insulin. About 50% of women with gestational diabetes will need insulin. Recent studies have shown that metformin can achieve glycaemic control in about 50% of women who would otherwise need insulin.

Early diagnosis of complications More frequent antenatal visits are necessary. Congenital abnormalities should be sought on an 18-week ultrasound. Fetal surveillance in the third trimester is necessary in order to detect placental insufficiency. The frequency of testing (e.g. cardiotocography, ultrasound) depends on the period of gestation, severity of the disease and the presence of other factors likely to influence fetal wellbeing (e.g. hypertension, renal insufficiency). Ultrasonography should generally be carried out at 28 and 34 weeks’ in prepregnancy diabetes to assess fetal growth (macrosomia or placental insufficiency). In gestational diabetes, fetal surveillance may be clinical only if sugar control is very good and clinical parameters

satisfactory. The clinician should have a low threshold for ultrasound assessment for either placental insufficiency or macrosomia.

MANAGEMENT OF BIRTH Timing of birth Complications such as fetal compromise or preeclampsia may necessitate preterm delivery. Otherwise delivery should take place at 38 to 39 weeks’ gestation in women with prepregnancy diabetes. In women with gestational diabetes and no evidence of fetal macrosomia, delivery at 40 weeks’ is reasonable, but allowing the pregnancy to proceed significantly beyond the due date would mostly not be recommended on the basis of increasing risks of stillbirth and macrosomia. This data is observational as there has not been a sufficiently powered randomised controlled trial to assess the outcomes in gestational diabetes at postdates gestations.

Mode of birth Elective caesarean section will usually be preferred to induction of labour where there is malpresentation or a previous caesarean section. The incidence of caesarean section is about 50% in large reported series for prepregnancy diabetes and about 25% for women with gestational diabetes. As diabetes in pregnancy is an independent risk factor for shoulder dystocia, elective caesarean section is also recommended for severe fetal macrosomia (e.g. estimated fetal weight > 4250 g). If an elective caesarean section is planned, it should be performed as the first case of the morning. On the day of operation, the morning dose of insulin is withheld, and insulin and dextrose infusions are administered. These will need to be continued postoperatively until bowel function returns and the woman is able to tolerate oral nutrition.

Intrapartum care Where insulin has been used antenatally, a plan should be made antenatally regarding management of the woman’s insulin requirements in labour. In labour, the woman should be able to maintain sufficient energy intake orally. All urine should be tested for the presence of ketones. If ketonuria is present, the energy intake should be increased, if necessary by intravenous dextrose infusion. Blood glucose levels during labour are most readily controlled by a sliding scale of subcutaneous insulin. Routine intravenous dextrose infusion is not necessary for most women. Vigilant assessment of the progress of labour is indicated in anticipation of dystocia. Continuous electronic fetal monitoring is indicated. Epidural analgesia may be recommended in anticipation of a long labour. In addition, an epidural may also aid in blood glucose control, by reducing the level of circulating catecholamines. The delivery should be performed in the lithotomy position by an experienced accoucheur in anticipation of 189

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possible shoulder dystocia. Pushing in the second stage is contraindicated in the presence of diabetic proliferative retinopathy. The umbilical cord should be clamped early to decrease the risk of neonatal polycythaemia.

MANAGEMENT IN THE PUERPERIUM Diabetes management Immediately after vaginal delivery, the insulin infusion should be ceased. In a woman with prepregnancy diabetes, it is simplest to revert to her prepregnancy dose of insulin the following day and await the establishment of lactation to fine tune glycaemic control. Lactation necessitates an additional 50 g of carbohydrate per day. Women with gestational diabetes requiring insulin therapy can cease insulin after delivery. They should then be monitored with blood glucose levels for 48 hours. Levels > 10 mmol/L will require further treatment, and should be reported to the endocrinologist.

Neonatal management The baby of a diabetic mother is often macrosomic (excess fat and fluid), flabby, sleepy and difficult to feed. Because of immature behaviour, the baby is usually treated in a similar manner to the premature baby. In addition, a close watch is kept on blood glucose levels (tendency to hypoglycaemia) and respiratory function (atelectasis, respiratory distress syndrome). A careful check for congenital malformations should be made as well as for birth trauma. With more advanced disease, the baby often shows the features of intrauterine growth retardation, with attendant complications of wasting, asphyxia and meconium aspiration. Breastfeeding is not contraindicated, although this may be more difficult initially. The parents should be counselled regarding the inheritance risks of type 1 diabetes, which is 2% if the mother has diabetes but 6% if the father has diabetes, and 30% if both have type 1 diabetes mellitus.

FOLLOW-UP OF GESTATIONAL DIABETES All women with GDM should have a GTT at approximately 6 weeks postpartum to ensure resolution of the

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diabetes. Long-term follow-up of gestational diabetics has shown incidences of diabetes requiring specific therapy at approximately 25% by 15 years. Predictive factors in development of overt diabetes are: 1. persistence of abnormal glucose tolerance in the puerperium; 2. recurrence of gestational diabetes in a subsequent pregnancy; and 3. persistent obesity. From the mother’s viewpoint, the major advantage of the diagnosis of gestational diabetes is that follow-up offers the possibility of early diagnosis and prevention of the vascular complications of overt diabetes. All women with former gestational diabetes should be encouraged to continue the diet and exercise regimen adopted during pregnancy. Ongoing surveillance for the development of diabetes can most conveniently performed by annual measurement of Hb A1c. Levels > 6.5% are diagnostic of diabetes mellitus. FURTHER READINGS Crowther CA, Hiller JE, Moss JR, et al. Effect of treatment of gestational diabetes mellitus on pregnancy outcomes. New Eng J Med 2005;352:2477–86. HAPO Collaborative Research Group. Hyperglycemia and adverse pregnancy outcomes. New Eng J Med 2008;358:1991–2002. International Association of Diabetes and Pregnancy Study Groups Consensus Panel. International Association of Diabetes and pregnancy study groups recommendations on the diagnosis and classification of hyperglycemia in pregnancy. Diabetes Care 2010;33:676–82. Landon M, Spong C, Thom E, et al. A multicenter, randomized trial of treatment for mild gestational diabetes. New Eng J Med 2009;361:1339–48. Lee AJ, Hiscock RJ, Wein P, et al. Gestational diabetes mellitus: clinical predictors and long-term risk of developing type 2 diabetes: a retrospective cohort study using survival analysis. Diabetes Care 2007;30(4):878–83. Moses RG, SanGil F, Morris G, et al. Impact of the potential new diagnostic criteria on the prevalence of gestational diabetes mellitus in Australia. Med J Aust 2011;194:338–40.

Chapter 24  NEUROLOGICAL DISEASE Susan Walker

KEY POINTS There are a wide range of neurological conditions predating pregnancy that require obstetric management in partnership with the woman’s neurologist. Prepregnancy counselling is invaluable in optimising the maternal outcome in conditions such as epilepsy, multiple sclerosis and spinal cord injury, Care of women with epilepsy includes provision of reliable contraception, optimisation of antiepileptic drug regime, prepregnancy folate, surveillance for congenital abnormalities in pregnancy and attention to times of increased seizure risk, particularly intrapartum and postpartum. Conditions such as myasthenia gravis and myotonic dystrophy may have important fetal implications which need to be considered prior to, and during, pregnancy. Migraines tend to improve during pregnancy. Ergotamine is contraindicated in pregnancy, and triptans are not recommended. Pregnancy is a risk factor for both ischaemic and haemorrhagic stroke. Peripheral neuropathies such as carpal tunnel syndrome and Bell’s palsy are more common in pregnancy but are mostly self-limiting.

MULTIPLE SCLEROSIS Multiple sclerosis (MS) is a chronic degenerative condition caused by autoimmune-mediated demyelination of the brain and spinal cord. MS is more common in women than men, and the diagnosis is most commonly made between 15 and 50 years of age. Accordingly, a typical patient will be a woman of childbearing age.

PREPREGNANCY PLANNING The major issue facing women with MS planning a pregnancy is making a decision regarding disease-modifying drugs (DMDs). Beta interferon is the most commonly used agent and this is not recommended periconceptually, or during pregnancy and lactation. Nevertheless, for women who have conceived unknowingly on interferon,

the available data is reassuring, and would not generally be considered grounds for recommending abortion. The best prognosis is for women with well-controlled disease, as pregnancy and postpartum relapses are more common among women who have had a relapse in the 12 months prior to pregnancy. Reliable contraception is recommended to optimise pregnancy timing, with regard to both disease stability and to ensure women and their families are able to plan adequate support for the pregnancy, depending on both the physical and psychological needs of the woman during pregnancy and postnatally with her new baby.

MULTIPLE SCLEROSIS IN PREGNANCY In common with other autoimmune conditions, MS disease activity decreases during pregnancy. This may be

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due to the relative immune-tolerant state of pregnancy. This decrease is offset by an increased rate of relapse in the first 12 weeks postpartum, with up to 30% of women with relapsing MS having a postpartum relapse, presumably due to the return of immunocompetence. When the protective effects of pregnancy and the increased postpartum risks are combined, the overall effect of pregnancy is for no increase in the risk of MS exacerbations. Women who experience a relapse in pregnancy should be managed as usual, with the mainstay of therapy pulsed corticosteroid therapy. MS has little or no effect on important pregnancy outcomes such as preterm birth or fetal growth restriction.

LABOUR AND DELIVERY Most women with MS can expect to have a normal vaginal delivery. Spinal or epidural anaesthesia is not contraindicated, although a predelivery anaesthetic consult is recommended to discuss pain relief in labour and document any preexisting neurological deficit.

Postpartum Breastfeeding is not contraindicated in women with MS, and more stable disease has been reported in association with lactation, presumably due to the stable hormonal state induced by lactational amenorrhoea. The benefits of breastfeeding need to be weighed against the need to remain off DMDs during lactation. The importance of good psychosocial support in the postpartum period cannot be overemphasised.

EPILEPSY PREPREGNANCY PLANNING Women of reproductive age with epilepsy should avoid unplanned pregnancy with reliable contraception. The efficacy of hormonal contraception may be reduced by enzyme inducing antiepileptic drugs (AEDs), such as phenobarbitone, primidone, phenytoin, carbamazepine, oxcarbazepine and topiramate. When pregnancy is planned, AED medication should be optimised and adequate folic acid supplementation instituted.

PREGNANCY CARE First seizure In women who present during pregnancy with their first seizure, consideration should also be given to alternative diagnoses, such as eclampsia, a primary neurological event, metabolic disturbance or drug toxicity or a seizure complicating a vaso-vagal faint.

Seizure frequency Most studies suggest that pregnancy has little or no impact on seizure frequency. If seizure control deteriorates in pregnancy, potential contributors that should be 192

considered include: decreased medication compliance because of concern about teratogenesis; decreased drug absorption because of nausea and vomiting; impaired sleep; and decreased drug levels because of the increased volume of distribution in pregnancy.

The impact of seizures on pregnancy outcomes While the fetus is relatively resistant to short hypoxic episodes, prolonged convulsive seizures may result in sustained fetal hypoxia. While there are legitimate concerns about teratogenicity of AEDs, the potential benefit of ceasing or changing medication must be weighed against a risk of increased seizure frequency, with the attendant risk to the patient, her fetus and possibly other children.

Congenital malformations The risk of congenital malformation is higher among women with epilepsy (WWE), higher among treated compared to untreated women and highest among those using polytherapy rather than monotherapy. The risk of major congenital malformation associated with individual AEDs as monotherapy are estimated at approximately 3% for lamotrigine, 5% for carbamazepine and phenobarbitone, 7% for phenytoin and more than 10% for valproate. There is limited data on newer anticonvulsants such as levetiracetam, topiramate and gabapentin. As a single agent, valproate (particularly in doses > 1100 mg/ day) appears to be associated with the highest risk and this is further amplified when combined with other AEDs.

Surveillance for birth defects In WWE, especially those taking AEDs, an ultrasound examination should be offered at 11 to 13 weeks’. Acrania (the precursor of anencephaly) should be recognised at this gestation, and an increased nuchal translucency is also a useful screening test for cardiac and other structural defects. At second trimester, an expert morphological assessment should be performed.

LABOUR AND DELIVERY Labour and delivery is a relatively high-risk time for seizure recurrence. The reasons for this are multifactorial including poor bioavailability and compliance with AEDs, sleep deprivation, anxiety and hyperventilation in labour. Key management issues for managing women with epilepsy in labour are summarised in Box 24.1.

POSTPARTUM CARE Most AEDs are compatible with breastfeeding. WWE and all their maternity care providers should be aware of the risk of postpartum seizures, particularly in the setting of sleep deprivation. Upon discharge, WWE will be anxious about the prospect of having a seizure while caring for a

Chapter 24  Neurological Disease

BOX 24.1  Intrapartum care of women with epilepsy. Intravenous access should be secured in labour in anticipation of a seizure. Women should continue to take their usual AEDs in labour. Hyperventilation and maternal exhaustion should be avoided. Labouring in water is not recommended for women with epilepsy. Generalised tonic–clonic seizures are associated with hypoxia, and continuous CTG tracing is recommended in the event of a seizure. An intravenous benzodiazepine (e.g. diazepam and midazolam) is recommended to terminate the seizure. In the event of benzodiazepine (e.g. diazepam and midazolam) being used to terminate the seizure, loss of baseline variability of the fetal heart rate tracing can be expected to follow for approximately 1 hour. Women should deliver in a centre with adequate facilities for neonatal resuscitation.

triggers are the mainstay of treatment in pregnancy. The triptans are also not recommended for use in pregnancy although registry data for sumatriptan is largely reassuring following exposure in pregnancy.

SECONDARY HEADACHES Secondary headaches are those due to an underlying cause such as space-occupying lesions, vascular disorders, infections or other systemic illness. ‘Red flag’ symptoms such as postural headache, headache provoked by Valsalva or exertion, ‘thunderclap’ headache or headache accompanied with neurological signs warrant further investigation.

CEREBROVASCULAR DISEASE IN PREGNANCY Stroke in pregnancy may be haemorrhagic or nonhaemorrhagic. Pregnancy and the postpartum period are recognised risk factors for both haemorrhagic and ischaemic stroke, due to the increase in cardiac output, and changes in vessel tone, coagulation factors and endothelial function. Preeclampsia/eclampsia is an important independent risk factor for both haemorrhagic and ischaemic stroke. Haemorrhagic causes of stroke include subarachnoid haemorrhage or intracerebral haemorrhage. Con­ tributors to intracerebral haemorrhage include preeclampsia/eclampsia, arteriovenous malformations and aneurysmal rupture. Non-haemorrhagic stroke includes arterial ischaemic stroke and cerebral vein thrombosis.

• baby at home alone. To minimise the risk of harm if a seizure occurs, changing or feeding the baby on the floor is recommended, the use of baby slings should be avoided, stair climbing should be minimised where possible and bathing the baby should be avoided when alone. The importance of adequate postnatal social supports cannot be overemphasised.

HEADACHE IN PREGNANCY TENSION HEADACHES Tension headaches are the most common form of headache and there does not appear to be any change in headache frequency or character during pregnancy. Tension headaches may be difficult to differentiate from pregnancy-specific disorders, such as preeclampsia. As a general rule, any patient over 20 weeks’ with a headache not resolved with simple analgesics should be evaluated for preeclampsia.

MIGRAINES Migraines may be triggered by hormonal fluctuations associated with menstruation, puberty and menopause. The stable hormonal environment in pregnancy may be the reason that many migraine sufferers experience an improvement in symptoms during pregnancy. Simple analgesics and avoiding known dietary and lifestyle



INTRACRANIAL HAEMORRHAGE Subarachnoid haemorrhage and intracerebral haemorrhage have clinical features similar to those seen in nonpregnant populations. The causative aneurysm or vascular malformation can be managed by surgical clipping or embolisation. Women with a known vascular malformation should undergo treatment prior to attempting pregnancy; these women can undergo normal labour and delivery. If women with untreated vascular malformations are considering vaginal delivery, regional anaesthetic and instrumental delivery to minimise pushing in the second stage is recommended.

CEREBRAL VENOUS THROMBOSIS Cerebral venous thrombosis (CVT) is most common in the postpartum period. Risk factors include dehydration, infection and hypercoagulable states. CVT usually presents with a diffuse severe headache, followed by vomiting, seizures, confusion, focal neurological deficits and impaired conscious state. Management involves anticoagulation, initially with intravenous heparin or 193

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subcutaneous low molecular weight heparin, followed by warfarin for at least 6 months.

supports during pregnancy and following delivery of the baby.

NEUROIMAGING IN PREGNANCY

MYOTONIC DYSTROPHY

Neuroimaging may involve CT scan or MRI. CT scanning is useful for diagnosing intracranial bleeding, trauma and cerebral oedema, while MRI may provide further information on vascular malformations, tumours, small infarcts, cerebral vein thrombosis and inflammatory processes. MRI has the advantage of not using ionising radiation. The MRI contrast agent gadolinium crosses the placenta and is generally withheld during pregnancy.

SPINAL CORD INJURY Fertility is usually preserved in women with spinal cord injury. Important considerations in pregnancy include managing anaemia and avoiding upper tract urinary sepsis. The need for thromboprophylaxis should be individualised, weighing the increased in venous thromboembolism risk in pregnancy against the increased risk of preterm—and possibly silent—labour. Women with lesions between T5 and T10 may have painless labours and delivery. Serial cervical examinations or fetal fibronectin testing may be used to assist with detecting silent uterine activity, and hospitalisation may be necessary close to term. A serious complication among women with lesions above T6 is autonomic dysreflexia (ADR). ADR is caused by sympathetic hyperactivity below the level of the spinal lesion in response to stimuli such as distended bowel or bladder, urinary infection or labour. Uncontrolled sympathetic discharge results in severe hypertension, headache and cardiac arrhythmia. ADR may be complicated by intracranial haemorrhage or myocardial infarction in the mother, and uteroplacental vasoconstriction can result in acute fetal compromise. Management involves removing the noxious stimulus, sitting the patient upright to lower blood pressure and aggressive antihypertensive treatment.

Myotonic dystrophy (MD) does not generally worsen in pregnancy and is not associated an increased rate of pregnancy complications. Its importance lies in that the inheritance is autosomal dominant. The phenotype of MD can be extremely variable, and congenital myotonic dystrophy, associated with polyhydramnios, neonatal hypotonia, feeding and breathing difficulties, can occur in infants of mothers with relatively mild symptoms. Prenatal diagnosis is possible, although predicting prognosis may be difficult. Genetic counselling is recommended for families where either parent is known to have myotonic dystrophy.

MYASTHENIA GRAVIS Myasthenia gravis is an immune-mediated disorder with antibodies directed against the acetylcholine receptor on the neuromuscular endplate of skeletal muscle. Maternal myasthenia may run a variable course in pregnancy. It is important that women with myasthenia gravis receive specialised care, since transplacental passage of the ACh receptor antibodies may cause congenital myasthenia, a potentially life-threatening condition in the newborn.

PERIPHERAL NEUROPATHIES CARPAL TUNNEL SYNDROME Carpal tunnel syndrome is characterised by numbness and tingling in the distribution of the median nerve as a result of median nerve compression as it travels in the carpal tunnel, exacerbated by the weight gain and fluid retention of pregnancy. Wrist splints may provide symptomatic relief. Steroid injections or surgical release is not usually necessary as most resolve spontaneously over the weeks to months following delivery.

CEREBRAL PALSY

BELL’S PALSY

Cerebral palsy (CP) describes a group of non-progressive motor disorders characteristically appearing in infancy or early childhood. The degree of postural and motor dysfunction will vary according to the CP subtype, but intelligence is often normal. Along with motor disability, common comorbidities with CP include epilepsy, hypertension and bladder dysfunction. Management of women with CP in pregnancy will need to address potential problems with: 1. increased seizures and muscle spasticity, particularly bladder dysfunction; 2. attention to skin care; 3. surveillance for urinary sepsis; 4. managing the relevant comorbidities of hypertension and epilepsy; and 5. addressing any additional mobility aids and social

Bell’s palsy is also more common in pregnancy. Corticosteroids, as prescribed in non-pregnant patients, can be given in pregnancy.

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FURTHER READING Algra AM, Klijn CJ, Helmerhorst FM, et al. Female risk factors for subarachnoid hemorrhage: a systematic review. Neurology 2012;79(12):1230–6. Coyle PK. Pregnancy and multiple sclerosis. Neurol Clin 2012;30(3):877–88. Lu E, Wang BW, Guimond C, et al. Disease-modifying drugs for multiple sclerosis in pregnancy: a systematic review. Neurology 2012;79(11):1130–5.

Chapter 24  Neurological Disease

MacGregor EA. Headache in pregnancy. Neurol Clin 2012;30(3):835–66. Pearce CF, Hansen WF. Headache and neurological disease in pregnancy. Clin Obstet Gynecol 2012;55(3):810–28. Scott CA, Bewley S, Rudd A, et al. Incidence, risk factors, management, and outcomes of stroke in pregnancy. Obstet Gynecol 2012;120(2 Pt 1): 318–24.

Semere LG, McElrath TF, Klein AM. Neuroimaging in pregnancy: A review of clinical indications and obstetric outcomes. J Matern Fetal Neonatal Med 2013;26(14):1371–9. Walker S, Permezel M, Berkovic S. The management of epilepsy in pregnancy. BJOG 2009;116:758–67. Wlodarczyk BJ, Palacios AM, George TM, et al. Antiepileptic drugs and pregnancy outcomes. Am J Med Genet 2012;Part A 158A:2071–90.

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Chapter 25  MENTAL HEALTH DISORDERS DURING THE PERINATAL PERIOD Megan Galbally and Martien Snellen

KEY POINTS Identifying and treating mental illness is an integral component of quality maternal care and essential for the delivery of best outcomes for mother and baby. Assessment of mental illness in pregnancy is important to ensure better outcomes for mothers and babies. However, the form that psychosocial assessment ideally takes is open to debate. Use of psychopharmacological treatments for mental illness in pregnancy and lactation must weigh the risks and benefits for both mother and child. Postpartum blues affect at least 50% of women, most commonly approximately 3 to 5 days postpartum. Postnatal depression affects approximately 10% of women and requires consideration of pharmacological therapy if of moderate severity. Puerperal psychosis is a rare condition (0.1% of pregnancies) but a psychiatric emergency.

INTRODUCTION Mental illness has been one of the leading indirect causes of maternal mortality in Australia1 and, in particular, postnatal depression is one of the most common complications of childbirth, with prevalence rates of between 10 to 20%.2,3 Yet a study of obstetric-gynaecology outpatients in the United States found that while 20% met the criteria for mental illness, only 23% of these women had been recognised within the service,4 and a more recent study in Australia of midwives, GPs and maternal and child health nurses (MCHNs) found all practitioners were more likely to identify depression during the postpartum rather than in pregnancy.5 It is now accepted that identifying and treating women with mental illness is an integral component of quality maternity care, whether this is best through universal or targeted screening or through other forms of psychosocial assessment is still unclear. This arises out of the recognition that untreated mental illness during pregnancy impacts not just women but also their developing babies. Mental illness has been associated with an

increased risk of pregnancy complications such as prematurity, low birth weight and preeclampsia.6,7 Untreated mental illness in pregnancy and the postpartum has also been associated with poorer long-term developmental outcomes for children.8 Therefore, early detection and effective management are crucial to ensuring best outcomes for mothers and their children.

EMOTIONAL WELLBEING IN PREGNANCY The birth of a child represents a major life event that demands psychological, emotional, practical and relational adjustment. Early work in the area suggested that this transition should be considered to be a crisis moment for the family unit due to the dramatic need for change and reorganisation. However, more recent conceptualisations of the entry into parenthood offer the view that this transition is associated with the experience of stress as well as the satisfactions and rewards of parenting. Frequently, there are discrepancies between women’s and

Chapter 25  Mental Health Disorders during the Perinatal Period

men’s expectations about how parenting would affect their lives and how they would fare in their parenting role, and their actual experiences. Adjustment has been found to be more difficult when parenting expectations exceeded experiences in the following domains: relationship with spouse, physical wellbeing, maternal competence and maternal satisfaction. The recent focus has been on how the transition into parenthood affects the marital relationship and it has revealed a tendency towards a decline in marital satisfaction. Common areas of dispute and dissatisfaction relate to differing expectations regarding household duties, childcare, finances and sex. An Australian study of first-time fathers found that pregnancy was a time of greater emotional stress for men than the postnatal period and this was associated with changes in the marital relationship.9 Most studies find that sexual interest and frequency of sexual activity remain below prepregnancy levels for up to a year after delivery.10 The majority of couples have resumed sexual intercourse by the time their baby is 3 months old, and it isn’t uncommon for a couple to delay resumption until the 6-week check-up where reassurances are required and permission sought. While most couples successfully negotiate the transition into parenthood, many continue to struggle. During the postnatal period, simple questions that enquire into a woman’s experience of her transition into parenthood can easily identify those who are struggling and allow the activation of pathways to appropriate care.

IDENTIFICATION AND ASSESSMENT OF MENTAL ILLNESS IN PREGNANCY Whether or not to screen for antenatal and postnatal depression has been the subject of an international debate.11,12 The apprehensions regarding screening have focused on the choice of measures, with concerns that the most commonly used tool, the Edinburgh Postnatal Depression Scale (EPDS) (Box 25.1), has been reported to display a wide-ranging sensitivity and specificity.12 There has also been concerns about whether this results in a reduction in morbidity, the cost-effectiveness, whether women will take up treatment following screening and whether as a result of the high falsepositive rate we potentially risk overpathologising women.13 While many maternity services and maternal child health centres in Australia have taken up routine antenatal and postnatal screening with the EPDS, other services internationally have not, with the 2014 NICE guidelines in the United Kingdom recommending the EPDS be considered only for targeted use, not universal use, and as part of a full assessment.14 In addition, a recent Cochrane review that focused on the role of antenatal psychosocial screening found that screening did not lead to a reduction of maternal morbidity and better outcomes.15

BOX 25.1  The ten questions of the Edinburgh Postnatal Depression Scale. 1. I have been able to laugh and see the funny side of things. 2. I have looked forward with enjoyment to things. 3. I have blamed myself unnecessarily when things went wrong. 4. I have been anxious or worried for no good reason. 5. I have felt scared or panicky for no very good reason. 6. Things have been getting on top of me. 7. I have been so unhappy that I have had difficulty sleeping. 8. I have felt sad or miserable. 9. I have been so unhappy that I have been crying. 10. The thought of harming myself has occurred to me. Source: Cox JL, Holden JM, Sagovsky R. Detection of postnatal depression: development of the 10-item Edinburgh Postnatal Depression Scale. Br J Psychiatry 1987;150:782–6. Wisner KL, Parry BL, Piontek CM. Postpartum Depression. N Engl J Med 2002 July 18;347(3):194–9.

Regardless of depression screening, it is important for maternity services to recognise that this is not the only mental illness that needs to be considered as part of good obstetric care. Schizophrenia and bipolar disorder, for instance, also carry risks in pregnancy from the illnesses themselves, as well as the medications used to treat them.16 Therefore, clinical assessment of past and present symptoms of mental illness, as an addition to screening measures in antenatal care, is critical for the identification of women who may be at risk of perinatal mental illness. While the focus of the debate around screening and psychosocial assessment in pregnancy and the postpartum revolves around maternal mental health, an ideal assessment should be broader and contain three key elements: 1. a focus on a woman’s emotional wellbeing; 2. her relationship and bonding with her fetus/baby; and 3. a wider focus on her relationship with her partner or key supports. This can be done simply through enquiry at relevant points during pregnancy and potentially integrated within routine antenatal care appointments.

SPECIFIC DISORDERS OF THE PERINATAL PERIOD MATERNITY BLUES The maternity blues are thought to occur in at least 50% of women. The disorder generally coincides with days 3 197

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to 5, which is often the time of onset of lactation, and is regarded as a self-limiting condition which remits within days with reassurance alone. It is characterised by lowered mood, anxiety, tearfulness, indecisiveness and insomnia. However, it is important that clinicians distinguish this from emerging depression or anxiety disorders.

showed a reduction in relapse in women with a past history of puerperal psychosis by commencing lithium at delivery.21

ANTENATAL AND   POSTNATAL DEPRESSION

Despite schizophrenia and bipolar disorder being lowprevalence mental illnesses (1% and 2.5% respectively), they have the potential to be high-impact disorders within the perinatal setting. Both the illnesses themselves and their pharmacological treatment significantly elevate the risk of poor outcomes for both mother and child. Unplanned and unwanted pregnancies are common and relapse rates of both disorders are significantly elevated when pharmacological treatment is suspended (i.e. 37% for patients with bipolar disorder who continue mood stabiliser medication versus 85% for those who cease treatment).22 Poor nutrition, lack of social supports, decreased attendance for antenatal obstetric review, substance abuse and single motherhood frequently complicate the scenario further. It is becoming increasingly clear that these disorders elevate obstetric and neonatal risks with significantly higher rates of low birth weight, intrauterine growth retardation, preterm delivery, gestational diabetes, preeclampsia, instrumental delivery, lower Apgar scores, stillbirth, infant malformation, need for neonatal resuscitation, admission to the neonatal intensive care unit and infant death. Active psychotic symptoms, in particular, have been found to increase these risks. In addition, the medications used to treat these illnesses (anti­ psychotics and mood stabilisers) may be associated with complications such as teratogenicity, pregnancy complications, neonatal complications and concerns about effects on longer-term adverse neurodevelopmental. Pregnancy-related changes in pharmacokinetics may also decrease medication serum levels to the point of being subtherapeutic. A range of other mental illnesses such as borderline personality disorder, eating disorders and anxiety disorders have also been associated with particular risks across pregnancy and the early postpartum.

Depression across the perinatal period affects approximately 10% of women.2,3 The risk factors that have been identified include depression/anxiety during pregnancy, stressful life events during pregnancy, low level of social support and past history of depression. Depressive illness can be difficult to distinguish from a normal increase in emotional lability often associated with pregnancy and the postpartum. Key distinguishing symptoms include: anhedonia (loss of enjoyment and pleasure); depressive cognitions that involve a sense of worthlessness, inadequacy and hopelessness; and suicidal ideation. Common symptoms of depression such as insomnia, lethargy and appetite disturbance are less pathognomonic of depression in pregnancy, as pregnancy itself can also affect these functions. Untreated maternal depression has been associated with a range of pregnancy complications and poorer child developmental outcomes. These include gestational hypertension, preeclampsia, prematurity, low fetal growth and poorer child development.7,8 There is some evidence that ceasing antidepressant treatment during pregnancy in women who are stable increases their risk of relapse,17 although this remains controversial.18 While specific studies of efficacy for depression treatments in pregnancy are limited, the general research findings recommend that for mild depression, psychological and pharmacological treatment are equally efficacious. However, moderate to severe depression often requires consideration of pharmacotherapy. The difference in pregnancy is that careful consideration needs to be given to the risks and benefits for both mother and child should she be either treated or untreated.

PUERPERAL PSYCHOSIS Puerperal psychosis occurs in approximately 0.1% of women, and most who develop this condition do so within the first 4 weeks following delivery.19 The condition is regarded as a psychiatric emergency as it usually develops rapidly with psychotic symptoms, disorganised behaviour and cognitive impairment, and is associated with infanticide and suicide.20 Both lithium carbonate and electroconvulsive therapy (ECT) have been demonstrated to be effective treatments.20 Women with a history of puerperal psychosis have a high risk of relapse after subsequent deliveries.20 However, Bergink et al. 198

SCHIZOPHRENIA AND   BIPOLAR DISORDER

MANAGEMENT OF MENTAL ILLNESS IN PREGNANCY Management of mental illness, regardless of diagnosis, is typically conceptualised as having a biopsychosocial approach. In pregnancy and the postpartum, it is also important to consider the fetus/infant and the wider family unit as an essential part of effectively managing mental illness across this period. Comorbidities such as smoking, alcohol and substance abuse, and commonly occurring risk factors such as inadequate nutrition and obesity, should always be addressed and systems established that encourage attendance at antenatal

Chapter 25  Mental Health Disorders during the Perinatal Period

appointments. Co-existing domestic violence can be present and must be addressed. Perinatal mental healthcare plans developed in pregnancy for management across delivery and the early postpartum are effective tools for multidisciplinary communication. The important components are contained in Box 25.2.

PHARMACOLOGY Pharmacological treatments of mental illness include antidepressants, antipsychotics (typical and atypical), mood stabilisers (anticonvulsants and lithium carbonate), anxiolytics and hypnotics. Although coverage of the pharmacological treatment of mental illness and the evidence of risks in pregnancy is beyond the scope of this chapter, it is important for all clinicians to understand the principles of weighing benefits and risks in pregnancy and to ensure that where medication is prescribed, there is adequate monitoring and care and that informed consent is sought.23 The aim should always be to seek the minimal effective dose; however, the emphasis should be on effective rather than minimal, and polypharmacy avoided wherever possible. Pharmacological treatment in pregnancy involves balancing both the risks associated with untreated mental illness for both mother and unborn child against the relatively unknown effects that pharmacological treatment of mental illness may pose for the child. In particular, there is a paucity of long-term developmental studies that examine for effects beyond pregnancy from exposure to psychopharmacological treatments. For many medications, any comfort we may have prescribing them in pregnancy and breastfeeding comes from the relative

BOX 25.2  Perinatal mental health plan. Patient name, expected date of delivery, treatment team, consideration of setting of delivery depending on risks Pharmacological and other treatments; monitoring and dosage requirements/changes Recommendations for lactation (related to risks with any pharmacological treatments and/or extra supports if appropriate), supports and rest in the early postpartum Length of stay; will be determined by clinical need, in particular related to observation and risks for the neonate and ensuring adequate support and monitoring of mental state for the mother Discharge planning that includes partner and family or other key supports in postpartum care; consideration of supports for early parenting skills and identification of pathways to care should relapse occur

absence of negative data rather than the presence of positive data. However, for many women pharmacological treatment is essential for them to maintain mental health. For depression, this was recognised with joint guidelines for the treatment of depression in pregnancy developed and published by the American College of Obstetricians and Gynaecologists in collaboration with the American Psychiatric Association. Likewise, women with schizophrenia and bipolar disorder often cannot cease or alter their treatments as the risks of relapse are high with serious health implications. The medications used to treat these conditions (antipsychotics and mood stabilisers) do have implications for antenatal monitoring and care.16 A summary is contained in Table 25.1. Again, it needs to be remembered that pregnancyrelated physiological and pharmacokinetic changes frequently decrease the effectiveness of medications, particularly in the third trimester, and dose adjustments may need to be made.

PSYCHOLOGICAL THERAPIES Psychological therapies have been found to be equally as effective as medications for mild depression and for anxiety disorders. Both the United Kingdom’s NICE guidelines and the Australian beyondblue/NHMRC guidelines support a range of psychological treatments for depression and anxiety. A recent Cochrane review also found preliminary evidence to support specific psychological interventions for the prevention of postnatal depression. A cautionary note is their role in prevention of the deleterious effects of maternal depression on child development with a Cochrane review failing to find any beneficial effect for child outcomes.24 There are a wide range of psychological models for addressing the parent–infant relationship25 and new research into better understanding the underlying mechanisms.26 Interestingly, a review of psychological interventions for women with schizophrenia that focused on the mother– infant relationship identified that no specific models of care have been published. Regardless of this, pharmacological treatment of mental illness should always be accompanied by psychotherapy, whether it is supportive, psycho-educational, focused on cognitive behaviour or psychodynamic, in order to both maintain mental health and negotiate the patient’s transition into motherhood.

ELECTROCONVULSIVE THERAPY Where women present with severe or life-threatening depressive illness, where other treatments have failed and where the mother may pose a risk to herself and her unborn infant, consideration may be given to treatment with electroconvulsive therapy (ECT) during pregnancy. The risks that have been associated with such treatment in pregnancy include fetal bradycardia, fetal distress, placental abruption, onset of premature labour, maternal 199

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TABLE 25.1  PREGNANCY MONITORING FOR ANTIPSYCHOTICS AND MOOD STABILISERS (AEDS AND LITHIUM CARBONATE). Stage

Antipsychotic

Lithium carbonate

AEDs

First trimester

FBE; U&E; TFT; LFT; B12/ folate; vitamin D; iron studies; Ca; fasting glucose and lipids; BMI; BP; ECG high-resolution ultrasound; early GTT

FBE; U&E; TFT; LFT; B12/folate; vitamin D; iron studies; lithium levels every 4 weeks; highresolution ultrasound and Doppler flow studies

FBE; U&E; TFT; LFT; B12/folate; vitamin D; iron studies; drug level; high-resolution ultrasound for NT assessment (if inadequate maternal/ amniotic fluid); alpha-fetoprotein

Second trimester

Weight; BP; high-resolution ultrasound

Lithium level every 4 weeks; U&E; TFT; growth monitoring; morphological scan and fetal echo

Drug level; FBE; LFT; highresolution ultrasound; growth monitoring

Third trimester

Weight; BP; high-resolution ultrasound

Lithium level weekly; U&E; TFT

Drug level; FBE; LFT

After delivery

Observe baby for withdrawal, toxicity, sedation; postpartum GTT if indicated

Maternal lithium level; U&E; TFT; cord blood: lithium; TFT; U&E

Drug level; observe baby for adverse effects and careful morphological examination

Abbreviations: AEDs = antiepileptics; BP = blood pressure; Ca = calcium; ECG = electrocardiography; FBE = full blood examination; GTT = glucose tolerance test; LFT = liver function test; NT = nuchal translucency; TFT = thyroid function tests; U&E = urea and electrolytes. Source: Adapted from Galbally M, Snellen M, Walker S, Permezel M. Management of antipsychotic and mood stabilizer medication in pregnancy: recommendations for antenatal care. Aust N Z J Psychiatry 2010 Feb;44(2):99–108.

status epilepticus and maternal aspiration if she is not intubated. To ensure safety, consultation with experts in anaesthesia of pregnancy, perinatal psychiatrists and recommendations and monitoring by obstetrics is recommended before proceeding. REFERENCES 1) Austin MP, Kildea S, Sullivan E. Maternal mortality and psychiatric morbidity in the perinatal period: challenges and opportunities for prevention in the Australian setting. Med J Aust 2007;186(7):364–7. 2) Buist AE, Austin MP, Hayes BA, et al. Postnatal mental health of women giving birth in Australia 2002–2004: findings from the beyondblue National Postnatal Depression Program. Aust N Z J Psychiatry 2008;42(1):66–73. 3) Bennett HA, Einarson A, Taddio A, et al. Prevalence of depression during pregnancy: systematic review. Obstet Gynecol 2004;103(4):698–709. 4) Spitzer RL, Williams JBW, Kroenke K, et al. Validity and utility of the PRIME-MD patient health questionnaire in assessment of 3000 obstetric-gynecologic patients: the PRIME-MD Patient Health Questionnaire ObstetricsGynecology Study. Am J Obstet Gynecol 2000;183(3):759–69. 5) Buist A, Bilszta J, Milgrom J, et al. Health professional’s knowledge and awareness of 200

6)

7)

8) 9)

10) 11)

12)

perinatal depression: results of a national survey. Women Birth 2006;19(1):11–16. Jablensky AV, Morgan V, Zubrick SR, et al. Pregnancy, delivery, and neonatal complications in a population cohort of women with schizophrenia and major affective disorders. Am J Psychiatry 2005;162(1):79–91. Kurki T, Hiilesmaa V, Raitasalo R, et al. Depression and anxiety in early pregnancy and risk of pre-eclampsia. Obstet Gynecol 2000; 95:487–90. Deave T, Heron J, Evans J, et al. The impact of maternal depression in pregnancy on early child development. BJOG 2008;115:1043–51. Condon JT, Boyce P, Corkindale CJ. The First Time Fathers Study: a prospective study of the mental health and wellbeing of men during the transition to parenthood. Aust N Z J Psychiatry 2004;38(1):56–64. Snellen M. Rekindling: your relationship after childbirth. Melbourne: Text Publishing; 2010. Buist AE, Barnett BE, Milgrom J, et al. To screen or not to screen—that is the question in perinatal depression. Med J Aust 2002;177(Suppl.): S101–5. Gibson J, McKenzie-McHarg K, et al. A systematic review of studies validating the Edinburgh Postnatal Depression Scale in antepartum and postpartum women. Acta Psychiatr Scand 2009;119(5):350–64.

Chapter 25  Mental Health Disorders during the Perinatal Period

13) Matthey S. Are we overpathologising motherhood? J Affect Disord 2010;120(1–3):263–6. 14) NICE. Identifying and assessing mental health problems in pregnancy and the postnatal period. Manchester, UK: National Institute for health and Care Excellence; 2014. 15) Austin MP, Priest SR, Sullivan EA. Antenatal psychosocial assessment for reducing perinatal mental health morbidity. Cochrane Database Syst Rev 2008;(4):CD005124. 16) Galbally M, Snellen M, Walker S, et al. Management of antipsychotic and mood stabilizer medication in pregnancy: recommendations for antenatal care. Aust N Z J Psychiatry 2010;44(2):99–108. 17) Cohen LS, Altshuler LL, Harlow BL, et al. Relapse of major depression during pregnancy in women who maintain or discontinue antidepressant treatment. JAMA 2006;295(5):499–507. 18) Yonkers KA, Gotman N, Smith MV, et al. Does antidepressant use attenuate the risk of a major depressive episode in pregnancy? Epidemiology 2011;22(6):848–54. 19) Kendell R, Chalmers J, Platz C. Epidemiology of puerperal psychoses. Br J Psychiatry 1987;150(5):662–73. 20) Sit D, Rothschild AJ, Wisner KL. A review of postpartum psychosis. J Womens Health 2006;15(4):352–68.

21) Bergink V, Bouvy PF, Vervoort JS, et al. Prevention of postpartum psychosis and mania in women at high risk. Am J Psychiatry 2012;169(6):609–15. 22) Viguera AC, Whitfield T, Baldessarini RJ, et al. Risk of recurrence in women with bipolar disorder during pregnancy: prospective study of mood stabilizer discontinuation. Am J Psychiatry 2007;164(12):1817–24, quiz 923. 23) Galbally M, Snellen M, Lewis AJ. A review of the use of psychotropic medication in pregnancy. Curr Opin Obstet Gynecol 2011;23(6):408–14. 24) Dennis CL, Dowswell T. Psychosocial and psychological interventions for preventing postpartum depression. Cochrane Database Syst Rev 2013;2. 25) Galbally M, Lewis AJ, Ijzendoorn M, et al. The role of oxytocin in mother-infant relations: a systematic review of human studies. Harv Rev Psychiatry 2010;19(1):1–14. 26) Anderson EL, Reti IM. ECT in pregnancy: a review of the literature from 1941 to 2007. Psychosom Med 2009;71(2):235–42. FURTHER READING Galbally M, Snellen M, Lewis A. Psychopharmacology and pregnancy: treatment efficacy, risks and guidelines. Heidelberg, Germany: Springer; 2014.

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Section 2.6 COMMON CLINICAL SCENARIOS AND PRESENTING PROBLEMS IN PREGNANCY Chapter 26

Common problems in pregnancy

Chapter 26  COMMON PROBLEMS IN PREGNANCY Michael Permezel and Megan Di Quinzio

KEY POINTS Pregnancy is associated with substantive physiological changes, consequent on the physical presence of the pregnancy itself but also the consequential haemodynamic changes and the large amounts of hormones emanating from the placenta. While all these changes have important roles in facilitating a healthy pregnancy, they can also have undesirable consequences for maternal comfort and sometimes serious sequelae for the mother and/or developing fetus. Whether minor or serious, it is imperative that all care providers are attentive to maternal symptomatology, are able to distinguish the normal from the abnormal, take pains to alleviate symptoms where possible and provide ongoing maternal support where difficulties persist. Oesophageal reflux is particularly common and responds to antacids, H2-antagonists or proton pump inhibitors for the more severe cases. Constipation should be avoided with appropriate dietary advice but mild laxatives can and should be used if needed. Abdominal pains of varying sorts are extremely common in pregnancy but usually ‘fleeting’ if not of clinical consequence. More substantive abdominal pain requires clinical evaluation to exclude potentially serious causes that might impact adversely on pregnancy.

OESOPHAGEAL REFLUX (HEARTBURN) PATHOPHYSIOLOGY This is a very common symptom of pregnancy and arises from relaxation of the gastro-oesophageal sphincter under the influence of progesterone and is further exacerbated in late pregnancy with pressure of the gravid uterus on the stomach. Vomiting in pregnancy will aggravate the condition but is sometimes also a consequence of severe reflux.

MANAGEMENT The following measures can help minimise heartburn. 1. Meals should be light and avoid those foods found to be most likely to provoke heartburn. 2. The bed should be raised at the head some 15 to 20 cm, and an extra pillow used if this is compatible with a good sleep. Even though the reflux may be more symptomatic during the day, less reflux at night may help daytime symptomatology. 3. Drug therapy involves antacid preparations (e.g. aluminium hydroxide/magnesium hydroxide, Mylanta),

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which can be taken liberally according to the manufacturer’s recommendations. The H2-antagonist, ranitidine, can also be used in pregnancy. There is less experience with proton pump inhibitors in early pregnancy but they are commonly prescribed in late pregnancy for refractory cases not responding to other medication.

CONSTIPATION PATHOPHYSIOLOGY Constipation is a common feature of pregnancy and presumably relates to the relaxant effect of progesterone on the gastrointestinal smooth muscle. It may be aggravated by dehydration with excessive vomiting in early pregnancy, iron supplementation and any relative immobility.

CLINICAL CONSEQUENCES Constipation commonly causes general abdominal discomfort and is rarely severe. Excessive straining may aggravate haemorrhoids and is intuitively unwise if there is any reason to suspect cervical insufficiency.

MANAGEMENT Constipation should be alleviated with the following strategies. 1. Increase of dietary fibre (bran, green vegetables, dried fruit) should be the focus of therapy. The woman troubled with constipation should become familiar with the fibre content of specific foods and also what is effective for her. 2. Fluid and exercise may assist. 3. Laxatives are indicated if diet, fluid and exercise are insufficient. Suitable agents would include bulkproducing compounds (Fybogel, Metamucil, Normacol), magnesium hydroxide (milk of magnesia) and lactulose (e.g. Duphalac). Stimulant laxatives such as senna (Senokot) are also safe in pregnancy and may be appropriate.

ABDOMINAL PAIN IN PREGNANCY DIFFERENTIAL DIAGNOSIS There are conditions specific to pregnancy in addition to those that are possible in any woman. It is best to think of the differential diagnosis in terms of the likely organ involved and then secondarily what might cause pain at that location. A framework for this is as follows. Uterine. Round ligament pain, miscarriage or labour, red degeneration of a fibromyoma, placental abruption, chorioamnionitis.



204

• • • • • • •

Urinary tract. Urinary tract infection, urinary calculus. Ovary. Complication of an ovarian cyst (THIN-RIM: torsion, haemorrhage, infection, necrosis, rupture, incarceration, malignancy). Tube. Ectopic pregnancy. Hepatobiliary. Preeclampsia, cholecystitis, cholelithiasis. Peritoneum. Endometriosis, haemoperitoneum from any cause (uterine rupture, splenic artery aneurysm rupture, hepatic rupture). Gastrointestinal. Gastroenteritis, appendicitis, Crohn’s disease, bowel obstruction. Pancreatic. Pancreatitis.

ROUND LIGAMENT PAIN Clinical features Pregnant women often report lower abdominal pain and tenderness in the second trimester, at approximately 15 to 20 weeks’ gestation. The pain is usually lateral to the uterus, in the groin and overlying the round ligament, which can be palpated as a tender cord. The pain is usually unilateral and is more often left-sided, perhaps associated with dextrorotation of the uterus bringing the left ligament into apposition with the peritoneum of the left anterior abdominal wall. The pain is often initiated or accentuated by sudden movement (standing up, bending, coughing, sneezing).

Treatment Treatment is to rest in a position of comfort and take analgesia with paracetamol. Occasionally the pain necessitates absence from work. Usually the condition abates completely within 2 to 3 weeks, although hypertrophy and stretching of the ligaments continue.

RED DEGENERATION OF A UTERINE FIBROMYOMA Clinical features This is usually an acute presentation with severe localised abdominal pain that can be readily confused with appendicitis or a placental abruption. Known presence of a fibromyoma is extremely helpful in making the diagnosis, as is point tenderness over an area of the uterus in the context of an obviously healthy fetus.

Treatment After exclusion of more sinister causes, treatment is conservative with simple analgesia. Resolution of pain occurs over a few days.

UTERINE CONTRACTIONS OF LATE PREGNANCY Differential diagnosis Braxton Hicks contractions are contractions in late pregnancy that do not culminate in labour. They are most

Chapter 26  Common Problems in Pregnancy

commonly completely asymptomatic but the woman may recognise a palpable tightness of the uterus that may be associated with mild discomfort. Sometimes Braxton Hicks contractions are more significant and the woman needs to briefly stop what she was doing. When that discomfort is more severe but still does not result in labour, the contractions may be termed threatened preterm labour when before 37 weeks’ and spurious labour when they occur at term.

Management Braxton Hicks contractions require only an explanation and a reminder of the signs of labour. Threatened preterm labour and spurious labour are, by definition, retrospective diagnoses and will not generally be distinguishable from genuine labour until they are observed over time and labour is found not to eventuate. Recurrent spurious labour at term is a risk factor for adverse perinatal outcome and should be managed with increased fetal surveillance and consideration given to induction of labour.

UPPER RESPIRATORY TRACT INFECTION

FIGURE 26.1

Varicose veins of the leg in pregnancy. Source: Courtesy of Prof. Norman Beischer.

This is as common in pregnancy as at other times but may be more severe and of longer duration in view of the general immunosuppression of pregnancy. For example, bronchitis is probably more common, which may have implications for women who suffer from bronchial asthma (see Ch 17).

EPISTAXIS This is often related to oestrogen-induced engorgement of the profuse network of veins lining the nasal passages. Usual measures, such as pressure and ice packs, will be sufficient. Only very rarely is cautery of specific vessels is needed.

VARICOSE VEINS PATHOPHYSIOLOGY The prime cause of varicose veins in pregnancy is probably a relaxant effect of progesterone on vascular smooth muscle, added to by increased pressure within the venous system as a consequence of the arteriovenous shunting effect of the placenta and direct pressure of the uterus on the pelvic veins. Incompetence of the valves in the upper leg occurs, causing further aggravation. Although there is a strong hereditary tendency, each pregnancy makes the condition worse. Some 10 to 20% of women suffer varicose veins of the legs, with higher figures occurring in multiparas and those over 30 years (Fig 26.1). Varicosities of the vulva occur in about 2% of pregnancies and are also more common with increasing parity (Fig 26.2).

FIGURE 26.2

Severe varicose veins of the vulva.

Source: Reproduced with permission from the Royal Women’s Hospital, Parkville Victoria.

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CLINICAL CONSEQUENCES

HAEMORRHOIDS

The main complaint is of aching, tiredness or pain in the legs, night cramps and fullness/oedema. The fullness related to vulval varicosities may create alarm in the patient but a strong postural dependence (only apparent on standing) makes diagnosis relatively easy and the woman can be reassured that complete resolution is extremely likely in the puerperium. Thrombophlebitis (thrombosis) occurs in 5% of women with varicose veins, usually in the puerperium. Haemorrhage will occur if the vein is damaged and bleeding can be profuse but, being of low pressure, is readily controlled by direct pressure. If a varix in the leg is bleeding, the woman must lie down, elevate the leg and have pressure applied to the bleeding site. Significant bleeding may eventuate during delivery if an episiotomy incision or tear involves vulval or vaginal varicose veins.

PATHOPHYSIOLOGY

MANAGEMENT Antenatal

If prolapse has occurred, replacement is carried out with the aid of a rectal lubricant. If prolapse is immediately recurrent, repeated replacement is obviously unhelpful. Bleeding from haemorrhoids is common during pregnancy and the puerperium. It is important that a rectal

Reassurance is the hallmark of management of varicose veins in pregnancy. The veins will improve after pregnancy but this can take several months and not usually right back to the pre-pregnancy state. The following strategies may minimise worsening of lower limb varicose veins in pregnancy. 1. Weight-bearing exercise should be minimised. An understanding of the incompetence of the perforating veins will make it obvious that exercise will aggravate the condition. Similarly, long periods of standing will aggravate the condition. Swimming will not have the same effect as the lower limb venous pressure will be less and therefore becomes the preferred mode of exercise for these women. 2. Support stockings may be helpful but a tight roll occluding veins at the top of the stocking should be avoided. 3. Surgical management is virtually never needed in relation to pregnancy.

This term describes varicose enlargement of the veins of the anal canal (inferior haemorrhoidal plexus). The aetiology and behaviour during pregnancy are the same as described above. The main aggravating factors are constipation (see above) and prolonged pushing down during the second stage of labour.

CLINICAL CONSEQUENCES Bleeding may occur as well as thrombosis. The former is usually associated with the passage of a hard motion, and is rarely severe. Haemorrhoids are often particularly painful in the postnatal period but usually rapidly resolve during the puerperium (Fig 26.3).

MANAGEMENT

Intrapartum Care should be taken at the time of delivery to minimise laceration to varicosities. In extreme cases, a midline episiotomy may be considered, recognising the atten­ dant risk of sphincter damage. Any haemorrhage from damaged vulval varices should be controlled by simple pressure until medical assistance is obtained.

Puerperium Superficial thrombophlebitis is both common and painful. A low-molecular-weight heparin may speed resolution, as may anti-inflammatory drugs. 206

FIGURE 26.3

Haemorrhoids. Oedematous painful haemorrhoids in association with a sutured episiotomy that has probably been sutured too tight, leading to oedema of the suture line. Source: Reproduced with permission from the Royal Women’s Hospital, Parkville Victoria.

Chapter 26  Common Problems in Pregnancy

examination is performed when the woman reports bleeding and if bleeding persists after pregnancy, further investigation with sigmoidoscopy is indicated to exclude other bowel pathology.

BREAST SORENESS

MANAGEMENT Oedema usually subsides after resting at night and is aggravated by prolonged standing. The condition is managed largely by increasing the rest periods, with the legs well elevated; diuretics are contraindicated.

PATHOPHYSIOLOGY

COMPRESSION NEUROPATHIES

As a result of the stimulatory effects of oestrogen and progesterone on the breast parenchyma, as well as a general increase in vascularity, the woman often experiences fullness, discomfort and tenderness in the breasts.

PATHOPHYSIOLOGY

MANAGEMENT The main aspects of management are reassurance regarding the cause of the symptoms and their temporary nature. Symptomatic relief is obtained by adequate breast support and local warmth.

OEDEMA PATHOPHYSIOLOGY This is a very common finding, especially in hot weather. It is due to the increased venous pressure consequent on both the arteriovenous shunt through the placenta and extrinsic compression of the great veins by the uterus. It is more common in preeclampsia but in that condition the oedema is usually generalised, involving fingers and face as well as the lower limbs (Fig 26.4).

The most troublesome of these is the carpal tunnel syndrome, so called because the median nerve (which supplies the ‘thumb half’ of the hand) passes through the bony-aponeurotic tunnel at the wrist and becomes compressed if there is swelling, which often occurs in pregnancy. A similar phenomenon can occur with the lateral cutaneous nerve of the thigh and is known as meralgia paraesthetica.

CLINICAL FEATURES The usual symptoms are numbness, tingling and a burning sensation.

MANAGEMENT With median nerve compression, rest of the wrist during the day will alleviate nocturnal numbness, tingling and pain. Splinting of the wrist is often helpful in ensuring the wrist is rested. Only very rarely is surgery needed during pregnancy to relieve the pressure by incising the fibrous roof of the tunnel.

HEADACHE PATHOPHYSIOLOGY This is a common complaint, and must be attributed to intracranial vascular changes related to oestrogen and progesterone.

CLINICAL FEATURES Headache tends to be most troublesome in the second trimester but in some women persists throughout pregnancy.

MANAGEMENT FIGURE 26.4

Gross pitting oedema in a 34-year-old para 7 at 38 weeks’ gestation. She had iron deficiency anaemia with haemoglobin of 7.8 g/dL.

Analgesics can be used as needed—most commonly paracetamol but with codeine or even morphine if necessary. Metoclopramide 10 mg is useful if there is associated nausea and vomiting. Investigation is required if the attacks are frequent, severe or persistent or are associated with localising neurological symptoms or signs. 207

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FAINTING PATHOPHYSIOLOGY Progesterone-induced vasodilatation of pregnancy, with or without varicose veins, leads to venous pooling in the lower limbs with reduced venous return and consequent risk of a hypotensive syncope. In late pregnancy, syncope can be induced by pressure on the inferior vena cava by the gravid uterus, the supine hypotensive syndrome.

CLINICAL FEATURES The effect is compounded by heat (vasodilatation) and standing (failure of muscles to pump venous blood back to the heart). Although a relationship between fainting and fetal sequelae is not established, anaphylaxis and other examples demonstrate that the fetus is exquisitely sensitive to sustained maternal hypotension.

MANAGEMENT Although syncope is not unusual in pregnancy, strategies are needed to reduce the occurrence and promptly minimise the duration of hypotension should a faint occur. 1. Avoidance of predisposing factors. It is important that the woman recognises potential predisposing factors (e.g. standing in a queue at the checkout in a supermarket) and takes steps to avoid these situations (e.g. dad does the shopping). 2. First aid treatment consists of lying down, preferably with the legs elevated. Such action should be initiated at the first sign of giddiness. 3. Supine hypotension is avoided by advising women and their carers of the inadvisability of lying supine (on the back) for any length of time during the third trimester. Much fuss is made in the common press regarding the ‘dangers’ of sleeping supine in pregnancy. While this could be true, it would appear more likely that sleep apnoea poses the greater risk and the woman that develops supine hypotension during sleep is most likely to experience discomfort and instinctively move to a more suitable position.

FATIGUE PATHOPHYSIOLOGY Fatigue during pregnancy is exceedingly common, particularly in the first and third trimesters, with a window of greater energy between. The mechanism is unclear but there is good evidence that excessive exertion results in lower birth weights and occupational physical labour is associated with a higher incidence of preterm birth.

MANAGEMENT Although the precise evidence is lacking, the overwhelming view is that fatigue is an evolved mechanism to 208

reduce activity in the interests of the pregnancy. Resting would therefore seem to be the appropriate response.

SACROILIAC PAIN PATHOPHYSIOLOGY The hormones of pregnancy soften the three key joints of the pelvis (two sacroiliac and the symphysis pubis) in order to enable some ‘give’ in these joints during parturition. Therefore, it is not surprising that a majority of pregnant women complain of a backache or sense of strain in the lower back, most commonly to one side or the other. During weight-bearing exercise, the entire upper body is supported through this joint that is normally ‘fixed’ but has been ‘loosened’ by the hormones of pregnancy.

CLINICAL FEATURES Sacroiliac joint strain can be confirmed by elicitation of tenderness over the posterior aspect of the joint. Often this is maximal around mid-pregnancy, implying a hormonal basis as much as a mechanical one.

MANAGEMENT Assessment is indicated, as in rare cases the back pain is related to a vertebral apophyseal joint or an intervertebral disc. 1. Rest is the most important form of treatment, particularly avoiding activities that aggravate the condition. Very often the pain is worse at night, following increased activity during the day. Every patient with the condition must be made aware of the mechanism and the obvious imperative of avoiding weightbearing exercise. Swimming is good to enable exercise that does not strain the joint. 2. Analgesia in the form of paracetamol can be used if necessary but as the condition is likely to be long standing during pregnancy, management by avoidance of causative factors is key. 3. Maternity belts or corsets are commonly advocated by physiotherapists and may benefit some women. 4. While massage, manipulation or exercises sometimes provide short-term relief, they are unlikely to be helpful in the longer term.

MUSCLE CRAMPS PATHOPHYSIOLOGY Muscle cramps, particularly in the calf muscles, are very common in pregnancy, affecting approximately 33% of women; they are severe in 5% of women. The exact cause is not known, but must be related either to a temporary shunt of blood away from the muscle (ischaemic cramp) or to a change in the pH or electrolyte milieu (tetanic cramp).

Chapter 26  Common Problems in Pregnancy

CLINICAL FEATURES Cramps usually occur late in pregnancy and are worse at night. The attacks are often precipitated by ‘stretching’ in the early morning.

MANAGEMENT Placing a pillow at the foot of the bed to remind the woman not to ‘stretch’ the legs (i.e. plantar flex the ankle joints). Many find that magnesium or vitamin B complex supplementation is helpful.

SKIN CONDITIONS IN PREGNANCY These may be related to a specific condition, such as drugs, jaundice, malignant disease, infestations or bites. Often, no cause can be found and the condition must be assumed to be related to other metabolic products, skin stretching or altered neurovascular sensitivity. Three conditions specific to pregnancy should be remembered.

ISOLATED ABDOMINAL PRURITUS This is common in the second half of pregnancy and is not associated with a rash. It may or may not be associated with abdominal striae (stretch marks).

3. Delivery is indicated at 37 to 38 weeks’ but earlier if there is deteriorating hepatic function. Delivery is indicated even if biochemistry has normalised on ursodeoxycholic acid.

PRURITIC URTICARIAL PAPULES AND PLAQUES OF PREGNANCY Pathogenesis The pathogenesis of pruritic urticarial papules and plaques of pregnancy (PUPPP) is poorly understood. Preponderance in first pregnancies is suggestive of an immune aetiology.

Clinical features PUPPP is the most common rash in pregnant women. It normally occurs in first pregnancies during the third trimester, with an average onset of 35 weeks’. The rash commonly begins on the abdomen but spreads to breasts, thighs and arms (Fig 26.5). Just as the name suggests, it is very itchy, red and raised and is rarely vesicular. Unlike cholestasis, there is no risk to the mother or baby and the condition resolves in the early puerperium.

Management

This is an effect of the pregnancy steroid hormones on the liver. Raised circulating bile salts cause generalised pruritus.

PUPPP can be extremely itchy and a caring approach is needed, with more frequent antenatal visits to provide general patient support. 1. Symptomatic relief is all that is required for milder cases: lukewarm shower and dab dry, and oral antihistamines. 2. Corticosteroids can also be used: betamethasone cream for moderate severity, oral prednisolone for the more severe cases.

Diagnosis

HERPES GESTATIONIS

The serum levels of the hepatocellular enzymes (e.g. AST, ALT) are commonly elevated along with the bile salts.

This extremely rare but serious condition occurs mainly in the second and third trimesters. Crops of papillae become bullous, initially on the trunk and spreading to the limbs (Fig 26.6). Treatment is by oral steroids.

CHOLESTASIS OF PREGNANCY Pathophysiology

Clinical features The pruritus is generalised but often worst on the palms and soles. Jaundice is rare. Most importantly, there is an increased risk of still birth—the mechanism of which is uncertain but is more likely be through placental insufficiency than a direct effect on the fetal heart.

Management The following need to be considered with cholestasis in pregnancy. 1. Ursodeoxycholic acid alleviates symptoms and restores biochemistry. However, the risk of stillbirth may remain increased. 2. Fetal surveillance should be intensified through increased maternal vigilance with respect to fetal movements, ultrasound and cardiotocography (e.g. weekly).

PRURITUS VULVAE DIFFERENTIAL DIAGNOSIS Pruritus vulvae in pregnancy may be due to: infections, particularly Candida, which are increased in pregnancy chemical irritation (e.g. soaps, detergents) dermatological conditions such as lichen sclerosus, lichen planus.

• • •

MANAGEMENT Assessment through clinical examination is essential as well as the vulval swab for culture if the diagnosis is 209

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A

B

C

D

FIGURE 26.5

Pruritic urticarial papules and plaques of pregnancy (PUPPP). A Typical periumbilical sparing and distribution of the lesions along the abdominal striae. B Early PUPPP shows urticarial lesions in the abdominal striae. C Lesions with microvesiculated appearance on the forearm in PUPPP. D Widespread PUPPP may resemble a toxic erythema.

Source: James D, Steer PJ, Weiner CP, Gonik B. High Risk Pregnancy. 4th ed. Philadelphia: Saunders, 2011. Copyright © 2011 Saunders, An Imprint of Elsevier. Figure 51.16A–D. Photographs courtesy of Helen Raynham, MD.

uncertain. Treatment will depend on aetiology but all women should be given advice to avoid chemical irritation from soaps, inappropriate creams and, most importantly, perspiration.

VAGINAL DISCHARGE DIFFERENTIAL DIAGNOSIS Increased vaginal discharge is a common condition in pregnancy and the following should be considered in the differential diagnosis. 1. Leucorrhoea is a normal increase in the vaginal discharge as a consequence of the impact of oestrogen on the lower genital tract. It is commonly white 210

(hence the name) and non-offensive. There is no specific treatment other than maternal reassurance. 2. Infections may produce vaginal discharge of which Candida is most likely. 3. Premature rupture of the membranes is an important differential diagnosis. 4. Discharge of the cervical mucus plug or ‘show’ is common in late pregnancy. It may be only mucoid or blood-stained.

ASSESSMENT A careful history and clinical examination (including speculum examination) is essential. Sometimes it will become apparent that it is not a vaginal discharge at all but an

Chapter 26  Common Problems in Pregnancy

of the enlarging uterus. Typically, it is most apparent in early pregnancy when the uterus has a pelvic location, and again in late pregnancy when the head enters the pelvis and presses on the bladder. Nocturia may also be due to nocturnal return of increased tissue fluid (oedema) to the vascular system. This will improve with measures that reduce lower limb oedema in pregnancy, mainly avoiding prolonged standing.

ASSESSMENT All women should have a urine microscopy and culture requested at the first antenatal visit to exclude asymptomatic bacteriuria. If urinary frequency is troublesome, particularly if combined with other features suggestive of infection (e.g. dysuria, scalding, more than a trace of protein on dipstick), the urine culture should be repeated.

INSOMNIA IN PREGNANCY FIGURE 26.6

Herpes gestationis. Rash at 32 weeks’. Commenced on soles of feet at 26 weeks’. Spread generally with vesicles on legs and feet. Responded to oral then topical steroids and delivered at term. Source: Courtesy of Monash Health.

episode of urinary stress incontinence, which is extremely common in late pregnancy. History features that would suggest membrane rupture are discussed elsewhere but include a profuse watery discharge that is ongoing and may be associated with predisposing factors in the pregnancy. Sterile speculum examination reveals a ‘washed-out appearance’. A vaginal swab for microscopy and culture should be taken from all women with a vaginal discharge but if there is doubt about rupture of the membranes, specific biochemical tests can be performed on the discharge, including placental alpha microglobulin-1 (e.g. AmniSure). Tests relying on the higher pH (more alkaline) of amniotic fluid are less reliable as serum extravasate from an extra-amniotic blood clot and semen will also both be alkaline.

URINARY FREQUENCY AND NOCTURIA DIFFERENTIAL DIAGNOSIS Urinary tract infections are more common in pregnancy and it is important to exclude them; however, urinary frequency is a common symptom of pregnancy even in the absence of an infection. It probably is simply a consequence of reduced bladder capacity through pressure

DIFFERENTIAL DIAGNOSIS Pathophysiology Disturbances to the sleep rhythm may be a direct hormonal effect on sleep rhythm. Other contributing factors will be nocturia (see above) and the sheer physical size of the uterus later in pregnancy (Fig 26.7). Sleeping in the afternoon as a consequence of general fatigue may lead to insomnia at night, which in turn creates greater need for the afternoon nap. Backache, nocturia, nocturnal cramps and heartburn are all common and may aggravate the sleep disturbance. Less commonly, insomnia may be a presentation of depression in pregnancy (see Ch 25).

Clinical features Physiological insomnia is particularly apparent in the third trimester and very common.

Management Women are often distressed by insomnia in late pregnancy. It is important that the clinician takes the matter seriously and works with the woman to manage the problem as follows. 1. Reassurance regarding the normality of the condition is often all that is required. 2. Avoidance of the afternoon nap can certainly aid sleeping at night and break a cycle of daytime sleep and nocturnal wakefulness. 3. Symptomatic alleviation of heartburn, nocturnal cramps and so on as discussed elsewhere may also assist. 4. Experiment with dietary changes (e.g. avoiding a late meal) or an exercise regimen (e.g. an evening walk) may assist some women. 5. Sleeping tablets are generally used only as a last resort as other measures are preferred and are mostly 211

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reasonably effective. Doxylamine is safe in pregnancy. Temazepam is sometimes used sparingly in late pregnancy for refractory insomnia not responding to other measures.

FIGURE 26.7

Triplets at 35 weeks’ gestation in a 25-year-old para 2. The midline scar was from a previous ovarian cystectomy. She delivered 4 days later of babies weighing 2601 g, 2195 g and 2140 g. The placenta tissue weighed 1340 g.

212

FURTHER READING Centers for Disease Control and Prevention. Prevention of perinatal Group B streptococcal disease. Revised Guidelines from CDC; 2010. International Association of Diabetes and Pregnancy Study Groups. Recommendations on the diagnosis and classification of hyperglycaemia in pregnancy. Diabetes Care 2010;33(3):676–82. Katzberg HD, Khan AH, So YT. Assessment: symptomatic treatment for muscle cramps (an evidence-based review): report of the Therapeutics and Technology Assessment Subcommittee of the American Academy of Neurology. Neurology 2010;74(8):691–6.

Section 2.7 LABOUR AND BIRTH Section 2.7.1 Normal labour and birth Chapter 27

The physiology of parturition

Chapter 28

Management of normal labour

Section 2.7.2 Induction of labour, instrumental delivery and casearean section Chapter 29

Induction of labour, including cervical ripening

Chapter 30

Episiotomy and vaginal outlet tears

Chapter 31

Instrumental delivery

Chapter 32

Caesarean section and trial of labour after caesarean

Section 2.7.3 Intrapartum clinical problems Chapter 33

Intrapartum fetal compromise

Chapter 34

Failure to progress in labour

Chapter 35

Malpresentation and malposition

Chapter 36

Postpartum haemorrhage

Chapter 37

Maternal collapse

Chapter 38

Obstetric analgesia and anaesthesia

Section 2.7.4 The puerperium and lactation Chapter 39

The physiology of the puerperium and lactation

Chapter 40

Normal postpartum care

Chapter 41

Puerperal disorders

Chapter 42

Maternal and perinatal mortality and morbidity and global reproductive health

Chapter 43

Australian Indigenous women’s health in pregnancy

Section 2.7.1 NORMAL LABOUR AND BIRTH

Chapter 27  THE PHYSIOLOGY OF PARTURITION Michael Permezel and Megan Di Quinzio

KEY POINTS Labour (or parturition) is defined as the process in which the fetus, placenta and secundines are expelled from the birth canal after a minimum period of 20 weeks. Before this, the term ‘miscarriage’ or ‘abortion’ is applied. From early in the third trimester, the uterus progressively delineates into a thick upper segment and a thin lower segment. By the time labour commences, there has been a general softening of the connective tissues of the pelvis: joint ligaments, cervix and other pelvic connective tissue. The increase in elasticity facilitates dilatation of the cervix and the passage of the baby through the birth canal. The onset of labour is the consequence of dominance of factors promoting uterine activity over contrasting factors promoting uterine quiescence. Having reached this threshold, a series of positive feedbacks further expand factors promoting activity and suppress those causing quiescence. Labour is described in three stages. The first stage comprises the slower latent phase when the cervix is effacing and beginning to dilate, and the more rapid active phase up until full cervical dilatation. The second stage concludes with birth of the fetus and the third stage with delivery of the placenta and membranes.

ANATOMICAL AND PHYSIOLOGICAL CHANGES IN LATE PREGNANCY STRUCTURAL CHANGES OF THE UTERUS At the end of pregnancy the uterus fills most of the abdominal cavity. Its length has increased from around 7.5 cm to 40 cm and its weight from around 60 g to 900 g. There is usually some rotation of the uterus to the right side, so that at caesarean section the left round liga­ ment is seen more readily than the right. There is general thickening of the ligaments supporting the uterus and the blood vessels are greatly enlarged, especially the veins (Fig 27.1).

The upper and lower uterine segments In early pregnancy, the uterus has two distinct compo­ nents: the uterine body and the cervix. As indicated in Chapter 1, the uterine body is predominantly muscular but the cervix is only 20% muscle and 80% connective tissue. From approximately 26 to 28 weeks’ gestation, there is progressive development of a lower uterine segment (LUS) by stretching of the uterine tissues between the histological and anatomical internal os of the cervix. Like the cervix, the LUS has a fibromuscular composition and is easily recognised as it is covered by loose peritoneum. In contrast, the upper uterine segment (UUS) is thicker, muscular and covered by a serosal layer that is firmly adherent to the underlying muscularis (Fig 27.2). At term, before labour has commenced, the LUS will commonly measure around 6 cm in length. In normal

Chapter 27  The Physiology of Parturition

labour, there is progressive stretching of the LUS making it both broader and thinner. The junction of the LUS and UUS is commonly around the level of the symphysis pubis prior to labour but rises during labour as the LUS is stretched. In obstructed labour, the junction of UUS and LUS may be as high as the umbilicus as the LUS becomes very broad and thin and may even rupture if the obstruction is not alleviated. This is more common in an obstructed multiparous labour than a nulliparous labour. In obstructed labour, the thin LUS may ‘balloon’ outwards, sometimes making the junction of UUS and LUS visible on abdominal examination—a ‘retraction ring’ (see Chapter 34).

The cervix FIGURE 27.1 

Distended ovarian and uterine veins lateral to the left round ligament. This is a common finding at caesarean section. This woman was undergoing repeat elective caesarean section. Source: Courtesy of Prof. Norman Beischer.

The cervix is approximately at the level of the ischial spines and begins to shorten and dilate prior to labour. The cervical canal shortens from above down, until only the external os remains as a thin rim (Fig 27.3). This sequence is classically seen in the nullipara; in the multipara, effacement and dilatation may occur simultaneously.

INITIATION OF LABOUR Factors favouring uterine activity and uterine quiescence Rather than there being a single cause for the onset of labour, labour ensues when the factors favouring uterine activity overcome those factors favouring uterine quiescence. The factors are listed in Table 27.1. Most important would appear to be rises in corticotrophin releasing factor and oestrogen efficacy (through changes in the oestriol:oestradiol ratio) and a reduction in pro­ gesterone efficacy (through changes in the progesterone receptors).

Positive feedback loops

FIGURE 27.2 

The retractor in the midline subumbilical incision exposes the juntion of the upper and lower uterine segments. The loose peritoneum over the lower uterine segments abuts the firmly adherent serosa over the upper segment. Source: Courtesy of Prof. Norman Beischer.

Once the balance favours onset of labour, positive feed­ back loops rapidly amplify the factors promoting labour. Positive feedback is a powerful means to rapidly convert quiescence to labour so that, once it starts, it usually con­ tinues ‘full steam ahead’. Two examples of positive feed­ back at a biochemical level are given in Figures 27.4 and 27.5. At a mechanical level, Ferguson’s reflex is also positive feedback. Distension of the cervix and upper vagina cause increased release of oxytocin, which in turn triggers more contractions and more cervical and vaginal distension.

Biochemical changes in the myometrium, cervix and membranes prior to and in early labour The above mechanisms then act through the key organs responsible for successful parturition: the myometrium, 217

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A

B

C

D

FIGURE 27.3 

Changes in the cervix during the first stage of labour. A Cervix at term—no dilatation or effacement. B Cervical effacement (‘taking up’ to become part of the lower uterine segment) has commenced. C The endocervical canal has disappeared as effacement of the cervix is complete. The external os is 2 to 3 cm dilated. D The cervix is almost fully dilated and the intact bag of forewaters bulges into the vagina.

TABLE 27.1  ONSET OF LABOUR VERSUS UTERINE QUIESCENCE. Factor

Favouring onset of labour

Favouring uterine quiescence

Stress

Biological stress through bacterial colonisation

Antibacterial defences: vaginal pH, cervical mucus

Physical stress through mechanical stretch

Hormones

Oxidative stress

Antioxidants: thioredoxin, superoxide dismutase

Oestrogen

Progesterone

Corticotrophin-releasing factor (CRF) Cytokines

Pro-inflammatory cytokines: IL-1β, IL-6, IL-8, TNFα, MCP-1

Anti-inflammatory cytokines: IL-10

Transcription factors

Pro-inflammatory transcription factors: NFκB, MAPK, FOX-01

Anti-inflammatory transcription factors: SIRTs, PPARs

Prostaglandins

PGE2, PGF2α

PGHs

Proteases

Matrix metalloproteinases (MMPs)

Tissue inhibitors of MMPs (TIMPs)

218

Chapter 27  The Physiology of Parturition

Progesterone Placental CRH Oestrogen

Fetal and maternal pituitary ACTH

Fetal and maternal adrenal cortisol

FIGURE 27.4 

Placental corticotrophin-releasing hormone (CRH), adrenal cortisol and pituitary ACTH: a positive feedback loop.

in late pregnancy and early labour in parallel with the changes in the uterine muscle and the cervix. Through a process of apoptosis (programmed cell death) and release of connective tissue degradation enzymes (matrix metal­ loproteinases [MMPs]), the membranes progressively weaken. Interestingly, the process occurs almost exclu­ sively in the supracervical membranes and hardly at all at the sites distant from the cervix. The membranes may rupture prior to the onset of labour, during the first stage or in the second stage. Where an extreme preterm baby may be born with membranes still intact (‘born in a caul’), this is extremely uncommon at term due to the changes that occur in the supracervical membranes in late preg­ nancy and labour. Occasionally, the outer chorion may rupture before the amnion, creating a significant fluid leak (transudation across the amnion) suggestive of rup­ tured membranes but still clinically with membranes intact, as evidenced by bulging forewaters or a further ‘gush’ when the amnion ruptures.

The vagina, perineum and ligaments

NFKB, MAPK

SIRT

Pro-inflammatory cytokines TNF, IL-1, IL-6, IL-8

FIGURE 27.5 

Pro-inflammatory and anti-inflammatory transcription factors and cytokines interacting, producing positive feedback.

the cervix, the fetal membranes and the connective tissue of the birth canal.

The uterine muscle The uterine muscle exhibits an increase in oxytocin receptors and an increase in gap junctions (with an increase in collectively connexon proteins), which enhance the transmission of the contraction impulse through the myometrium.

The cervix Dissolution of collagen and elastin fibres and an increase in interstitial fluid produces a softening of the cervical substance so that it more readily shortens and dilates, progressively losing its ability to function as a mechanical sphincter retaining the fetus in utero.

The amniotic and chorionic membranes The fused amniotic and chorionic membranes line the cavity of the uterus and are attached to the endometrium except over the cervix. Changes occur in the membranes

The vagina and perineum share with the uterus a general increase in vascularity and markedly increased elasticity to allow passage of the fetus, mostly with only a minor degree of distension injury. The ligaments of the pelvic joints also soften to allow some increase in pelvic capacity.

Labour onset The strength and frequency of contractions are usually greater during the night and the peak incidence of labour onset is soon after midnight; nocturnal labours are usually shorter than day labours. The criteria used for the onset of true labour are: 1. rhythmic, regular contractions that show a progressive increase in amplitude and frequency, and are discomforting to the woman (unlike Braxton Hicks contractions); and 2. a ‘show’ of blood and mucus, which indicates that the cervical canal is opening (Figs 27.6 and 27.7). These features will usually distin­ guish true labour from false (spurious) labour.

Uterine contraction strength, duration and frequency The uterus has a baseline tone of approximately 5 mmHg. During the active phase of labour, uterine contractions will result in an increase in pressure of 25 to 60 mmHg. Contraction frequency in active labour is commonly 3 to 5 in 10 minutes and contraction duration of 40 to 60 seconds. The contractions exhibit ‘fundal dominance’ which causes a peristaltic wave forcing the contents of the uterus downwards. The contractions begin in pacemakers which are situated in the region of one or other uterine horn (near the attachment of the tubes).

The pain of uterine contractions Pain is not usually perceived until the contraction pres­ sure reaches approximately 25 mmHg. While some pain 219

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FIGURE 27.6 

At the onset of labour, dilatation of the cervix begins and the plug of mucus (operculum) which occluded the endocervical canal is shed (Fig 27.7). The show of blood at this time is due to the membranes being stripped off the uterine wall.

FIGURE 27.7 

An unusually long, thick, intact cervical mucus plug passed by a 26-year-old primigravida immediately before the head came on view. It is uncommon for an intact mucus plug to be passed in this way. Source: Courtesy of Prof. Norman Beischer.

undoubtedly arises from the uterine contraction itself, much of the pain of the first stage of labour arises from the forceful dilatation of the cervix. Clinical estimates of the duration of contractions are usually shorter than the real duration, since the beginning and end of the contrac­ tion are below the pain threshold.

How do uterine contractions produce cervical dilatation and presenting part descent? The uterus causes the cervix to dilate basically because the muscle of the UUS pulls the LUS and cervix up over the presenting part, stretching the LUS and cervix and forcing the presenting part downward (Fig 27.8). For this to occur, it is necessary for the uterus to be fixed in 220

A

B

FIGURE 27.8 

Changes in the uterus during the first stage of labour. The arrows mark the site of Bandl’s physiological ring between the upper and lower uterine segments. In obstructed labour, this ring rises and becomes visible as a pathological retraction ring. A At the onset of labour, there is neither taking up nor dilatation of the cervix. B On completion of the first stage, the vagina, cervix and lower uterine segment form a continuous surface; the cervix no longer acts as a ledge preventing descent of the presenting part.

position in relation to the pelvis. If the uterus was floating free within the abdominal cavity, the uterus would rise up as the muscle fibres shorten rather than the presenting part go down. Fixation of the uterus within the abdominal cavity is provided by the supports which are attached in the region of the cervix: the transverse cervical ligaments laterally, the uterosacral ligaments posteriorly and the pubocervi­ cal ligaments anteriorly. It is with these ligaments to pull against that the uterus can push the baby through the soft tissues (pelvic and perineal floors) and hard structures (bony pelvis) that constitute the birth canal. Descent occurs in an oscillatory fashion, as anyone familiar with the terminal phases of labour has observed. With each contraction the baby descends, but because of the resistance of the birth canal structures, it loses some of this ground during the relaxation phase. However, with each contraction some descent is maintained, however small, and this gain is secured by retraction of the uterine muscle. With retraction of the UUS myome­ trium, the muscle does not relax to its original length, but stays at a new shorter length.

THE STAGES OF LABOUR Three stages of labour are traditionally described: first, from the onset of regular contractions to full dilatation of the cervix; second, from full dilatation to delivery of the baby; and third, from birth of the baby until delivery of the placenta.

Chapter 27  The Physiology of Parturition

THE FIRST STAGE OF LABOUR

Duration of the first stage of labour

The latent phase The latent phase is usually defined as being from the onset of labour until both contractions are established and the cervix is 3 cm dilated and effaced. The latent phase varies greatly in duration, more so in the nullipara than a multipara. It may be almost non-existent when contractions quickly establish in the presence of a cervix that has ripened (anterior, soft, dilated and effaced with a low presenting part) in late pregnancy. In contrast, the latent phase may last many hours or days when labour begins with irregular contractions or episodes of spurious labour and an unripe cervix (posterior, firm, long and closed with a high presenting part).

The active phase Once active contractions occur and the cervix is 3 cm dilated and effaced, labour characteristically proceeds quickly until full dilatation (Fig 27.9). The 90th percentile for rate of dilatation is at least 0.9 cm/hr in the nullipa­ rous woman and 1.2 cm/hr in the multipara. This rapid progress can be attributed to some of the positive feed­ back mechanisms referred to earlier where the estab­ lished labour enhances both the release and responsiveness to prostaglandins and oxytocin. Prior to rupture of the membranes, there is a ten­ dency for the force of uterine contractions to be dispersed equally on all points of the uterine cavity. Following rupture of the membranes, the presenting part is directed forcefully against the cervix.

The major problem in determining an average duration of the first stage of labour is defining the point of labour onset in those women in whom the latent phase is very prolonged and merges with the latter stage of pregnancy. A median first stage duration is much easier to deter­ mine. Approximate values are 8 hours in a nullipara and 4 hours in a multipara.

THE SECOND STAGE OF LABOUR The mechanism of a normal birth Figure 27.10 diagrammatically illustrates the progress of the head through the birth canal through successive steps of descent, internal rotation, extension and external rota­ tion (restitution).

Descent Descent of the fetal head into the pelvis has already occurred in most nulliparas in the later weeks of preg­ nancy. In parous women, significant descent usually occurs only after labour commences. Descent occurs because of the contractions of the uterus, which push the fetus down and at the same time stretch and draw up the muscle fibres of the lower uterine segment. Descent is continuous throughout labour unless an insuperable obstruction is present. After the membranes rupture, the uterus acts more directly on the fetus (fetal axis pressure), driving the head down more efficiently through the lower birth canal.

Cervical dilatation (cm)

10

8

Active phase of labour

6

4

2 Latent phase of labour

2

4

6

8 Hours

10

12

14

16

FIGURE 27.9 

The latent phase of labour, where a slow rate of cervical dilatation is followed by an active phase from about 3 cm of cervical dilatation with more rapid cervical dilatation. 221

FIGURE 27.10 

A

A

B

B

C

C

D

D

E

E

F

F

G

G

H

H

The mechanism of delivery from the left occipitolateral position. This is an explanation of the steps or movements the fetus undergoes to negotiate the birth canal. Each step is illustrated by paired diagrams of the pelvis viewed laterally and of the head as palpated from below during vaginal examination. A The head enters the pelvic brim with the posterior parietal bone presenting. Both fontanelles are shown at the same station, as would be the case if flexion was incomplete. B Lateral flexion of the head on the neck enables the head to descend and engagement has occurred. The head is now synclitic. C Further lateral flexion allows descent of the head past the pubic symphysis. Internal (anterior) rotation of the occiput by 90° is required. D The occiput has rotated 45° towards the front. The shoulders have rotated with the head, which is not always the case. The sagittal suture lies in the right oblique diameter of the pelvis. E Internal (anterior) rotation of the occiput is complete. Further descent has occurred with the head now distending the lower vagina and stretching the muscles of the pelvic floor (Fig 27.11). The sagittal suture lies in the anteroposterior diameter of the outlet. The head now begins to extend. F Birth of the head is due to extension, with the pubic symphysis acting as fulcrum. Restitution of 45° will now occur. G Restitution of the head is due to the twist on the neck (due to internal rotation) being undone. Had the shoulders not rotated 45° with the head (see D above) restitution would have been through 90°; 45° external rotation will now occur. H External rotation of the head is due to internal (anterior) rotation of the shoulders. This movement does not occur if the internal rotation of the head is unaccompanied by the movement of the trunk, as the shoulders are already in the anteroposterior diameter of the pelvis. Traction on the head directed posteriorly releases the anterior shoulder from beneath the pubic symphysis. 222

Chapter 27  The Physiology of Parturition

External urinary meatus

Vagina Ischiocavernosus

Levator ani

Bulbocavernosus

Central point of perineum

Superficial transverse perineal muscle Anal sphincter

FIGURE 27.11 

During delivery, the muscles of the pelvic diaphragm are pushed downwards and the aperture between the origins of the levatores ani muscles (from the back of the pubic bones) is greatly increased. The perineum bulges downwards and the tissues between vagina and anus are stretched to approximately double their previous length.

Engagement is defined as the station at which the maximum diameter of the presenting part has passed through the pelvic inlet. Although the maximum diame­ ter of the presenting part has not yet passed through the ischial spines (the narrowest part), engagement is of great importance as it suggests that a vaginal birth is highly likely (although not certain). Flexion of the head will be maintained and even increased during head descent as pressure on the vertex will lead a flexion rotation around the atlanto-occipital joint. With full flexion and a vertex presentation, the most favourable diameter presents (suboccipitobregmatic).

Internal rotation This means rotation of the head inside the pelvis prior to birth, most often to occipitoanterior from a previously occipitotransverse or even occipitoposterior position (Fig 27.12). Internal rotation is probably effected by the angulation of the pelvic floor through the shape of the levator ani muscles. It is also aided by the fact that the more angular shape of the anterior pelvis is a better fit for the angular occiput and the posterior pelvis is more suited to the flatter forehead (sinciput).

Extension The head remains flexed until the leading part reaches the perineum. As the head is crowned it follows the natural forward inclination of the birth canal and extends, the lower border of the symphysis pubis acting as a fulcrum (Fig 27.13). It follows that the occiput will appear initially, and as the process of extension continues, the vertex, forehead and finally the face will appear from beneath the posterior part of the vulval ring.

External rotation (restitution) The phase of external rotation of the head is also called restitution. It is simply the undoing or reversal of the

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FIGURE 27.12 

Restitution and external rotation from the left occipitoanterior position. A The head is born by extension and restitutes 45° to undo the twist on the neck. B The head externally rotates a further 45° in the same direction as restitution, due to internal violation of the shoulders through 45°. External rotation, although named for the head, is due to the shoulders and if prevented by the accoucheur, can result in impacted shoulders. C The face is directed laterally and the shoulders now lie in the anteroposterior diameter of the pelvic outlet.

head twisting which had taken place as described under internal rotation. The head will almost always birth occip­ itoanterior but the shoulders will pass through the pelvis in the anterior-posterior plane. That means, the head, once free on the perineum, will rotate to either left or right occipitotransverse, depending on which side the back is on. Restitution should happen spontaneously and does not need to be effected by the accoucheur.

Trunk delivery Because of the curve of the birth canal, the anterior shoul­ der appears first, and with further downward fetal axis pressure exerted by the uterus, the posterior shoulder follows the forward sweep of the canal and appears at the 223

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120 mmHg with the addition of 60 mmHg from mater­ nal effort.

Fetal compromise in the second stage of labour

FIGURE 27.13 

The position of the fontanelles and sagittal suture before birth of the head by extension of the neck. The posterior fontanelle is readily palpable anteriorly, but because the head is well flexed, the anterior fontanelle is situated out of easy reach in the hollow of the sacrum at a higher station. The bones and ligaments of the pelvic outlet are shown. Source: Courtesy of Prof. Norman Beischer.

fourchette. The remainder of the trunk is born by the process of lateral flexion or sideways bending of the spine. The initial movement, freeing the anterior shoul­ der, is usually assisted by downward and backward pres­ sure on the head by the accoucheur (Fig 27.10H). This means that the full bisacromial diameter (12.5 cm) does not transverse the vulval ring, the shorter acromio­ humeral diameter (10 cm) presenting. This is important in reducing the incidence of posterior vulval tears.

Secondary powers and the bearing-down reflex When the cervix is fully dilated, the second stage of labour is entered. The contractions are usually stronger, but may occur less frequently. With the cervix no longer offering resistance, the head has less resistance and descends more readily than in the first stage. A strong bearing-down reflex coincides when the presenting part is low enough to exert pressure on the rectum. This bearing down sensation can of course sometimes occur prior to full cervical dilatation. If bearing down occurs in this circumstance, it risks a cervical tear and may lengthen the ligaments supporting the cervix as it is pushed infe­ riorly by the added forces of maternal effort. The woman is therefore encouraged not to bear down until the cervix is fully dilated; if in doubt, full dilatation can be verified by vaginal examination. Bearing down uses both the diaphragm and abdomi­ nal wall muscles (‘secondary powers’). Peak intrauterine pressures of 60 mmHg may be further increased to 224

It is not uncommon for fetal compromise to develop in the second stage of labour. A reduction in uteroplacental blood flow with the increased intrauterine pressures may be compounded by compression of the umbilical cord as the presenting part descends through the pelvis. This makes the second stage of labour the most dangerous hour of almost every person’s life. Few will undertake activities during their lifetime associated with greater mortality and long-term consequences. During each uterine contraction, the high intra­ uterine pressures reduce uteroplacental blood flow. With the secondary powers also operative, the higher pressures lead to even greater reductions in uteroplacental blood flow and more fetal compromise than would oth­ erwise occur. The umbilical cord encircles the neck in around 25% of labours. Cord prolapse occurs in about 0.5% and true knots in around 1% of labours. Other cases have the cord trapped between the lower segment and the presenting part. In each case, there will be cord compression with each contraction that may become cord occlusion when the presenting part descends. The second stage is usually short (especially in a multipara) and the fetus is adapted to be able to tolerate short periods of reduced oxygenation. Fortuitously, in those cases where the second stage is not short, rapid instrumental delivery can usually be effected as soon as any fetal compromise is detected.

Duration of the second stage of labour The median duration of the second stage ranges from around 40 minutes in the nullipara to around 20 minutes in the multipara. Factors influencing the duration include the strength and coordination of uterine contractions, the strength of the mother’s secondary powers (ability to push), the resistance of the lower birth canal (high in the nullipara because it has not been distended previously) and the size, presentation and position of the presenting part. Epidural analgesia may prolong the second stage by removing the sensation to bear down.

Damage to the tissues of the pelvic floor During the second stage, the neuromuscular tissues, fascia and ligaments of the pelvic floor will inevitably undergo a combination of traction injury (particularly ligaments and muscles) and compression injury (particu­ larly nerves). Together, these injuries may leave a legacy of prolapse and varying degrees of urinary and faecal incontinence. The likelihood of long-term compression (nerve) injury will increase with the duration of the second stage and sustained compression. In contrast, traction injury will largely be a consequence of a

Chapter 27  The Physiology of Parturition

relatively large fetus and aggravated by a rapid forceful delivery as may occur either spontaneously or with instrumental birth.

THE THIRD STAGE OF LABOUR The third stage of labour is the period from the birth of the baby to the delivery of the placenta and membranes. Separation of the placenta usually occurs quickly after the birth of the baby because the marked reduction in size of the uterus produces a shearing force between the maintained surface area of the placenta and the reduced surface area of the uterine wall to which it is attached. Descent of the placenta then occurs, first into the lower segment and then into the vagina. The maternal circulation provides around 750 mL/ min to the placental bed. Following placental separation, in the absence of any haemostatic mechanism, there is the possibility of haemorrhage at this rate into the uterine cavity. As the maternal blood volume is only around 7 L, the woman would rapidly exsanguinate. It is therefore small wonder that in resource-poor settings maternal mortality approaches 1% of all births, and postpartum haemorrhage is paramount in causing this terrible statistic. Therefore, haemostasis is truly vital and effected in two ways: 1. compression of the uteroplacental blood

vessels by the retracted uterine muscle fibres; and 2. through normal vascular haemostasis through vasospasm, platelet aggregation and clot formation. The latter is enhanced by having specialised vessels that are particu­ larly able to effectively occlude in this manner, and the release of thromboplastins into the intervillous space on fracturing of the anchoring villi during placental separa­ tion. The positive pressure in the intervillous space with the sustained postdelivery uterine contraction will lead to thromboplastins refluxing back into the uteroplacental vessels and effecting haemostasis by interacting with the vascular endothelium.

Uterine atony in the third stage of labour The uterus contracts less well if there has been a pro­ longed labour with decreasing uterine contractions and ‘uterine exhaustion’. Other factors contributing to atony in the third stage of labour include uterine overdisten­ sion (polyhydramnios, multiple pregnancy, macrosomia) and high parity, particularly grand multiparity where the woman has been delivered of five or more children previ­ ously. Unfortunately, failure to provide family planning in resource-poor settings is frequently responsible for high parity and consequential maternal deaths from atonic postpartum haemorrhage in pregnancies that women might not have chosen to have, had family plan­ ning been available.

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Chapter 28  MANAGEMENT OF NORMAL LABOUR Michael Permezel

KEY POINTS The diagnosis of labour is not straightforward, as the spurious labour (that which does not establish) may mimic early labour in every respect. Women are usually able to telephone birth suite staff at the hospital to obtain advice on when they should come to hospital. On admission of a woman who presents in possible or probable labour, a detailed assessment should be made, aided by a copy of the woman’s antenatal obstetric record. Many centres recommend an admission cardiotocograph (CTG), recognising that it is wrong to conclude from the randomised controlled trials that an admission CTG confers no benefit. The place of birth is a personal choice based largely on two things: how risk averse or tolerant a woman is for perinatal risk and the priority a woman places on birth in a home-like setting. The vast majority of women are very risk averse and hospital is most appropriate. For a few less risk-averse women looking for a homelike birth experience, an alternative birth centre is often chosen. Only a very small number of women are so risk tolerant that homebirth is an acceptable option. Management of the first stage of labour should consider psychological support, assessment of the mother, assessment of fetal wellbeing, progress of the labour, fluid and nutrition, position and mobility, analgesia and any extra requirements such as antibiotics for women who are colonised with Group B streptococci (GBS). Where there are no risk factors, fetal surveillance may be by auscultation or continuous cardiotocography according to guidelines. Indications for an obligatory recommendation for continuous cardiotocography are generally agreed. Semirecumbent is the most common position for normal birth in Western hospitals. Assistance in the birth by an accoucheur has the primary objective of reducing perineal trauma. Active third-stage management focuses on the administration of an oxytocic, awaiting placental separation and then assisting delivery of the placenta. A ‘non-actively’ managed third stage has double the rate of postpartum haemorrhage.

Chapter 28  Management of Normal Labour

THE ASSESSMENT OF A WOMAN WHO MAY BE IN LABOUR There are several key issues that must be addressed when a woman presents in labour or possibly in labour. As in all clinical medicine, each question is resolved through history, examination and investigations.

ISSUES TO BE ADDRESSED BY THE ADMISSION ASSESSMENT Is the woman in labour? Labour is defined as progressive painful uterine contractions resulting in the expulsion of the products of conception after 20 weeks’ gestation. As discussed in the previous chapter, the latent phase of labour may blend in with the last days of prelabour such that in some women, there may be no clear point where the antenatal period ended and labour began.

Spurious labour As the definition is dependent on a result, at the time of admission it may be unclear whether the painful contractions are going to progressively increase in strength, duration and frequency (true labour) or subside before the active phase of labour establishes (spurious labour). While some associated features make true labour more likely, in many cases there is no way of being certain whether the current episode of painful contractions is the real thing or not. Happily, in most cases this is not a critical diagnosis and a period of observation will determine whether the labour is ‘establishing’ or not.

What is the gestational age? Determining gestational age is important for a number of reasons, including for deciding whether continuous cardiotocography (CTG) is to be recommended (< 37 weeks’ or ≥ 41 to 42 weeks’ gestation). Prolonged pregnancy is associated with an increase in many complications (see Ch 13). Gestational age will be determined by reference to the expected date of delivery as calculated in early pregnancy based on obstetric ultrasound and/or menstrual dates.

Are there any complications of relevance? These may be from the current pregnancy or from past obstetric, gynaecological, medical or surgical history. Most often the information can be obtained from the medical record or a referral letter if the patient has come from antenatal care elsewhere.

How is fetal wellbeing? This should have been assessed at each antenatal visit but requires further evaluation on admission in labour. The key objective at this point is whether continuous CTG is to be recommended in labour.

THE CLINICAL ASSESSMENT The precise admission procedure differs from hospital to hospital. If the woman is in significant discomfort from strong contractions, the admission procedures should be expedited, and finalised when she has become settled.

History The woman should be asked about all features of the contractions: frequency, duration and intensity. In general, contractions that the woman can still talk through or continue performing a task through are unlikely to be labour pains. The presence of a show or rupture of the membranes increases the likelihood that labour has begun. Fetal movements should be specifically inquired about. Most relevant history of the current pregnancy and past history can be reliably obtained from the antenatal record.

Examination A general examination is carried out, with attention being paid to the abdomen. The blood pressure is recorded, as are the temperature, pulse rate and respiratory rate. The abdomen should be examined systematically, determining the fundal height and the lie, presentation and station of the fetus (Fig 28.1). The station is particularly important as it will act as a baseline for the assessment of progress and a low station assists in the diagnosis of true rather than spurious labour. The strength, duration and frequency of contractions are observed. The perineal pad should be inspected to determine if there is any evidence of amniotic fluid and, if so, whether meconium is present. A vaginal examination should be performed in the absence of any contraindications such as an undiagnosed antepartum haemorrhage (risk of causing haemorrhage from a placenta praevia) or ruptured membranes with a plan to manage conservatively (risk of introducing infection). The introitus is first examined and any abnormalities noted such as vulval varices. The labia are parted and a digital vaginal examination performed. Attention should be paid to the following: excessive discomfort that maybe suggestive of vaginismus any abnormalities such as a vaginal septum, vaginal cyst (e.g. Gartner’s) or cervical anomalies (rarely, cervical cancer may be first diagnosed in labour) the cervical consistency, position, dilatation, effacement and how well it is applied to the presenting part (Fig 28.2) the nature, station and position of the presenting part (Fig 28.3) the degree of caput and moulding; the latter can be scored from 0 (nil) to +++ depending on the degree of apposition/overlap of the fetal skull bones

• • • • •

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A

B

C

D

E FIGURE 28.1

Examination of the abdomen. A The height of the fundus is noted. B The fetal pole occupying the fundus (usually the breech) is palpated. C Lateral palpation (‘umbilical grip’) detects the fetal back on one side and flexed limbs on the other. D The presenting part is identified and its station noted. This fetus is large and there is a retraction ring visible below the umbilicus and above the distended lower uterine segment. E Pelvic palpation is useful in labour to follow descent of the presenting part. Source: Courtesy of Prof. Norman Beischer.

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Chapter 28  Management of Normal Labour



the abnormality of the bony pelvis such as undue prominence of the ischial spines, the sacral promontory or an unusually narrow pubic arch (Fig 28.4). After the vaginal examination has concluded, a sterile perineal pad should be applied and the woman allowed to adopt whichever position gives her most comfort: walking, sitting, squatting on all fours, resting in bed and so on.

Investigations In the uncomplicated pregnancy, no specific investigations are indicated other than possibly an admission cardiotocograph.

A

The admission cardiotocograph The question of whether to perform an admission cardiotocograph (CTG) is a fraught with controversy. Only a very small number of women will benefit by virtue of detecting serious fetal compromise not otherwise evident. If performed routinely, it is an inconvenience to a large number of women and inevitably leads to a proportion of women having continuous CTG throughout their labour when they would not otherwise have had it. Opponents of the admission CTG point to these disadvantages and the failure of randomised controlled trials to show benefit. Advocates of the admission CTG point to a small number of unequivocal ‘saves’ detected

B

C

FIGURE 28.2

Assessment of the cervix. A Primigravida prior to labour with an unfavourable cervix; the cervix is long, undilated and not effaced. B Primigravida in early labour. In most primigravidas the cervix is well effaced before cervical dilatation begins. C Multipara in early labour. The cervix typically begins to dilate before it is completely effaced.

Not engaged

Engaged

Narrow pelvic plane

Past narrow pelvic plane

FIGURE 28.3

Station of the head. The fetal scalp is on view when the maximum diameters of the head (biparietal and suboccipitobregmatic) reach the narrow pelvic plane and this is the level of a low-forceps delivery.

FIGURE 28.4

Palpation of the right ischial spine.

Source: Courtesy of Prof. Norman Beischer.

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on admission CTG and the deficiencies of randomised controlled trials in the assessment of clinically important but rare outcomes.

MANAGEMENT OF THE FIRST STAGE OF LABOUR WHERE SHOULD THE WOMAN BE LOCATED? When should the woman come in to hospital in labour? If a hospital birth is planned, the woman in early labour will commonly ring the hospital, relate her particular circumstances and seek advice as to when she should come to hospital. In very early labour and in the absence of risk factors, there is no immediate rush to come to hospital. Issues to be considered in advising when to come in include the: 1. presence of any risk factors; 2. strength, frequency and duration of contractions; 3. ability of the woman to cope and potential need for pain relief; and 4. time from the hospital in the event that labour suddenly accelerates. Although perinatal death in the latent phase of the first stage of labour is very uncommon, there are good reasons why it is more likely than at any time antenatally for the following reasons. First, a placenta that is only just maintaining fetal oxygenation will have a further reduction in uteroplacental blood flow with the onset of contractions. Second, early labour may be associated with significant descent of the presenting part, which in turn may produce serious cord compression in the event that the cord had already been tight around the neck prior to any descent. Third, the precipitating factor for labour initiation is sometimes an event that is associated with fetal compromise such as fetal hypoxia, chorioamnionitis or a placental abruption. For these reasons, and also for reassurance, the very risk-averse woman in early labour merits a timely assessment.

The place of birth Homebirth Homebirth lacks the immediate availability of potentially life-saving therapeutic procedures, should they be needed. Unfortunately, serious obstetric complications such as acute fetal compromise and postpartum haemorrhage may occur both profoundly and without warning. A small increase in maternal and perinatal morbidity and mortality would therefore be expected. As a randomised controlled trial of sufficient size is unachievable, perinatal outcome with homebirth can only be assessed in case-control and population studies. Unfortunately such studies are easily manipulated by each side of the homebirth debate and it is difficult to obtain accurate estimations on how often the place of birth causes mortality or long-term morbidity of either mother or infant. A figure of an additional 1 in 1000 230

for perinatal death would appear likely for homebirth, a risk that would appear to be acceptable for some women in order to have a better birth experience.1,2 If homebirth is undertaken, there should be counselling regarding the attendant risks, strict guidelines should be followed and a clear contingency put in place for rapid transfer to an adequately resourced hospital should complications develop.

Alternative birthing centres Alternative birthing centres (ABCs) offer many women birthing in a home-like environment but with closer proximity to emergency care than would be available to a homebirth. Women are screened for the presence of risk factors and transferred to conventional care according to agreed guidelines in the event that complications occur. Transfer rates vary among centres, but approximately one-third of women booking in an ABC might expect to be transferred antenatally and a further one-third of the remainder transferred in labour. This means that often only a little over half of all women booking in an ABC will actually remain there. Population studies of births in ABCs suggest that perinatal mortality is not significantly higher than the conventional birth centre, but these are not randomised studies and matching for equivalent risk is very difficult (Figures 28.5 and 28.6).

WHO SHOULD CARE FOR THE WOMAN IN LABOUR? Obstetricians and midwives Women are generally cared for by a midwife or obstetric nurse, overseen to varying extents by an obstetrician. In many labours there is no need for the obstetrician to attend at all but in most countries, only an obstetrician will perform caesarean sections or any instrumental delivery other than the most straightforward. If a midwife is caring for a woman in labour, an obstetrician will need to be consulted in the event of complications according to agreed guidelines.

Unregulated birth attendants A number of perinatal deaths under the care of unregulated birth attendants led South Australia to legislate in 2013 that only a medical practitioner or midwife can provide healthcare to a woman in labour in that Australian state. At the time of writing, other states have not yet followed, but somewhat controversial legislation does emphasise the need for knowledge, skills and attitudes in the care of a woman and her fetus in labour.

Partner, family and friends A supportive partner giving psychological support has been shown to reduce the analgesic requirements of women in labour. The partner can help with relaxation, psychoprophylactic techniques and timing of contractions. Extension to a broader circle of family and friends is most often unhelpful. Some women will want a second

Chapter 28  Management of Normal Labour

FIGURE 28.5

Birth centre in a major teaching hospital. Note the absence of the usual hospital equipment. Source: Courtesy of Prof. Norman Beischer.

or third person present but it is uncommon to want more. If children are to be present, this needs to be a considered decision with significant antenatal preparation.

ASPECTS OF CARE IN THE FIRST STAGE OF LABOUR Psychological support Psychological support is very important in labour. The needs of every woman are different and a perceptive carer will be responsive to the woman’s psychological needs. As discussed in the previous section, the partner (and possibly others) will contribute to the psychological support.

Assessment of the mother The following observations are routinely performed (more frequently if abnormal). Temperature is recorded 4-hourly. A rise in temperature is common in a long labour but a significant pyrexia mandates continuous CTG and antibiotic administration. Blood pressure and pulse rate are taken hourly. Respiratory rate is recorded 4-hourly.

• • •

Assessment of the labour Uterine contractions The intensity, duration and frequency of uterine contractions are recorded every 30 minutes in the first stage of labour and every 10 minutes in the second stage. The intensity of contractions can be measured using an intrauterine pressure catheter as a research tool but in practice, the intensity of contractions is assessed subjectively by abdominal palpation of the uterus by the midwife. With weak contractions, the uterus can readily be indented, whereas with strong contractions, the uterus feels rigid. Long duration (e.g. 60 secs) and high frequency (e.g. 4 to 5 in 10 mins) usually (but not always) parallel high intensity.

Abdominal station A formal assessment of the descent of the presenting part by abdominal examination should be made every 1 to 2 hours, according to circumstances.

Vaginal examination Vaginal examination is commonly performed about every 4 hours in the active phase of the first stage of labour. In the latent phase of labour, this may be less often but 231

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FIGURE 28.6

A father holds his newborn daughter whom he has delivered in a birth centre. The mother is witnessing the birth and receiving support and encouragement from friends.

approaching second stage, it is common to re-examine to confirm full dilatation of the cervix, say, 2 hours after a cervical dilatation of 8 or 9 cm has been diagnosed. The rate of cervical dilatation is the benchmark of adequate progress in labour. Other important features include the station of the presenting part, rotation of the presenting part (if not occipitoanterior) and any signs of obstructed labour including caput, moulding and cervical oedema.

Fetal membranes The state of membranes and nature of the liquor should be recorded along with the time of membrane rupture. The presence of meconium in the liquor should be reported immediately.

Assessment of fetal wellbeing Clinical assessment of fetal condition in labour is performed by observation of the amniotic fluid (oligohydramnios, meconium staining), as already mentioned, 232

and auscultation of the fetal heart rate. Some practitioners favour amniotomy in labour when cervical dilatation has reached 4 to 6 cm or more, to exclude the passage of meconium and also because the process of labour may thus be accelerated and its duration lessened.

Auscultation of the fetal heart Auscultation of the fetal heart rate should be performed every 15 to 30 minutes in the first stage of labour and after every contraction in the second stage of labour. Auscultation optimally occurs with a hand-held Doppler device, begins before the end of the contraction and continues for at least 60 seconds. The landmark randomised controlled trial upon which a policy of allowing auscultation as an alternative to continuous CTG is based used 15-minutely auscultation in the first stage, and this is preferred in some jurisdictions. When there is slowing of the heart rate during a contraction or delay in return to the normal rate (120 to

Chapter 28  Management of Normal Labour

160 bpm) after it has ceased, then CTG is indicated (Figs 28.7, 28.8 and 28.9) unless delivery is imminent.

Continuous cardiotocography Continuous electronic fetal heart rate monitoring (CTG) is indicated where there are risk factors for fetal compromise—either apparent antenatally or having occurred in labour. The indications for continuous CTG are listed in Box 28.1. Particularly risk-averse women without any complications may still choose continuous CTG to monitor their fetus in labour. They should be

informed that this may increase the likelihood of instrumental birth, particularly in units where fetal blood sampling is not available or not commonly used in labour.

Ambulation and position There is some evidence that ambulation in early labour will shorten the duration of labour. When mothers are given free choice, they will usually sit up or ambulate until the cervix is 5 to 6 cm dilated, and thereafter will often recline on their side in bed. Squatting positions,

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FIGURE 28.7

A Normal baseline and variability. In this case, the absence of accelerations could be due to early fetal hypoxia or fetal sleep, or it may be due to the use of morphine, pethidine or other pain relief in labour. B Absent variability of the fetal heart rate in labour. This is almost always due to near-terminal fetal hypoxia but may also be seen with fetal tachyarrhythmias or fetal brain death. 200

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FIGURE 28.8

A Baseline tachycardia with accelerations and normal variability. The tachycardia could be due to maternal fever, which in turn may be a consequence of either infection or obstructing labour. B Baseline bradycardia with normal variability. This is not uncommon with prolonged gestations (e.g. 41+ weeks’) and is likely to be a normal variation if there are no other features suggesting fetal hypoxia. 233

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FIGURE 28.9

A Variable decelerations. These are due to cord compression in labour. The abrupt onset and rapid recovery distinguish variable decelerations from early decelerations. B Late decelerations with tachycardia and reduced variability. This unequivocally suggests fetal hypoxia. The sharp spikes may be fetal ectopic beats.

BOX 28.1  Indications for continuous CTG in labour. Antenatal risk factors ✚ Abnormal antenatal CTG ✚ Abnormal Doppler umbilical artery velocimetry ✚ Suspected or confirmed intrauterine growth restriction ✚ Oligohydramnios or polyhydramnios ✚ Prolonged pregnancy ≥ 42 weeks’ ✚ Multiple pregnancy ✚ Breech presentation ✚ Antepartum haemorrhage ✚ Prolonged rupture of membranes (≥ 24 hours) ✚ Known fetal abnormality which requires monitoring ✚ Uterine scar (e.g. previous caesarean section) ✚ Essential hypertension or preeclampsia ✚ Diabetes where medication is indicated or poorly controlled, or with fetal macrosomia ✚ Other current or previous obstetric or medical conditions which constitute a significant risk of fetal compromise (e.g. cholestasis, isoimmunisation, substance abuse) ✚ Decreased fetal movements ✚ Morbid obesity (BMI ≥ 40) ✚ Maternal age ≥ 42 ✚ Abnormalities of maternal serum screening associated with an increased risk of poor perinatal outcomes (e.g. low PAPP-A < 0.4MoM) Intrapartum risk factors ✚ Induction of labour with prostaglandin/oxytocin ✚ Abnormal auscultation or CTG ✚ Oxytocin augmentation 234



Regional anaesthesia (e.g. epidural or spinal) and paracervical block ✚ Abnormal vaginal bleeding in labour ✚ Maternal pyrexia: recommend ≥ 38°C ✚ Meconium or blood-stained liquor ✚ Absent liquor following amniotomy ✚ Prolonged first stage of labour ✚ Prolonged second stage as defined by referral guidelines ✚ Preterm labour < 37 completed weeks’ ✚ Tachysystole (more than five active labour contractions in 10 minutes without fetal heart rate abnormalities), ✚ Uterine hypertonus (contractions lasting more than 2 minutes in duration or contractions occurring within 60 seconds of each other, without fetal heart rate abnormalities) ✚ Uterine hyperstimulation (either tachysystole or uterine hypertonus with fetal heart rate abnormalities) Other conditions where a recommendation for continuous cardiotography should be considered, particularly if multiple conditions are present ✚ Pregnancy gestation 41.0 to 41.6 weeks’ gestation ✚ Gestational hypertension ✚ Gestational diabetes mellitus without complicating factors ✚ Obesity (BMI 30–40) ✚ Maternal age ≥ 40 and < 42 ✚ Maternal pyrexia ≥ 37.8°C and < 38°C ✚

Chapter 28  Management of Normal Labour

unless practised, are usually too tiring to maintain for any length of time. Many women like to have a shower during labour but water immersion is controversial for two reasons. First, there are increased difficulties delivering care during the first stage (see below). Second, rapid birth may ensue, resulting in a location where there will be considerable difficulty in the management of complications such as unexpected shoulder dystocia, maternal collapse or haemorrhage.

Nutrition and fluid intake An intravenous infusion should be considered in any long labour (e.g. more than 12 hours). The woman may eat in early labour but this is usually not encouraged in established labour due to gastric slowing, a tendency to experience nausea and vomiting late in labour, and the risk of inhalation of stomach contents in the unlikely event that the woman suffers a grand mal convulsion or requires general anaesthesia.

Analgesia The subject of pain relief is addressed in Chapter 38.

Antibiotics These maybe indicated prophylactically for any of the following indications: Group B streptococcal colonisation on vaginal/ perianal swab in late pregnancy prolonged rupture of the membranes (≥ 18 hours) suspected chorioamnionitis (temperature ≥ 37.8°C in labour) perceived risk of infective endocarditis (e.g. cardiac valve disease).

• • • •

Bladder and bowels Although the days of the routine enema on admission are thankfully long gone, attention to urinary tract and bowel activity remains a necessary component of intrapartum care. 1. Bladder. The bladder should be emptied every 2 hours. Each specimen of urine should be assessed for volume, glucose, ketones and protein. If urine retention develops, a urinary catheter should be passed. This is almost inevitable with epidural analgesia and many units will have a policy of routine urinary cauterisation whenever epidural analgesia is used. 2. Bowels. All bowel actions are recorded. If the rectum is obviously loaded on admission, a low volume enema or glycerine suppositories are recommended.

MANAGEMENT OF THE SECOND STAGE OF LABOUR The same principles that were applied to the first stage of labour should continue in the second stage, including

attention to maternal surveillance, labour progress assessment, fetal surveillance, maternal positioning, fluid intake, analgesia, antibiotics (if indicated) and bladder care. The posture usually adopted is one of semi­ recumbency. Squatting is not easy to maintain unless practised.

THE SECOND STAGE PRIOR TO BIRTHING Recognising the onset of the second stage of labour At or near the end of the first stage, the woman may exhibit one or more of the following: shivering, hiccups, vomiting, flushing and a small amount of vaginal bleeding. As the presenting part descends to the pelvic floor, the woman will experience a desire to ‘bear down’ or ‘push’. At this point, no head should be palpable abdominally. If there is doubt regarding whether there is full cervical dilatation, a vaginal examination should be performed to confirm that there is no cervix palpable.

Management of the normal second stage of labour prior to the actual birth If progress is satisfactory, it is probably unnecessary to exhort the woman to push, until the presenting part has reached the pelvic floor. This is particularly so if she has had an epidural anaesthetic. It is probably safer for the woman to push naturally, not close her glottis, and not push continuously for more than 6 to 8 seconds. The actual pushing is best effected by the woman partially sitting and grasping the backs of the thighs, the legs being well separated. After pushing, the woman is encouraged to exhale fully and take another deep breath to take advantage of the contraction. Confusion as to the true amount of progress may arise in breech presentations if a limb (or limbs) presents; it may have slipped through the not fully dilated cervix. In multiparas, strong pushing can sometimes cause the presenting part to descend to the level of the outlet, even though the cervix is not fully dilated. Finally, gross moulding and caput formation resulting from cephalopelvic disproportion can simulate deep descent of the head. The woman is much helped by sympathetic handling and encouragement, and wiping the face and neck with a cool wet sponge is soothing. If pressure on the presenting part of the rectum causes the expulsion of faecal material, this should be removed with a pad and the perineum swabbed. Towards the end of the second stage, the presenting part will reach the perineum and begin to distend it. The woman is now ready for delivery. If continuous CTG is not being used for fetal surveillance, auscultation should be carried out after each contraction as described above. There is much debate as to a reasonable duration of the second stage before recommending instrumental 235

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birth. In a multipara, there is a small risk of uterine rupture with prolonged pushing and an upper limit of pushing for 1 hour is generally recommended. In a nullipara, 2 hours of pushing is generally accepted, providing fetal surveillance is instituted after the first hour. The nullipara may be permitted an hour or more in second stage without pushing for the head to descend to the pelvic floor, particularly if there is effective epidural analgesia.

CONDUCT OF A NORMAL DELIVERY Preparation for birth Universal precautions The risk of exposure to blood-borne viruses during birth has potentially serious consequences for staff attending the birth. Precautions will include the use of gloves for procedures such as venepuncture or changing bedpans, with sterile gloves, aprons or gowns and eye protection routinely used for birth.

Instruments Instruments and surgical drapes should be placed in readiness for birth when the woman enters the second stage. Minimum instrumentation should include clamps for the umbilical cord and scissors to cut the cord.

Position of the woman There are a number of positions that may be recommended to the woman at this stage of labour. Squatting. This is more physiological than the other positions and allows better pushing by the mother. It is associated with a widening of the pelvic outlet through hyperflexion and abduction of the hip joint, causing movement at the sacroiliac joint. Many women find the position difficult to sustain for any length of time. Semirecumbent (modified dorsal). This is the most common position for a woman to birth in hospital. The woman lies on her back in a semi-sitting position, the knees and hips are flexed, and the legs are widely separated. This combines the pelvic advantages of hyperflexion and abduction of the hip joint but without necessitating the muscular strength needed for squatting. Lithotomy. Although less popular and less comfortable, this position is more likely to be used for instrumental birth since assessment of position and required manipulations are facilitated. When shoulder dystocia (impacted shoulders) is anticipated, the dorsal position is unfavourable because downward traction, which is required to free the anterior shoulder from beneath the symphysis pubis, is prevented by the bed. The lithotomy position permits easy downward traction towards the floor. On all fours. This position has a number of disadvantages. In general, there is poor access of the accoucheur









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to the perineum, meaning little control over the birthing process and an increased risk of damaging tears. Auscultation of the fetal heart can be more difficult and various manoeuvres in the management of shoulder dystocia impossible. Most relevant is that the fetus is being pushed ‘uphill’ (against gravity) and without the pelvic advantages of hyperflexion of the hip joint. All this adds up to temporarily delaying pressure on the perineum (supporters say that the woman is more comfortable) and prolongation of the second stage, which is undesirable from both maternal and fetal perspectives. Standing or sitting. These positions may be used but some support to the back is usually required.



Antisepsis Cotton wool or gauze swabs soaked in antiseptic solution are used to clean the perineum prior to birth. Aqueous chlorhexidine 0.1% is commonly used for this purpose.

The birth The role of the accoucheur at the time of birth is illustrated in Figure 28.10. There is a series of steps that ensure safe delivery of the neonate with minimisation of trauma to the pelvic floor.

Delivery of the head The position of the accoucheur will depend on the position of the woman. The following description applies to birth in the semirecumbent (dorsal) position. The left hand is placed so that the fingers are spread over the vertex, usually with the base of the hand applied to the back of the occiput and the fingers spread forwards over the parietal bones. The purpose of this manoeuvre is not to exert backward pressure on the head (which will delay birth), but rather to prevent sudden expulsion of the head, which will produce increased perineal damage. The hand should also act as a barometer of progress that enables the accoucheur to inform the woman of optimum ‘bearing-down force’ to achieve a steady, controlled birth of the head and thereby minimising perineal trauma. As the occiput descends under the symphysis pubis, extension occurs and progressively the forehead, nose, mouth and finally chin emerge from beneath the posterior ring of the vulval opening. If the perineum is tight, the chin may need freeing by slipping the index finger under the baby’s mandible and elevating it. Blood and mucus maybe wiped from the baby’s mouth and nose.

Cord around the neck A finger of the right hand is run up past the occiput to ascertain whether the cord is looped around the neck (approximately 25% of fetuses). If the cord is present, it is drawn down over the head; other loops are treated similarly. If there is undue tension, two clamps are placed on the cord approximately 2 cm apart and the cord is cut between them. The release of additional loops can be achieved quite easily by unwinding the clamped ends around the neck.

Chapter 28  Management of Normal Labour

A

B

FIGURE 28.10

A The posterior shoulder is delivered by lateral flexion of the trunk in an anterior direction. Note that the overemphasis of external rotation is no longer applied and so the head faces laterally. B The baby is born and held head downwards. He is covered with vernix and is very slippery; it is necessary to hold his head as shown since his weight could cause his feet to slip from the grasp of the other hand. Source: Courtesy of Prof. Norman Beischer.

Delivery of the shoulders and trunk Following external rotation (restitution) of the fetal head, the shoulders should be delivered. Delivery of the shoulders can traumatise the perineum, so care is needed. Usually the anterior shoulder slips from under the symphysis pubis aided by downward and backward traction of the head. This can be firm but not strong traction, because of the risk to the brachial nerve plexus (Erb’s) palsy. If difficulty is experienced, the woman should be positioned over the edge of the bed so that traction can occur towards the floor in a manner that will release the anterior shoulder from behind the symphysis pubis. If further difficulty is experienced, the birth should be managed as shoulder dystocia (see Ch 34). After the anterior shoulder is freed, the direction of traction is more in the line of the lower birth canal— upwards and forwards. Further gentle and steady trac­ tion allows the posterior shoulder to emerge over the perineum. The latter structure should be watched carefully during this time. The rest of the birth follows easily. It is usually best, when the shoulders are delivered, to change the hold on the baby’s head, the right hand securing it behind the neck while the left hand grasps the feet at the ankles. Some babies are thickly covered with vernix and are quite slippery. They should never be held with only one hand and should always be placed so that a fall would be harmless if the grip is lost.

‘Hands-off’ management of birth In this technique, the baby is delivered ‘naturally’ with little in the way of assistance from an accoucheur. Of course, this will commonly occur without great incident but there is an expectation that uncontrolled birthing will be associated with increased rates of perineal injury. As yet, trials of sufficient size have not been undertaken to quantify any additional adverse outcomes in association with a ‘hands-off’ technique.

MANAGEMENT OF THE THIRD STAGE OF LABOUR Management of the third stage is of vital importance in minimising postpartum haemorrhage, retained placenta, maternal morbidity and maternal death. As indicated in Chapter 27, postpartum haemorrhage is the major cause of maternal death worldwide, particularly so in resourcepoor settings where women lack access to family planning and achieve a high parity with associated increased risk of atonic postpartum haemorrhage.

CLAMPING OF THE CORD After the baby has been delivered and attended to, the cord is doubly clamped and divided. If the baby is held below the level of the placenta, blood will transfuse from 237

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the placental circulation into the fetus. This has benefits for the fetus in terms of improved iron stores but it will aggravate the level of jaundice commonly seen in the first few days of life. Both early and delayed clamping are therefore acceptable strategies. In either event, issues around cord clamping should not delay active management of the third stage of labour.

CORD BLOOD Specific tests on cord blood Cord blood will be collected into appropriate tubes if there are conditions where tests are indicated. The most common reason is the Rh-negative mother where a cord blood group will reveal whether or not the mother requires the administration of prophylactic anti-D. A direct Comb’s test is also commonly performed in this situation to determine whether there are anti-red cell antibodies adherent to the fetal red cells. Cord blood may also be required in certain maternal disorders (e.g. maternal immune thrombocytopenic purpura).

Donation for stem cell storage Cord blood is particularly rich in stem cells. The blood is usually collected by needling of the cord with the placenta still in situ. Approximately 80 mL of cord blood rich in stem cells can be obtained. Two sorts of cord stem cell donations are possible. First, there is a public cord blood bank that can be accessed by a suitably ‘antigenically matched’ member of the community in need of a stem cell transfusion (e.g. in the management of leukaemia). This has universal support. There is also a facility for private donation; that is, an individual pays quite a large sum to have the cord blood stored specifically for their own future use or a nominated family member. This is more controversial because of an uncertain likelihood of future need for the cord stem cells. At the time of writing, there are a number of possible future uses but none as yet in established clinical practice. Each woman must weigh the cost and inconvenience against an uncertain future benefit.3

There are essentially four alternatives for oxytocic in third-stage management. Oxytocin (5 or 10 units administered intravenously or intramuscularly) has a more rapid onset of action (approximately 30 seconds after intramuscular administration) but shorter duration of action (approximately 20 minutes). The only significant adverse effect is a tendency to hypotension in a few women. This is thought to be an anti-vasopressin effect, oxytocin obviously being structurally similar. Ergometrine (0.5 mg intramuscularly) has a slower onset of action than oxytocin (approximately 2 minutes) but it lasts longer (approximately 60 minutes). Side effects include nausea, vomiting and hypertension. It is therefore contraindicated if there is preexisting hypertension. It is also contraindicated if there is diminished cardiac reserve as the intense arteriolar spasm increases afterload and both the venular spasm and profound uterine contraction increases preload. Ergometrine is now uncommonly used in third stage management other than in combination with oxytocin (below). Oxytocin-ergometrine in combination intramuscularly (e.g. Syntometrine: oxytocin 5 units, ergometrine 0.5 mg) combines the early onset of oxytocin and the longer duration of action of ergometrine. A Cochrane review has shown oxytocin-ergometrine in combination to be superior to oxytocin alone in the prevention of postpartum haemorrhage greater than 500 mL, but not better in the prevention of PPH greater than 1000 mL.4 However, it has all the adverse effects of ergometrine and the same contraindications. Misoprostol (400 mcg rectally) has been shown to be less effective than oxytocin or ergometrine but in resource-poor settings, misoprostol can be given orally or rectally and is likely to save many lives as it is progressively introduced to areas where injections of oxytocin or ergometrine are not feasible.









ACTIVE MANAGEMENT OF THE THIRD STAGE OF LABOUR

Await uterine contraction, placental separation and descent

There are three aspects to active management of the third stage of labour: 1. administer an oxytocic; 2. await uterine contraction, placental separation and descent; and 3. assist delivery of the placenta and membranes.

The uterus is not massaged or prodded unless there is excessive bleeding. A sterile basin or bedpan is placed against the perineum which serves to contain the umbilical cord and to enable blood loss to be assessed. The cord is drawn down until resistance is felt. If there is a perineal wound, it should be compressed with a gauze pad if it is obviously bleeding. The signs of placental separation and descent are classically as follows: 1. show of blood; 2. lengthening of the cord; and 3. the uterus assumes a more globular shape and greater mobility. These signs may occur with partial separation and may not all be present when complete separation has occurred.

Oxytocic administration Immediately after the birth of the child, it is customary to palpate the uterus to exclude a second twin, although this will be an extremely unlikely occurrence if the woman has had multiple ultrasound examinations during pregnancy. Administration of a bolus oxytocic with a fetus still in utero will produce profound fetal anoxia and possibly uterine rupture. 238

Chapter 28  Management of Normal Labour

Assist delivery of the placenta and membranes Controlled cord traction After separation and descent, delivery of the placenta is most physiologically and painlessly effected by controlled cord traction. The essentials of this method are as follows. The cord is reclamped near to the vulva and steadied with one hand while the other hand is used to push the uterine fundus upwards (Fig 28.11). This will confirm that the placenta has separated, since the cord will not then follow the upward movement of the uterus. If separation has occurred, a combined movement is made of downward and backward traction on the cord and upward displacement of the uterus, provided that the latter is firmly

contracted. The abdominal hand is the controlling factor since it holds the fundus and prevents the possibility of inversion of the uterus; this only occurs when cord traction is performed with an uncontracted uterus. If the placenta does not advance, there are two possibilities: it is still attached to the uterus (perhaps only partially) or it has become trapped in a tightly contracted uterus. In such cases, the accoucheur must be patient and repeat the procedure at intervals of some minutes, resisting the temptation to massage the uterus if bleeding is not excessive. If the umbilical cord vessels are congested, the clamp can be removed and the blood drained out. This reduces the size of the trapped placenta. If there is a delay in delivery of the placenta, urethral catheterisation may be performed, although it is doubtful whether this actually makes a difference. Usually, the membranes readily follow the placenta. If they begin to tear, the placenta should be rotated to cause a bunching up of the membranes near the vulva; a wide clamp is then applied and a steady traction exerted (Fig 28.12). Experienced assistance must be sought if the placenta is not delivered within 10 minutes, or earlier if bleeding is excessive. The further management of these complications is considered later.

A

B FIGURE 28.11

Delivery of the placenta by controlled cord traction. A The contracted uterus is pushed upwards as traction is exerted on the cord in the direction of the curve of the birth canal. B The abdominal hand ‘palms’ the fundus as the folded placenta appears fetal-surface first. Another method of holding cord and clamp is shown. Source: Courtesy of Prof. Norman Beischer.

FIGURE 28.12

The trailing membranes are detached from the uterine wall and delivered complete by careful traction with a seesaw action. Source: Courtesy of Prof. Norman Beischer.

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Fundal expression of the placenta If the cord has snapped, an alternative method of placental delivery is fundal expression. Here, fundal pressure on the contracted uterus is used as a piston to push the placenta downwards from the lower segment or upper vagina. Too much force will cause pain to the mother and stretching of the supports of the uterus.

PASSIVE MANAGEMENT OF THE THIRD STAGE OF LABOUR A few women will choose not to have active management of the third stage of labour. They should be informed that this is associated with a twofold increase in the risk of postpartum haemorrhage (8% instead of 4%).

INSPECTION OF THE PLACENTA AFTER DELIVERY The placenta is examined carefully and methodically. 1. The maternal surface is inspected to see if there are any missing cotyledons (Fig 28.13). 2. The fetal surface is examined to determine if there could be a missing section of the placenta. That is, if a vessel runs to the edge of the placenta and the membranes there are ragged or absent, the presence of a succenturiate lobe should be suspected (Fig 28.14). Whitish areas are common in the subchorial region and these usually represent fibrin deposition, not infarcts. The weight of the placenta is

recorded, together with the time of its delivery and any significant anomaly. 3. The membranes are inspected for completeness. Ideally, there is a circular hole where the fetus emerged and the membranes are otherwise complete. The distance of the hole from the edge of the placenta indicates how close the placenta was to the internal os; if less than the length of the lower uterine segment, then the placenta was partially praevia. Often the membranes are ‘ragged’; that is, incomplete. In such cases, an estimate should be made of how much of the membranes remains in the uterus. The membranes may insert on the surface of the placenta rather than at its edge (circumvallate placenta) and this should be recorded (Fig 28.15); in this condition the placenta is unusually thick but has a reduced diameter, as though excessive regression of chorionic villi had occurred, with later extension of the remainder beyond the original edge of the placental disc. Placenta membranacea is the converse and much less common condition, where the chorionic villi persist over most or all of the circumference of the chorion, the placenta being wide but thin (Fig 28.16).

Management of an incomplete placenta If part of the placenta is missing (Fig 28.13) or a succenturiate lobe is suspected, exploration of the uterus should be made (Fig 28.14). If this is not done, there is a risk of later secondary postpartum haemorrhage in relation to infection of retained products of conception.

FIGURE 28.13

A missing placental cotyledon was noted at routine inspection of the placenta. Although there was not excessive postpartum blood loss, manual exploration of the uterine cavity was performed under anaesthesia and the missing cotyledon removed. Source: Courtesy of Monash Health.

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FIGURE 28.14

Fetal surface of a placenta succenturiata. Several large vessels pass across the membranes to the succenturiate lobe. The condition is termed vasa praevia when such vessels pass over the region of the internal os. Source: Courtesy of Prof. Norman Beischer.

Chapter 28  Management of Normal Labour

INSPECTION OF THE VULVA, VAGINA AND PERINEUM AFTER BIRTH A gentle but thorough inspection is made for injuries to the vulva and vagina, especially tears in the region of the vulval ring. Occasionally, the epithelium may be intact but a haematoma may have developed in the deeper tissues. After operative vaginal deliveries, or if bleeding is abnormal, the whole length of the vagina and the cervix must be inspected. Any episiotomy or birth canal injury should be repaired in a timely manner (see Ch 30).

FURTHER CARE IN THE EARLY POSTNATAL PERIOD Maternal observations and investigations FIGURE 28.15

Circumvallate placenta; the amnion forms a double fold as it attaches to the placenta and obscures the vessels at the outer rim of the fetal surface. A mild accidental haemorrhage occurred at 38 weeks’ gestation. Source: Courtesy of Monash Health.

Routine observations of temperature, pulse rate and blood pressure are made, the frequency depending on whether the preceding labour was normal or complicated. Palpation of the uterine fundus for atony and inspection of the perineal pad should be made every 15 minutes for at least 2 hours after birth. If there is voiding difficulty or the bladder is palpable after voiding, a urinary catheter should be passed. If the woman is Rh-negative, her blood will be sent for a blood group antibody screen in order to confirm that she has not developed anti-D antibodies in late pregnancy. REFERENCES 1) Wax JR, Lucas FL, Lamont M, et al. Maternal and newborn outcomes in planned home birth vs planned hospital births: a metaanalysis. Am J Obstet Gynecol 2010;203: 243.e1–8. 2) Walker SP, McCarthy EA, Ugoni A, et al. Cesarean delivery or vaginal birth: a survey of patient and clinician thresholds. Obstet Gynecol 2007;109(1):67–72. 3) RANZCOG. Statement on provision of routine intrapartum care in the absence of pregnancy complications. July 2014. Online. Available: ; [17 Dec 2014]. 4) McDonald SJ, Abbott JM, Higgins SP. Prophylactic ergometrine-oxytocin versus oxytocin for the third stage of labour. Cochrane Database Syst Rev 2004;(1):CD000201.

FIGURE 28.16

Placenta membranacea; the chorionic villi have persisted over the entire surface of the gestation sac. Source: Courtesy of the Estate of Dr. Ian MacIsaac.

FURTHER READING RANZCOG. Statement on umbilical cord blood banking. May 2013. Online. Available: ; [17 Dec 2014]. 241

Section 2.7.2 INDUCTION OF LABOUR, INSTRUMENTAL DELIVERY AND CASEAREAN SECTION

Chapter 29  INDUCTION OF LABOUR, INCLUDING CERVICAL RIPENING Michael Permezel and Gillian Paulsen

KEY POINTS In approximately 25% of pregnancies, the clinical circumstances reach a position where the risk–benefit equation of induction versus remaining in utero favours the former. Elective caesarean section should be considered as an alternative to induction of labour where the situation is such that vaginal birth is contraindicated or where the likelihood of achieving a vaginal birth is low. The suitability of the cervix for induction should be assessed with a cervical score. The cervical score may influence the decision as to whether induction of labour is recommended in a particular clinical situation. If induction is still recommended with an unfavourable cervix, mechanical or pharmacological cervical ripening agents will increase the likelihood of vaginal birth. Each technique for induction of labour has its own side effect profile. Of particular concern is the possibility of excessive uterine muscular activity with the use of oxytocic drugs, particularly prostaglandins.

BACKGROUND INCIDENCE Induction of labour takes place in approximately 25% of pregnancies but can vary considerably in different health services and care models.

THE RISK–BENEFIT EQUATION WITH INDUCTION OF LABOUR The decision regarding a recommendation for induction of labour will depend on the following factors that need to be carefully assessed in each individual: indication for induction of labour gestational age suitability for induction of labour maternal tolerance of risk in order to avoid medical procedures around childbirth.

• • • •

Indication for induction of labour The indication for induction should be a circumstance or condition that may benefit from delivery before spontaneous labour. A list of all the conditions that might benefit from early birth is extensive and could include almost every obstetric or medical (including psychological) condition (Box 29.1). Other benefits might be legitimately social where, for example, the partner has only a specific window of leave before returning to a military service position overseas. Almost regardless of the indication, the perceived benefit needs to be balanced against the risks (potential adverse consequences) of labour.

Risks of birth occurring earlier than it would have occurred spontaneously The risks of birth occurring earlier than it would have without induction are the common problems of prematurity, particularly respiratory distress, poor feeding and so on (see Ch 12).

Beischer & MacKay’s: Obstetrics, Gynaecology and the Newborn

BOX 29.1  Common indications for induction of labour. Prolonged pregnancy Hypertensive disorders ✚ Essential hypertension, gestational hypertension, preeclampsia Diabetes mellitus ✚ Gestational diabetes mellitus, prepregnancy diabetes mellitus Other medical conditions ✚ Renal disease, liver disease, cholestasis of pregnancy, red cell isoimmunisation, thrombophilia, anticoagulation in pregnancy, substance abuse, neurological (e.g. myotonic dystrophy) Placental insufficiency suspected or likely ✚ Fundus less than dates, poor late fetal growth, ultrasound suggesting placental insufficiency, oligohydramnios, fetal movements decreased, previous placental insufficiency, low PAPP-A in first trimester Prelabour rupture of the membranes Multiple pregnancy Antepartum haemorrhage with normally sited placenta Gynaecological ✚ Long-standing infertility, may be particularly risk averse Musculoskeletal conditions ✚ Disabling ligamentous pain in late pregnancy Psychological or mental health issues may sometimes benefit from labour induction Social ✚ Most commonly partner availability

Risks related to the method of induction of labour These will be discussed with each method but include, for example, cord prolapse after artificial rupture of the membranes and excessive uterine muscular activity after administration of oxytocics such as prostaglandins or oxytocin.

compared to awaiting spontaneous labour. Repeated randomised clinical trials have shown either no increase in caesarean section or actually a reduction in caesarean section. Examples include the Hannah randomised controlled trial of induction versus observation of the post41 weeks’ pregnancy and the HYPITAT trial of the management of hypertension in late pregnancy.1,2

Assessment of gestational age Accurate ultrasound dating is important because of not only the risks of prematurity complications but also because the hazards of remaining in utero in many conditions escalate exponentially in late pregnancy.

Assessment of suitability for induction of labour If the head is high and mobile, induction of labour is relatively contraindicated due to the small risk of a cord prolapse with rupture of the fetal membranes. A caesarean section may be a wiser option if delivery is needed. Most attention is usually paid to the state of the cervix through assessment of the cervical (Bishop’s) score (see Ch 13). A ‘ripe’ cervix increases the likelihood of an uncomplicated vaginal birth following induction of labour. If the cervix is ‘unripe’, various methods may be used to improve the cervical score (mechanical or pharmacological) but these have some morbidity attached and an unfavourable cervix affects the risk–benefit of induction of labour.

Assessment of maternal factors: how much fetal risk is the woman prepared to take in order to avoid induction of labour? Most women are relatively intolerant of fetal risk and prepared to accept obstetric procedures such as caesarean section or induction of labour in order to minimise fetal risk. There is, however, a small group of women who are particularly averse to ‘medicalisation’ of birth and more tolerant of fetal risk in order to avoid induction of labour.3 This should also be considered in the risk–benefit model when recommending induction of labour.

Risk of caesarean section after attempted (‘failed’) induction of labour

CONTRAINDICATIONS TO INDUCTION OF LABOUR

The term ‘failed’ should probably be eliminated from obstetric terminology as it has the connotation that either the woman or her carers have somehow not met expectations. In truth, it is perfectly reasonable to attempt induction of labour in the knowledge that caesarean section is a possibility or even a probability. It is a persisting misconception that induction of labour makes a caesarean section more likely when

It is self-explanatory that those conditions unsuitable for vaginal birth will also be unsuitable for induction of labour. Examples include malpresentation, placenta praevia, previous classical caesarean section, vasa praevia and active genital herpes simplex infection.

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CONTRAINDICATIONS TO VAGINAL BIRTH

Chapter 29  Induction of Labour, Including Cervical Ripening

CONTRAINDICATIONS TO ADMINISTRATION OF AN OXYTOCIC (OXYTOCIN OR PROSTAGLANDINS) Conditions that predispose to uterine rupture are relative contraindications to oxytocic administration (particularly prostaglandins). Examples include grand multiparity and a previous uterine scar.

CONTRAINDICATIONS TO ARTIFICIAL RUPTURE OF THE MEMBRANES A high mobile presenting part risks a cord prolapse with artificial rupture of the membranes (ARM).

TECHNIQUES FOR LABOUR INDUCTION ASSESSMENT PRIOR TO INDUCTION OF LABOUR A detailed history should already have been taken paying particular attention to those factors that will most impact on the risk–benefit equation with respect to labour induction. Abdominal examination will reveal whether the presenting part is fixed. A vaginal examination to assess the cervical score is paramount in determining the most appropriate method and whether cervical ripening is advisable.

The cervical (Bishop’s) score The cervical score gives an idea of the likelihood of induction being successful in achieving labour; that is, painful regular uterine contractions associated with progressive dilatation of the cervix. There are several variants of the cervical score but an example is given in Table 29.1. The cervical score is calculated by summing the score in each of the five categories as determined on vaginal examination prior to induction of labour. Where the cervical score is ≤ 5, cervical ripening with either prostaglandin or a transcervical catheter is recommended to increase the likelihood of a successful induction.

Assessment of fetal wellbeing The fetus will be assessed clinically and may already have had some investigations antenatally (depending on the clinical circumstances). Regardless of prior assessments, a (further) cardiotocograph should be performed prior to cervical ripening or labour induction as each of the techniques may further compromise the fetus at risk.

CERVICAL RIPENING As indicated already, some form of cervical ripening is preferred where the cervix is ‘unripe’ (cervical score ≤ 5) in order to increase the probability of a vaginal birth. The two common techniques for cervical ripening are pharmacological (prostaglandin therapy) or mechanical (transcervical catheter, e.g. Foley). Where the cervix is ‘favourable’ (ripe) (cervical score > 5), neither of these agents is required and they will unnecessarily delay birth. In addition, the administration of prostaglandins in the presence of a favourable cervix will further increase the likelihood of a precipitate (rapid) labour and/or uterine hyperstimulation (excessive uterine activity associated with fetal compromise). Sometimes, a cervical ripening agent alone has caused labour to begin but ‘augmentation’ (Ch 34) with ARM and/or oxytocin may still be required as the effect of the ripening agent may wear off before labour is established. If the cervix is favourable (whether cervical ripening agents have been used or not) and labour not yet established in a woman scheduled for induction, labour is commonly induced with ARM followed by an oxytocin infusion. It is normal practice not to administer an oxytocin infusion until after the ARM. This is because there may be a relatively sudden increase in sensitivity to oxytocin after rupture of the membranes, with all the potential consequences of uterine hyperstimulation.

FETAL SURVEILLANCE FOLLOWING CERVICAL RIPENING OR INDUCTION OF LABOUR Regardless of which agent is selected, even if the indication for induction of labour does not mandate a

TABLE 29.1  CERVICAL SCORE. 0

1

2

3

Cervical dilatation

0 cm

1–2 cm

3–4 cm

> 5 cm

Cervical effacement

0–30%

31–50%

51–80%

> 80%

Cervical position

Posterior

Intermediate

Anterior

Cervical consistency

Firm

Intermediate

Soft

Presenting part station

–3

–2

–1, 0

+1, +2 245

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recommendation for continuous cardiotocography, continuous cardiotocography is indicated when labour begins. All agents used to induce labour can have direct or indirect effects on fetal wellbeing.

SPECIFIC AGENTS Prostaglandins Which prostaglandin? There are four structural groups of prostaglandins (A, B, E and F). Each of these is further subdivided into 1 or 2, depending on the number of saturated bonds between the carbon atoms, and alpha or beta, depending on their spatial arrangement. Only the E1, E2 and F2 compounds are of obstetric therapeutic interest. The routes of administration can be oral, intravenous, extra-amniotic, intraamniotic, intracervical or high vaginal but for cervical ripening at term, the intravaginal route is most commonly used. Dinoprostone (prostaglandin E2 gel) Intravaginal dinoprostone (prostaglandin E2) gel is commonly used to ripen the unfavourable cervix on the day prior to planned induction of labour. A dose of 1 mg would be recommended initially and 1 or 2 mg (depending on response) 6 hours later as long as the cervix remains unfavourable, uterine contractions have not established and fetal wellbeing is satisfactory. In some circumstances a third dose of dinoprostone may be required; however, the total dose should not normally exceed 5 mg. Dinoprostone slow-release pessary Controlled-release pessaries are designed to deliver approximately 4 mg of dinoprostone over a 12-hour period. A string attached to the pessary enables easy removal of the pessary in the event of hyperstimulation. A slow-release vaginal pessary containing misoprostol is also available. Misoprostol tablets These come in 200-mcg tablets formulated for the treatment of peptic ulcers. Misoprostol is highly effective in cervical ripening and induction of labour. The 200-mcg dose is commonly used orally or vaginally 4 hourly for second trimester induction of labour but almost inevitably causes hyperstimulation of the uterus at term, with consequent severe fetal compromise and sometimes even uterine rupture. A dose of 12.5 to 25 mcg can be obtained by dissolving the misoprostol in solution and administering only aliquots of 1/16 or 1/8 of the mixed solution.

excessively frequent (> 5 in 10 minutes) or of excessive duration (> approximately 70 seconds), placental oxygenation will fall and the fetus will become first hypoxic and then acidotic. Excessively frequent contractions is termed uterine tachysystole. Where this results in fetal compromise, it is termed uterine hyperstimulation. The other consequence of excessive uterine muscular activity is the possibility of excessive thinning of the lower uterine segment as the upper segment contracts (and retracts) vigorously around the fetus. This can result in uterine rupture, most commonly from a tear within the lower uterine segment. A less than full thickness tear can result in a uterine vein being torn, with intrauterine pressure forcing amniotic fluid into the maternal blood stream. The catastrophic consequences of amniotic fluid embolism are covered in Chapter 36. Management of excessive uterine muscular activity Uterine tachysystole mandates continuous cardiotocography and consideration of any oxytocic cessation. If the contractions are relatively low intensity and with some interval between, some clinicians will refrain from immediately withdrawing the oxytocic and opt for vigilant observation of the fetal wellbeing. Where there is any evidence of fetal compromise (uterine hyperstimulation), any oxytocic must be discontinued (e.g. cessation of any oxytocin infusion, removal of a dinoprostone pessary or attempted removal of dinoprostone gel from the vagina) and consideration given to the administration of a tocolytic in order to suppress the excessive uterine activity. Alternative tocolytic regimens are given in Table 29.2.

Contraindications to prostaglandin administration The following are relative contraindications to administering prostaglandins for cervical ripening or induction of labour. Conditions that predispose to uterine rupture. Grand multiparity and previous uterine scar are predisposing factors for uterine rupture and are relative contraindications to prostaglandin administration.



TABLE 29.2  ACUTE TOCOLYSIS FOR UTERINE HYPERSTIMULATION. Drug

Dose

Salbutamol

50 mcg slowly intravenously; repeated if necessary up to 250 mcg, but one or two doses usually sufficient

Terbutaline

250 mcg subcutaneously

Glyceryl trinitrate

400 mcg sublingual or buccal spray; may be repeated once if necessary

Adverse effects of prostaglandins

Excessive uterine muscular activity The principle concern with prostaglandin administration is the risk of excessive uterine muscular activity. The clinical consequences are twofold. First, there is a reduction in uteroplacental blood flow with every uterine contraction. If the sufficiently intensive contractions are 246

Chapter 29  Induction of Labour, Including Cervical Ripening



Any situation where there is concern that fetal compromise will develop in the presence of increased uterine muscular activity. An unfavourable cervix in the presence of suspected placental insufficiency is probably best managed with a transcervical balloon catheter rather than prostaglandins as the likelihood of sudden severe fetal compromise with uterine tachysystole will be reduced.

Pre- and post-prostaglandin fetal surveillance A reactive antenatal cardiotocograph should immediately precede the administration of prostaglandins, both the first dose and any subsequent doses. Some units have protocols that recommend repeat cardiotocographs approximately 6 hours after the administration of prostaglandins to detect fetal compromise related to uterine activity that is not otherwise apparent. All women need continuous cardiotocography in any labour subsequent to prostaglandin administration.

Transcervical balloon catheter In women in whom the cervix is unfavourable, a 30-mL Foley balloon catheter is passed through the cervix. The balloon is then insufflated with saline in the lower segment of the uterus. This is most often done on the evening before planned induction of labour in the presence of an unfavourable cervix. The Foley balloon is usually expelled from the lower uterine segment through the cervix overnight, leaving a cervix ripe for induction of labour the next morning.

Adverse effects of a transcervical balloon catheter Infection The main concern when using a catheter for cervical ripening is that infection may be introduced and chorioamnionitis may result. In practice, this does not appear to be a significant problem. However, given that even a very small number of cases of chorioamnionitis would be clinically important, those employing this technique should be vigilant in their aseptic technique and be alert to any increase in incidence of chorioamnionitis.

Artificial rupture of the membranes Mechanism of action Artificial rupture of the membranes (ARM) probably works in two ways. First, there is likely to be an increase in endogenous prostaglandin release which both directly augments uterine muscular activity and also increases receptivity to endogenous or exogenous oxytocin. Second, prior to ARM intrauterine pressure is directed evenly in all directions as per any fluid-filled cavity. Following ARM, contraction will exert a more direct pressure on the fundal pole of the fetus, forcing the presenting part down against the cervix, which will assist mechanically with cervical dilation and, via the Fergus reflex (Ch 27), will promote endogenous oxytocin release.

Technique An aseptic technique should be performed, first swabbing the vulva and vagina with aqueous chlorhexidine and then using chlorhexidine lubricant, sterile gloves and sterile implements. The instrument used for the procedure depends on the preference of the operator. Most commonly, the specially designed AmniHook is used but alligator forceps are an alternative, particularly if the procedure is difficult in the presence of a cervical score that is lower than usual. After the procedure, a check for cord prolapse is made, and the fetal heart is auscultated. If the amount of liquor is greater than normal, the hand should be kept in the vagina and the liquor released slowly. It is preferable not to perform an ARM when the head is mobile. Sometimes, however, it is necessary and wise to make sure the presenting part remains over the pelvic brim and the liquor drains away. Early use of an oxytocin and vertical posturing will make it less likely that the presenting part drifts into one or other iliac fossa.

Adverse effects of ARM

Cord prolapse This will be most likely when ARM is performed with a high mobile presenting part, a malpresentation or polyhydramnios. Infection ARM should be performed aseptically, as indicated.

Oxytocin infusion for induction of labour Regimen This should almost always be preceded by spontaneous or artificial rupture of the membranes, as indicated. The concentration and infusion rate will be dictated by local preference. A widely used regimen places 10 units per 1000 mL normal saline or Hartmann solution (10 units/L). An infusion pump line is usually inserted into the routine intravenous drip line. Beginning with an infusion rate of approximately 12 mL/hr (0.12 units/hr, 2 milliunits per minute), the infusion rate is increased by 12 units at intervals until regular contractions of moderate intensity are occurring at a rate of approximately four in 10 minutes. If there is good progress of labour (cervical dilatation of at least 1 cm/hr) or more than four contractions in 10 minutes, the oxytocin infusion rate should not be increased. It is wise to increase the oxytocin dose only every 30 minutes, since it takes this time for plasma levels of oxytocin to reach a steady state. During the infusion, the frequency and nature of contractions should be assessed every 15 minutes.

Adverse effects of an oxytocin infusion

Excessive uterine muscular activity This may result from overdosage or unusual sensitivity to oxytocin. The latter is particularly prevalent when 247

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prostaglandins have been used for cervical ripening. As a consequence, the oxytocin infusion rate should be commenced at a lower rate after prostaglandin use. Hypotension Oxytocin has a mostly mildly hypotensive effect but some women exhibit greater sensitivity to this side effect. This side effect presumably relates to the fact that the structure of oxytocin is analogous to the vasoconstrictor vasopressin. Water intoxication In contrast to an apparent antagonism of the vasoconstrictor effect of vasopressin, oxytocin has an agonistic effect with respect to water retention. Where high doses of oxytocin are used, hyponatraemia can be a problem. This is now very uncommon; however, prior to the availability of prostaglandins very high doses and prolonged use of oxytocin frequently caused serious water intoxication. Postpartum haemorrhage Oxytocin, like other hypothalamo-pituitary peptides, down-regulates its own receptor. This means that there will be reduced sensitivity to endogenous oxytocin if the high levels of infused oxytocin are ceased. This can

248

be particularly important after birth. The oxytocin infusion used for induction or augmentation should be continued for at least an hour after birth to assist in maintaining uterine tone and preventing postpartum haemorrhage. REFERENCES 1) Koopmans CM, Bijlenga D, Groen H, et al.; HYPITAT study group: Induction of labour versus expectant monitoring for gestational hypertension or mild pre-eclampsia after 36 weeks’ gestation (HYPITAT): a multicentre, open-label randomised controlled trial. Lancet 2009;374(9694):979–88. 2) Hannah ME, Hannah WJ, Hellmann J, et al. Induction of labor as compared with serial antenatal monitoring in post-term pregnancy. A randomized controlled trial. The Canadian Multicenter Post-term Pregnancy Trial Group. N Engl J Med 1992;326(24):1587–92. 3) Walker SP, McCarthy EA, Ugoni A, et al. Cesarean delivery or vaginal birth: a survey of patient and clinician thresholds. Obstet Gynecol 2007;109(1): 67–72.

Chapter 30  EPISIOTOMY AND VAGINAL OUTLET TEARS Michael Permezel and Gillian Paulsen

KEY POINTS An episiotomy is a valuable adjunct to the management of a vaginal birth but should only be used when clearly indicated. Indications for episiotomy include to avoid a major perineal tear, expedite birth, reduce traction needed during instrumental birth and improve access for manipulative deliveries. Midline episiotomies have only a very limited place in clinical practice as there is a higher likelihood of extension into the anal sphincter. Third- and fourth-degree perineal tears require an experienced surgeon with good lighting and adequate analgesia. A cervical tear should be expected if there is brisk bleeding immediately after delivery of the baby and before the placenta has separated. A vulvovaginal haematoma usually requires a urinary catheter and conservative management is generally preferred.

EPISIOTOMY An episiotomy is an incision made in the perineum and vagina that enlarges the introitus and lessens the curve of the birth canal to facilitate the birth of the fetus.

INDICATIONS The liberal rather than the restricted use of episiotomy for normal delivery does not appear to offer any benefits. However, judicious use can avoid serious complications of vaginal birth. The potential benefits are as follows.

Avoidance of major perineal tear Perineal tear already occurring early with head crowning; instrumental birth A small perineal tear is clearly associated with less discomfort than an episiotomy. However, an episiotomy may

avoid a large tear, a ragged tear that does not heal well or a tear in areas of particular disadvantage such as in the anterior compartment around the urethra or clitoris and involving the anal sphincter (see the section on third- and fourth-degree tears later in this chapter). There is little doubt that enlarging the posterior compartment with an episiotomy will reduce anterior tears (Fig 30.1). The evidence for avoiding third- and fourth-degree tears is less clear.

Expedite birth Fetal compromise and/or inadequate progress with the head on the perineum; vaginal breech delivery It is common, especially in a nulliparous woman, that an inelastic perineum will considerably delay birth, with possible consequences in terms of fetal compromise and compression injury to the nerves of the pelvic floor.

Beischer & MacKay’s: Obstetrics, Gynaecology and the Newborn

Traction force reduction

involved. Analgesia can be provided with local infiltration in the absence of a regional or pudendal block.

Instrumental birth; breech extraction A tight perineum can add considerably to the traction forces necessary to effect an instrumental birth or even a breech extraction. An episiotomy will reduce the traction required, with obvious benefits for the fetus. If the perineum is not particularly ‘tight’, an episiotomy may not be necessary.

Improve access for manipulative delivery Shoulder dystocia; vaginal breech delivery Occasionally, a tight perineum may make manipulative birth more difficult. Examples of this include delivery of the posterior arm in a case of shoulder dystocia (Ch 34) or delivery of the after coming head of a breech (Ch 15).

THE PROCEDURE Prior to the episiotomy Before episiotomy is carried out, it is important to explain to the woman the reason for the procedure and what is

Clitoris

External urinary meatus

Technique of the surgical incision Mediolateral episiotomy A finger should be inserted into the vagina to guard the fetal head during local anaesthetic infiltration of the perineum when the perineum bulges downwards during a contraction (Fig 30.2). The incision is made when the head bulges the perineum because it is easier to judge the proper length, the anal sphincter is displaced and blood loss is less. One blade of the scissors is inserted inside the vagina with the cutting angle resting on the fourchette. The incision is made posterolaterally at a 45° angle (at a position equivalent to 7.30 on the clock). Make a single cut during a contraction (Fig 30.3). It is important not to begin the incision away from the midline as Bartholin’s duct may be inadvertently damaged. If delivery is not immediate, bleeding from the cut edges can be controlled by firm pressure with a gauze swab while awaiting the next contraction.

Midline episiotomy A midline episiotomy has the major disadvantage that extension through the anal sphincter is significantly more common. The advantages of this technique are less bleeding, greater ease of repair, less pain during healing and a lower incidence of subsequent dyspareunia. If vulval varicosities are particularly severe, a midline episiotomy will reduce blood loss compared to a mediolateral episiotomy. Median

Mediolateral J-shaped

Internal pudendal artery

Para-urethral tear due to failure to cut an episotomy

Inferior rectal artery

FIGURE 30.1 

Anterior vulval tear in the para-urethral region. An episiotomy may well have avoided this painful injury. The area near the urethral meatus and clitoris is very vascular and careful suturing is required. 250

FIGURE 30.2 

Types of episiotomy incision. If the incision extends past the anus, it enters the area innervated by the perforating cutaneous nerves which are not affected by a pudendal nerve block.

Chapter 30  Episiotomy and Vaginal Outlet Tears

A

B

C FIGURE 30.3 

Technique of episiotomy. A Local analgesia was provided by perineal infiltration (trickle of blood marks site of injection) when the head bulged the perineum. Note anal dilatation during a contraction. B The scissors are in position at the fourchette. C The incision being made during a contraction. Source: Courtesy of Prof. Norman Beischer.

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REPAIR AND MANAGEMENT OF AN EPISIOTOMY Prior to surgical closure The main principles in repair are to identify key structures and extent of the lesion, obtain haemostasis, align the edges anatomically and not suture too tightly. The woman is usually in the lithotomy position but a small lesion can be repaired in the dorsal position. There must be sufficient vision to be able not only to perform the surgical repair but also to clearly identify the structures involved, particularly whether the anal sphincter has been affected (see the section on third- and fourthdegree tears later in this chapter). The operative field is prepped, draped and well illuminated. Perineal infiltration with lignocaine 0.5 to 1% through the cut surface of the wound is performed if anaesthesia is inadequate. Synthetic absorbable sutures are used throughout. Catgut and chromic catgut have been shown to produce more pain in the early postnatal period.

A FIGURE 30.4 

Surgical closure Repair of the vaginal epithelium The first step is the repair of the vaginal epithelium, and for this a continuous suture is used (Fig 30.4A). A gauze pack may be introduced into the vagina to aid exposure. The structures to be sutured are identified and vaginal lacerations sought. Arterial bleeding is dealt with by clamping and ligating the vessel, but oozing from epithelial and skin edges is controlled by the pressure applied by the sutures. Haemostasis is imperative, otherwise extensive bruising and haematoma formation can occur with the subsequent complications of pain, infection and disruption of the wound. Sutures are placed at about 1-cm intervals and a good bite of epithelium and submucosa is taken to obliterate dead space. Vaginal lacerations are also repaired. Sutures should not be tied too tightly because of the swelling which occurs in the following 24 to 48 hours. Three markers should be used for accurate opposition: the vaginal apex, the hymen and the mucocutaneous junction.

B

Repair of episiotomy. A The vaginal incision has been sutured from apex down to the introitus. B Interrupted sutures have been inserted in the perineal muscles. Finally, the skin will be closed with a subcuticular continuous suture. Source: Courtesy of Prof. Norman Beischer.

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Occasionally, the episiotomy incision extends high up the vagina, usually due to difficulty with the delivery of the shoulders. If the upper limit of the vaginal incision cannot be seen, a stitch is inserted as high as possible and tied; traction upon this stitch then exposes the upper limit of the incision, which is sutured.

Approximation of the perineal muscles The second step is approximation of the perineal muscles. Interrupted sutures are used (Fig 30.4B) because they control bleeding and reduce dead space, thus preventing haematoma formation. Usually two to three sutures are sufficient. The anatomical distortion inevitable with the mediolateral incision should be allowed for as the lower elements of the levator ani muscle and the bulbocavernosus muscle are sutured. The ultimate strength of the repaired pelvic floor depends mainly upon this layer.

Closure of the perineal skin The third step is closure of the perineal skin, which is performed with a continuous subcuticular suture beginning posteriorly and working back towards the fourchette with absorbable suture material.

Immediately after surgical closure Once surgical closure is complete, a vaginal examination ensures that no pack remains and a rectal examination excludes stitches in the rectum or anal canal. If there is persistent oozing from an episiotomy wound and/or vaginal lacerations after repair, haemorrhage can usually be controlled by insertion of a gauze pack (10 cm × 2 m) into the vagina. This is removed 12 to 24 hours later. If a pack is used, an indwelling catheter is inserted because the pack will occlude the urethra and prevent voiding. If packing is required, an antibiotic should be prescribed.

Care in the early puerperium Analgesia is needed for the first 48 to 72 hours. Pain is greater with larger episiotomies and much external suturing, long second stage, operative delivery and perineal bruising. An icepack during the first 24 hours will reduce bruising and swelling. The wound should be kept clean and dabbed dry after showering. Non-steroidal antiinflammatory drugs (NSAIDs) are beneficial if discomfort is significant.

Complications of an episiotomy Infection Infection is relatively uncommon considering the nature of the area. It usually takes the form of a stitch abscess or infected haematoma, but occasionally infection of the ischiorectal fossa may occur.

Wound breakdown This is usually the result of poor suturing technique (e.g. knots too tight) or an infected haematoma. Management is usually to await healing without resuturing but with a

large wound some approximation of the wound edges is needed, which can be achieved with two or three large sutures with entry points well away from the wound edges.

PERINEAL TEARS CLASSIFICATION Perineal tears are classified in degrees from 1 to 4, as shown in Table 30.1.

PREDISPOSING FACTORS Rapid second stage of labour Instrumental birth; precipitate birth The connective tissue and muscles of the perineum have proportionately more tearing and less stretching, the more rapid the birth. Prevention In both the above situations, the accoucheur is responsible for effecting delivery in a controlled manner. This extends back to antenatal education and preparation of the woman for the second stage of labour.

Large presenting part or shoulders Large fetus; malpresentation with unfavourable diameter presenting (face to pubis) Occasionally the fetus may present with an arm alongside the head, leading to a sudden expansion of the perineum as the flexed elbow delivers. A ‘face to pubis’ birth is almost always associated with increased tearing in the absence of a large episiotomy. Prevention This can be prevented in two ways: 1. employ strategies to reduce macrosomia such as dietary advice and selected induction of labour; and 2. avoid ‘face to pubis’

TABLE 30.1  CLASSIFICATION OF PERINEAL TEARS. Degree

Structures involved in the perineal tear

1st

Skin, subcutaneous tissue and superficial fascia

2nd

Muscles of the perineum

3rd

Anal sphincter

  3A

  < 50% of the external anal sphincter

  3B

  ≥ 50% of the external anal sphincter

  3C

  internal anal sphincter involvement

4th

Anorectal mucosa 253

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instrumental delivery by either rotation before vaginal birth or caesarean section.

Perineum less elastic Nulliparity; scarring from a previous perineal tear or episiotomy Approximately 80% of women having their first baby will have a perineal tear. The major modifications to connective tissue during pregnancy are just sufficient in most women to allow passage of the fetus through the introitus with only minor perineal tears (first or seconddegree). Following the first birth, an increased ability of the perineum to ‘stretch’ is retained and perineal tears are much less common with a second or subsequent birth. There are also presumably inherent individual characteristics of connective tissue that make tearing more or less likely under the same stretch impulse. There are no known effective pharmacological techniques to make the perineum more elastic and therefore prevent tears. Devices that mechanically stretch the perineum in late pregnancy may have a role but studies examining long-term consequences with respect to prolapse are awaited. A timely episiotomy may avoid anterior tears (Fig 30.1) or major perineal tears by directing the stretch away from the sphincters. However, if performed too early and too small, all the stretch will be taken in that part of the perineum and an extension, possibly through the sphincter, becomes even more likely than if there was no episiotomy at all.

COMPLICATIONS Anorectal incontinence may occur if there is unrecognised disruption of the anal sphincter and therefore inadequate restoration of the normal anatomy. Transient incontinence is most often a result of neuropraxia and recovers after the first couple of weeks. An unrepaired anal sphincter injury will produce continuing symptoms with incontinence of flatus and possibly faeces. A rectovaginal fistula will occur with breakdown of a fourth-degree tear but can also occur if a repair suture is placed too deep so that the suture hole can form a fistulous track.

REPAIR AND MANAGEMENT OF FIRST- AND SECOND-DEGREE PERINEAL TEARS These are managed as for an episiotomy.

REPAIR AND MANAGEMENT OF THIRD- AND FOURTH-DEGREE PERINEAL TEARS Prior to surgical closure Third- and fourth-degree tears have a particularly significant risk of long-term sequelae related to anorectal 254

continence and it seems likely that such continence is affected by the quality of the repair. Therefore, the following special measures are usually undertaken for the repair of a third- or fourth-degree tear. Anaesthesia. The procedure is usually performed under regional or general anaesthesia. Local anaesthesia is inadequate. Positioning. The patient is placed in the lithotomy position. Lighting and exposure. Adequate lighting and exposure are used. This usually means that the procedure is performed in an operating theatre or a room in the birth suite that is equipped for such a purpose. Clinician expertise. The procedure should be either performed or supervised by an appropriately trained obstetrician.

• • • •

Surgical closure The external anal sphincter (EAS) and internal anal sphincter are best repaired with a monofilament suture such as polydiaxanone (PDS). Clear identification of the defect is critical. Approximation can occur either by a direct end-to-end apposition or an overlapping technique. The remainder of the repair is as for an episiotomy.

Care in the early puerperium The use of postoperative laxatives is recommended to reduce the incidence of postoperative wound dehiscence. Intraoperative and postoperative broad-spectrum antibiotics are recommended to reduce the risk of infection, which in turn may lead to anal incontinence and fistula formation. Inclusion of metronidazole is advisable to cover the possible anaerobic contamination from faecal matter.

Follow-up care Follow-up visits for assessment of second- and thirddegree tears and identification of continence problems should be recommended 3 to 6 months postpartum. Endo-anal ultrasound may be required. Counselling for future births should be considered for women with thirdand fourth-degree tears, with consideration of caesarean section for future births, especially in women with anal incontinence.

CERVICAL LACERATIONS CLINICAL FEATURES The characteristic feature of a cervical laceration is a steady loss of bright red blood, which commences soon after delivery of the baby. Unless the uterus is also damaged, it is firmly contracted. These features help to distinguish traumatic and placental-site bleeding.

Chapter 30  Episiotomy and Vaginal Outlet Tears

MANAGEMENT Control of blood loss before repair If the loss is heavy, bimanual compression should be employed (vaginal hand pressing firmly against the front of the cervix and lower segment, abdominal hand pressing the back of the uterus downwards and forwards against the vaginal hand). Packing may be used as an emergency, but must be properly performed; it often wastes time and blood, and bimanual compression is preferable.

Technique of repair The vaginal walls are well retracted by an assistant and a systematic inspection is made of the vagina and cervix. If the bleeding is from a vaginal laceration, it is closed with a continuous or interrupted chromic catgut suture. If the bleeding is from a cervical laceration, the cervix is grasped with two or more sponge forceps and drawn down until the apex of the tear is visible. A suture is placed just beyond this to secure haemostasis and the repair is completed with either a continuous or interrupted suture. Cervical lacerations are common during normal delivery (as seen in gynaecological practice when cervical cytology is performed), but seldom cause persistent haemorrhage requiring repair.

If the bleeding is coming from inside the cervical canal, it is likely that its origin is from the placental site or a tear in the uterus; exploration will determine this.

VULVAL OR VAGINAL HAEMATOMA The incidence of significant haematoma formation is approximately 1/1000 deliveries. The bleeding in this case is into the tissues, rather than external. It is caused by continued bleeding from vessels that have retracted into the deep paravaginal and vulval tissues (Fig 30.5). There may or may not be an overlying tear that has been repaired. Obviously, it is preferable to secure any deep bleeding point at the base of a tear or episiotomy to avoid haematoma formation. Rarely, the haematoma may be associated with uterine rupture, in which case the vaginal haematoma will usually extend up into the broad ligament. The degree of discomfort to the woman is proportional to the size of the haematoma; if large, severe pain is experienced (classically perirectal) and shock may result. Management is most often conservative as incision and draining may alleviate ‘tamponade’ of a deep-bleeding vessel and cause further bleeding which is difficult to control. The alternative is to attempt drainage of the

FIGURE 30.5 

Vulval haematoma seen 3 hours after a normal delivery due to failure to achieve haemostasis during repair of an episiotomy. An indwelling catheter was required because of urinary retention. The haematoma was evacuated and the woman was transfused with four units of packed cells. Source: Reproduced with permission from the Royal Women’s Hospital, Parkville, Victoria.

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haematoma with insertion of a vaginal pack to tamponade against further bleeding. A urinary catheter will be needed if a vaginal pack is inserted. FURTHER READING de Leeuw JW, de Wit C, Kuijken JP, et al. Mediolateral episiotomy reduces the risk for anal sphincter injury during operative vaginal delivery. BJOG 2008;115(1):104–8.

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Rezaei Z, Haghighi Z, Haeri G, Hekmatdoust A. A comparative study on relieving post-episiotomy pain with diclofenac and indomethacin suppositories or placebo. J Obstet Gynaecol 2014;34(4):293–6.

Chapter 31  INSTRUMENTAL DELIVERY Michael Permezel and Gillian Paulsen

KEY POINTS Approximately 12% of births are instrumental vaginal deliveries. Common indications include fetal compromise and delay in the second stage of labour. They are also used if the mother is not advised to ‘push’ and for the aftercoming head of a vaginal breech delivery. An instrumental birth can only be contemplated if the cervix is fully dilated and both the presentation and station are favourable. A favourable presentation is usually a vertex but can be a deflexed vertex (usually occipitoposterior) or a face in the mentoanterior position. The ‘station’ required is engagement, which means that the maximum diameter of the presenting part is through the pelvic inlet. Engagement is determined by both abdominal palpation and vaginal examination. With a vertex presentation at engagement, there is no head palpable abdominally and the vertex has reached the level of the ischial spines in the absence of caput or moulding. Prior to embarking on an instrumental birth, the membranes should be ruptured, uterine contractions present, the bladder emptied and appropriate anaesthesia in place. Perineal infiltration may be adequate for a vacuum but not for a forceps delivery. The choice between forceps and vacuum is often an individual one but each obstetrician should be able to do both types of instrumental birth. Simplistically, the vacuum is less traumatic for the mother as forceps need extra room beside the head. However (and importantly), the vacuum is associated with the very serious neonatal side effect of subaponeurotic (subgaleal) haemorrhage.

HISTORY The forceps, first brought into use in the 17th century by the Chamberlens, a Huguenot family, represent one of the milestones in obstetrical practice. The story of the invention is a fascinating one, in that it was hidden from general use for generations for personal profit by the family. James Young Simpson is credited with designing the first vacuum-like instrument in 1848, which he referred to as an ‘Air Tractor’. However, it was not until 1954 that

Tage Malmström in Sweden perfected and introduced the vacuum into clinical practice.

CHOICE BETWEEN INSTRUMENTS: FORCEPS OR VACUUM? In some centres, the vacuum extractor has almost entirely replaced the forceps; in others, it is hardly used at all. The correct situation is probably a balance between the two.

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The pros and cons of the two instruments are given in Table 31.1.

INCIDENCE There is a very wide range according to variations in the facilities available and different philosophies of practice. A common incidence would be approximately 12%. Centres with a high rate of epidural analgesia for pain relief in labour will generally have a higher rate due to a large number of ‘lift out’ instrumental births where the epidural has prevented the mother from being able to push the fetus over the perineum. Units that prefer a caesarean section to a rotational or mid-cavity instrumental delivery will have a lower instrumental rate but a higher caesarean section rate.

INDICATIONS The classical indications for instrumental birth are given below.

PROLONGED SECOND STAGE OF LABOUR This is the most common indication yet also the most contentious. The issue is discussed in more detail in Chapter 33 but, simplistically, a long second stage is undesirable because it increases the risk of fetal compromise and also increases the likelihood of compression injury to the structures (especially nerves) of the pelvic floor. The former can largely be averted by a policy of continuous cardiotography where second stage is prolonged but pelvic floor damage remains an issue. The usual time limits for the ‘active’ second stage (i.e. ‘pushing’) are 2 hours for nulliparas and 1 hour for multiparas, although it should be remembered that these are merely guidelines and will depend on the condition of the mother and fetus as well as the nature and progress of the labour.

FETAL COMPROMISE The fetus is more prone to hypoxia in the second stage of labour for two reasons. First, as a result of the reduced maternal uteroplacental blood flow caused by the high intrauterine pressures during frequent, strong contractions with additional pressure rise from maternal pushing. Second, umbilical cord compression is very common in the second stage of labour with descent of the presenting part. This is rarely a consequence of cord prolapse and much more commonly the cord is tightened around the neck or shoulder or is between a fetal body part and the uterine wall.

MOTHER NOT ABLE TO BEAR DOWN (PUSH) Where the mother is not able to perform Valsalva manoeuvre (strain, push, bear down), an instrumental delivery will be necessary to effect birth. It is very uncommon for the lower birth canal and pelvic floor to allow birth with uterine contractions alone. Almost always some additional forces are required, either maternal effort from above or instrumental traction from below. Conditions where maternal straining is contra­ indicated include severe hypertension, preeclampsia/ eclampsia, cardiac disease, diabetic proliferative retinopathy, subarachnoid haemorrhage, Marfan’s syndrome (risk of aortic dissection) or a tumour or arteriovenous malformation that may haemorrhage under the added pressures of a maternal Valsalva.

AFTERCOMING HEAD OF A VAGINAL BREECH DELIVERY Forceps are often applied to the aftercoming head of the breech, to facilitate delivery (Fig 31.1). It should be noted that traction is being applied to the more brittle parietal

TABLE 31.1  FORCEPS VERSUS VACUUM. Forceps delivery

Vacuum delivery

More

Less

  skull fracture and intracranial haemorrhage

Rare

Extremely rare

  subgaleal haemorrhage

Rare

Uncommon

Analgesia requirement

Regional or general

Perineal infiltration mostly adequate

Contraindications

Those for vaginal birth

Face, preterm < 34 weeks’

Failure rate in the absence of cephalopelvic disproportion

Very low

Low

Maternal trauma Serious fetal injury

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bones in this circumstance rather than around the exceptional hard base of skull. At caesarean section, forceps may be used to deliver the baby’s head through the uterine incision (see Ch 32).

FIGURE 31.1

Forceps delivery of the aftercoming head of a vaginal breech delivery with the assistant holding the baby up by the legs. Source: Courtesy of Prof. Norman Beischer.

STATION PRIOR TO INSTRUMENTAL BIRTH The ‘station’ is the level of descent of the presenting part within the birth canal. The expected difficulty of instrumental birth can be to some extent anticipated by the station of the presenting part at the commencement of the procedure. (See Fig 31.2.) 1. Outlet station (or ‘lift-out’). The head has reached the pelvic floor, the position is anterior and the scalp can be seen at the introitus without parting the labia. 2. Low station. The maximum diameter of the head is through the narrowest plan of the pelvis—the bispinous diameter. Prior to a low-instrumental birth, in the case of a vertex presentation the presenting part will be at least 3 cm below the ischial spines in the absence of caput and moulding. 3. Mid-cavity station. The head is ‘engaged’; that is, the maximum diameter of the presenting part has passed through the pelvic inlet. No head will be palpable abdominally and the vertex has at least reached the level of the ischial spines in the absence of caput and moulding. It is extremely important to realise that in the case of a mid-cavity instrumental birth, the maximum diameter of the head is not yet through the narrowest part of the pelvis. It is still possible that the head may not fit through the pelvis and a caesarean section might be needed if instrumental birth is not easily effected. 4. High station. The head is not engaged.

1 2

A

3

B

C

FIGURE 31.2

Types of forceps delivery and direction of traction. A Station of the head for mid-forceps (1), low forceps (2) and outlet forceps (3) deliveries. The arrows show how the direction of traction must change as the head descends, in order to follow the curve of the birth canal. B The usual type of mid-forceps delivery: the lowest part of the presenting part (vertex) is past the level of the ischial spines and the maximum diameter of the head is through the pelvic inlet. C Outlet forceps: the greatest diameter of the head is past the narrow pelvic plane. Delivery is completed by extension of the head around the symphysis pubis. 259

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DESCRIPTION OF THE INSTRUMENTS OBSTETRIC FORCEPS The obstetric forceps consists of two pieces, joined together by a locking mechanism. Each piece has a handle and this

is connected to the blade by the shank (Fig 31.3). The lock is usually situated at the junction of the handle and shank; it is usually of fixed type but may be sliding, as in Kielland forceps. There is often a projection at the lower end of the handle called the shoulder, which is used for assisting traction and/or rotation of the baby’s head. The blades of the forceps, which are applied to each side of the head, are

A

B FIGURE 31.3

A Barnes forceps are shown on the left and Kielland forceps on the right. The cephalic curve of the blades is similar in each. The different locking mechanisms are shown. B Lateral view showing that Barnes forceps have a much larger pelvic curve than Kielland forceps. Source: Courtesy of Prof. Norman Beischer.

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usually open (fenestrated). In all forceps there is a cephalic curve which fits the contour of the baby’s head, and a pelvic curve, which allows for the concave shape of the sacrum. In forceps primarily designed for rotation of the head (e.g. Kielland forceps), the pelvic curve is minimal. By means of the cephalic and pelvic curves, each forceps blade can be designated as left or right, according to which side of the maternal pelvis it is applied.

VACUUM EXTRACTION DEVICE (‘VENTOUSE’) The principle of use is that a suitably sized plastic or metal cup is applied as near the occiput as possible (to maintain flexion during traction) and a vacuum is created inside the cup by means of a hand or electric pump. Ideally the cup should be placed over the posterior fontanelle symmetrically (i.e. the sagittal suture is evenly overlapped on either side by the cup). The suction draws the loose scalp of the fetus into the cup in the form of a ‘chignon’. Traction is then applied by means of a chain or cord attached to the cup with a handle on the other end. Pressure tubing passes from (or along) the traction handle to the source of suction. A pressure gauge indicates the pressure developed in the system.

THE PROCEDURE OF INSTRUMENTAL DELIVERY PREREQUISITES The traditional description is FORCEP, as follows. 1. Favourable presentation, position and station. Position: the vertex should be occipitoanterior unless using Kielland or similar forceps. If the station is low, it is possible to perform a forceps delivery ‘face to pubes’ with the occiput remaining posterior. In the rare event that a forceps delivery is performed with a face presentation, the necessary position is mentoanterior. Station: the head must be ‘engaged’. This is defined elsewhere in the chapter. 2. Os (cervical) fully dilated. 3. Ruptured membranes. 4. Contractions present: the absence of contractions after a long labour and uterine exhaustion increases the likelihood of an atonic postpartum haemorrhage; in this situation, an oxytocin infusion should be commenced before beginning the instrumental birth 5. Empty bladder. 6. Pelvic and perineal analgesia. It is apparent that steps 3 to 6 can be accomplished with therapeutic procedures but 1 and 2 need to be present. That is, the decision as to whether an instrumental birth

can be contemplated requires FO: a favourable presentation and station with the cervix fully dilated.

PRIOR TO COMMENCING AN INSTRUMENTAL BIRTH The woman should be fully informed of the reason for the procedure and what is involved, but a specific written consent form is not required in most centres. The indication should be clear and also that the basic requirements are met in terms of station, presentation and full dilatation of the cervix.

TECHNIQUE The woman is usually in the lithotomy position and full antiseptic preparations and draping are carried out; precaution against the supine hypotensive syndrome (pelvic tilt) may be indicated as for caesarean birth. Anaesthesia may be local (perineal infiltration), regional (pudendal nerve block, epidural or spinal) or general (Chapter 38) depending on the station and position of the head, and the anticipated difficulty of the procedure. Perineal infiltrate may be adequate for a low vacuum birth but not for a forceps delivery. The bladder is catheterised and then emptied. A careful examination is made to determine the state of the membranes, dilatation of the cervix, presentation, station and position of the head, presence of caput and moulding and the tightness of fit of the head in the pelvis. The forceps are applied left blade first into the hollow of the sacrum and wandered over to the left side of the fetal head. The same on the opposite side occurs with the right blade, followed by locking the two together (Figs 31.4 and 31.5).

Outlet and low forceps delivery Here the blades are applied to the sides of the baby’s head, the left blade being inserted first. A check is made that the forceps are applied correctly and symmetrically. If this is the case, the two blades come together and lock easily (Fig 31.5); the sagittal suture lies midway between the blades and parallel to them. Minor rotation may be necessary to bring the sagittal suture to the anteroposterior position. Traction is applied at the time of contractions and with the mother bearing down. The direction of traction follows the direction of the birth canal. The fetal heart should be auscultated between contractions. As the head distends the perineum, the direction of traction moves horizontally and then upwards in line with the birth canal. An episiotomy is preformed unless there is little perineal resistance and no sign of tearing. The blades are carefully removed as the head is about to pass through the expanded vulva, and the rest of the procedure is carried out as for a normal delivery.

Mid-cavity forceps delivery The general procedure is similar to that outlined in the outlet forceps, the main difference being in the rotation of the fetal head. The first essential is an accurate appraisal 261

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A

B

C

D

E

F

G FIGURE 31.4

Technique of forceps application.  Note that forceps are held with the handle in the palm of the hand when being applied; in these pictures the instrument is held by the shank to show the movements of the handle. A Introduction of the left blade. The handle is rotated through a wide circle to avoid trauma by the blade as it rotates into position around the head. B The handle is lowered and the blade passes the fetal cheek and temple. C The blade in position when applied to the head with its pelvic curve coinciding with that of the birth canal. D Introduction of the right blade which is inserted in the midline. E The blade passing fetal cheek and temple. F The forceps in position and locked. G The biparietal diameter of the fetal head is enclosed within the widest diameter of the forceps and the tips overlie the fetal cheeks. The head is well flexed (posterior fontanelle readily palpable). Source: Courtesy of Prof. Norman Beischer.

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A

B

C

D

FIGURE 31.5

Forceps application and delivery. A This primigravida had delay in the second stage of labour with the head on view. An outlet forceps was performed. The left forcep blade is first inserted between the fetal head and the hollow of the sacrum. Note lubrication of the forceps and the fingers of the left hand protecting the vaginal wall. B The right forcep blade is then inserted into the same position and wandered 90° to the right in the same way as the left. C The forceps have been locked into position and a right mediolateral episiotomy is performed, commencing at the fourchette in the midline. D Delivery of the head by traction. Source: Courtesy of Prof. Norman Beischer.

of station, flexion and position. This is aided by the usual measures of palpation of sutures and fontanelles. If there is any uncertainty, additional palpation of the ear and occipital ridge is essential (Fig 31.6). Ultrasound may be used to confirm fetal position but will rarely be needed by an experienced accoucheur. If the position is not occipitoanterior, rotation of the head is achieved either manually or by means of forceps. If manual rotation is performed, the head is held in the anterior position and the forceps blades are applied. Great care is necessary to ensure that they are symmetrically placed on the baby’s head, since this is the key to successful delivery and a baby in good condition. Traction is often much greater than that required for outlet forceps. Because of the higher station in the pelvis, the correct direction of pull is aided by exerting downward pressure on the shanks of the forceps with traction (Pajot’s manoeuvre) or applying the axis traction apparatus.

If forceps rotation is to be attempted, a larger episiotomy is usually made and the Kielland forceps employed. The blades are applied to the fetal head in the posterior or occipitolateral (transverse) position, usually by ‘wandering’ the anterior blade over the baby’s face (the sinciput being smoother than the occiput offers less resistance to the forceps blade as it is rotated into position), and directly applying the posterior blade. The handles of the instrument are pushed downwards against the perineum and the occiput is rotated to the front by means of a rotational force applied to the shoulders on the blades. While traction forces are applied to the very hard bones at the base of skull, rotational forces are applied over the softer parietal bones. Fetal damage (skull fracture and/or intracranial haemorrhage) may be the consequences, and rotational forceps should only be undertaken with caution and under the direction of an experienced obstetrician. 263

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A

B

FIGURE 31.6

Diagnosis of position of the fetal head. A The anterior fontanelle is readily palpated when the head is deflexed (unless there is considerable caput). B When the position is occipitolateral, the ear may be palpated below the pubic symphysis. The root of the ear indicates whether the occiput is to the left or right.

Vacuum birth The cup, lubricated with obstetric cream, is inserted into the vagina—preferably at the time of a contraction. Perhaps the single most important factor in safety and success is placement of the cup in the proper area of the fetal skull. The application of the vacuum cup is at the flexion point, which is 3 cm anterior to the posterior fontanelle. The edge of the cup should abut the edge of the posterior fontanelle. After a negative pressure of 0.1 to 0.2 kg/cm2 is reached, a check is made that there is no interposed maternal tissue under the cup edge. Traction is applied coincident with uterine contractions and maternal effort. If the position of the fetal head is not occipitoanterior, the direction of pull is the same but the occiput should rotate to the front spontaneously during descent. The vacuum should not be applied for more than 15 minutes and should also be ceased if there is no progress with active pulling with three contractions. If birth has not been achieved, either caesarean section or forceps delivery should be performed. Vacuum birth followed by forceps delivery has the highest complication rates but becomes the only option if the head has reached a low station but the vacuum has been unsuccessful.

NON-VERTEX PRESENTATIONS Face presentation The same principles apply as with vertex presentations; however, greater care is necessary to avoid damage to the facial structures during placement of the blades. Obviously, a vacuum cannot be used with a face presentation.

Brow presentation In most cases of brow presentation at full dilatation, a caesarean section is still the preferred option. However, some brows will descend deeply into the pelvis and behave 264

more as a particularly deflexed occipitoposterior position. In these cases, rotation with Kielland’s through 180° may lead to flexion of the fetal head and a relatively easy delivery of a vertex in the occipitoanterior position.

TRIAL OF INSTRUMENTAL DELIVERY A trial of instrumental delivery is done in the operating theatre, with everything ready for caesarean section should the instrumental delivery not succeed. There are several advantages to being in the operating theatre for what may be either a difficult instrumental birth or a failed instrumental birth and caesarean section. Fetal condition is commonly compromised by a trial of instrumental birth. This is thought to be a consequence of a vagal reaction to the application of either vacuum or forceps. The consequent bradycardia can cause hypoxia and acidosis as a consequence or reduced fetal placental blood flow. If a difficult instrumental vaginal delivery is successfully accomplished, both shoulder dystocia and lower genital tract tears are common. Both these conditions benefit from the superior anaesthesia, lighting and assistance available in the operating theatre.





FAILED INSTRUMENTAL BIRTH ‘Failed instrumental birth’ is an undesirable term as it implies some deficiency in management when in fact the opposite is more likely. The astute clinician is aware that it is very difficult to predict which mid-cavity instrumental birth can be effected easily with minimal risk to mother and fetus and which cannot. The wise course of action in these circumstances is obviously to attempt an instrumental birth but if unexpected difficulty is encountered at any step (application, rotation or traction), abandon the procedure and move to prompt caesarean section.

Chapter 31  Instrumental Delivery

Forceps delivery after failure of vacuum A particular situation is where the vacuum fails to obtain an airtight seal and traction keeps resulting in the seal being broken and the cup falling off. Many clinicians will then appropriately apply the forceps, particularly if the station is low. Criticism that a caesarean section should have been performed would appear ridiculous if the station is low and the forceps performed without difficulty.

ADVERSE EFFECT OF INSTRUMENTAL BIRTH MATERNAL High vaginal and cervical tears, third- and fourth-degree perineal tears Even with a meticulous technique, tears are to some extent unpreventable. Every effort should be made to perform procedures slowly to enable tissues to stretch rather than tear.

Postpartum haemorrhage This may be from genital tract trauma (at any level) but also from an atonic postpartum haemorrhage. It is not uncommon to perform an instrumental birth for delay in the second stage related to uterine exhaustion. Having delivered the baby with forceps or vacuum, the uterus remains atonic in the third stage of labour. For this reason, contractions should be reinstated with an oxytocin infusion prior to embarking on an instrumental birth.

FETAL Skull fracture and/or intracranial haemorrhage Incorrect application of the forceps may cause abnormal distortions of the skull architecture with potential rupture of large intracranial veins. Mostly this is inadvertent and a consequence of excessive moulding of the fetal head, rather than incorrect technique. It happens that with the unmoulded fetal head in the occipitoanterior position, the tips of the forceps (where traction is applied) serendipitously come to lie on the extremely hard mastoid and petrous temporal bones at the base of the skull. However, with a posterior position or excessive moulding, traction may be exerted over the softer occipital bones with resulting risk to the integrity of the skull and the underlying intracranial vessels. Also, during rotation, there are forces applied to the parietal and frontal bones that are less able to take these stresses (Fig 31.7). Damage to the cervical spine and/or vertebral arteries may occur with rotational births. Complete uterine relaxation (often assisted pharmacologically) is essential before embarking on a rotational forceps. Direct damage to structures such as the eye, nose and ear is more likely (Fig 31.8). Occasionally, pressure

FIGURE 31.7

Depressed fracture of the left frontal bone in a 1-day-old 3100 g male infant born after a Kielland forceps rotation. The fracture was elevated after four days and the outcome was (surprisingly) good. Source: Courtesy of Prof. Norman Beischer.

of the forceps blade on the facial nerve as it passes forwards in front of the ear causes temporary paralysis of that side of the face. Abrasions are not uncommon, but these heal quickly.

Sub-aponeurotic haematoma (subgaleal haemorrhage) The scalp is an aponeurosis that slips easily over the underlying skull. This property reduces the risks of abrasive injury with bumps to the head. The absence of any firm attachment between scalp and underlying skull means that there is a large potential space into which bleeding can occur. The volume can be more than 500 mL and result in fatal hypovolaemia in a neonate with total blood volume not much more than a litre. This most commonly occurs with vacuum birth when the scalp is lifted from the skull, potentially tearing veins. Early diagnosis is essential and there are recommended guidelines for close neonatal surveillance after anything other than very straightforward vacuum births.

Soft tissue injury The vacuum causes a large oedematous lump on the scalp (chignon). This disappears in the first 24 hours. Of longer duration is a cephalhaematoma which is due to subperiosteal bruising (Fig 31.9). This can last many weeks but eventually resolves. It is particularly common after forceps delivery but also may occur after vacuum birth or even spontaneous vaginal birth.

Shoulder dystocia While not strictly a consequence of the instrumental birth, if the head just makes it through the pelvis it is 265

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A FIGURE 31.9

Bilateral cephalhaematoma in a 4-day-old infant of birth weight 4170 g born by mid-cavity forceps from the occipitoanterior position. These can be expected to resolve spontaneously without long-term sequelae. Source: Courtesy of Prof. Norman Beischer.

possible that the shoulders may not. Anticipation of possible shoulder dystocia should accompany every mid-cavity instrumental birth undertaken for failure to progress. This is particularly so if the position is occipitoanterior, as it is genuine cephalopelvic disproportion causing the slow progress rather than an unfavourable presenting diameter as occurs with a posterior position. B FIGURE 31.8

A Periorbital haematoma in a 4-kg male infant aged 4 days. He was born by rotational forceps. B Corneal opacity beneath the orbital haematoma, related to a corneal abrasion. Two weeks later the corneal opacity had resolved but vision was impaired in that eye at follow-up. Source: Courtesy of Prof. Norman Beischer.

266

FURTHER READING RANZCOG. College statement: instrumental vaginal delivery (C-Obs 16); Nov 2012. Online. Available: . RANZCOG. College statement: rotational forceps (C-Obs 13); Nov 2012. Online. Available: . RANZCOG. College statement: prevention detection and management of subgaleal haemorrhage in the newborn (C-Obs 28); July 2012. Online. Available: .

Chapter 32  CAESAREAN SECTION AND TRIAL OF LABOUR AFTER CAESAREAN Michael Permezel

KEY POINTS Caesarean section is the mode of birth in approximately 30% of pregnancies. The overall rate is surprisingly uniform across Western countries, with the Scandinavian countries having notably lower rates than others. The rise in the caesarean section rate over the last 50 years has generated much political debate. There are essentially two reasons for this rise. The first is an increasing incidence of conditions more likely to lead to caesarean section such as advanced maternal age and increasing maternal obesity. The second and more important reason is the evolution of a more risk-averse population. In the past, a less risk-averse maternity sector would attempt vaginal birth with conditions that had a ‘low’ incidence of poor outcome that could have been averted by caesarean section. For most women now, unless the likelihood of an adverse outcome as a consequence of vaginal birth is ‘extremely low’, caesarean section will be preferred. The most common reason for a caesarean section is that the woman has had one previously. The first caesarean section most commonly had been performed for obstructed labour, poor progress in labour and/ or fetal compromise or a malpresentation. Approximately 99% of caesarean sections are performed through a transverse incision in the lower uterine segment. The classical incision is a vertical incision in the upper uterine segment and the consequent uterine scar is 20 times more likely to rupture in the next pregnancy in comparison to the lower-segment incision. Overall, a woman who has had a single transverse lower uterine segment caesarean section has a 1 in 200 risk of uterine rupture if she tries to birth vaginally in her next pregnancy and approximately 1 in 5 of these will be associated with a perinatal death. The improved perinatal outcome with repeat caesarean section is partly due to avoiding uterine rupture but even more attributable to the lower perinatal mortality if born at 39 weeks’ gestation rather than awaiting spontaneous labour beyond that date. If labour is occurring after a previous caesarean section, assessment of both fetus and progress should be vigilant, with early recourse to caesarean section if progress is inadequate or there is acute fetal compromise.

DEFINITION Caesarean section is the surgical technique whereby the fetus is delivered through an incision in the uterus.

INCIDENCE There is considerable variation in the incidence of caesarean section between types of hospitals, with higher rates

in the tertiary centres and private sector. The overall caesarean section rate in most OECD countries is in the 28 to 32% range; Australia is fairly typical. Much has been made of the continuing rise in caesarean section rate. Clearly, it is not unique to Australia. There are essentially two reasons for this rise. First, there is a change in profile of the pregnant population that makes them more likely to need a caesarean section. The most obvious changes are increases in maternal age,

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maternal obesity and gestational diabetes mellitus (in part linked to the first two). The other and more important reason for the worldwide increase in caesarean section is that women are becoming more ‘risk averse’. That is, most women are relatively intolerant of even small risks to their fetus in order to achieve a vaginal birth.1 This means that where previously most women would be accepting of the very small added risks of, say, vaginal breech delivery, most women now will opt for a caesarean section in that circumstance. Other obstetric conditions carry similar small risks with vaginal birth (e.g. previous caesarean section) and many women now choose caesarean section over attempted vaginal birth in such situations.

TYPES OF OPERATION UTERINE INCISION Lower uterine segment caesarean section The lower uterine segment caesarean section (LUSCS) is by far the most common technique (98%). The approach is nearly always a transverse one through the lower uterine segment after opening the peritoneal cavity and then the loose peritoneum over the lower uterine segment. Rarely, an extraperitoneal approach is used.

Classical caesarean section This was the only type of operation used for several centuries, hence the term ‘classical section’ but is now performed in only approximately 1% of caesarean sections. A vertical incision is made in the upper part (i.e. body) of the uterus (Fig 32.1). Common indications include a transverse lie with the back down and extreme prematurity where there the lower uterine segment is not as yet formed. Classical caesarean section has a much higher rate of uterine rupture in subsequent pregnancy, both antenatally

A FIGURE 32.1

and in labour. If vaginal birth is attempted after a classical caesarean section, uterine rupture can be expected in about 10% of cases (compared to only 0.5% after a transverse lower uterine segment caesarean section).

Vertical lower uterine segment caesarean section This is a ‘compromise’ technique where the lower segment is not yet fully formed but is long enough to deliver a preterm infant. Rupture rates in a subsequent pregnancy are probably less than for a classical incision.

ELECTIVE/EMERGENCY CAESAREAN SECTION An elective caesarean section is both planned antenatally and performed before the onset of labour. An emergency caesarean section is either performed in labour or unplanned in the antenatal period. A repeat elective caesarean section at 39 weeks’ on a routine operating list would be elective, but a caesarean section performed for fetal compromise or obstructed labour would be an emergency. The distinction is not always clear as a woman with a previous caesarean section may develop preeclampsia and the following day have a previously unscheduled caesarean section—this could be classified either as emergency or elective.

INDICATIONS There are few more contentious issues in medicine than the decision to have a caesarean section rather than a vaginal birth. Passions run high on both sides of the decision equation. As indicated earlier, this is not a unique situation in any geographic location and not confined to the developed world. China and Brazil both have relatively high caesarean section rates while the rates in Scandinavian countries are relatively low compared to others in Europe.

B

A The lower uterine segment incision. Note the thin uterine muscle and incision in the lower uterus just above the retractor. B The classical caesarean section incision. The skin is still incised transversely above the symphysis but the uterine incision is vertically through the thick muscle of the upper uterine segment. 268

Chapter 32  Caesarean Section and Trial of Labour after Caesarean

THE DECISION EQUATION FOR CAESAREAN SECTION VERSUS VAGINAL BIRTH Like all decisions in medicine, the decision for caesarean section is a balance of pros and cons. A model for the decision equation for caesarean section is given in Figure 32.2. In many cases, the maternal (e.g. major placenta praevia) or fetal (e.g. cord prolapse) advantage of caesarean section is so overwhelming that a maternal preference for vaginal birth does not materially affect the decision.

Maternal preference for a mode of birth and maternal risk tolerance There are many situations where the maternal or fetal advantages of caesarean section are much more subtle, and a maternal preference for vaginal birth in a relatively risk-tolerant woman appropriately becomes the determining factor in recommending attempted vaginal birth. Equally, in a similar clinical equation that is relatively evenly balanced and where the mother has no strong preference for vaginal birth but is particularly risk averse, it is appropriate for her preference to become the determining factor in favour of a caesarean section.

The influence of intended and likely future parity In a discretionary situation, where both attempted vaginal birth and caesarean section appear reasonable options, the likely and intended future parity are of great importance. Of all the adverse effects of caesarean section, the most grave is the possibility of placenta accreta in a subsequent pregnancy. The likelihood of such an outcome

increases almost exponentially as parity (and the further number of caesarean sections) increases. Recommendations in a 43 year old may therefore be quite different to those made to a 22 year old who is intent on having a large family.

COMMON INDICATIONS FOR CAESAREAN SECTION These conditions are covered in the various chapters as indicated.

Uterine scar Repeat elective caesarean section versus trial of vaginal birth after caesarean is addressed later in this chapter. There is less information regarding risks posed by other uterine scars but ruptures have certainly been recorded after myomectomy (especially if the scar is full myometrial thickness), uterine perforation at curettage and hysteroplasty for fusion abnormalities of the Müllerian system.

Obstructed labour (Ch 34) True obstructed labour is now relatively uncommon as most labours progress slowly before developing signs of obstruction and the caesarean section is performed for slow progress before all signs of obstruction have developed.

Inadequate progress in labour and/or fetal compromise (Ch 33) Inadequate progress in labour and fetal compromise commonly occur together. Typically, inadequate progress leads to an oxytocin infusion, which may not be tolerated if there is already borderline fetal compromise. The oxytocin has to be ceased in the interests of fetal wellbeing

Psychological Neonatal RDS Maternal risks of index pregnancy Maternal risks of subsequent pregnancy

Pelvic floor damage Perinatal moridity and mortality

Planned vaginal Birth

Elective caesarean section

FIGURE 32.2

The risk–benefit equation for planned delivery versus elective caesarean section. 269

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but then there are inadequate contractions to achieve progress. The result is commonly a caesarean section. Fetal compromise can, of course, occur in the absence of an oxytocin infusion for many reasons, as discussed in Chapter 33.

Malpresentation (Ch 15) A transverse or oblique lie in labour will almost always require a caesarean section. A breech presentation can be safely delivered vaginally, but only after a full and satisfactory assessment, including an ultrasound to exclude fetal abnormality or head extension (Ch 15). Most brow presentations will have a caesarean section, but some will effectively be a very deflexed posterior position and respond to rotation with full flexion and therefore deliver vaginally. Although a mentoanterior face presentation may deliver vaginally, a mentoposterior face presentation will almost invariably require caesarean section.

Antepartum haemorrhage (Ch 10) A major degree of placenta praevia requires caesarean section. If the lower placental edge impinges on the lower uterine segment but is more than 2 cm away from the internal cervical os, vaginal birth may still be possible. Where the placenta does not cover the os (grade 1 or 2) on a 32-week scan, a repeat ultrasound at around 36 weeks’ will establish whether expansion of the lower uterine segment has sufficiently displaced the placenta upwards to enable a vaginal birth. Minor degrees of placental abruption can usually deliver vaginally. A ‘moderate abruption’ (tense tender uterus or blood loss > 200 mL with a live fetus) may benefit from caesarean section on diagnosis, as rapid fetal deterioration can occur with further placental separation. A severe abruption is defined as sufficient placental separation to cause fetal death. Heavy blood loss is the rule and disseminated intravascular coagulation (DIC) will almost inevitably develop over the next few hours. There are two schools of thought. The first avoids caesarean section so that there is not a surgical wound in addition to the placental bed from which to bleed when the DIC develops. The second view is to perform an early caesarean section to avoid the development of DIC. Both strategies probably have a place, and a considered recommendation should be made given an understanding of the pathophysiology and the circumstances of the individual case.

Severe preeclampsia and eclampsia (Ch 16) Preeclampsia is not in itself an indication for caesarean section. However, when severe preeclampsia occurs at very or extreme preterm gestations, the cervix is commonly unripe and in the presence of preeclampsiaassociated placental insufficiency, induction of labour without fetal compromise is often unachievable and a caesarean section is the preferred option. 270

Multiple pregnancy (Ch 14) Multiple pregnancy does not mandate a recommendation for caesarean section. However, intrauterine manipulation (internal version and breech extraction) is reasonably likely to be needed between birth of the first and second twins. If this is contraindicated (e.g. previous caesarean section), elective caesarean section is usually preferred. Malpresentation of the first twin is also common in multiple pregnancy and a caesarean section is recommended. Note that malpresentation of the second twin does not usually affect the recommendation regarding mode of birth.

Probable cephalopelvic disproportion (Ch 33) It is almost axiomatic that it is not possible to predict cephalopelvic disproportion antenatally and attempted vaginal birth is the best approach, even if obstructed labour and an emergency caesarean section is a likely outcome. Certainly, there is little current credibility with attempts to predict outcome of labour with a combination of estimating fetal size on ultrasound and the maternal pelvis radiologically. There are, however, some situations where a successful vaginal birth is so unlikely that caesarean section is the appropriate recommendation. This will most often be where either mother or fetus is at the extremes of normality. An estimated fetal weight of ≥ 5 kg might lead to a recommendation for abdominal delivery unless the mother was obviously very tall with a likely large pelvis. Maternal height < 150 cm might similarly lead to a caesarean section recommendation unless the fetus was obviously small. Somewhere between is the primigravida with a high mobile head at 40 weeks’ or beyond. There is unequivocally a much higher rate of caesarean section in these cases and many clinicians will recommend elective caesarean section rather than a trial of labour, but both options are reasonable.

Caesarean section on maternal request Increasingly, some women are requesting caesarean section in the absence of a specific additional risk to mother or fetus. Most clinicians will respond favourably to such a request but have an obligation to ensure that the decision is a well-informed one. In particular, the woman should be apprised of the pros and cons of her request; of prime importance would be the future risk of placenta accreta if high parity is intended.

THE PROCEDURE PREPARATION FOR CAESAREAN SECTION Consent for an elective procedure is usually obtained at a late antenatal visit. The woman needs to be aware of two things: 1. what is going to happen prior to, during

Chapter 32  Caesarean Section and Trial of Labour after Caesarean

and after the procedure; and 2. any potential adverse consequences of the procedure. The gestation selected for a repeat elective caesarean section is usually at approximately 39 weeks, balancing the risk of neonatal respiratory distress against the undesirability of performing the procedure so late that the woman comes into labour and the operation then done as an emergency with increased attendant risks. Fasting is required before the procedure. For elective operations, the woman is admitted on the day of surgery. For morning surgery, the woman fasts overnight. If the operation is in the afternoon, she can have a light breakfast at least six hours before planned surgery. Blood tests are conducted prior to surgery. Two units of blood are cross-matched if an above-normal loss is expected (e.g. placenta praevia); otherwise, in many centres the blood is typed and screened for unexpected antibodies and cross-matched only if required (blood group and antibody screen). Only 1% of women will require a blood transfusion because of excessive haemorrhage at elective caesarean section; it is noteworthy that this rate is less than the rate of transfusion after vaginal delivery! Gastric acidity reduction is required for emergency caesarean section in labour. In active labour, gastric emptying is delayed, and so emergency caesarean section is always regarded as having a risk of aspiration of gastric contents. It is common to administer an H-1 selective antihistamine (e.g. ranitidine) or an antacid such as sodium citrate prior to emergency caesarean section. Regional analgesia, usually spinal, is the safest technique for mother and baby, and is used in the vast majority of elective procedures and in emergency procedures where possible if there is no existing epidural block. In emergency procedures, if there is an existing epidural block for labour this can be ‘topped up’ for the caesarean section. It is uncommon for general anaesthesia to be necessary, and it has many disadvantages (Ch 38). An intravenous infusion is commenced if it is not already running. Blood loss at caesarean section is often unpredictable, and can be heavy. In addition, the resulting haemoconcentration and trauma predispose to thromboembolism. Antibiotic prophylaxis at the time of caesarean section significantly reduces the incidence of endometritis and wound infection. There is some conflict regarding the timing of antibiotic administration. Early administration is most effective in preventing infection but risks anaphylaxis with the fetus in utero—with potentially disastrous consequences for the fetus. There is no evidence that combinations of antibiotics or more than one dose offer any advantage over a single dose of one antibiotic. The standard drug used is cephazolin 2 g prior to skin incision (2 g if the mother’s weight is > 80 kg, 3 g if maternal weight is > 120 kg). The instruments and drapes required are those for any abdominal operation, together with special requirements for caesarean section: abdominal retractor;

curved retractor; obstetric forceps; curved scissors; suturecutting scissors; Green–Armytage forceps (at least 4); tissue forceps (e.g. Allis); needle holders; sucker and tubing; diathermy; needles; sutures; sponge forceps; scalpel handles; scalpel blades; curved artery forceps; straight artery forceps; toothed dissecting forceps; swabs; and packs (should have a radio-opaque strip). Suction is required for the anaesthetist and operator and for neonatal resuscitation. A neonatal resuscitation table is set aside for the management of the infant after birth.

SURGICAL TECHNIQUE After the woman is anaesthetised, she is placed in partial Trendelenburg position and the right hip is elevated to relieve pressure of the uterus on the great vessels. The abdomen is prepared with a suitable antiseptic solution (e.g. alcoholic chlorhexidine solution) and drapes are applied. The Pfannenstiel incision (Fig 32.3) is used in 99% of caesarean operations. It is popular for cosmetic reasons

FIGURE 32.3

Pfannenstiel incision at the postnatal visit 7 weeks after caesarean section. The wound is well-healed. Source: Courtesy of Prof. Norman Beischer.

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and has the advantages of less postoperative pain (better convalescence) and lower risks of wound dehiscence and incisional hernia. The vertical subumbilical incision is indicated if hysterectomy is likely (e.g. known placenta accreta) since it provides better exposure. A transverse incision is made through the subcutaneous fat and rectus sheath. The bellies of the rectus muscle are then separated and the peritoneal cavity entered. The lower segment is exposed with the aid of a curved retractor and the loose peritoneum over it is cut with curved scissors. The peritoneum is reflected downwards, carrying the bladder with it. The muscle of the lower segment is incised with a scalpel in a transverse direction. The initial incision is extended either with scissors or by stretching with fingers at each angle. The retractor is removed and the baby is delivered either manually or with forceps. The cord is clamped and cut. A midwife or doctor will take the baby in a sterile wrap to the resuscitation table where, in the absence of a need for resuscitation, the baby can be quickly dried and wrapped before being given to the parents. Forceps, usually the Green–Armytage type, are sometimes applied to the edges of the uterine incision for traction and to control bleeding. After an oxytocic has been administered (e.g. oxytocin), the placenta is removed and the uterine cavity is explored. A finger or cervical dilator may be passed down through the internal os to ensure adequate patency. The uterus is closed in two layers with a synthetic absorbable suture (e.g. chromic catgut or polyglycolic acid) (Fig 32.4). Additional sutures may be required to control bleeding. At

this point an examination of the ovaries and uterine tubes is made to exclude such pathology (e.g. an ovarian cyst). The parietal peritoneum is usually closed but the visceral parietal peritoneum is left unsutured to reconstitute spontaneously. The rectus sheath is closed with a synthetic absorbable suture, as are the subcutaneous tissues and skin. Subcuticular suturing of the skin produces a superior cosmetic result to the use of staples or non-absorbable sutures. The skin is dressed with an occlusive waterproof dressing. The vagina is checked to ensure that there is no significant ongoing vaginal bleeding. The urinary catheter, if still indwelling, is usually left until the following day.

Difficulties that may be encountered at the time of caesarean section Adhesions from a previous caesarean section or pelvic surgery may render access difficult. A poorly formed lower uterine segment is more common early in the third trimester, and may necessitate a vertical incision. Difficulty with delivery of the fetal head from deep in the pelvis can be remedied by the administration of a tocolytic (e.g. glyceryl trinitrate or salbutamol) and upward pressure on the vertex from the vagina by an assistant. Occasionally, the skin incision has been too small and will need to be enlarged. Rarely, the breadth of the lower uterine segment proves inadequate for the aftercoming head of a breech presentation, and an ‘inverted T’ incision in the uterus is necessary to safely deliver the aftercoming fetal head. It is preferable in this situation to perform a vertical lower segment or classical incision from the start, as the junction of a ‘T’ becomes a point of future weakness and potential rupture.

Additional procedures that may be performed concurrently Hysterectomy Hysterectomy is required in about 1 in 150 women who have a caesarean section. The usual indications are an otherwise uncontrolled primary postpartum haemorrhage or a placenta accreta (Ch 36). The operative procedure differs in no way from that used in the non-pregnant woman except that haemorrhage is more likely and tissue planes are easier to identify.

Sterilisation To save an additional operation, tubal sterilisation can be performed after completion of the caesarean section. The Pomeroy technique is commonly performed (Fig. 32.5) but it is possible that salpingectomy may reduce the incidence of future ovarian cancer (Ch 63). FIGURE 32.4

Closing the uterus at caesarean section using running locking stitch.

Source: Pfenninger JL, Fowler GC. Pfenninger and Fowler’s Procedures for Primary Care. 3rd edn. Philadelphia: Saunders, 2010. Copyright © 2010 Saunders, An Imprint of Elsevier. Figure 162.16.

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POSTOPERATIVE CARE Post-caesarean observations include pulse rate, blood pressure and respiratory rate and should be recorded as for any major surgical procedure: half-hourly for 4 hours, and thereafter 4 hourly for 24 hours. Additionally, the

Chapter 32  Caesarean Section and Trial of Labour after Caesarean

cases of an excessively narcotised mother falling asleep and inadvertently smothering the baby. If the bowels have not opened by the third day, an aperient is usually given night and morning until this is remedied. Other nursing measures are the same as for general puerperal and routine postoperative care. Silk tie

FIGURE 32.5

Pomeroy sterilisation. A knuckle of tube is ligated with absorbable suture, and a small segment is being excised. Source: Gabbe SG, Niebyl JR, Galan HL, et al. Obstetrics: Normal and Problem Pregnancies. 6th edn. Philadelphia: Saunders, 2012. Copyright © 2012 Saunders, An Imprint of Elsevier. Figure 20.23.

ADVERSE EFFECTS OF CAESAREAN SECTION Maternal and perinatal mortality are difficult to separate from the indication for the caesarean section. With purely uncomplicated repeat elective caesarean sections, maternal mortality appears to be no different from attempted vaginal births and perinatal mortality is almost certainly less. The main reason for avoiding caesarean sections is largely the risk of placenta accreta in subsequent pregnancies.

Immediate (at the time of the procedure) vaginal loss should be checked and abdominal palpation used to ensure that the uterus is not atonic. An intravenous infusion will be in place. Typically, the woman will receive 8-hourly saline or Hartman’s solution until tolerating oral fluids. The woman usually has nothing by mouth for 6 hours and then a light diet only until bowel sounds are heard and flatus passed. At this point, the intravenous infusion can be discontinued and a normal diet commenced. A urinary catheter is left in the bladder postoperatively, usually until the following morning. This avoids the woman having to mobilise immediately following surgery, when the epidural will make mobilisation difficult. Analgesia should be effective in the interests of maternal comfort and will assist with mobilisation, thus reducing the risk of thromboembolism. Most commonly administered is a combination of oral paracetamol, a nonsteroidal anti-inflammatory drug (NSAID) and opioids. If epidural or spinal analgesia has been used, there will be a pain-free period immediately after the operation. Mobilisation is important in the prophylaxis of postoperative complications such as thromboembolism and atelectasis/pneumonia. Leg movements, deep breathing and coughing are encouraged from 2 hours postoperatively and the mother will normally be encouraged to fully mobilise, shower and care for the baby from the morning immediately following surgery. Anticoagulation with a low-molecular-weight heparin is commonly administered routinely after caesarean section until discharge from hospital, to further minimise the risk of thromboembolism. Breastfeeding/nursing can commence in the recovery room and the mother should be allowed to feed and nurse the baby as desired on the first day. If the mother is taking narcotic analgesia on the day of surgery, she should be supervised at all times with the baby as there have been

For the mother, immediate complications include those related to the anaesthetic (drug overdose, hypoxia, apnoea, aspiration of gastric content), the operation (haemorrhage, damage to bladder or bowel) or the condition necessitating the operation (hypertensive disease, diabetes, uterine infection). Laceration to the fetus is uncommon but can occur if entry is difficult and if vision is impaired by excessive bleeding.

Early postoperative complications (in the week or so after surgery) Infection may occur in the abdominal wound, uterus, urinary tract or chest. Local infection is related to the duration of membrane rupture and labour, number of pelvic examinations and surgical technique (haemostasis and so on). Thromboembolism, ileus, secondary haemorrhage and wound dehiscence are less common early complications. The baby may be adversely affected by the operation itself; for example, hypoxia from the supine hypotensive syndrome if the mother is not positioned properly. If a general anaesthetic is used, the baby will usually be born under the influence of the anaesthetic. Respiratory distress is more common, which may be related to the fact that amniotic fluid is not squeezed out of the lung as in vaginal delivery (‘wet lung’).

Late sequelae Late complications relate principally to a subsequent pregnancy.

Uterine rupture This occurs consistently in about 1 in 200 pregnancies where a mother attempts to deliver vaginally after one previous caesarean section and no other vaginal births. The rate is higher if labour is induced and higher again if prostaglandins have been used for cervical 273

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ripening. More than one caesarean section is associated with a progressively increased risk of uterine rupture but probably only to approximately 1 in 70 pregnancies after two previous caesarean sections. The statement ‘you will rupture your uterus if you try and have a vaginal birth’ is most unwise as the vast majority will not rupture their uterus; it is just that sensible risk management means that a caesarean section should be strongly recommended.

Figure 32.2. Added to this is a component related to the likelihood of achieving vaginal birth. In those attempted VBACs where there is a much lower likelihood of vaginal birth (see below), the balance becomes tilted more towards elective caesarean section.

Placenta praevia and placenta accreta

This will occur in about 1 in 200 attempted VBACs but only approximately 1 in 5 of these will have a perinatal death. Serious morbidity is harder to estimate but may be a similar figure (a further 1 in 5), as is the number who will need a hysterectomy.2

Both placenta praevia and placenta praevia accreta increase with each caesarean section. Approximate rates are given in Table 32.1 and probably represent the single greatest argument against maternally requested caesarean section in a woman likely to have more than one future pregnancy.

TRIAL OF LABOUR AFTER A CAESAREAN SECTION THE DECISION EQUATION Trial of labour after a caesarean section (TOLAC) is also referred to as attempted vaginal birth after caesarean section (attempted VBAC). The following discussion refers largely to an attempted vaginal birth after a single lower uterine segment caesarean section. As stated already, the risks after more than one caesarean section or a single classical caesarean are much higher. Deciding between a repeat elective caesarean section and an attempt at vaginal birth after caesarean is an extension of the simple decision equation given in

TABLE 32.1  INCREASING LIKELIHOOD OF BOTH PLACENTA PRAEVIA AND PLACENTA ACCRETA WITH INCREASING NUMBERS OF PREVIOUS CAESAREAN SECTIONS. Number of previous caesarean sections

Praevia (%)

0

0.5

2

1

1

10

0.1

2

2

30

0.6

3

4

50

2

4

10

70

7

274

Accreta (% of those with praevia)

Accreta (% of all pregnancies) 0.01

Against an attempted VBAC Uterine rupture

Perinatal mortality and morbidity This is undoubtedly higher than for an elective caesarean section but the 1/1000 perinatal deaths consequent on uterine rupture is the lesser contributor. The added perinatal death rate from awaiting spontaneous labour is about 1 in 600,3 with a further significant morbidity related to awaiting vaginal birth and labour4.

Against a repeat elective caesarean section Placenta accreta in a subsequent pregnancy In a purely clinical sense, the greatest argument in favour of VBAC is the risk of accreta in subsequent pregnancies (see above). Therefore, expected future parity is an overwhelming consideration. If the current pregnancy is likely to be the last, the clinical balance strongly favours repeat caesarean section. If two or more further pregnancies are expected, the recommendation should mostly be for attempted vaginal birth. For those that perhaps will have one further pregnancy, the clinical equation is pretty balanced; there is a very small risk of accreta if the patient has a repeat elective caesarean, and a similar small risk of adverse perinatal outcome if VBAC is attempted.

Likelihood of achieving a vaginal birth if attempted after a previous caesarean section The overall success rate for attempted vaginal delivery ranges from 50 to 80% depending on local guidelines around the management of the labour (i.e. minimal accepted rates of progress, the use or non-use of oxytocin to induce or augment labour) and the selection of cases. Women with morbid obesity are not ideal candidates for caesarean section but the success rate with attempted VBAC is as low as 10%. Women who have had a previous vaginal delivery, either before or subsequent to a caesarean section, are more likely to have a successful outcome.

Chapter 32  Caesarean Section and Trial of Labour after Caesarean

MANAGEMENT OF LABOUR AFTER A PREVIOUS CAESAREAN SECTION Place of birth Trial of labour following caesarean section is a safe procedure only when conducted in an appropriate hospital setting that can perform an immediate caesarean section in the unlikely event of a uterine rupture.

First stage of labour management The first stage of labour management follows a standard regimen as outlined in Chapter 28. Key aspects are worth some emphasis. Assessment of progress of labour should be vigilant and at least 1 cm/hr in the active phase. Delivery should be achieved within 12 hours of the onset of labour. Slow progress would generally not be augmented with oxytocin. Maternal surveillance with respect to scar tenderness or pain is generally not helpful as both these clinical features are very common in the absence of rupture. A ‘ripping’ or ‘tearing’ sensation is more concerning and more likely to be a genuine rupture. Fetal surveillance with continuous cardiotocography is mandatory and a sudden deterioration in the fetal heart tracing is often the first sign of uterine rupture. A group and antibody screen should be performed and an intravenous line inserted. Epidural analgesia can be used.

REFERENCES 1) Walker SP, McCarthy EA, Ugoni A, et al. Cesarean delivery or vaginal birth: a survey of patient and clinician thresholds. Obstet Gynecol 2007;109(1):67–72. 2) Appleton B, Targett C, Rasmussen M, et al. Vaginal birth after caesarean section: an Australian multicentre study. VBAC Study Group. Aust N Z J Obstet Gynaecol 2000;40(1):87–91. 3) Vashevnik S, Walker S, Permezel M. Stillbirths and neonatal deaths in appropriate, small and large birthweight for gestational age fetuses. Aust N Z J Obstet Gynaecol 2007;47(4):302–6. 4) Badawi N, Kurinczuk JJ, Keogh JM, et al. Intrapartum risk factors for newborn encephalopathy: the Western Australian case-control study. BMJ 1998;317(7172):1554–8. FURTHER READING Crowther CA, Dodd JM, Hiller JE, et al; Birth After Caesarean Study Group. Planned vaginal birth or elective repeat caesarean: patient preference restricted cohort with nested randomised trial. PLoS Med 2012;9(3):e1001192.

Second stage of labour management There is concern with prolonged pushing in the second stage of labour. An upper limit of 1 hour of active pushing before instrumental delivery is wise.

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Section 2.7.3 INTRAPARTUM CLINICAL PROBLEMS

Chapter 33  INTRAPARTUM FETAL COMPROMISE Michael Permezel and Julia Francis

KEY POINTS Intrapartum fetal compromise may cause both perinatal death and permanent disability in the child. However, both are very rare outcomes (approximately 1 in 2000) of well-resourced intrapartum care. During each uterine contraction, there is a substantial impairment of uteroplacental blood flow. With a healthy placenta and normal uterine activity, this is well tolerated by the fetus. Causes of intrapartum fetal compromise include maternal hypoxia, maternal hypotension, excessive uterine muscular activity, placental abruption, placental insufficiency, cord complications and fetal conditions including haemorrhage from vasa praevia. The management of acute fetal compromise includes prompt intrauterine resuscitation, and assessment and treatment of any cause, then re-evaluation of the fetal condition and delivery if necessary. Where urgent delivery is indicated, instrumental birth may be attempted if there is a favourable presentation (vertex) and station (engaged) and the cervix is fully dilated. If these circumstances are not present, a caesarean section is required.

AETIOLOGY In the pathway from mother to fetus, there are essentially seven mechanisms which may impair fetal oxygenation (Fig 33.1).

seen in conditions such as fainting and the supine hypotensive syndrome (where it is usually transient; Fig 33.2), shock (where it may be prolonged) and epidural analgesia. Box 33.1 outlines the causes of maternal hypotension.

MATERNAL OXYGENATION

Fetal compromise after epidural anaesthesia

An inadequate oxygen content of the maternal blood may result from poor gas exchange in the lungs (poorly administered anaesthesia, lung pathology), cardiac failure or anaemia.

MATERNAL HYPOTENSION Placental gas exchange is dependent on adequate maternal blood flow through the placenta. A reduction in maternal blood pressure to deliver blood to the fetus is

Placental perfusion appears particularly sensitive to maternal hypotension and may participate in the vasoconstrictor response to reduced blood pressure. This means that even though the blood pressure may not be recorded as particularly low, the vasoconstriction that is maintaining the blood pressure is impairing uteroplacental blood flow. Once the spinal or epidural block is effective, the uteroplacental circulation will be within the field of block and therefore no longer participating in the vasoconstriction response.

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Maternal hypoxia

BOX 33.1  Causes of maternal hypotension.

Maternal hypotension Placental abruption

Placental insufficiency

Fetal conditions

Umbilical cord compression



Spinal or epidural anaesthesia Supine hypotension Vasovagal syncope Hypovolaemia Sepsis Cardiogenic (e.g. arrhythmia, valve disease) Anaphylaxis Pharmacological effect (e.g. antihypertensive, phenothiazine) Pulmonary embolism (thrombotic or amniotic)

FIGURE 33.1 

Mechanisms for the pathogenesis of impaired fetal oxygenation.

Placenta

PLACENTAL ABRUPTION

Fetus

Separation of the placenta from the decidual lining of the placental bed will diminish the area available for gas exchange. Placental abruption is more common in labour because: 1. the abruption may have caused the woman to labour; and 2. an intrapartum event that causes marked reduction in uterine size (e.g. rupture of membranes when there is polyhydramnios or following delivery of the first twin) predisposes to abruption (Ch 10).

CHRONIC PLACENTAL INSUFFICIENCY

Aorta L4

Inferior vena cava

FIGURE 33.2 

Postural (supine) hypotension syndrome. The inferior vena cava is compressed by the gravid uterus.

UTERINE HYPERSTIMULATION The pressure in the uterine wall (approximately 60 mmHg) during a contraction will impair uteroplacental blood flow. During pushing in second stage (approximately 120 mm Hg, depending on the maternal blood pressure) there may be cessation of uteroplacental and umbilical blood flow. If the contractions are of excessive frequency and/or duration, there will be inadequate time for gas exchange and the fetus will become hypoxic. When excessive uterine muscular activity (uterine tachysystole) is associated with fetal compromise, the situation is termed uterine hyperstimulation. 278

Placental insufficiency has multiple causes (Ch 11) but becomes almost inevitable in every pregnancy as the gestation advances beyond the due date. Serious placental insufficiency may begin early in the second half of pregnancy. In the best possible scenario, a pregnancy may not develop placental insufficiency until beyond 42, or even 43, weeks’ gestation. As elsewhere in the body, the arteries develop a disease process similar to atherosclerosis. The process is accelerated in the presence of such conditions as hypertension, preeclampsia, diabetes and chronic renal disease. The result is reduced blood flow and sometimes thrombosis of the vessel. Starved of oxygenation, the corresponding section of the fetal side of the placenta undergoes vasospasm and may infarct (Fig 33.3). Regardless of the aetiology, chronic placental insufficiency may lead to acute fetal compromise in labour. The reduction in uteroplacental blood flow with even normal uterine activity may not be tolerated by the fetus with a diseased placenta. As the uterine contractions progressively increase in frequency, duration and intensity during labour, there will be a point where the uteroplacental blood flow no longer maintains fetal oxygenation.

UMBILICAL CORD This is the final supply link to the fetus, and blood flow may be diminished or cut off by entanglements about the

Chapter 33  Intrapartum Fetal Compromise

BOX 33.2  Fetal causes of fetal compromise in labour. Fetal hypotension: acute fetal haemorrhage (vasa praevia bleeding) Fetal anaemia: for example fetomaternal haemorrhage, red cell isoimmunisation Fetal infection: for example bacterial chorioamnionitis, CMV Fetal cardiac disease

FIGURE 33.3 

Placenta from a case of placental insufficiency in a woman with essential hypertension and superimposed preeclampsia. The mother had an intrauterine death in her only previous pregnancy. Caesarean section was performed at 33 weeks’ gestation. The severely growthrestricted infant weighed only 1260 g, with the multiply infarcted placenta weighing only 280 g. Source: Courtesy of Prof. Norman Beischer.

body of the fetus, knotting, presentation or prolapse (Fig 33.4). The cord is looped around the fetal neck in at least 25% of deliveries and approximately 1% have a true knot. These seldom cause fetal death in utero before the onset of labour since the knot tightens only when contractions cause descent of the head (Fig 33.4). Cord compression when there is cord entanglement, oligohydramnios or compression between the presenting part and the uterine wall is a common cause of so-called ‘variable’ fetal heart rate decelerations seen on cardiotocography.

FETAL CONDITIONS Box 33.2 lists some fetal causes of acute fetal compromise in labour. Vasa praevia may be associated with acute bleeding at the time of membrane rupture and very rapid fetal deterioration as it exsanguinates from the torn vessels. Acute bacterial chorioamnionitis (e.g. Group B streptococcus) will produce villus oedema and impair placental gas exchange.

CONSEQUENCES OF INTRAPARTUM FETAL COMPROMISE The hypoxic fetus will become acidotic and develop ischaemic damage to vital organs including the brain, heart

and kidneys. Death will eventually ensue. A common compounding effect is the failure of the compromised neonate to establish respiration at birth. In the absence of skilled neonatal resuscitation, neonatal asphyxia will further contribute to the hypoxic damage prior to birth.

PERINATAL DEATH Perinatal death is a very uncommon result of labour at term. Where the fetus is alive at the onset of labour in a well-resourced setting, the perinatal mortality during labour is possibly only 1 per 2000 births. In home birth (less well resourced), the perinatal mortality is approximately doubled.1

CEREBRAL PALSY Much is made of the fact that most cerebral palsy is not the product of birth asphyxia. Studies have estimated that only approximately 10% of cerebral palsy has an intrapartum origin and only a proportion of that is potentially preventable with astute care. However, it is also noteworthy that cerebral palsy is much less common after elective caesarean section at term than after vaginal birth or emergency caesarean section.2 This leads to the hypothesis that at least some cerebral palsy at term would appear to be related to late pregnancy (after 39 weeks’) placental insufficiency but prior to the onset of labour.

MANAGEMENT OF ACUTE INTRAPARTUM FETAL COMPROMISE Acute intrapartum fetal compromise can be managed with a stepwise approach as follows. 1. Perform general intrauterine resuscitation. 2. Assess and treat the underlying cause. 3. Reassess. 4. If there is no response, prepare for immediate delivery. 279

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A

B

FIGURE 33.4 

Delivery of a face presentation by forceps in a case of fetal death after a 17-hour labour at 42 weeks’ gestation in a 17-year-old primigravida. The fetus weighed 3220 g and had three tight loops of cord around the neck. Labour was monitored by auscultation alone. Fetal death occurred 4 hours into the labour, presumably due to tightening of the loops of nuchal cord as the head descended. Source: Courtesy of Prof. Norman Beischer.

General intrauterine resuscitation The immediate response to acute intrapartum fetal compromise is to institute general measures to improve fetal oxygenation. These include the following. Reposition the woman with a view to minimising supine hypotension and also possibly reducing cord compression. Most commonly, the best position is left lateral but it may sometimes be better in right lateral. Oxygen can be administered by mask although evidence is lacking as to whether this has any fetal benefit, given that the mother’s haemoglobin would normally have 100% oxygen saturation. Intravenous fluid (e.g. normal saline) bolus of, say, 250 mL. This will reduce hypotension and improve cardiac output if there is some maternal dehydration (not uncommon in labour). Oxytocic withdrawal should occur, with any oxytocin infusion ceased and any prostaglandin that remains vaginally removed if possible. Tocolytic administration should be considered. Common regimens include salbutamol 100 mcg

• • • • •

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intravenously, terbutaline 250 mcg subcutaneously, and glyceryl trinitrate spray 400 mcg sublingually.

Assess and treat the underlying cause The causes of acute fetal compromise are listed earlier in this chapter. In an acute situation, the assessment requires a high level of clinical skill so as to be rigorous in establishing the most likely cause, while at the same time not delaying further treatment. Assessment must include some knowledge of the antenatal history as well as intrapartum progress. Vital signs and abdominal examination can be quickly established but often the most important step is the vaginal examination. This is because the most common cause of acute fetal compromise is cord compression as the head descends in the second stage of labour. What then is the most common finding on vaginal examination in the presence of acute severe fetal compromise in labour? Although it may rarely be a cord prolapse, the most common finding will be that the woman is in second stage and fortuitously suitable for instrumental birth if

Chapter 33  Intrapartum Fetal Compromise

the fetal compromise continues and spontaneous birth is not imminent. Maternal hypotension most often follows epidural anaesthesia and will respond to intravenous volume infusion. Excessive uterine muscular activity should respond to cessation of any oxytocic and administration of a tocolytic as described earlier.

Reassess the fetal condition Cardiotocography Has there been a dramatic response to treatment? A detailed discussion of cardiotocographs (CTGs) is given in Chapter 11. Intrapartum CTGs can be described as ‘reactive’ or ‘reassuring’ (fetal heart rate accelerations present with normal variability, normal baseline and no adverse decelerations). The intermediate level of concern is ‘non-reactive’. In these cases, there are no accelerations and often some reduced variability. This trace may be due to early fetal hypoxia but more commonly is a pharmacological effect of drugs administered in labour such as pethidine, morphine or even magnesium sulfate being administered for management of preeclampsia or neuroprophylaxis. Severe hypoxia is very unlikely in the absence of ominous features as the uterine contractions should lead to late decelerations. A CTG pattern with a higher probability of fetal hypoxia or acidosis is called ‘non-reassuring’ or ‘ominous’. The term chosen is a glass half-empty or half-full situation—an appropriate analogy given that late decelerations will commonly be associated with fetal acidosis in about half the cases. Units that use the term ‘nonreassuring’ place emphasis on the fact that half of these cases do not have significant fetal compromise. Those using the term ‘ominous’ are emphasising that half the fetuses are indeed acidotic. Apart from late decelerations, other patterns that have a high probability of acidosis are complicated variable decelerations, absent variability and sinusoidal traces.

Fetal blood sampling The degree of fetal acidosis can be measured reasonably accurately with the technique of fetal blood sampling. The fetal base deficit or lactate level can be assessed. Indications This procedure is indicated where there is significant uncertainty regarding fetal condition. Many units almost never perform fetal blood sampling in labour. A few units obligate fetal blood sampling prior to a caesarean section for fetal compromise. The right course of action is somewhere inbetween. If there is a high probability of severe fetal compromise, delivery should be expedited and not delayed by attempts at fetal blood sampling. The pros and cons of fetal blood sampling are listed in Box 33.3. Contraindications Fetal blood sampling is contraindicated if there is clear evidence of serious sustained fetal compromise on the CTG. It is also contraindicated if there is a known fetal

BOX 33.3  Pros and cons of fetal blood sampling. Pros ✚ Randomised controlled trials suggest that fetal blood sampling can reduce the caesarean section rate for fetal compromise as not all fetuses with CTGs suggestive of hypoxia are actually acidaemic. Cons









✚ ✚





Delays during fetal blood sampling may aggravate fetal compromise. Requires use of equipment that may fail or not be available. Technically difficult if < 3 cm dilated. Blood-borne virus transmission may occur from mother to fetus. There is a risk of fetal haemorrhage from a scalp wound, particularly if there is unexpected fetal thrombocytopenia (e.g. NAIT, see Ch 22).

bleeding disorders, the gestational age is < 34 weeks’ or there is a non-vertex presentation or a risk of viral transmission from mother to fetus (HIV, hepatitis viruses, herpes simplex viruses). Technique After cleansing of the vagina, an appropriately sized amnioscope is inserted gently through the cervix until the presenting part comes into view. The area in view is wiped clean and sprayed with ethyl chloride. A sample of capillary blood is obtained by piercing the scalp with a small disposable blade and drawing the blood into a fine tube treated to prevent clotting. If a coincident acidosis is suspected in the mother, a sample of her blood should also be taken for analysis. The normal pH value is > 7.25; the more depressed the reading below this, the more likely the baby is to be suffering from hypoxia. A value below 7.20 is definitely pathological and calls for close review. A normal lactate is < 4.2 mmol/L. A level 4.2 to 4.8 is concerning and > 4.8 should mandate delivery.

Amniotic fluid quantity and meconium-staining Passage of meconium occurs because asphyxia stimulates the vagus nerve, which supplies the gut. This has occurred in approximately 20% of pregnancies prior to birth, most often during labour. In about half the cases, the meconium is not apparent until after delivery because the presenting part seals the vagina like a plug. Premature infants are less likely to pass meconium in the presence of asphyxia and post-term infants more likely to pass meconium without any evidence of asphyxia. Thick 281

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meconium implies an element of oligohydramnios combined with meconium passage and makes significant asphyxia more likely. Meconium not only makes fetal acidaemia more likely but also increases the possible consequences of fetal hypoxia. As gasping during hypoxic episodes may result in neonatal meconium aspiration syndrome, the threshold for delivery should be lowered by the presence of meconium liquor—particularly if thick meconium.

Other strategies for evaluating fetal condition Digital stimulation of the fetal scalp during a vaginal examination will commonly provoke an acceleration if the fetus is not acidaemic. Electrocardiography (ECG) requires the application of a fetal scalp electrode and may reveal ST segment and T-wave changes in the presence of hypoxia. A fetal pulse oximeter can be placed alongside the fetal cheek in labour for continuous measurement of the fetal oxygen level. Both the fetal ECG and pulse oximeter are yet to become established in clinical practice and remain areas for research.

Delivery or continued observation? The decision equation Factors to consider in deciding between delivery versus continued observation include: 1. likely severity of fetal compromise 2. likelihood that the fetal compromise will respond to measures put in place (e.g. supine hypotension, uterine hyperstimulation) or progressively worsen as labour progresses (e.g. cord compression, placental insufficiency) 3. adverse consequences of operative birth (e.g. outlet instrumental birth or episiotomy would be regarded as less adverse than caesarean section, whereas caesarean section in a high maternal age pregnancy would be regarded as a better outcome than the same procedure in a young woman with expected high future parity).

version and breech extraction is an alternative to be considered (Ch 14).

Urgency of birth Animal experiments have examined the effects of complete anoxia in the term primate fetus. Anoxia of up to 10 minutes’ duration appears to be well tolerated without apparent long-term neurological damage. More than 20 minutes is commonly fatal. These numbers are an approximate guide only to the human situation. Importantly, most situations will be hypoxia of varying degrees (rather than anoxia), suggesting that times may be a good deal longer. However, often the human fetus has already suffered some pre-morbid hypoxia, which the same experiments have shown reduces tolerance to acute insults.

UMBILICAL CORD ACCIDENTS PROLAPSE

Prolapse occurs where the cord lies beside the presenting part (occult prolapse) or below it (frank prolapse), the membranes having ruptured. The condition may or may not be preceded by cord presentation, where the cord is similarly placed but the membranes are still intact (Figs 33.5 and 33.6).

Incidence and predisposing factors Cord prolapse occurs in approximately 0.5% deliveries (cephalic presentations). It is more common in breech presentations (approximately 2%) and multiple pregnancy (approximately 4%). Other predisposing factors include transverse of oblique lie, polyhydramnios and artificial rupture of the membranes in the presence of a high mobile presenting part.

Diagnosis Cord presentation (Fig 33.5) may be diagnosed on antenatal ultrasound or very occasionally with a particularly

Mode of birth If delivery is urgent and the head is on the perineum, an episiotomy may rapidly effect birth. In other circumstances, the choice will lie between instrumental birth and caesarean section. Essentially, if there is a favourable presentation (vertex or deflexed vertex) and station (‘engaged’) and the cervix is fully dilated, an instrumental delivery can be performed. If the presentation is nonvertex, the head not engaged or the cervix not fully dilated, a caesarean section is required. The mid-cavity deflexed vertex with a posterior position is a special circumstance. Ideally, any attempt at instrumental birth should be performed in the operating theatre so that there is rapid access to caesarean section if the instrumental birth is not successful. In the event of fetal distress between the birth of twins, an internal 282

FIGURE 33.5 

Cord presentation; the membranes are intact.

Chapter 33  Intrapartum Fetal Compromise

6. Mode of birth is as described for acute fetal compromise: instrumental birth only if there is a favourable presentation and station and the cervix is fully dilated (breech extraction of the second twin being an obvious possible exception). If the fetus is already deceased, vaginal birth is preferred.

CORD ENTANGLEMENT AND TRUE KNOTS Incidence

FIGURE 33.6 

Prolapse of the cord in labour, with the cervix almost fully dilated.

Cord around the baby’s neck is relatively common. One loop of cord around the neck occurs in about 25% of pregnancies, two loops in 2.5%, three loops in 0.5% and more than three loops in 0.1%. Cord around the body is present in approximately 2% (Fig 33.7). True knots of the cord occur in approximately 1% of pregnancies but approximately 4% of stillbirths (Fig 33.8).

astute vaginal examination in labour. Cord prolapse (Fig 33.6) should be excluded by immediate vaginal examination when the membranes rupture in the presence of any of the aetiological factors listed previously (i.e. malpresentation, multiple pregnancy, high presenting part or polyhydramnios). Occasionally, the cord may pass through the introitus and its presence is reported by the woman. Cord compression typically results in variable decelerations of the fetal heart rate during a uterine con­traction with sustained bradycardia when the cord compression becomes continuous and causes complete occlusion.

Management An immediate assessment is made of the nature of the labour contractions, dilatation of the cervix, and pulsations of the cord (together with fetal cardiac activity). Treatment is immediate delivery when the fetus is alive and at a viable gestation (> 24 weeks’). If the cervix is not fully dilated, this will be by immediate caesarean section but, surprisingly often, the cord will be noticed first at full dilatation and an instrumental birth can be effected. The presence of a cord prolapse with a live fetus at a viable gestation should initiate the following. 1. Assistance should be summoned; it is likely that an anaesthetist and paediatrician will also be needed. 2. The knee–chest position will reduce pressure on the cord. 3. The presenting part is pushed upward via sterile gloved hand in the vagina to further reduce pressure on the cord. 4. The cord is replaced in the vagina if prolapse to the exterior has occurred. 5. Acute tocolysis (see earlier in the chapter) can be administered to reduce uterine contractions.

FIGURE 33.7 

Knotting of the umbilical cord around the ankle caused the death of this 3040 g infant. The mother had reported cessation of movements at 36 weeks’ gestation. A fetal death was confirmed and labour induced, delivering this fetus with some maceration 2 days after fetal movements had ceased. Source: Courtesy of Prof. Norman Beischer.

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Pathogenesis There is generally an excess of fluid and/or a long cord, and the occurrence is probably related to freedom of fetal movement. Tangling is common (20 to 25%) in monochorionic monoamniotic twins.

Complications There is often some compromise to umbilical blood flow if the cord is tight, and a variable deceleration pattern is seen if a CTG is being carried out in labour. Apgar scores are usually lower, and cord entanglement is occasionally a cause of stillbirth (Fig 33.4). The disposition of the fetus in utero can be disturbed by the effect of the cord traction (e.g. deflexion or malpresentation) or the head fails to descend in labour. Cord entanglement is more likely to cause intrauterine death before labour than the cord around the fetal neck, since the latter usually tightens only during descent in the second stage of labour.

SHORT CORD This has many of the features of cord entanglement. The shortening may be absolute (e.g. less than 30 cm) or relative, due to looping around the fetus. Features include fetal hypoxia, fetal death, placental abruption, breech presentation, delayed onset of labour and/or poor progress and occasionally cord rupture. FIGURE 33.8 

This healthy 3585 g male infant was delivered by forceps because of delay in the second stage of labour. There was no evidence of fetal compromise in labour but the cord was wrapped twice around the baby’s neck and contained two loose true knots. The cord was unusually long at 76 cm, which is associated with both an increase in nuchal encirclements and more true knots.

REFERENCES 1) Wax JR, Lucas FL, Lamont M, et al. Maternal and newborn outcomes in planned home birth vs planned hospital births: a meta-analysis. Am J Obstet Gynecol 2010;203:243.e1–8. 2) Badawi N, Kurinczuk JJ, Keogh JM, et al. Intrapartum risk factors for newborn encephalopathy: the Western Australian case-control study. BMJ 1998;317(7172):1554–1558.

Source: Courtesy of Prof. Norman Beischer.

FURTHER READING RANZCOG. Intrapartum fetal surveillance guidelines. 3rd ed. East Melbourne: RANZCOG; 2014.

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Chapter 34  FAILURE TO PROGRESS IN LABOUR Michael Permezel and Julia Francis

KEY POINTS Prolonged labour is associated with a number of undesirable consequences including maternal and fetal infection, fetal traumatic injury, postpartum haemorrhage and damage to the maternal pelvic floor. Progress is carefully monitored in all labours. Where progress is inadequate, available options are: 1. ongoing observation; 2. augmentation of the labour with an oxytocin infusion; or 3. delivery. Where delivery is indicated, a caesarean section will be needed if there is not a favourable presentation (vertex) or station (engaged) or the cervix is not fully dilated. If all these criteria are met, an instrumental birth can be considered. Augmentation of labour with an oxytocin infusion is contraindicated by fetal compromise or conditions that predispose to uterine rupture such as high parity or a scar on the uterus. Shoulder dystocia should be anticipated, especially where there are predisposing factors such as maternal obesity, diabetes mellitus, prolonged pregnancy, fetal macrosomia or an extensively moulded fetal head. Management of shoulder dystocia consists of a series of steps undertaken sequentially until delivery is accomplished. Adverse consequences of shoulder dystocia include an upper brachial plexus palsy (Erb’s), birth asphyxia and maternal trauma.

DYSTOCIA Dystocia is abnormal or difficult labour and usually refers to slow progress in labour.

AETIOLOGY Traditionally, the causes of dystocia are the powers (uterine muscular activity), the passenger (fetus) and the passages (bony and soft tissues of the birth canal). However, in many cases all three combine to produce dystocia, the most obvious example being a large fetus in the posterior position in a small woman.

The powers This is also known as uterine muscle dysfunction. The major criteria for normal uterine activity during labour

are fundal dominance, synchronisation in the spread of the excitation wave, progressive increase in amplitude, duration and frequency of contractions, and, finally, relaxation between contractions. Uterine muscular dysfunction can be incoordinate or hypotonic. In the latter case, the uterine contractions are weak and/or occur infrequently; if tocographic measurements are being made, the pressures will be below 30 mmHg. The net result is that the work performed by the uterus is less than normal, the cervix fails to dilate and the presenting part fails to descend. In uterine inertia, the contractions are abnormal throughout labour and never establish properly. The condition is more common in nulliparas, but strangely, is also common in women of high parity (grand multipara). This dysfunction usually manifests as prolongation of the latent phase (cervical effacement) and presumably arises

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from inadequate development of the positive feedback loops that should see labour establish once it has begun (Ch 27). In some women, uterine overdistension or lack of a well-fitting presenting part contribute to uterine inertia. Uterine exhaustion is the term used when labour slows after being established. It is a protective action taken by the uterus against rupture (usually in the nullipara) and occurs when there is a serious relative or absolute obstruction to labour.

The passages Bony pelvis The different anatomical shapes and pelvic measurements are described in Chapter 2. Pelvic contraction will most commonly be diagnosed when associated with marked shortness of stature. Rarely, there may be a history of conditions that affect pelvic shape such as spina bifida, untreated congenital dislocation of the hip, rickets or severe pelvic trauma (Fig 34.1).

Soft tissues A uterine fibromyoma in the cervix or lower uterine segment may prevent descent of the presenting part, as may an ovarian mass in the hollow of the sacrum. The non-pregnant uterine horn of a uterus didelphys is a very rare example of a soft tissue mass that may obstruct labour (see Ch 21, Fig 21.2). Previous cervical surgery can leave cervical scar tissue which is resistant to cervical dilatation (cervical dystocia). A vaginal septum usually will run in the anteroposterior plane in the midline and commonly obstructs labour in the second stage, at which point it is easily divided. It is best divided antenatally as it can avulse during labour with major vaginal trauma.

The passenger The fetal causes of cephalopelvic disproportion are fetal macrosomia, malpresentation causing larger diameters to present (brow, deflexed vertex, shoulder) or fetal abnormalities (Fig 34.2).

OBSTRUCTED LABOUR Obstructed labour is the result of ‘cephalopelvic disproportion’. That is, the presenting part is unable to pass through the birth canal. Most commonly it is disproportion between bony skull of the fetus and the bony pelvis but, as indicated above, obstructed labour can be due to soft tissue obstruction or a fetal anomaly or malpresentation.

Natural consequences of obstructed labour Where the presenting part cannot negotiate the pelvis, two consequences are possible: 1. obstructed labour, sepsis, fetal death, genital tract fistula; and 2. obstructed labour, uterine rupture, maternal death and potential fetal death.

Obstructed labour, sepsis, fetal death, genital tract fistula

FIGURE 34.1 

Two years previously this woman was in a motor vehicle accident and suffered severe injury, including fractures of the pelvis (pubis, Ischium and iliac crest) and intraperitoneal and extraperitoneal rupture of the bladder. This film at 38 weeks’ shows distortion of the left side of the pelvis. A living infant (2950 g) was delivered by elective lower-segment caesarean section. The operation was difficult because of adhesions between the bladder, uterus and anterior abdominal wall. Source: Courtesy of Prof. Norman Beischer.

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This series of events is most common in primigravidae. The presenting part is forced against the pelvis, producing ischaemic necrosis of the soft tissues (vaginal or uterine wall, bladder, bowel) between the bony skull and pelvis. The uterus develops uterine exhaustion and the contractions wane in frequency and intensity. The necrotic tissues become infected. The ensuing sepsis leads to fetal death. With fetal death, the fetal skull collapses and the fetus is passed vaginally. Necrosis of the tissues of the pelvic brim may result in an obstetric fistula; this is most commonly vesicovaginal, but it can be rectovaginal or both. This sequence of events remains common in areas of the world with no access to medical care and caesarean section for obstructed labour. Medical practitioners applaud the work of those who are trying to provide care for these women, not only to treat their fistulae but also to put measures in place that reduce the likelihood of future women suffering these terrible consequences of obstructed labour.

Chapter 34  Failure to Progress in Labour

A

B

C

FIGURE 34.2 

A Dicephalic fetus. The incidence of this extremely rare congenital anomaly is 1 in 40 000 births. In this unusual case there were also two anuses separated by a tail, and the double heart was in the neck due to absence of the normal attachment of pericardium to diaphragm. B Sacrococcygeal teratoma associated with fetal and placental hydrops. The mother was a 23-year-old primipara. Labour was induced at 26 weeks’ gestation when she developed polyhydramnios and severe preeclampsia. The fetus weighed 1865 g and the placenta 1250 g. C Compound presentation (breech and hands) accounts for the extensive bruising and oedema shown by this 2320 g infant whose 24-year-old primigravid mother was admitted in premature labour at 32 weeks’ gestation. This photograph was taken shortly after birth by caesarean section. The next day a left Erb’s palsy was noted, which resolved as the bruising subsided. Source: Reproduced with permission from the Royal Women’s Hospital, Parkville, Victoria.

Obstructed labour, uterine rupture, maternal death This series of events is most common in a multigravida. The presenting part is forced against the pelvis but the uterus continues to contract strongly. The lower uterine segment gets thinner and thinner as the junction of the upper and lower uterine segments is drawn higher and higher by retraction of the muscle fibres of the upper segment. Eventually, the lower segment ruptures and the fetus is extruded into the maternal abdomen. The placenta separates with the reduction in intrauterine volume, and the woman exsanguinates from the uterine tear, with the fetus lies dead within the peritoneal cavity.

Signs of obstructed labour Neither of the scenarios just discussed is allowed to eventuate where obstetric care is provided. Poor progress in labour in conjunction with the signs of obstructed labour will lead to delivery of the fetus before rupture or fistula can develop. The signs of obstructed labour (Box 34.1) are largely the consequences of the pressure of the presenting part on the pelvic inlet. The maternal pyrexia, maternal tachycardia, fetal tachycardia and haematuria are consequences of pressure on the soft tissues at the pelvic brim. The retraction ring forms and rises as the upper segment retracts and pulls the ballooned lower segment upwards (Fig 34.3). The cervix becomes oedematous, as does the fetal scalp (caput formation), and the fetal bones 287

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BOX 34.1  Signs of obstructed labour. Lack of progress (contractions, cervical dilatation, station) in association with: Maternal tachycardia Fetal tachycardia Maternal pyrexia Macroscopic haematuria Retraction ring on abdominal examination Cervical oedema Caput Moulding

FIGURE 34.3 

overlap in an attempt to ‘mould’ the fetal head to the pelvis.

AUGMENTATION OF LABOUR Rationale It has proved extremely difficult with intrauterine pressure transducers to reliably quantify contraction intensity. As a result, it is generally assumed that lack of progress in a primigravida is due to inadequate uterine muscular activity. The response to poor progress in the primigravida is therefore to augment contractions, initially with artificial rupture of the membranes and then an oxytocin infusion. This assumption seems excessive when first encountered, but the practice has stood the test of time and almost certainly reduces problems related to slow progress in labour.

A 25-year-old primigravida seen before caesarean section, which was indicated by fetal distress (meconium in liquor, early decelerations, fetal tachycardia), incoordinate uterine action and obstructed labour due to an occipitoposterior position. Labour began spontaneously at 42.2 weeks’ gestation. The woman required epidural analgesia for pain relief; two top-ups were given during the 18 hours of labour. Note the subumbilical flattening immediately above the ballooned lower segment of the uterus. The urinary catheter was required because the woman had been unable to void. Note also the wedge under the mattress to tilt the woman, thus minimising the risk of vena cava occlusion. The infant was born in good condition, birth weight 3510 g. This is the most common clinical situation seen in women having primary (first) caesarean sections; the combination of posterior position, incoordinate and obstructed labour, often in association with evidence of fetal compromise on the cardiotocograph. Source: Courtesy of Prof. Norman Beischer.

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Adverse effects Increasing the frequency, duration and intensity of uterine contractions has potential adverse consequences as follows. 1. Fetal compromise. As indicated in Chapter 33, there is a reduction in uteroplacental blood flow consequent on the increase in intrauterine pressure during contractions. If that reduction exceeds the threshold for that feto-placental unit, there will be a failure of fetal oxygenation. Timely cessation or reduction of the oxytocin infusion is likely to restore fetal oxygenation. 2. Uterine rupture. This is an uncommon consequence of augmentation of labour and will be more common in the multigravida. A partial thickness tear may result in amniotic fluid embolism with often fatal consequences for both mother and baby.

Contraindications Augmentation is contraindicated where there is already fetal compromise or the risk of uterine rupture is increased such as in multiparity (especially grand multiparity) or a uterine scar (usually previous caesarean section).

Regimen An artificial rupture of the membranes (ARM) is almost always performed prior to commencement of the oxytocin infusion. First, ARM may direct the mechanical forces of uterine contractions against the cervix and better achieve cervical dilatation. Second, when the membranes do rupture, there may be a release of endogenous prostaglandins, which can lead to hyperstimulation if an oxytocin infusion is running. The oxytocin infusion regimen is usually as for induction of labour (Ch 29).

DEFINING INADEQUATE PROGRESS IN LABOUR Latent phase of labour As indicated in Chapter 27, it can be almost impossible to define when labour begins in late pregnancy. Augmentation during the latent phase of labour is more akin to induction than augmentation. However, recurrent presentations with early/spurious labour is a known risk factor for stillbirth and induction is a reasonable step at that point.

First stage of labour The 90th percentile for cervical dilation in the active phase of labour is 0.9 cm/hr in a primigravida and 1.2 cm/ hr in a multigravida. Instituting treatment for lack of progress should be tied to the risks of prolonged labour such as chorioamnionitis, compression injury to the tissues and nerves of the pelvic floor, uterine exhaustion with postpartum haemorrhage and, rarely, the consequences of neglected obstructed labour (discussed later).

A rate of cervical dilatation of less than 1 cm/hr in the active phase of labour would generally be regarded as ‘inadequate progress of labour’ and merit consideration of augmentation (primigravida) or delivery (multigravida).

Second stage of labour A primigravida will usually be allowed 2 hours in the second stage with 1 hour of active pushing before obstetric delivery is considered. Augmentation is a very reasonable alternative if the uterine contractions appear inadequate. Only 1 hour of second stage is recommended in a multigravida given the much higher risk of uterine rupture.

CONSEQUENCES OF A PROLONGED LABOUR Maternal complications Maternal complications of a prolonged labour may include the following. Chorioamnionitis. The barrier effect of the cervical plug of mucus and the fetal membranes is lost once active labour commences. Microorganisms, which are prevalent in the vagina, pass upwards into the amniotic cavity and cause an amnionitis, with later spread to the uterus and para-uterine tissues. Postpartum haemorrhage. This is more common because of uterine exhaustion and infection. Uterine rupture or vesicovaginal fistula. These are the ultimate consequences of neglected obstructed labour (as stated previously) and should not occur with appropriate obstetric care.



• •

Fetal complications Fetal complications of a prolonged labour are as follows. Fetal hypoxia. As indicated previously (Ch 33), there is a marked reduction of uteroplacental blood flow with each uterine contraction. Under normal circumstances, the fetus is adequately oxygenated during the time between contractions. However, in a prolonged labour, there may be a cumulative effect of the repeated mild hypoxia such that the reduction in uteroplacental blood flow with contractions is no longer tolerated and hypoxia develops. The other hypoxic impetus may be repeated cord compression. Again, mild degrees of cord compression that are well tolerated for short periods may be much less well tolerated in a long labour, and hypoxia may ensue. Fetal infection. The fetus may develop sepsis in association with maternal chorioamnionitis with inhalation of infected liquor. Pneumonitis, meningitis, pyelonephritis and so on may follow. Fetal trauma. A prolonged labour is more likely to be associated with a difficult birth. The head may be extensively moulded, enabling vaginal birth, but shoulder dystocia then becomes more common. The



• •

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extensively moulded head deep in the pelvis after prolonged obstructed labour may be difficult to deliver by either vaginal or abdominal routes.

MANAGEMENT OF INADEQUATE PROGRESS OF LABOUR General management This is similar to that outlined under the normal care of the woman in labour (Ch 28). Fetal surveillance with cardiotocographic monitoring should be considered if not indicated prior to this time. Intravenous fluid replacement is warranted if there are any signs of dehydration. A broad-spectrum antibiotic is indicated after the membranes have been ruptured for longer than 18 hours.

Assessment Objectives of assessment The following issues should be addressed. 1. Are there signs of obstructed labour? 2. Is obstruction of labour inevitable (e.g. massive fetus in a small woman, brow presentation)? 3. Is augmentation contraindicated by either fetal compromise or an increased risk of uterine rupture?

History and examination If the mother has had previous children, there will often be a history of prolonged labour and operative birth. Examination should be directed to maternal height, estimated fetal size and an assessment of fetal presentation. Careful assessment should be made of all facets of the labour—powers, passenger, passages—to determine whether any other abnormality, particularly disproportion, exists.

Treatment: first stage of labour 1. Obstructed labour present or inevitable caesarean section Delivery is indicated by the most appropriate means. In the first stage of labour, this will be a caesarean section.

2. Inadequate progress but augmentation contraindicated Observe then reassess. Labour would usually be observed for longer but with persistent failure to progress, delivery is indicated.

3. Inadequate progress and augmentation not contraindicated Augment then reassess. The assumption is made that powers are inadequate for the labour. Augmentation takes place with an oxytocin infusion in addition to an ARM. Many of these women will have minor disproportion, with or without malpositions (usually posterior position of the occiput), or minor deflexion attitudes (vertex or bregma presentations). Improved uterine activity is 290

often sufficient to produce normal anterior rotation and/ or flexion of the head, and thus oxytocin infusion is the treatment of choice (acceleration of labour) once significant disproportion has been excluded. Amniotomy alone is usually not effective. If satisfactory progress has not occurred in 2 hours (multigravida) or 4 hours (primigravida), a caesarean section is indicated. Note that if the woman is multiparous, particular caution is needed with the oxytocin infusion in that progress must quickly establish as normal, with reassessment after only 2 hours. Some clinicians will almost never use oxytocin to augment a multiparous labour but most obstetricians will do so with great caution where the contractions are infrequent and of short duration.

Treatment: second stage of labour In the second stage of labour, there may be four alternatives rather than just the three listed earlier: caesarean section; observation and reassess; augmentation and reassess; or instrumental birth. Note that just as an instrumental birth cannot be performed if the head is too high (not engaged), a caesarean birth is extremely difficult if the head is low. When an instrumental birth is possible in the second stage of labour, this is usually the preferred option. However, if a primigravida has a posterior position that is only just engaged, augmentation with oxytocin is probably the wisest recommendation, provided fetal well­ being is satisfactory. This will potentially allow for an easier instrumental birth or sometimes even a spontaneous birth if the oxytocin is particularly effective. In the situation of a posterior position that is only just engaged and needs delivery, obstetricians would be fairly evenly divided as to whether an attempt at instrumental delivery should be recommended or to proceed straight to caesarean section.

SHOULDER DYSTOCIA (IMPACTED SHOULDERS) Impaction of the shoulders is present when there is obstruction to the passage of the shoulders through the bony pelvis, the head having already been delivered. This complication is particularly important, since it can occur unexpectedly in cephalic presentations and there may be no time to summon help. The obstetric attendant should always be on guard for this emergency in any obese or diabetic woman, or one whose labour is prolonged despite good contractions. Impacted shoulders should not be confused with difficulty with the shoulders due to a small head passing through an incompletely dilated cervix; this can occur with anencephaly, microcephaly or fetal death with skull collapse. In this circumstance, the head is not delivered but is in the vagina. Treatment is to await full cervical dilatation when spontaneous delivery will occur; attempts to extract the fetus when the cervix is not fully dilated may result in rupture of the uterus.

Chapter 34  Failure to Progress in Labour

PATHOPHYSIOLOGY Shoulder dystocia is usually the result of large fetal shoulders in relation to the fetal head in a situation where the head just makes it through the birth canal, but the shoulders cannot. The fetal head delivers, often with difficulty, but the neck and shoulders fail to appear. The chin burrows into the maternal perineum. The posterior shoulder is usually in the hollow of the sacrum with the anterior shoulder trapped behind the symphysis pubis. Less commonly, both shoulders may be above the pelvic inlet.

ADVERSE CONSEQUENCES Facial purpuric rash The infant may develop a facial purpuric rash as a consequence of the intense venous congestion that follows delivery of the head with the body trapped in the birth canal.

Fractured clavicle Although this is more common with shoulder dystocia, a fractured clavicle may occur during a normal delivery and be unnoticed apart from a ‘click’ as the shoulders are delivered and a palpable lump over the mid-clavicle in the neonatal period. There are no long-term consequences.

Brachial plexus injury Excessive traction on the shoulders will lead to a traction injury of the upper segments (C5 to C7) of the brachial plexus—Erb’s palsy. The child cannot abduct the arm at the shoulder and has weakness of elbow flexion (Fig 34.4). Many cases of Erb’s palsy will undergo partial or complete resolution in the days and weeks after birth but severe brachial plexus palsy will produce permanent disability of the affected arm.

FIGURE 34.4 

Total brachial plexus palsy due to impacted shoulders in a 4-day-old baby following difficult mid-forceps delivery. His birth weight was 4950 g. Complete resolution did not occur. The more common nerve palsies (total incidence 2 per 1000 births) involve upper brachial plexus (Erb C5, 6, 50%) facial nerve (45%), total brachial plexus (3%) and lower brachial plexus (Klumpke C7, C8, T1, 2%). They are associated with impacted shoulders, breech extraction and difficult forceps delivery. More than 90% recover completely, usually within a few days. Source: Courtesy of Prof. Norman Beischer.

Birth asphyxia

PREDISPOSING FACTORS

Once the head has been delivered, there is increasing risk of fetal asphyxia as time elapses. This has commonly been ascribed to sustained compression of the umbilical cord within the birth canal, creating an anoxic situation for the fetus and a medical emergency. However, in many cases the cord is subsequently found to have been high above the pelvic brim and the reason for the asphyxia is unclear. Critical to fetal tolerance of transient asphyxia is the ‘pre-morbid’ fetal condition. If the fetus has been well throughout labour, the short period of hypoxia during management of shoulder dystocia is likely to be well tolerated. However, a fetus that has had a difficult labour will be much more likely to suffer long-term consequences of hypoxia at birth.

Conditions that predispose to shoulder dystocia are either associated with unusually large shoulders or unusually small head for the body size (Box 34.2). Anticipation of shoulder dystocia in the presence of one or more of the predisposing factors just discussed is key to the prevention of adverse sequelae. An experienced obstetrician and paediatrician should be present at delivery and the woman positioned such that the manoeuvres referred to in the next section can be accomplished without excessive difficulty.

Maternal traumatic injury Severe maternal trauma (including uterine rupture) can be caused during the various manipulations.

MANAGEMENT Shoulder dystocia is an obstetric emergency and all staff that may need to manage shoulder dystocia should know and rehearse the various manoeuvres. 1. Call for assistance. In anticipation of difficulty, an obstetrician or obstetric registrar experienced in the 291

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BOX 34.2  Conditions that predispose to shoulder dystocia. Relatively large shoulders ✚ Shoulder dystocia in previous pregnancies ✚ Maternal diabetes mellitus ✚ Maternal obesity and excessive weight gain in the pregnancy ✚ Macrosomia ✚ Prolonged pregnancy Relatively small head ✚ Moulded head with prolonged labour ✚ Microcephaly or anencephaly

management of shoulder dystocia should be summoned, along with a paediatrician. 2. Specific manoeuvres. Key to the prevention of brachial plexus injury is the avoidance of excessive downward traction on the fetal head. However, traction needs to be firm to effect timely delivery in order to minimise the risk of asphyxial damage.

1. Position the woman in McRobert’s position at the edge of the bed Marked flexion of the mother’s legs will decrease the inclination of the pelvis and some rotation at the sacroiliac joints may enlarge the pelvic outlet. Positioning on the edge of the bed to enables downward traction towards the floor. Traction in this direction has the greatest likelihood of releasing the shoulder from behind the symphysis pubis. Apply firm but not excessive downward traction. This should alleviate approximately 50% of cases of shoulder dystocia.

2. Apply suprapubic pressure and again apply firm downward traction This manoeuvre is shown in Figure 34.5.

3. Rotation of the shoulders Perform a vaginal examination to check alignment of the shoulders is in the AP diameter. The examining hand can rotate the shoulders if misaligned. If traction in the AP plane is not successful, traction after rotation to 45° may be attempted. Older books talk of rotating the shoulders 180° to make the posterior shoulder anterior but this is rarely attempted and more rarely successful. These manoeuvres may be referred to with eponyms such as Ruben’s 2, Woods’ screw and reverse Woods’ screw.

4. Delivery of the posterior arm An episiotomy is cut or extended and the accoucheur’s hand is passed into the hollow of the sacrum and grasps the humerus below the shoulder joint. The arm is swept 292

FIGURE 34.5 

Application of suprapubic pressure in association with downward traction in an attempt to release the anterior shoulder from behind the symphysis pubis.

across the fetal chest until the forearm can be grasped. This is then brought down and delivered posteriorly. An alternative technique is to pass a rubber tube (e.g. Foley catheter) into the posterior axilla and exert downward traction to deliver the posterior shoulder. Once the posterior arm is out, the anterior shoulder readily follows and delivery of the posterior arm is the most common successful manoeuvre in the management of severe shoulder dystocia. After delivery, the episiotomy must be repaired, together with any cervical or vaginal lacerations that may have occurred (these are common unless the episiotomy is extensive). Manual exploration of the uterus may be indicated to exclude uterine rupture; in any case, a careful check on the condition of the mother must be kept for postpartum bleeding and infection. The infant will usually require resuscitation, special observation and possibly treatment for brachial plexus and skeletal injury, particularly fractures of the clavicle and humerus (Figs 34.4 and 34.6).

5. Cleidotomy If all the preceding manoeuvres are unsuccessful, the situation is usually desperate. Cleidotomy will collapse the fetal shoulder girdle and can be effected with scissors but is very difficult to accomplish and carries a high risk of maternal trauma.

Chapter 34  Failure to Progress in Labour

6. Symphysiotomy Surgical division of the symphysis pubis is still practised in some resource-poor countries in the management of obstructed labour, as an alternative to caesarean section. It obviously carries a risk of surgical damage to the urethra and haemorrhage. However, in experienced hands, it has been successfully used in the management of severe shoulder dystocia.

7. Caesarean section Replacement of the head back into the vagina and performing a caesarean section will only be an alternative in those cases where there has been little cord compression and the head replaces easily. Both these circumstances

may apply in the situation where neither shoulder has entered the pelvis and both are firmly resting on the pelvic inlet. Note: Repositioning onto all fours has been recommended by some guidelines but in the author’s experience is unhelpful and often counterproductive in that the woman is positioned where further steps become extremely difficult. The acronym HELPERR has been popularised by the ALSO course and is given in Box 34.3. This acronym has received some criticism, including the early emphasis on episiotomy, failure to prompt movement of the patient to the edge of the bed and, finally, the recommendation of positioning on all fours.

BOX 34.3  Acronym for shoulder dystocia management (HELPERR). Help Evaluate for episiotomy Legs Pressure Enter Remove posterior arm Roll

Call for assistance McRobert’s: hyperflexion of hips; reposition over edge of bed Suprapubic pressure Vaginal examination to check alignment of shoulders and consider rotational manoeuvre(s) Most reliable technique when simple measures fail Position on all fours: doubtful benefit and can be counterproductive (see above)

FIGURE 34.6 

This clavicle was fractured during delivery of impacted shoulders; the newborn was otherwise unharmed. Source: Courtesy of Prof. Norman Beischer.

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Chapter 35  MALPRESENTATION AND MALPOSITION Julia Francis and Michael Permezel

KEY POINTS Axial pressure on the vertex within the birth canal results in rotation around the atlanto-occipital joint and a fully flexed vertex presentation in approximately 85% of pregnancies. This produces the smallest possible fetal diameters for birth. A deflexed vertex presentation complicates approximately 15% of labours and occurs almost always in association with a posterior position of the fetal occiput. Approximately 60% will rotate to anterior during labour; a very small number deliver ‘face to pubis’ but the remainder require some form of assistance to birth in the form of manual rotation, vacuum, forceps or caesarean section. Brow presentation is uncommon (about 1 in 500 deliveries), but should be recognised because obstructed labour is usual and caesarean section is usually necessary. Face presentation occurs in approximately 1 in 800 deliveries and may be due to increased extensor tone, a neck tumour or anencephaly. Because the presenting diameter (submentobregmatic) is similar to that in the fully flexed fetus (suboccipitobregmatic) there is a much greater likelihood of vaginal delivery than in brow presentation.

DEFLEXION OF THE FETAL HEAD PATHOPHYSIOLOGY The four cephalic presentations As the head starts to extend from fully flexed, through minor extension, partial extension and then fully extended, the presenting part will move forwards from the vertex, to deflexed vertex, brow and face. The presenting diameters and approximate measurements at term are given in Table 35.1 and Figure 35.1. Of greatest importance is the increase in presenting diameters as the head becomes progressively deflexed but then returns to 9.5 cm with complete extension (face presentation).

What causes flexion of the fetal head? When the fetus presents cephalically, there are two essential factors that maintain the flexed attitude of the head. The first, which acts throughout pregnancy and labour, is the normal predominance of flexor tone in the baby, which is seen not only in the relation of head to chest but also in relation to the limbs and trunk (Fig 35.2). Occasionally, this is reversed and a predominant extensor tone exists (‘flying fetus’, Figs 35.3 and 35.4). The second factor usually comes into operation in late pregnancy and especially in labour; it depends on the fact that the atlantooccipital joint, on which the head flexes and extends on the trunk, is not centrally placed at the base of the skull but rather more towards the back. As the vertex meets the pelvic floor, the pressure leads to flexion of the head at the atlanto-occipital joint. With a breech presentation,

Chapter 35  Malpresentation and Malposition

TABLE 35.1  PRESENTING DIAMETERS AND APPROXIMATE MEASUREMENTS AT TERM. Presentation

Presenting diameter

Approximate measurement at term (cm)

Prevalence

Vertex

Suboccipitobregmatic

9.5

85%

Deflexed vertex

Occipitofrontal

11.5

15%

Brow

Verticomental

13.5

1 in 500

Face

Submentobregmatic

9.5

1 in 800

Suboccipitobregmatic diameter (9.5 cm) Occipitofrontal diameter (11.5 cm)

Suboccipitobregmatic diameter (9.5 cm)

supraoccipital-mental diameter (13.5 cm)

FIGURE 35.1

Sagittal diameters of the fetal skull.

the same will occur but through pressure of the fundus on the vertex as the mother bears down with pushing in the second stage of labour.

DEFLEXED VERTEX PRESENTATION AND THE OCCIPITOPOSTERIOR POSITION The deflexed vertex presentation may also be called an anterior fontanelle presentation or military position. It is almost only ever seen in association with a posterior position, so these will be covered together. Extension of the fetal head in association with a posterior position may be more apparent than real. This is a consequence of the angle of inclination of the pelvis, placing a more anterior point on the head in the middle of the pelvis with a posterior position than an anterior position. The effect is the same as deflexion with the larger occipitofrontal diameter presenting (approximately 11.5 cm). This larger diameter has to negotiate the birth canal and is responsible for the majority of longer labours, with a higher incidence of forceps delivery and caesarean section.

FIGURE 35.2

The fetal attitude of universal flexion at term. In this case, the mother died undelivered from cardiac disease. Source: Reproduced with permission from the Royal Women’s Hospital, Parkville, Victoria.

The occiput of the fetus lies posterior to the transverse diameter of the pelvic brim in about 15% of women at the onset of labour. In half it corrects to anterior but in the other half, there is persistence of a posterior or transverse position with its attendant deflexed vertex presentation and larger diameters of the fetal head that must negotiate the maternal pelvis.

AETIOLOGY The most likely and logical explanation for the posterior position is that of mutual configuration; that is, the larger posterior segment of the head fits better into the larger posterior segment of the maternal pelvis. This is particularly so where the heart shape of the pelvis is exaggerated through a marked sacral promontory. In addition, the normal anterior rotation may be impeded if 295

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FIGURE 35.3

Face presentation due to head extension (‘flying fetus’). Source: Courtesy of Prof. Norman Beischer.

fontanelle back towards the sacrum. The orbital ridges maybe just palpable under the symphysis pubis but if they are easily palpable, deflexion has occurred to a brow presentation.

SEQUELAE OF A POSTERIOR POSITION AT THE START OF LABOUR

FIGURE 35.4

Two neonates born on the same day. The infant on the left presented by the vertex and was born normally. The one on the right exhibited extension of the neck due to a brow presentation and required a caesarean section. Source: Courtesy of Prof. Norman Beischer.

the transverse diameter of the pelvis is reduced. If the placenta is situated anteriorly in the uterus, a posterior position of the baby is favoured, since there is more room for the prominent occiput posteriorly.

DIAGNOSIS On abdominal examination, fetal limbs are palpable anteriorly. The fetal shoulder (and loudest place for fetal heart auscultation) is out towards the flank, usually on the right (Fig 35.5). Vaginal examination reveals a prominent anterior fontanelle central within the pelvis with the posterior 296

There are several possible outcomes, depending on factors such as the size and shape of the pelvis and fetal head, and the strength and coordination of uterine contractions (Fig 35.6). 1. Anterior rotation occurs in about 60% of labours that are posterior positions at the start of labour. With this ‘self-correction’ during labour, the occiput rotates all the way to anterior as it descends through the pelvis. It is thought that the rotation is effected by the angulation of the pelvic floor as the head descends, deflecting the occiput towards the front. If there is failure of descent, there will also be failure of rotation. Where rotation does occur, there is usually a vaginal birth as having successfully descended the upper birth canal with large diameters of a posterior position, the smaller diameters of the now anterior position find a relatively comfortable passage through the lower pelvis. 2. Transverse arrest occurs in about 20% of posterior positions. 3. Posterior arrest occurs in about 15% of posterior positions. 4. ‘Face to pubis’ birth occurs in about 5% of posterior positions (i.e. approximately 0.75% of all births). In this circumstance, the larger diameters extend the perineum creating a high likelihood of extensive perineal trauma.

Chapter 35  Malpresentation and Malposition

Each of these strategies has complex pros and cons with respect to mother and fetus, which are covered in other chapters. The recommendation will be appropriately influenced by the expertise of the accoucheur and the particular circumstances of the labour (e.g. duration, station, position, fetal size, signs of obstruction). There may also be considerable differences between women in the relative priority of avoiding caesarean section (e.g. high parity anticipated, resource-poor settings, personal aversion to caesarean birth) versus risk minimisation (e.g. older woman, subfertility, particular aversion to perineal trauma and the consequences thereof).

THE OCCIPITOTRANSVERSE POSITION This is also termed the occipitolateral position and has two quite different situations. Normal labour. A lateral position is normal early in labour as the pelvic inlet is wider transversely than in the anterior–posterior diameter. It is actually uncommon for the head to engage directly occipitoanterior. With descent of the head through the pelvis, the shape of the pelvic floor against the occiput rotates it from lateral to anterior. It is very uncommon for this not to occur or for the rotation to be directed posteriorly. Partial rotation of a posterior position. Most occipitotransverse positions with inadequate progress began as posterior positions but failed to complete the rotation to anterior. Management is as for a posterior position but with a higher likelihood of successful spontaneous correction, manual rotation or vacuum rotation.



• FIGURE 35.5

In occipitoposterior positions, the anterior shoulder is palpated well out from the midline to the right. This contrasts with an occipitoanterior position where the anterior shoulder is usually palpated close to the midline on the left.

MANAGEMENT First stage of labour Anticipation of a longer labour will influence many of the recommended practices in the first stage of labour. Heightened vigilance is required in the assessment of mother, fetus and progress. Analgesia and food/fluid intake should consider the greater likelihood of both a prolonged labour and operative birth. Lack of adequate progress is managed along standard lines (see Ch 34).

Transverse or posterior position with inadequate progress in the second stage A number of options are available: 1. manual rotation; 2. instrumental rotation (Kielland forceps or vacuum); 3. instrumental birth ‘face to pubis’; 4. caesarean section; 5. oxytocin augmentation; or 6. continue to await progress.

BROW PRESENTATION In this complication, the brow (area between the anterior fontanelle and root of the nose) forms the presenting part. It is the most unfavourable of all of the deflexion attitudes since the large mentovertical diameter (13.5 cm) is presenting: in the mature fetus this usually prevents vaginal birth. However, as indicated below, rotation may occur with subsequent flexion, enabling a vaginal birth.

INCIDENCE Including transient situations, confirmed by vaginal examination in labour, brow presentation occurs about once in 500 pregnancies.

AETIOLOGY A failure of flexor tone in the fetus may lead to the brow presenting (Fig 35.7). In these cases, pressure from the pelvic floor on the presenting part will neither flex nor extend the head as the brow is positioned over the atlantooccipital joint. The head is therefore ‘stuck’ as a brow 297

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Right occipitoposterior

20% short (45°) t i rotation t ti posterior

20% transverse arrest aer 45° rotation

60% long (135°) anterior rotation

FIGURE 35.6

From a right occipitoposterior position in early labour, the incidence of rotation to other positions is approximately 60% anterior, 20% transverse and 20% posterior.

FIGURE 35.7

The neonate on the right presented occipitoanterior but the neonate on the left presented in labour as a brow. This photo is taken at 2 days of age and illustrates a persistence of the extensor attitude and prominence of the brow. Source: Courtesy of Prof. Norman Beischer.

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Chapter 35  Malpresentation and Malposition

presentation that is unable to fit through the pelvis because of the very large presenting diameter (13.5 cm).

DIAGNOSIS A brow presentation will rarely be diagnosed on abdominal palpation. On vaginal examination, a prominent anterior fontanelle gives the impression of a posterior position but further exploration (usually anteriorly under the symphysis) reveals the root of the nose in the midline and the orbital ridges laterally (Fig 35.8).

CLINICAL SEQULAE A brow presentation will almost always obstruct and be associated with signs of inadequate progress and then of obstructed labour. Unless extremely small (e.g. extreme prematurity), it will rarely deliver vaginally as a brow (Fig 35.9).

A

FIGURE 35.8

Brow presentation in labour.

B

FIGURE 35.9

A This neonate of birth weight 2960 g presented by the brow. The prominence of the brow is obvious. In this case, the fetus delivered vaginally as a brow, a rare outcome of brow presentation. B This contrasts with the elongation of a normally shaped head due to moulding in a term neonate that had presented by the vertex in an occipitoanterior position during labour and birth. Source: Courtesy of Prof. Norman Beischer.

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Rarely will a brow presentation spontaneously correct or deliver vaginally, almost always after rotating 180° from what was effectively a very deflexed posterior position to occipitoanterior.

MANAGEMENT With great caution, correction may be attempted in the second stage of labour by manual rotation with Kielland forceps rotation from a brow in the mentoanterior position that flexes to a vertex occipitoanterior during rotation. Much more commonly, a caesarean section will be performed to minimise risk to both mother and fetus.

FACE PRESENTATION This is maximal extension but paradoxically, a favourable diameter again presents to the pelvis (the submento­ bregmatic, 9.5 cm), which is the same as the most favourable diameter when the head is fully flexed (the suboccipitobregmatic).

INCIDENCE Excluding cases of anencephaly (which are now mostly diagnosed on ultrasound early in pregnancy), a face presentation only occurs about once in every 800 deliveries, so it is much less common than a brow presentation (Fig 35.10).

FIGURE 35.10

Maternal abdominal X-ray showing hyperextension of the fetal neck and a face presentation. Source: Courtesy of Normal Beischer.

AETIOLOGY Unless a distinctive cause such as anencephaly or tumour of the fetal neck is present, the usual cause will again be heightened extensor tone (Fig 35.11).

DIAGNOSIS As for brow presentation, diagnosis on antenatal abdominal examination is most unlikely but some will be diagnosed antenatally in the course of an ultrasound being performed for another reason. Most commonly, the face presentation will be diagnosed on vaginal examination in labour. A partly soft, partly firm, irregular contour will be noted which is easy to confuse with a breech presentation. The most useful landmarks are the orbital ridges, the nose, and the mouth and alveolar ridges. Unless a caput has formed, the general consistency is much firmer than in a breech presentation. If in doubt, prodding should not be vigorous because of possible damage to the baby’s eyes. Ultrasound may assist in early labour where diagnosis may be uncertain in the presence of minimal cervical dilatation.

CLINICAL SEQUELAE The labour is usually longer than normal, probably as a result of the poorer fit of the face in the lower uterine 300

FIGURE 35.11

Extension of the neck causing a face presentation in association with thyroid gland enlargement. The mother also had a goitre but was not on treatment. The condition resolved without treatment. Source: Courtesy of Monash Health.

Chapter 35  Malpresentation and Malposition

segment, poorer moulding and the fact that full extension is less easily achieved than full flexion. The face at birth is commonly bruised, blue, oedematous and quite disfigured but recovers very quickly over a few days in the absence of any direct trauma from an amniotomy, fetal electrode placement or fetal blood sampling.

MANAGEMENT Antenatal If a face presentation is suspected in pregnancy, an ultrasound should be performed to determine any predisposing factors such as anencephaly or a tumour of the neck. An elective caesarean section will usually be recommended because of the limitations on intrapartum care and the higher likelihood of needing an emergency caesarean section.

Intrapartum The progress of labour is followed by abdominal and, if necessary, vaginal examination. Application of a fetal scalp electrode or fetal blood sampling should be avoided. Otherwise, the management and labour is similar to that described for the woman with a normal vertex presentation. For birth, the chin rotates around under the symphysis pubis, and the brow, vertex and occiput will in turn sweep over the perineum. Unlike in the vertex presentation, there will be no chin to pick up below the coccyx, only the top of the baby’s head. After delivery of the head, the rest of the baby is managed as in a normal birth (Fig 35.12). A mentoposterior position will generally not correct during labour (Fig 35.13) and a caesarean section is recommended. Forceps or manual rotation of a face to mentoanterior is rarely performed. A vacuum is obviously absolutely contraindicated but a direct forceps delivery of a mentoanterior position may be appropriate for delayed second stage or usual maternal or fetal indications. However, it should be remembered that engagement will not have occurred until the face is at least 3 cm below the ischial spines.

FIGURE 35.12

Face presentation: mechanism of delivery. A The chin is anterior and has descended until the fetal hyoid bone is at the level of the symphysis pubis. B The head pivots on the symphysis pubis and is born by flexion. The chin appears first, followed by the nose, brow, vertex and occiput.

FIGURE 35.13

Persistent mentoposterior position: delivery cannot occur if the chin remains posterior. Delivery will only be effected vaginally if the chin rotates anteriorly.

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Chapter 36  POSTPARTUM HAEMORRHAGE Michael Permezel

KEY POINTS Postpartum haemorrhage (PPH) occurs in about 4% of pregnancies and accounts for about 10% of direct maternal deaths. The key to management is to act without delay in implementing the sequence of steps necessary to control the bleeding. The common causes are ‘tone’ (uterine atony), ‘tissue’ (retained placental tissue), ‘trauma’ (birth canal laceration) and ‘thrombin’ (coagulopathy). Active management of the third stage of labour (including the administration of an oxytocic), reduces the likelihood of uterine atony. Although most cases occur unexpectedly in women without risk factors, there are pregnancies where PPH should be anticipated: previous PPH, chorioamnionitis, placental abruption, placenta praevia, uterine overdistension (including multiple pregnancy), prolonged labour and instrumental birth. Initial management of a PPH in the birth suite will focus on summoning appropriate personnel, resuscitation, contracting the uterus (massage and oxytocics), emptying the uterus and excluding a lower traumatic site for the bleeding. If the PPH is persistent, the patient is taken to the operating theatre. Resuscitation continues with anaesthetic support monitoring volume, haemoglobin and clotting, and replacing as needed. Exploration of the uterus is performed to exclude retained products or high genital tract injury to the uterus, cervix or upper vagina. Ongoing bleeding is managed with further oxytocics and other measures as deemed necessary including balloon tamponade, compression sutures, vessel ligation and hysterectomy. Secondary PPH is almost always due to infection, often in combination with some retained products of conception. Microbiological assessment, ultrasound and antibiotics are required but only a minority of cases will need curettage.

PRIMARY POSTPARTUM HAEMORRHAGE Primary postpartum haemorrhage (PPH) is defined as bleeding of 500 mL or more from the birth canal in the first 24 hours after delivery of the baby. Major PPH is variously defined but most easily as blood loss of greater than 1000 mL. It remains the major cause of maternal death on a global basis—mostly in women of high parity who did not want to be pregnant. The consequences of

sustained haemorrhagic shock in a pregnant woman are discussed in Chapter 37 but include disseminated intravascular coagulation which will further add to the bleeding.

INCIDENCE There are many inaccuracies in the estimation of blood loss around the time of birth, but the best approximations would suggest 4% PPH with active management of the third stage and 8% if active management is omitted.

Chapter 36  Postpartum Haemorrhage

AETIOLOGY A PPH arises from either the placental site or a traumatic site. Possible aetiologies are in Box 36.1 and each is discussed later in this chapter.

MANAGEMENT OF ACUTE BLOOD LOSS AT BIRTH INITIAL MANAGEMENT IN THE   BIRTH SUITE 1.  Summon assistance Significant haemorrhage requires more than one pair of hands and experienced help can be lifesaving. The woman should never be left alone and a second person will be needed to obtain the necessary drugs, equipment and so on.

2.  Simultaneous resuscitation The resuscitation should take place simultaneously with manoeuvres to arrest the haemorrhage. An intravenous line is needed and blood should be taken for cross-match if not already done. Fluid infusion should be compatible with blood lost.

3.  Contract the uterus There is an old saying that ‘an empty contracted uterus will not bleed’. While this is not always true, achieving a strong uterine contraction should be the priority when faced with brisk bleeding after birth. a. Uterine massage (‘Rub up the fundus’). This is usually an effective means of contracting the uterus and at the same time, one gains an impression of whether the uterus is atonic. b. Oxytocic administration. What is used will depend on what has already been administered for the third stage of labour. A common regimen might be: ergometrine 0.25 mg slowly intravenously and

repeated after 5 minutes if necessary; oxytocin 40 units in 1 L over 4 hours and misoprostol 1000 mcg rectally. If atony is likely and bleeding persistent, dinoprost (prostaglandin F2α), 1 mg intramyometrial may be given with careful supervision. Note that asthma and hypertension are contraindications.

4.  Empty the uterus If the placenta is retained, a further attempt is made to deliver it by controlled cord traction (if the cord is still attached) or fundal pressure (if the cord has been avulsed). If the placenta has been delivered, it is rechecked carefully for completeness and the presence of a transected feeding vessel in the membranes, which might indicate a missing succenturiate lobe.

5.  Check the lower birth canal Check the lower birth canal, looking for an obvious traumatic bleeding site in the low vagina or perineum.

6.  Prepare for the operating theatre if the bleeding is continuing Bimanual compression will reduce blood loss while preparations are being made for theatre. Haematology should be investigated, including a full blood examination and clotting studies, as well as checking the availability of compatible blood products.

SUBSEQUENT MANAGEMENT   IN THE OPERATING THEATRE 1.  Summon further assistance if needed An anaesthetist will be needed in theatre to manage the resuscitation. Consideration should be given to the whereabouts of other personnel who may be needed, including experienced surgical assistance and haematology/blood bank expertise.

2.  Simultaneous resuscitation BOX 36.1  Causes of primary postpartum haemorrhage. 1. Placental site a. Uterine atony: grand multiparity, overdistension (e.g. twins), long labour b. Retained placenta c. Placenta praevia d. Placenta accreta e. Uterine inversion f. Bleeding tendency 2. Traumatic site a. Uterine rupture b. Cervical tear c. Vaginal or perineal laceration

The anaesthetist will be responsible for maintaining blood volume, coagulation and platelets. Resuscitation should take place simultaneously with manoeuvres to arrest the haemorrhage. An intravenous line is needed and blood should be taken for cross-match if not already done. Fluid infusion should be compatible with blood lost.

3.  Explore the uterus Look for either retained products of conception or a traumatic site of bleeding in the uterus (manual exploration), cervix or upper vagina (under vision). Good anaesthesia and good lighting are essential.

4.  Contract the uterus Contract the uterus as mentioned previously. The anaesthetist should be overseeing an oxytocin infusion. Up to 303

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1 mg of ergometrine may be given in 250-mcg aliquots. Misoprostol will have been administered rectally and up to a total of 3 mg of dinoprost (prostaglandin F2α) can be given intramyometrially in 1-mg aliquots at least 5 minutes apart.

it takes to perform these procedures does not irrevocably compromise the patient. It should not be attempted by a surgeon inexperienced in the technique.

5.  Balloon tamponade or packing

Hysterectomy is generally regarded as an operation of last resort but a timely hysterectomy can be lifesaving, while procrastination for too long with other approaches may increase the likelihood of a maternal death.

Balloon tamponade (Fig 36.1) or packing should next be considered if the bleeding appears to be from the placental site and is persistent. On rare occasions, there is uncontrollable bleeding from multiple vaginal tears that require packing for control of venous ooze after arterial bleeding has been arrested with sutures.

6.  Compression sutures (e.g. B-Lynch) Compression sutures can be lifesaving if the bleeding is from a placental site in the upper uterine segment (Fig 36.2). A B-Lynch will not be effective if the bleeding is from a low-lying placental site, but alternative styles of compression sutures have been suggested for that situation.

7.  Internal iliac ligation or placental site radiological embolisation

8.  Hysterectomy

PPH FROM THE PLACENTAL SITE UTERINE ATONY Contraction of the uterus after placental separation causes the vessels supplying the placental bed to occlude. Inadequate contraction and failure of this critically important mechanism is the most common cause of PPH. Uterine atony is less common with ‘active management of the third stage of labour’, comprising the Fallopian tube

These measures may be employed in an attempt to further control persistent bleeding and preserve the uterus. Specific expertise is needed and care taken so that the time

Round ligament Broad ligament

INSERTION OF SUTURES

SUTURE TIED

FIGURE 36.1 

The Bakri balloon tamponade for control of postpartum haemorrhage.

Source: Gabbe SG, Niebyl JR, Galan HL, et al. Obstetrics: Normal and Problem Pregnancies. 6th edn. Philadelphia: Saunders, 2012. Copyright © 2012 Saunders, An Imprint of Elsevier. Figure 19.10. Courtesy Cook Women’s Health.

304

FIGURE 36.2 

B-Lynch compression suture for control of massive PPH.

Source: James D, Steer PJ, Weiner CP, Gonik B. High Risk Pregnancy. 4th ed. Philadelphia: Saunders, 2011. Copyright © 2011 Saunders, An Imprint of Elsevier. Figure 75.12. From B-Lynch C, Coker A, Lawal AH, et al. The B-Lynch surgical technique for the control of massive postpartum hemorrhage: An alternative to hysterectomy? Five cases reported. Br J Obstet Gynaecol 1997;104:372–5.

Chapter 36  Postpartum Haemorrhage

administration of oxytocic drugs and then assistance with the delivery of the placenta. Women choosing to have a ‘natural third stage’ are about twice as likely to have an atonic PPH. A number of factors may interfere with normal uterine retraction after birth: chorioamnionitis, uterine ‘exhaustion’ after a prolonged labour, high parity and overdistension of the uterus prior to birth. Overdistension may be the result of a large baby, multiple pregnancy or polyhydramnios, and in the first two cases will also be associated with an increased placental blood flow. Management is as described for an acute primary PPH. It is important not to assume atony without pursuing the possibility of other causes of placental site bleeding or a traumatic site.

RETAINED PRODUCTS OF CONCEPTION Non-separation and retention of part or whole of the placenta is also a common cause of PPH. Arteries and venous sinuses in the placental bed are inhibited from occluding even by relatively small amounts of placenta tissue (e.g. a cotyledon). This may be partly an effect on uterine contraction but may also be a failure of constriction of the arterioles and venous sinuses in the placental bed. Where the whole placenta, or a large portion, is retained, the diagnosis is obvious. Difficulty arises, however, if there is a small cotyledon retained (especially if the placenta is ragged) or if there is an additional (succenturiate) lobe (Fig 36.3). On occasions, large segments of retained membrane may act in the same way as

a cotyledon. In all women with significant ongoing bleeding, it is to be assumed that there ‘may’ be retained placental fragment and uterine exploration with adequate anaesthesia is indicated.

PLACENTA PRAEVIA AS A CAUSE   OF PPH With a placenta praevia, there is less muscle in the lower uterine segment and therefore less efficient contraction of the uterine wall around the vessels supplying the placental bed. This results in higher than usual blood loss from the placental bed if the placenta is located in the lower uterine segment. Fortuitously, this is usually at caesarean section where surgical measures can be instituted promptly. Sometimes sutures are directed specifically at bleeding points in the lower uterine segment but also a balloon catheter may be employed. Compression sutures are more difficult and those of the B-Lynch type are not suitable. Hysterectomy is necessary in about 1% of first caesarean sections for placenta praevia but the risk increases greatly where there are previous caesarean sections (see placenta accreta).

PLACENTA ACCRETA Pathology Placenta accreta implies morbid adherence of the placenta to the uterine wall. It is sometimes termed ‘percreta’ if the placenta completely traverses the uterine wall (often into the bladder).

FIGURE 36.3 

Missing placental cotyledon that was noted at routine inspection of the placenta after birth. Although there was no postpartum haemorrhage, a manual removal was performed and the missing cotyledon retrieved from the uterine cavity. Source: Courtesy of Monash Health.

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Predisposing factors This condition is usually associated with previous caesarean section (especially repeated) and may be tested for by estimation of serum alpha-fetoprotein (elevation) or by ultrasonography.

Clinical presentation The condition should be suspected clinically where there is a low-lying anterior placenta and a previous caesarean section. With placenta praevia and one prior caesarean section, the risk of accreta is about 25% but increases to 60% after two caesarean sections. Antenatal bleeding may be minimal or absent but separation of the placenta is difficult at caesarean section followed by heavy and persistent bleeding from the placental bed.

Management Placenta accreta is a life-threatening condition and all resources must be available to minimise maternal risk. Unless unavoidable by virtue of emergency substantial haemorrhage, a caesarean section for possible placenta accreta should only occur in a hospital equipped to manage massive haemorrhage and with the necessary surgical, anaesthetic, haematological and maybe radiological expertise available. Surgical approaches are varied and will depend on the specific circumstances and preference of the experienced obstetricians undertaking the procedure. Options include: 1. attempting to remove the placenta and control the bleeding, or 2. performing a high classical caesarean section and leaving the placenta in situ in the lower uterine segment. A hysterectomy may then be performed at that time. Alternatively, there may be attempted conservative management, waiting for the placenta to pass vaginally—which can take many weeks. The latter approach may be effective but a small number present with sudden haemorrhage days or weeks after the birth and this may be fatal.

inversion is a submucous fibromyoma projecting through the external os; this can be confused with partial inversion where the fundus may still be palpable abdominally. Bleeding may or may not be excessive, but shock is common if the uterus is not quickly replaced. Neurogenic shock usually ensues due to a massive parasympathetic output (vasovagal attack) consequent on traction on the infundibulopelvic ligaments as the ovaries are drawn down with the fundus of the uterus.

Management If recognised at the moment it occurs, immediate replacement can usually be effected. Otherwise, after shock has been corrected by intravenous therapy, an attempt is made to replace the uterus manually: with the fundus in the palm of the hand, strong upward pressure is exerted to place the uterine ligaments on the stretch; if this is maintained for 3 to 5 minutes the fundus will usually recede upwards as the ring widens. It is then pushed upwards with the clenched fist. The placenta, if still attached to the fundus, is manually removed after the inversion has been replaced; it provides a firmer base to press upon and lessens the risk of uterine rupture. Alternatively, O’Sullivan’s hydrostatic method may be used: here, sterile saline at body temperature is run into the upper vagina while the forearm occludes its egress below; the vagina balloons, the ring stretches and the fundus returns to its normal position. If the constricting ring feels tight, it may be relaxed with a slow intravenous bolus of 2 g of magnesium sulfate. Rarely, abdominal surgery may be necessary.

UTERINE INVERSION Pathophysiology The fundus of the uterus descends through the cervix and lies either in the vagina or outside the introitus. The placenta is usually still adherent, either totally or partially. This condition is extremely rare with active management of the third stage of labour including the routine administration of an oxytocic. Uterine inversion usually occurs in the presence of a fundal placenta with cord traction applied to an uncontracted uterus (Fig 36.4). It may also occur during a manual removal and at caesarean section.

Clinical features A large mass is felt or seen and there is no uterus palpable in the abdomen. The only condition which simulates 306

A FIGURE 36.4 

B

Uterine inversion. Traction on the cord when the uterus is atonic and the placenta not separated produces initial dimpling of the fundus A and then inversion of the uterus through the cervix B.

Chapter 36  Postpartum Haemorrhage

COAGULATION DEFECT The impact of coagulopathy on peripartum blood loss highlights the fact that uterine contraction alone is not responsible for cessation of placental site bleeding after separation. Activation of the endothelium with vasospasm, platelet aggregation and clot formation are all important as well. In obstetric practice, disseminated intravascular coagulation is easily the most common cause of failure of blood clotting. The clinical conditions predisposing to this complication are placental abruption, fetal death in utero (more than 4 weeks), severe preeclampsia, amniotic fluid embolism, chorioamnionitis and sustained hypotension with poor tissue perfusion for any reason (Ch 20). All of these conditions act by massive release of thromboplastin into the circulation. Occasionally, other conditions such as severe thrombocytopenia or hereditary disorders of coagulation (e.g. von Willebrand’s) may present with postpartum haemorrhage. In all of these conditions, correction of the underlying haematological disturbance will be key to controlling the blood loss.

PPH FROM A TRAUMATIC SITE Any disruption of the birth canal may cause excessive bleeding, because of the increased vascularity in pregnancy. In general, tears of the uterus, cervix and upper vagina are more serious, because of the larger vessels that may be torn and the difficulty in gaining access to them. More common and usually more manageable are tears of the lower vagina, introitus and perineum. A high tear should be suspected if bleeding is coming down from the upper vagina immediately after birth and before any separation of the placenta.

FIGURE 36.5 

Uterine rupture at the site of a previous classical caesarean section scar (subtotal hysterectomy specimen). Source: Reproduced with permission from the Royal Women’s Hospital, Parkville, Victoria.

UTERINE RUPTURE Predisposing factors Uterine scar Upper uterine segment scars (classical caesarean section, hysterotomy) are more likely to rupture (Fig 36.5) than the transverse scar from a single lower uterine segment caesarean section (Fig 36.6). Management of labour after caesarean section is discussed in Chapter 32. Rupture may also occur after operation on the non-pregnant uterus, including myomectomy or perforation of the uterus at the time of curettage.

Obstructed labour Neglected obstructed labour may result in a uterine rupture, particularly as the parity increases. The lower uterine segment progressively thins as it is drawn up over the presenting part. Rupture may occur intraperitoneally or extend into the broad ligament.

FIGURE 36.6 

Intact fetal membranes bulging through a uterine scar dehiscence. Source: Courtesy of Prof. Norman Beischer.

Trauma A high-speed motor vehicle accident may cause uterine rupture, as may obstetric manipulation (e.g. internal version prior to breech extraction of a second twin). 307

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Clinical features The clinical picture depends on the extent of the haemorrhage. A dehiscence may be an incidental finding at the time of caesarean section. If there has been significant bleeding, fetal compromise may be evident. With a true ‘rupture’, if the fetus is alive it will rapidly show evidence of compromise and a hypoxic death will follow if the fetus or placenta are extruded into the peritoneal cavity through the tear. The mother will experience pain at the site of rupture followed by evidence of intraperitoneal bleeding (e.g. shoulder-tip pain) and subsequently hypovolaemic shock if the bleeding is not arrested. Rupture may present after a vaginal birth as persistent ongoing bleeding or unexpected maternal collapse.

Treatment Apart from the usual measures for haemorrhagic shock, a uterine rupture will usually require hysterectomy, although a small defect may be successfully repaired— albeit with a significant likelihood of rupture in a subsequent pregnancy.

CERVICAL LACERATIONS Predisposing factors for cervical lacerations include the following. Pushing on an undilated cervix. This can generally be avoided with patient instruction. If this is not effective, epidural anaesthesia will quell the desire to push against a cervix that is not fully dilated. A hypertonic labour. Rapid labour may have a similar effect but without necessarily being due to ‘pushing’. Traumatic tearing of the cervix. Instrumental vaginal birth (especially rotational forceps), internal podalic version (usually for a second twin) and treatment of impacted shoulders are all manipulations that may tear the cervix. The characteristic feature is a steady loss of bright red blood, which commences soon after delivery of the baby, but the diagnosis will not be confidently made until the cervix is carefully inspected under anaesthesia. With good exposure and lighting, ‘walking’ around the cervix with forceps will expose any cervical tear, which can then be repaired. It is difficult to effectively reduce haemorrhage from a cervical tear with packing but bimanual compression may be effective while awaiting access to an operating theatre.

• • •

HIGH VAGINAL WALL TEARS A high vaginal wall tear will have causes similar to cervical lacerations and they may occur together. Access to a tear high in the lateral fornix can be extremely difficult but may involve major vessels in the base of the broad ligament. Expert surgical repair, often followed by a need for tight packing of the vagina, is required. Packing can be very useful for emergency treatment of haemorrhage from vaginal lacerations as the pelvis is a bony basin that 308

has rigid walls to pack against. Two large ribbon gauze packs are tied together, moistened with obstetric cream and firmly packed, beginning high in the vagina. Since the packing occludes the urethra, an indwelling (Foley) catheter is required and a uterine balloon with catheter drainage may help reveal ongoing uterine bleeding. The pack is removed 12 to 24 hours later and healing of any unsutured vaginal lacerations is usually quite satisfactory.

Low vaginal, introital and perineal tears Tears may occur almost anywhere, including involving the anterior compartment of the perineum (around the urethra and clitoris) and posteriorly involving the sphincter and anal canal. Particularly heavy bleeding may result from an annular avulsion of the vulva from the lower vagina. Tears are more common where the fetus is large or the head extended, where delivery is rapid or instrumental (not allowing time for tissues to stretch) or where there is a need for difficult manipulations (e.g. delivery of the posterior arm with shoulder dystocia. While there is no place for ‘routine’ episiotomies, a timely incision to enlarge the introitus can save the woman tears causing considerable blood loss, significant perineal pain in the puerperium and sometimes followed by dyspareunia lasting months or years. Each layer should be carefully identified and sutured, and haemostasis secured. Where the anal sphincter is involved, this must be clearly identified and repaired in theatre with good lighting and adequate anaesthesia. Where there is persistent bleeding from deep in the perineum, packing is not possible because there is nothing to pack against. Pressure will be effective but difficult to maintain. A large ‘compression suture’ may be effective but needs to be removed within 12 to 24 hours.

VULVAL AND PARAVAGINAL HAEMATOMA In approximately 1 out of 1000 births there is extensive ‘concealed’ bleeding into the tissues of the perineum or vagina. It may or may not have been preceded by lacerations where a vessel has retracted or temporarily been hidden by vasospasm, only to open up after closure of the wound. If the haematoma is large, pain will be severe and may cause significant hypovolaemia. Treatment is usually conservative in the first instance as ‘tamponade’ by the tissues will generally arrest the bleeding. An indwelling urinary catheter is usually needed along with narcotic analgesia. Drainage after a few days may be needed for maternal comfort. If early drainage is performed, vaginal packing is usually needed to help tamponade a deep bleeding point that has not been readily identified.

THE RETAINED PLACENTA IN THE ABSENCE OF BLEEDING Sometimes the placenta has separated and is ‘trapped’ in the cervix. This can be readily palpated on vaginal

Chapter 36  Postpartum Haemorrhage

examination and if most of the placenta is in the vagina, it can be relatively easy to grasp and remove without significant maternal discomfort. If there is minimal bleeding, it is likely that the placenta has not separated and patience is required. The accoucheur should check for placental separation every 5 minutes of so as there is the risk of concealed haemorrhage when separation occurs and the placenta remains in situ. Where the placenta has been retained for more than 30 minutes, arrangements should be made for manual removal of the placenta, as retention longer than 60 minutes (approximately 2% of labours) carries a substantive risk of major PPH.

MANUAL REMOVAL OF THE PLACENTA Manual removal of the placenta will require either regional or general anaesthesia. Blood should have been taken for cross-match as a PPH is common at the time of manual removal, and can be severe if the placenta is particularly adherent. Fresh sterile gloves (preferably with a forearm extension), gown and drapes should be used. The fingers are brought into the shape of a cone and the hand follows the umbilical cord into the uterine cavity. An assessment is made of the degree of adherence of the placenta and the site of attachment. The fingers are then inserted at one edge of the placenta, with the external hand on the abdomen exerting firm counter-pressure. With sweeping movements, the placenta is stripped from the wall of the uterus (Fig 36.7). It is important that the procedure be carried out gently and methodically, the operator having a clear mental picture of the disposition and extent of the placenta on the uterine wall. Occasionally, the placenta may be morbidly adherent to the uterus (placenta accreta), either wholly or in part. In such cases, a plane of cleavage will not be found and bleeding is usually heavy (see above). Following manual removal, the uterine cavity should be carefully explored to exclude any retained fragments and to ensure the uterine wall was not torn during the procedure. An oxytocic is then administered along with prophylactic antibiotics. A check of the birth canal is undertaken and any tears repaired.

SECONDARY PPH A secondary PPH is defined as any bleeding in excess of normal lochial loss between 24 hours and 6 weeks postpartum. Most cases are due to infection that may be associated with retained fragments of placenta and/or membrane. Rarely, there may be other causes such as choriocarcinoma or a submucous fibroid. Bleeding is bright and can be heavy.

MANAGEMENT A full clinical assessment is needed to ascertain the degree of blood loss and whether any resuscitation is

FIGURE 36.7 

Manual removal of the placenta. The placenta is palmed as the fingers gently separate it from the uterine wall. The abdominal hand provides counter-pressure, which assists in finding the correct plane between placenta and uterine wall.

required. A haemoglobin check is needed and a vaginal swab is taken for microbiological study. Oxytocics (e.g. ergometrine, misoprostol) variably assist with controlling acute bleeding. Antibiotic therapy is commenced even if the woman is afebrile, since endometritis is likely. A serum hCG should be performed if the bleeding is unusual or persistent, suggesting trophoblastic disease. An ultrasound will be requested to exclude substantive retained products of conception that will require curettage for removal. Curettage carries a risk of perforation of the uterus softened by both involution and infection. In the longer term, there may be intrauterine adhesion formation, known as Asherman syndrome. FURTHER READING Angstmann T, Gard G, Harrington T, et al. Surgical management of placenta accreta; a cohort ser