Obstetric and intrapartum emergencies : a practical guide to management [Second ed.] 9781108807746, 1108807747

Citation preview

Obstetric and Intrapartum Emergencies

,

,

Obstetric and Intrapartum Emergencies A Practical Guide to Management Second Edition

Edited by

Edwin Chandraharan Global Academy of Medical Education & Training, London & Basildon & Thurrock University Hospital NHS Foundation Trust, Essex, UK

Sir Sabaratnam Arulkumaran St George’s University of London

,

University Printing House, Cambridge CB2 8BS, United Kingdom One Liberty Plaza, 20th Floor, New York, NY 10006, USA 477 Williamstown Road, Port Melbourne, VIC 3207, Australia 314–321, 3rd Floor, Plot 3, Splendor Forum, Jasola District Centre, New Delhi – 110025, India 79 Anson Road, #06–04/06, Singapore 079906 Cambridge University Press is part of the University of Cambridge. It furthers the University’s mission by disseminating knowledge in the pursuit of education, learning, and research at the highest international levels of excellence. www.cambridge.org Information on this title: www.cambridge.org/9781108790932 DOI: 10.1017/9781108807746 © Cambridge University Press 2021 This publication is in copyright. Subject to statutory exception and to the provisions of relevant collective licensing agreements, no reproduction of any part may take place without the written permission of Cambridge University Press. First published 2012 Second edition 2021 Printed in the United Kingdom by TJ Books Limited, Padstow Cornwall A catalogue record for this publication is available from the British Library. Library of Congress Cataloging-in-Publication Data Names: Chandraharan, Edwin, editor. | Arulkumaran, Sabaratnam, editor. Title: Obstetric and intrapartum emergencies : a practical guide to management / edited by Edwin Chandraharan, Sir Sabaratnam Arulkumaran. Description: Second edition. | Cambridge ; New York, NY : Cambridge University Press, 2021. | Includes bibliographical references and index. Identifiers: LCCN 2020047396 (print) | LCCN 2020047397 (ebook) | ISBN 9781108790932 (paperback) | ISBN 9781108807746 (ebook) Subjects: MESH: Pregnancy Complications – therapy | Delivery, Obstetric – methods | Emergency Treatment – methods | Emergencies | Obstetrics – methods Classification: LCC RG571 (print) | LCC RG571 (ebook) | NLM WQ 240 | DDC 618.3–dc23 LC record available at https://lccn.loc.gov/2020047396 LC ebook record available at https://lccn.loc.gov/2020047397 ISBN 978-1-108-79093-2 Paperback ................................................................................................................................ Cambridge University Press has no responsibility for the persistence or accuracy of URLs for external or third-party internet websites referred to in this publication and does not guarantee that any content on such websites is, or will remain, accurate or appropriate. Every effort has been made in preparing this book to provide accurate and up-to-date information that is in accord with accepted standards and practice at the time of publication. Although case histories are drawn from actual cases, every effort has been made to disguise the identities of the individuals involved. Nevertheless, the authors, editors, and publishers can make no warranties that the information contained herein is totally free from error, not least because clinical standards are constantly changing through research and regulation. The authors, editors, and publishers therefore disclaim all liability for direct or consequential damages resulting from the use of material contained in this book. Readers are strongly advised to pay careful attention to information provided by the manufacturer of any drugs or equipment that they plan to use.

,

Obstetric and Intrapartum Emergencies

at 20:20:27,

at 20:20:27,

Obstetric and Intrapartum Emergencies A Practical Guide to Management Second Edition

Edited by

Edwin Chandraharan Global Academy of Medical Education & Training, London & Basildon & Thurrock University Hospital NHS Foundation Trust, Essex, UK

Sir Sabaratnam Arulkumaran St George’s University of London

at 20:20:27,

University Printing House, Cambridge CB2 8BS, United Kingdom One Liberty Plaza, 20th Floor, New York, NY 10006, USA 477 Williamstown Road, Port Melbourne, VIC 3207, Australia 314–321, 3rd Floor, Plot 3, Splendor Forum, Jasola District Centre, New Delhi – 110025, India 79 Anson Road, #06–04/06, Singapore 079906 Cambridge University Press is part of the University of Cambridge. It furthers the University’s mission by disseminating knowledge in the pursuit of education, learning, and research at the highest international levels of excellence. www.cambridge.org Information on this title: www.cambridge.org/9781108790932 DOI: 10.1017/9781108807746 © Cambridge University Press 2021 This publication is in copyright. Subject to statutory exception and to the provisions of relevant collective licensing agreements, no reproduction of any part may take place without the written permission of Cambridge University Press. First published 2012 Second edition 2021 Printed in the United Kingdom by TJ Books Limited, Padstow Cornwall A catalogue record for this publication is available from the British Library. Library of Congress Cataloging-in-Publication Data Names: Chandraharan, Edwin, editor. | Arulkumaran, Sabaratnam, editor. Title: Obstetric and intrapartum emergencies : a practical guide to management / edited by Edwin Chandraharan, Sir Sabaratnam Arulkumaran. Description: Second edition. | Cambridge ; New York, NY : Cambridge University Press, 2021. | Includes bibliographical references and index. Identifiers: LCCN 2020047396 (print) | LCCN 2020047397 (ebook) | ISBN 9781108790932 (paperback) | ISBN 9781108807746 (ebook) Subjects: MESH: Pregnancy Complications – therapy | Delivery, Obstetric – methods | Emergency Treatment – methods | Emergencies | Obstetrics – methods Classification: LCC RG571 (print) | LCC RG571 (ebook) | NLM WQ 240 | DDC 618.3–dc23 LC record available at https://lccn.loc.gov/2020047396 LC ebook record available at https://lccn.loc.gov/2020047397 ISBN 978-1-108-79093-2 Paperback ................................................................................................................................ Cambridge University Press has no responsibility for the persistence or accuracy of URLs for external or third-party internet websites referred to in this publication and does not guarantee that any content on such websites is, or will remain, accurate or appropriate. Every effort has been made in preparing this book to provide accurate and up-to-date information that is in accord with accepted standards and practice at the time of publication. Although case histories are drawn from actual cases, every effort has been made to disguise the identities of the individuals involved. Nevertheless, the authors, editors, and publishers can make no warranties that the information contained herein is totally free from error, not least because clinical standards are constantly changing through research and regulation. The authors, editors, and publishers therefore disclaim all liability for direct or consequential damages resulting from the use of material contained in this book. Readers are strongly advised to pay careful attention to information provided by the manufacturer of any drugs or equipment that they plan to use.

at 20:20:27,

Obstetric and Intrapartum Emergencies

at 20:20:26,

at 20:20:26,

Obstetric and Intrapartum Emergencies A Practical Guide to Management Second Edition

Edited by

Edwin Chandraharan Global Academy of Medical Education & Training, London & Basildon & Thurrock University Hospital NHS Foundation Trust, Essex, UK

Sir Sabaratnam Arulkumaran St George’s University of London

at 20:20:26,

University Printing House, Cambridge CB2 8BS, United Kingdom One Liberty Plaza, 20th Floor, New York, NY 10006, USA 477 Williamstown Road, Port Melbourne, VIC 3207, Australia 314–321, 3rd Floor, Plot 3, Splendor Forum, Jasola District Centre, New Delhi – 110025, India 79 Anson Road, #06–04/06, Singapore 079906 Cambridge University Press is part of the University of Cambridge. It furthers the University’s mission by disseminating knowledge in the pursuit of education, learning, and research at the highest international levels of excellence. www.cambridge.org Information on this title: www.cambridge.org/9781108790932 DOI: 10.1017/9781108807746 © Cambridge University Press 2021 This publication is in copyright. Subject to statutory exception and to the provisions of relevant collective licensing agreements, no reproduction of any part may take place without the written permission of Cambridge University Press. First published 2012 Second edition 2021 Printed in the United Kingdom by TJ Books Limited, Padstow Cornwall A catalogue record for this publication is available from the British Library. Library of Congress Cataloging-in-Publication Data Names: Chandraharan, Edwin, editor. | Arulkumaran, Sabaratnam, editor. Title: Obstetric and intrapartum emergencies : a practical guide to management / edited by Edwin Chandraharan, Sir Sabaratnam Arulkumaran. Description: Second edition. | Cambridge ; New York, NY : Cambridge University Press, 2021. | Includes bibliographical references and index. Identifiers: LCCN 2020047396 (print) | LCCN 2020047397 (ebook) | ISBN 9781108790932 (paperback) | ISBN 9781108807746 (ebook) Subjects: MESH: Pregnancy Complications – therapy | Delivery, Obstetric – methods | Emergency Treatment – methods | Emergencies | Obstetrics – methods Classification: LCC RG571 (print) | LCC RG571 (ebook) | NLM WQ 240 | DDC 618.3–dc23 LC record available at https://lccn.loc.gov/2020047396 LC ebook record available at https://lccn.loc.gov/2020047397 ISBN 978-1-108-79093-2 Paperback ................................................................................................................................ Cambridge University Press has no responsibility for the persistence or accuracy of URLs for external or third-party internet websites referred to in this publication and does not guarantee that any content on such websites is, or will remain, accurate or appropriate. Every effort has been made in preparing this book to provide accurate and up-to-date information that is in accord with accepted standards and practice at the time of publication. Although case histories are drawn from actual cases, every effort has been made to disguise the identities of the individuals involved. Nevertheless, the authors, editors, and publishers can make no warranties that the information contained herein is totally free from error, not least because clinical standards are constantly changing through research and regulation. The authors, editors, and publishers therefore disclaim all liability for direct or consequential damages resulting from the use of material contained in this book. Readers are strongly advised to pay careful attention to information provided by the manufacturer of any drugs or equipment that they plan to use.

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Contents List of Contributors viii Preface: Why a Second Edition? xiii Preface to the First Edition xv Acknowledgements xvi

Section 1 General Principles 1

2

Anatomical and Physiological Changes in Pregnancy: Impact on Emergency Care 1 Niraj Yanamandra and Edwin Chandraharan Principles of Resuscitation for ‘Maternal Collapse’ During Pregnancy, Labour and Postpartum: Airway, Breathing and Circulation 10 Renate Wendler

Section 3 Intrapartum Emergencies 8

Uterine Rupture 51 Caroline Reis Gonçalves and Edwin Chandraharan

9

Breech Delivery 56 Enaya Mirza and Edwin Chandraharan

10

Umbilical Cord Prolapse Malik Goonewardene

11

Fetal Compromise: Diagnosis and Management 76 Anna Gracia Perez-Bonfils and Edwin Chandraharan

Section 2 Algorithms for Management of the Top Five ‘Direct Killers’

66

3

Management of Deep-Vein Thrombosis and Pulmonary Embolism: Antepartum, Intrapartum and Postpartum 17 Chu Chin Lim and Tahir A. Mahmood

12

Shoulder Dystocia: Diagnosis and Management 86 Edwin Chandraharan and Sabaratnam Arulkumaran

4

Management of Severe Preeclampsia and Eclampsia: Antepartum, Intrapartum and Postpartum 26 Peter von Dadelszen and Laura A. Magee

13

Twin Delivery 92 Deepal S. Weerasekera

14

Instrumental Vaginal Delivery 98 Vikram Sinai Talaulikar and Sabaratnam Arulkumaran

15

‘Crash’ Caesarean Section Leonie Penna

16

Unintended Trauma and Complications During Caesarean Section 116 Suganya Sukumaran and Edwin Chandraharan

17

Obstetric Emergencies in Midwife-Led Settings 120 Emma Spillane

5

Management of Massive Obstetric Haemorrhage: Antepartum, Intrapartum and Postpartum 35 Ana Pinas Carillo and Edwin Chandraharan

6

Management of Septicaemia and Septic Shock: Antepartum, Intrapartum and Postpartum 43 Karin Leslie and Sarah Hammond

7

Management of Amniotic Fluid Embolism 47 Derek Tuffnell, James Tibbott and Hlupekile Chipeta

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107

v

Contents

Section 4 Postpartum Emergencies 18

Acute Puerperal Uterine Inversion Hemantha Senanayake, Probhodana Ranaweera and Mohamed Rishard

133

19

Sudden Postpartum Maternal Collapse Becky Liu and Amarnath Bhide

20

Retained Placenta 147 Kapila Gunawardane and Chathura Ratnayake

21

139

Perineal Trauma 153 Stergios K. Doumouchtsis and Vasilios Pergialiotis

Fluid Overload and Underload 239 Renate Wendler

34

Section 5 Medical and Surgical Emergencies During Pregnancy

Transfusion and Anaphylactic and Adverse Drug Reactions in Pregnancy 245 Saba Al-Sulttan, Sohail Bampoe and Anthony Addei

35

Major Trauma, Including Road Traffic Accidents 252 Kirsty Crocker and Tim Patel

Palpitations During Pregnancy 159 Sourav Das and Edwin Chandraharan

23

Breathlessness in Pregnancy 164 Amanda Ali and Hassan Shehata

24

Abdominal Pain in Pregnancy Archana Krishna and Edwin Chandraharan

Section 7 Neonatal Emergencies and the Management of Immediate Neonatal Problems

168 36

Blurring of Vision and Sudden Loss of Vision in Pregnancy 178 Anomi Panditharatne and Edwin Chandraharan

26

Psychiatric Emergencies 185 Lorraine Cleghorn

27

Drug Overdose in Pregnancy Lakshman Karalliedde

28

Diabetic Ketoacidosis in Pregnancy 200 Dagmar Krueger and Ayona Wijemanne

29

Convulsions and Epilepsy Ingrid Watt-Coote

30

Musculoskeletal Considerations in Pregnancy 214 Hiran Amarasekera

31

Endocrine Emergencies in Pregnancy Madhushree Ghosh and Manilka Sumanatilleke

191

207

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vi

32

Section Editors: Anthony Addei and Rehana Iqbal General Anaesthesia and Failed Intubation 231 Matthew Evans, Sarah Hammond and Christina Wood

33

22

25

Section 6 Anaesthetic Emergencies During Pregnancy

221

Resuscitation of the Newborn 261 Sadaf Bhayat, Louise Davidson, Siromi Gunaratne and Nigel Kennea

Section 8 Management of Anticipated and Non-anticipated Emergencies in Pregnancy 37

Placenta Accreta Spectrum Disorders (Abnormal Invasion of the Placenta) 273 Ana Pinas Carrillo, Richard Hartopp and Edwin Chandraharan

38

Peri- and Postmortem Caesarean Section 279 Priyantha Kandanearachchi, Sunali Kandanearachchi and Edwin Chandraharan

39

Management of Established Preterm Labour and Rescue Cerclage 283 Leo Gurney, Gareth Waring and Vedrana Caric

Contents

40

Failed Operative Vaginal Delivery: Minimising Maternal and Fetal Morbidity 292 Naheed Tahir and Edwin Chandraharan

Section 9 Setting-Up Skills and Drills Training in Maternity Services and Reducing Avoidable Harm Section Editor: Susana Pereira 41

Addressing Human Factors in Obstetric Emergencies 297 Susana Pereira and Kim Hinshaw

42

Setting Up and Running Labour Ward Fire Drills 307 Jia Yan-Ju and Edwin Chandraharan

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43

Simulation Training for Obstetric Emergencies 311 Polly Hughes

44

Learning from Mothers and Babies: Reducing Risk Through Audits and Confidential Enquiries and ‘Each Baby Counts’ Reports 315 Susana Pereira and Edwin Chandraharan

45

Risk Management: Emergency Obstetric and Intrapartum Care 320 Jessica Moore

Index

327

vii

Contributors

Anthony Addei Consultant anaesthetist and obstetric anaesthesia, St George’s University Hospitals NHS Foundation Trust, London, UK Amanda Ali Consultant in materno-fetal medicine, Kingston University Hospital NHS Foundation Trust, Kingston upon Thames, Surrey, UK Saba Al-Sulttan Clinical fellow in anaesthesia, St George’s University Hospitals NHS Foundation Trust, London, UK Hiran Amarasekera Consultant orthopaedic surgeon, Colombo East Teaching Hospital, Malabe, Sri Lanka Sabaratnam Arulkumaran Professor emeritus, St George’s University of London, London, UK Sohail Bampoe Consultant in anaesthesia and perioperative medicine, University College London Hospitals NHS Foundation Trust, London, UK Sadaf Bhayat Specialist registrar in neonatology, St George’s University Hospitals NHS Foundation Trust, London, UK Amar Bhide Consultant obstetrician and subspecialist in fetal medicine, St George’s University Hospitals NHS Foundation Trust, London, UK Vedrana Caric Consultant obstetrician and fetal medicine, James Cook University Hospital, Middlesbrough, UK Edwin Chandraharan Consultant obstetrician and gynaecologist and Director, Global Academy of Medical Education and

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viii

Training, London and Consultant intrapartum care advisor, Basildon and Thurrock University Hospital NHS Foundation Trust, Essex, UK Chu Chin Lim Consultant obstetrician and gynaecologist, Ninewells Hospital, Dundee, Scotland, UK Hlupekile Chipeta Consultant obstetrician and gynaecologist, Leeds Teaching Hospitals NHS Trust, Leeds, UK Lorraine Cleghorn Specialist midwife in mental health, St George’s University Hospitals NHS Foundation Trust, London, UK Kirsty Crocker Anaesthetist, Western AustralianHealth Board, Australia Sourav Das Consultant obstetrician, St George’s University Hospitals NHS Foundation Trust, London, UK Louise Davidson Specialist registrar in neonatology, St George’s University Hospitals NHS Foundation Trust, London, UK Stergios Doumouchtsis Consultant urogynaecologist, Epsom and St Helier University Hospitals NHS Trust, Epsom, UK Matthew Evans Specialist registrar in Anaesthesia, St George’s University Hospitals NHS Foundation Trust, London, UK Madhushree Ghosh Consultant obstetrician and gynaecologist, St George’s University Hospitals NHS Foundation Trust, London, UK

List of Contributors

Malik Goonewardene Senior professor of obstetrics and gynaecology, Faculty of Medicine, University of Ruhuna, Galle, Sri Lanka

Archana Krishna Consultant obstetrician and gynaecologist, University Hospitals Birmingham NHS Foundation Trust, Birmingham, UK

Siromi Gunaratne Consultant paediatrician and neonatologist, Durdan’s Hospital, Colombo, Sri Lanka

Dagmar Krueger Senior registrar in maternal medicine, St George’s University Hospitals NHS Foundation Trust, London, UK

Kapila Gunawardane Professor in obstetrics and gynaecology, University of Peradeniya and Honorary Consultant Obstetrician and Gynaecologist, Teaching Hospital, Peradeniya, Sri Lanka Leo Gurney Subspecialty trainee in materno-fetal medicine, Birmingham Women’s Hospital, Birmingham, UK

Becky Liu Specialist registrar, St George’s University Hospitals NHS Foundation Trust, London, UK

Sarah Hammond Consultant anaesthetist and obstetric anaesthesia, St George’s University Hospitals NHS Foundation Trust, London, UK

Tahir A. Mahmood Consultant obstetrician and gynaecologist, Victoria Hospital, Kirkcaldy, Fife, Scotland, UK

Richard Hartopp Consultant anaesthetist and obstetric anaesthesia, St George’s University Hospitals NHS Foundation Trust, London, UK Kim Hinshaw Consultant obstetrician and gynaecologist, Sunderland Royal Hospital, Sunderland, UK Polly Hughes Consultant obstetrician, St George’s University Hospitals NHS Foundation Trust, London, UK Rehana Iqbal Consultant anaesthetist and obstetric anaesthesia, St George’s University Hospitals NHS Foundation Trust, London, UK Priyantha Kandanearachchi Consultant obstetrician and gynaecologist, West Wales General Hospital, Carmarthen, Wales, UK

,

Karin Leslie Consultant obstetrician, Ashford and St Peter's Hospitals NHS Foundation Trust, Chertsey, UK

Tim Patel Consultant Emergency Physician, Western Australian Health Board, Australia Laura A. Magee Professor, School of Life Course Sciences, King’s College University Hospital, London, UK Enaya Mirza Senior registrar in obstetrics and gynaecology, Croydon University Hospital NHS Trust, Croydon, UK Jessica Moore Consultant obstetrician, St George’s University Hospitals NHS Foundation Trust, London, UK Sunali Pandithakoralle - Kandanearachchi Specialty doctor in anaesthesia, Princess of Wales Hospital, Bridgend, Wales, UK

Lakshman Karalliedde Retired toxicologist, Guy’s and St Thomas’ NHS Foundation Trust, London, UK

Anomi Panditharatne Specialty doctor in ophthalmology, Royal Free Hospital NHS Foundation Trust, London, UK

Nigel Kennea Consultant neonatologist, St George’s University Hospitals NHS Foundation Trust, London, UK

Leonie Penna Consultant obstetrician and subspecialist in fetal medicine, King’s College Hospital NHS Foundation Trust, London, UK

ix

List of Contributors

Susana Pereira Consultant obstetrician and subspecialist in fetal medicine, Kingston University Hospital NHS Foundation Trust, Kingston upon Thames, Surrey, UK Vasilios Pergialiotis Academic fellow, National and Kapodistrian University of Athens, Athens, Greece Gracia Anna Perez-Bonfils Consultant obstetrician and gynaecologist, Hospital Quiron and Hospital General de l’Hospitalet, Barcelona, Spain Ana Pinas-Carrillo Consultant obstetrician, St George’s University Hospitals NHS Foundation Trust, London, UK Probhodana Ranaweera Senior lecturer, University of Colombo, and honorary consultant obstetrician and gynaecologist at De Zoysa Hospital for Women, Sri Lanka Chatura Ratnayake Senior lecturer, University of Peradeniya and honorary consultant obstetrician and gynaecologist, Teaching Hospital, Peradeniya, Sri Lanka Caroline Reis Gonçalves Consultant obstetrician and gynaecologist, Hospital Sofia Feldman and Neocenter Maternidade, BeloHorizonte, Brazil Mohamed Rishard Senior lecturer in obstetrics and gynaecology, University of Colombo and honorary consultant obstetrician and gynaecologist at De Zoysa Hospital for Women, Colombo, Sri Lanka Hemantha Senanayake Professor in obstetrics and gynaecology, University of Colombo, and honorary consultant obstetrician and gynaecologist at De Zoysa Hospital for Women, Colombo, Sri Lanka Hassan Shehata Consultant obstetrician and lead for maternal medicine, Epsom and St Helier University Hospitals NHS Trust, Epsom, UK

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x

Emma Spillane Consultant midwife, Kingston University Hospital NHS Foundation Trust, Kingston upon Thames, Surrey, UK Suganya Sukumaran Consultant obstetrician and gynaecologist, South Warwickshire NHS Foundation Trust, Warwick, UK Manilka Sumanatileke Consultant physician and head of Department of Endocrinology, National Hospital of Sri Lanka, Colombo, Sri Lanka Naheed Tahir Consultant obstetrician and gynaecologist, Royal Bolton Hospital NHS Foundation Trust, Bolton, UK Vikram Talaulikar Associate specialist in reproductive medicine, University College Hospital London, London, UK James Tibbott Specialist registrar in obstetrics and gynaecology, Bradford Hospital NHS Foundation Trust, Bradford, UK Derek Tuffnell Consultant obstetrician and gynaecologist, Bradford Hospital NHS Foundation Trust, Bradford, UK Peter von Dadelszen Professor, School of Life Course Sciences, King’s College University Hospital, London, UK Gareth Waring Consultant obstetrician and subspecialist in fetal medicine, Newcastle Royal Infirmary, Newcastle, UK Ingrid Watt-Coote Consultant obstetrician and lead for maternal medicine, St George’s University Hospitals NHS Foundation Trust, London, UK Deepal S. Weerasekera Consultant obstetrician and gynaecologist, Ninewells Hospital, Colombo, Sri Lanka Renate Wendler Consultant anaesthetist and obstetric anaesthesia, St George’s University Hospitals NHS Foundation Trust, London, UK

List of Contributors

,

Ayona Wijemanne Consultant obstetrician, St George’s University Hospitals NHS Foundation Trust, London, UK

Jia Yan-Ju Senior doctor in obstetrics and gynaecology, Tianjin Central Hospital of Obstetrics and Gynaecology, Tianjin, China

Christina Wood Consultant anaesthetist and obstetric anaesthesia, St George’s University Hospitals NHS Foundation Trust, London, UK

Niraj Yanamandra Consultant obstetrician and gynaecologist, Rainbow Children's Hospital and Perinatal Care, Hyderabad, India

xi

,

Preface

Why a Second Edition? Recent confidential enquiries into maternal deaths in the United Kingdom (MBBRACE, 2017) have concluded that deaths due to obstetric haemorrhage have nearly doubled during the past triennium. The latest ‘Each Baby Counts’ Report by the Royal College of Obstetricians & Gynaecologists (October 2017) has noted that approximately 76% of perinatal deaths and brain injuries could have been avoided by an alternative management. Lack of knowledge and human factors were the main contributory factors to poor outcomes. In addition, the National Maternal and Perinatal Audit Report in the UK (2017) has highlighted significant variation in maternal and perinatal outcomes, even in a ‘well-resourced’ setting. Pregnancy and childbirth should be a safe and rewarding experience for women and their families, as well as for maternity healthcare providers. However, it is estimated that globally more than 300 000 women die during pregnancy and childbirth every year, and sadly, substandard care continues to contribute to a significant proportion of these deaths, even in the United Kingdom. Substandard care is often due to ‘too little being done too late’, especially while managing emergencies during antepartum, intrapartum and postpartum periods. Failure to recognise warning symptoms and signs of complications, lack of knowledge and skills, failure to seek appropriate experienced or multidisciplinary input, failures in team working and ineffective communication contribute to maternal and perinatal morbidity and mortality. The book aims to promote evidence-based emergency obstetric and neonatal care both in wellresourced and less well-resourced countries. We have attempted to include ‘practical algorithms’ for quick reference, a scientific basis for proposed actions for obstetric and intrapartum emergencies and illustrations, where appropriate. In recognition of the fact that more than 90% of women die in less wellresourced countries with limited resources, we have at 20:20:26,

.001

included a section on suggested management in lowresource settings. In addition, ‘Key Facts’, ‘Pearls’ and ‘Pitfalls’ are included for easy reference. In response to recent reports, we have added a new section on Human Factors edited by Dr Susana Pereira. We have added new chapters on emergencies during home births. In view of recent negative media reports regarding fetal trauma (skull fractures) and deaths during second-stage caesarean sections, as well as NHS Resolution Report in September 2019 highlighting ‘difficult delivery of the fetal head during caesarean section’ as an important cause of neonatal admission in the United Kingdom, we have added a new chapter on failed operative vaginal births. We are greatly indebted to the authors, who come from diverse backgrounds and experience, for not only sacrificing their time, but also for sharing their wealth of knowledge and expertise. This textbook reflects a collective effort from midwives, trainee obstetricians and gynaecologists, senior obstetricians, anaesthetists, neonatologists, perinatal psychiatrists, toxicologists, physicians and surgeons, from both well-resourced and less well-resourced countries to make pregnancy and childbirth safer for women and their babies. We are indeed delighted and privileged to edit this textbook with contributions from such a diverse group of authors that truly reflect the multiprofessional and multidisciplinary care that every woman and her baby fully deserve during pregnancy and childbirth. We have attempted to structure the sections for easy reference, starting with anatomical and physiological changes during pregnancy and their implications for clinical practice, followed by algorithms for the management of the ‘top five killers’. In addition to common antepartum, intrapartum and postpartum emergencies, we have also included management of uncommon but potentially life-threatening emergencies such as drug overdose, road traffic accidents and endocrine and musculoskeletal emergencies.

xiii

Preface

We wish to thank our Section Editors for Anaesthetic Emergencies, Drs Anthony Addei and Rehana Iqbal for ensuring that common anaesthetic emergencies such as failed intubation, fluid underload and overload and transfusion reactions are addressed. Similarly, we thank our Section Editor for Human Factors, Dr Susana Pereira, for her hard work. The recent Each Baby Counts Report published by the Royal College of Obstetricians and Gynaecologists (RCOG) in March 2020 has concluded that in 72% of babies who were severely brain-damaged or died following an intrapartum hypoxic insult, a different care may have resulted in a different outcome. More recently, the Rapid Report on Learning from SARS-COV-2- related and associated maternal deaths in the United Kingdom from March to May 2020 published by the Mothers and Babies: Reducing Risk through Audits and Confidential Enquiries Across the UK (MBRRACE-UK) has concluded that the care provided to women was extremely variable (www.npe

.001

https://www.cambridge.org/core. 21 May 2021 at 20:20:26,

u.ox.ac.uk/assets/downloads/mbrrace-uk/reports/M BRRACE-UK_Maternal_Report_2020_v10_FINAL. pdf). Moreover, this report found that not only many women who died had minimal or delayed obstetric or midwifery input, but there was also a lack of senior and/or multidisciplinary approach to care. Effective management of obstetric and intrapartum emergencies involves continuous multidisciplinary training and education. The section ‘Setting-Up Skills and Drills in Maternity Services’ is aimed at aiding continuously improving care and outcomes for women and their babies. We hope this textbook will be useful for midwives, medical students, trainee as well as senior obstetricians, anaesthetists and neonatologists both in wellresourced and less well-resourced countries. Let us work together to ensure that no woman or her baby should die due to substandard care by optimising management of obstetric and intrapartum emergencies.

Preface to the First Edition

Pregnancy and childbirth should be a safe and rewarding experience for women and their families, as well as for maternity healthcare providers. However, it is estimated that globally over 300 000 women die during pregnancy and childbirth every year, largely due to substandard care. Even in the United Kingdom, the latest Confidential Enquiries into Maternal Deaths Report suggests that substandard care may contribute to approximately 70% of all maternal deaths. Substandard care is often due to ‘too little being done too late’, especially whilst managing emergencies during antepartum, intrapartum and postpartum periods. Failure to recognise warning symptoms and signs of complications, lack of knowledge and skills, failure to seek appropriate experienced or multi-disciplinary input, as well as failures in team working and effective communication, contribute to maternal and perinatal morbidity and mortality. The book aims to promote evidence-based emergency obstetric and neonatal care both in wellresourced and less well-resourced countries. We have attempted to include ‘practical algorithms’ for quick reference, a scientific basis for proposed actions for obstetric and intrapartum emergencies and illustrations, where appropriate. In recognition of the fact that over 90% of women die in less well-resourced countries with limited resources, we have included a section on ‘Suggested management in low-resource settings’. In addition, ‘Key facts’, ‘Pearls’ and ‘Pitfalls’ are included for easy reference. We are greatly indebted to the authors who come from diverse backgrounds and experience, for not only sacrificing their time, but also for sharing their knowledge and expertise. There has been a collective effort from midwives, trainee obstetricians and gynaecologists, senior obstetricians, anaesthetists,

at 20:20:27,

.002

neonatologists, perinatal psychiatrists, toxicologists, physicians and surgeons, from both well-resourced and less well-resourced countries to make pregnancy and childbirth safer for women and their babies. We are indeed delighted to edit this textbook with contributions from such a diverse group of authors that truly reflect the multi-professional and multi-disciplinary care that every pregnant woman and her baby fully deserve. We have attempted to structure the sections for easy reference, starting with anatomical and physiological changes during pregnancy and their implications on clinical practice, followed by algorithms for the management of the ‘Top five killers’. In addition to common antepartum, intrapartum and postpartum emergencies, we have also included management of uncommon but potentially life-threatening emergencies such as drug overdose, road traffic accidents and endocrine and musculoskeletal emergencies. We wish to thank our Section Editor for Anaesthetic Emergencies, Dr Anthony Addei for ensuring that common anaesthetic emergencies such as failed intubation, fluid underload and overload and transfusion reactions are addressed. Effective management of obstetric and intrapartum emergencies involves continuous multidisciplinary training and education. The section on ‘Setting up skills and drills in maternity services’ is aimed at aiding continuously improving care and outcomes for women and their babies. We hope this textbook will be useful for midwives, medical students, trainee as well as senior obstetricians, anaesthetists and neonatologists both in the well-resourced and less well-resourced countries. Let us work together to ensure that no woman or her baby should die due to substandard care by optimising management of obstetric and intrapartum emergencies.

xv

Acknowledgements

We have been very privileged to care for women and their babies during pregnancy and childbirth, and to be part of excellent and cohesive multidisciplinary teams in our careers. Women and babies have taught us the importance of a multidisciplinary team approach to ensure a timely diagnosis and instituting the most appropriate management of obstetric and intrapartum emergencies to optimize outcomes. The editors also would like to sincerely thank each and every author for their generous contribution of their time, knowledge and expertise. We are very grateful to Mr Nick Dunton, Ms Katy

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Nardoni, Ms, Camille Lee-Own, Ms Emily Jones and Ms Anna Whiting from Cambridge University Press for their invaluable support and professionalism as well as to Ms Theresa Kornak for copy editing and the team at Integra for production management. Our immense gratitude goes to our family: Anomi, Ashane and Avindri Chandraharan and Gayatri, Shankari, Nishkantha and Kailash Arulkumaran for their unconditional support, encouragement as well as for their sacrifice, which made this second edition possible.

Section 1

General Principles

Chapter

Anatomical and Physiological Changes in Pregnancy Impact on Emergency Care

1

Niraj Yanamandra and Edwin Chandraharan

Key Facts Pregnancy is associated with profound anatomical, physiological, biochemical and endocrine changes that affect multiple organs and systems. These changes are essential to help the woman to adapt to the pregnant state and to aid fetal growth and survival. However, such anatomical and physiological changes may cause confusion during clinical examination of a pregnant woman. Similarly, changes in blood biochemistry during pregnancy may create difficulties in interpretation of results. Conversely, clinicians also need to recognise pathological deviations in these normal anatomical and physiological changes during pregnancy to institute appropriate action to improve maternal and fetal outcomes.

Haematology Blood Volume There is an overall increase in plasma, red blood cells (RBCs) and total blood volume. Plasma volume increases by 15% during the first trimester; accelerates in the second trimester; peaks at around 32 weeks, reaching up to 50% above non-pregnant levels; and stays elevated until term. It returns to non-pregnant levels by 6 days post-delivery. There is often a sharp rise of up to 1 litre in plasma volume within the maternal circulation at 24 hours after delivery.

Red Blood Cell Volume RBC volume falls during the first 8 weeks of pregnancy, increasing back to non-pregnant levels by 16 weeks and then rising to 30% above non-pregnant levels by term. The relatively smaller increase in RBC compared with plasma results in haemodilution and ‘physiological anaemia’ of pregnancy. at 20:20:27,

Coagulation and Fibrinolysis in Pregnancy Plasma levels of factors VII, VIII, IX and XII, together with fibrinogen and fibrin degradation products, increase during pregnancy (fibrinogen from 2.5 to 4 g/L). Levels of factors XI and III decrease. These changes overall increase coagulability and make pregnancy a ‘hypercoagulable’ state.

Platelets Pregnancy is associated with enhanced platelet turnover. Thrombocytopenia(platelets < 100 × 109/L) occurs in 0.8%–0.9% of normal pregnant women, while increases in platelet factor and β-thromboglobulin suggest elevated platelet activation and consumption. Since there is no change in platelet count in the majority of pregnant women, there is probably an increase in platelet production to compensate for the increased consumption.

Cardiovascular System Heart The heart is pushed upwards and rotated forwards, with lateral displacement of the left border. All heart sounds are louder and the first sound is split. A systolic ejection murmur is normal and is due to turbulence secondary to increased blood flow through normal heart valves. A diastolic murmur is heard occasionally. Cardiac output is increased as a result of increased heart rate, reduced systemic vascular resistance and increased stroke volume. Heart rate is increased above non-pregnant values by 15% at the end of the first trimester. This increases to 25% by the end of the second trimester, but there is no further change in the third trimester. Stroke volume is increased by about 20% at 8 weeks and up to 30% by the end of the second trimester, and then remains level until term.

1

Section 1

General Principles

Chapter

Anatomical and Physiological Changes in Pregnancy Impact on Emergency Care

1

Niraj Yanamandra and Edwin Chandraharan

Key Facts Pregnancy is associated with profound anatomical, physiological, biochemical and endocrine changes that affect multiple organs and systems. These changes are essential to help the woman to adapt to the pregnant state and to aid fetal growth and survival. However, such anatomical and physiological changes may cause confusion during clinical examination of a pregnant woman. Similarly, changes in blood biochemistry during pregnancy may create difficulties in interpretation of results. Conversely, clinicians also need to recognise pathological deviations in these normal anatomical and physiological changes during pregnancy to institute appropriate action to improve maternal and fetal outcomes.

Haematology Blood Volume There is an overall increase in plasma, red blood cells (RBCs) and total blood volume. Plasma volume increases by 15% during the first trimester; accelerates in the second trimester; peaks at around 32 weeks, reaching up to 50% above non-pregnant levels; and stays elevated until term. It returns to non-pregnant levels by 6 days post-delivery. There is often a sharp rise of up to 1 litre in plasma volume within the maternal circulation at 24 hours after delivery.

Red Blood Cell Volume RBC volume falls during the first 8 weeks of pregnancy, increasing back to non-pregnant levels by 16 weeks and then rising to 30% above non-pregnant levels by term. The relatively smaller increase in RBC compared with plasma results in haemodilution and ‘physiological anaemia’ of pregnancy. at 20:20:26,

.003

Coagulation and Fibrinolysis in Pregnancy Plasma levels of factors VII, VIII, IX and XII, together with fibrinogen and fibrin degradation products, increase during pregnancy (fibrinogen from 2.5 to 4 g/L). Levels of factors XI and III decrease. These changes overall increase coagulability and make pregnancy a ‘hypercoagulable’ state.

Platelets Pregnancy is associated with enhanced platelet turnover. Thrombocytopenia(platelets < 100 × 109/L) occurs in 0.8%–0.9% of normal pregnant women, while increases in platelet factor and β-thromboglobulin suggest elevated platelet activation and consumption. Since there is no change in platelet count in the majority of pregnant women, there is probably an increase in platelet production to compensate for the increased consumption.

Cardiovascular System Heart The heart is pushed upwards and rotated forwards, with lateral displacement of the left border. All heart sounds are louder and the first sound is split. A systolic ejection murmur is normal and is due to turbulence secondary to increased blood flow through normal heart valves. A diastolic murmur is heard occasionally. Cardiac output is increased as a result of increased heart rate, reduced systemic vascular resistance and increased stroke volume. Heart rate is increased above non-pregnant values by 15% at the end of the first trimester. This increases to 25% by the end of the second trimester, but there is no further change in the third trimester. Stroke volume is increased by about 20% at 8 weeks and up to 30% by the end of the second trimester, and then remains level until term.

1

General Principles

Blood Pressure

Table 1.1 Normal arterial blood gas values in pregnancy

Systolic blood pressure does not show a significant drop in pregnancy. It may drop slightly, by 6%–8%. However, there is a marked drop in diastolic pressure. It is reduced in the first two trimesters by up to 20%–25% and returns to the non-pregnant level at term. This is due to the placenta acting as an arteriovenous shunt, together with peripheral vasodilating factors such as oestrogen, progesterone and increased endothelial synthesis of prostaglandin E2 and prostacyclins. Both blood pressure and cardiac output are reduced during epidural analgesia. In a supine position, 70% of mothers have a fall in blood pressure of at least 10%, and 8% have decreases of between 30% and 50%.

pH

7.40–7.45

PaCO2

3.7–4.2 kPa

PaO2

13.0–14.0 kPa

HCO3−

18–21 mmol/L

consumption increases by about 18%, from 250 to 300 mL/minute. Tidal volume increases gradually from the first trimester by up to 45% at term. Functional residual capacity is decreased by 20%– 30% at term due to reductions of 25% in expiratory reserve volume and 15% in residual volume.

Blood Gases

ECG Changes During Pregnancy The following changes are of no clinical significance: • Sinus tachycardia and atrial and ventricular ectopics. Rotation of the electrical axis of the heart to the left • ST segment depression and T-wave inversion in inferior and lateral leads Changes in echocardiograph during pregnancy: • Left ventricular hypertrophy by 12 weeks • 50% increase in left ventricular mass at term • 12%–14% increase in aortic, pulmonary and mitral valve sizes

Respiratory System Anatomical Changes Capillary engorgement of the nasal and pharyngeal mucosa and larynx begins early in the first trimester. This may explain why many pregnant women complain of difficulty in nasal breathing, experience more episodes of epistaxis and experience voice changes. The thoracic cage increases in circumference by 5–7 cm because of the increase in both the anteroposterior and transverse diameters from flaring of the ribs. The level of the diaphragm rises by about 4 cm early in pregnancy even before it is under pressure from the enlarging uterus. This would account for the decrease in residual volume, since the lungs would be relatively compressed at forced expiration.

Physiology During pregnancy minute ventilation increases by about 40%, from 7.5 to 10.5 L/minute and oxygen .003

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PaCO2 decreases to 3.7–4.2 kPa by the end of the first trimester and remains at this level until term. Metabolic compensation for the respiratory alkalosis reduces the serum bicarbonate concentration to about 18–21 mmol/L, the base excess by 2–3 mmol/L and the total buffer base by about 5 mmol/L. PaO2 in upright pregnant women is in the region of 14.0 kPa, higher than that in non-pregnant women. This is due to lower PaCO2 levels, a reduced arteriovenous oxygen difference and a reduction in physiological shunt. Pregnant women maintain a normal arterial pH of 7.4–7.45 (Table 1.1).

Renal System Kidney size increases by about 1 cm in length. There is marked dilatation of renal calyces, pelvis and ureters. Increase in glomerular filtration rate (GFR) by about 50% reaches a maximum at the end of the first trimester and is maintained at this augmented level until at least the 36th gestational week. The 24-hour creatinine clearance increases by 25% at 4 weeks after the last menstrual period and by 45% at 9 weeks. During the third trimester a consistent and significant decrease towards nonpregnant values occurs preceding delivery.

Gastrointestinal System Gums may swell and bleed easily. The incidence of caries is increased. Barrier pressure (lower oesophageal sphincter [LOS] pressure minus gastric pressure) is reduced significantly during pregnancy compared with the non-pregnant state, due to increased intragastric pressure and reduced LOS pressure. LOS pressure appears to return to normal by 48 hours post-delivery.

Anatomical and Physiological Changes in Pregnancy

Endocrine System Glucose Metabolism Pregnancy is associated with an insulin-resistant condition, similar to that of type 2 diabetes. Early in pregnancy, increasing oestrogen and progesterone levels, which lead to pancreatic β-cell hypertrophy and insulin excretion, alter maternal carbohydrate metabolism. Secretion of other hormones such as human placental lactogen, prolactin, cortisol, oestrogen and progesterone induce insulin resistance. These hormones are found to be in significantly greater levels in pregnant women.

Thyroid Gland There is increased synthesis of thyroxine-binding globulin (TBG) by the liver in pregnancy. This increase leads to a compensatory rise in serum concentrations of total thyroxine (T4) and triiodothyronine (T3). There is, however, no change in the amount of free circulating thyroid hormones. There is iodine deficiency as a result of loss through increased glomerular filtration and decreased renal tubular absorption. Active transport of iodine to the fetoplacental unit and fetal thyroid activity also deplete the maternal iodide pool further from the second trimester.

Pituitary Gland There is significant enlargement of the pituitary gland during pregnancy. The growth is a result of an increase in the number of prolactin-secreting cells, with the proportion of lactotrophs increasing from 1% to 40%. This results in elevated prolactin levels to up to 10–20 times those of normal, non-pregnant values. These return to normal by 2 weeks postpartum, unless the woman breastfeeds. Gonadotropin levels are suppressed by the high concentrations of oestrogen and progesterone and are undetectable during pregnancy. Levels of basal growth hormone and antidiuretic hormone remain unchanged during pregnancy.

Adrenal Gland Plasma corticosteroid binding globulin (CBG) concentrations increase during pregnancy. Levels of both

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free and bound cortisol also increase and levels of serum and urinary free cortisol increase three-fold by term. Adrenocorticotropic hormone (ACTH), which influences steroid secretion from adrenal cortex, remains within the normal range for nonpregnant women.

Skin During pregnancy the skin undergoes a number of changes, mainly thought to be due to hormonal changes. Hyperpigmentation: This occurs in up to 90% of women during pregnancy. This begins in the first trimester and is prominently noticed in areas of normal hyperpigmentation such as nipples, areola, perineum and vulva. Both oestrogens and progesterone, which have melanogenic stimulant properties, are thought to be responsible for this hyperpigmentation. Linea nigra: This appears as an area of pigmentation extending from the symphysis pubis to xiphisternum. Although the pigmentation fades after delivery it rarely returns to pre-pregnancy levels. Melasma: Develops in up to 70% of women, mainly in the second half of pregnancy. It appears as patches of light-brown facial pigmentation usually over the forehead, cheeks, upper lip, nose and chin. Spider naevi: These present as a central red spot and reddish extensions which radiate outwards like a spider’s web and occur on the face, the trunk and arms. Most appear in early pregnancy and regress following delivery, although in up to 25% of women they may persist. Recurrences are known to occur at the same site in subsequent pregnancies. Striae gravidarum: These appear perpendicular to skin tension lines as pink linear wrinkles. They fade and become white and atrophic, although never disappear completely. Palmar erythema: Palmar erythema is reddening of the palms at the thenar and hypothenar eminences. This is thought to be due to high levels of oestrogen in pregnancy and is seen in up to 70% of women by the third trimester and fades within 1 week of delivery.

3

General Principles

Table 1.2 Pregnancy-specific ranges for serum biochemistry

Biochemistry

Pregnancy-specific ranges

Full blood count Hb White blood cell count Platelets

10.5–14.0 g/dL 5–11.0 g/dL 100–450 × 109/L

Liver function Alkaline phosphatase Alanine transaminase Aspartate transaminase Albumin Bilirubin

24 hours) PPH > 1 L or blood transfusion

Fewer than two risk factors

Lower risk

Note: if persisting or more than three risk factors, consider extending thromboprophylaxis with LMWH

Mobilisation and avoidance of dehydration

BMI, body mass index; LMWH, low-molecular-weight heparin; PPH, postpartum haemorrhage; VTE, venous thromboembolism.

• •

•

Prolonged treatment without confirming the diagnosis Vascular team not being involved in the management of massive PTE where embolectomy could make a difference Timing of inserting or removing regional anaesthesia catheter

• •

•

Key Pearls •

•

•

All staff providing care to pregnant women should be aware of the seriousness and presentations of VTE and initiate appropriate management as soon as possible. Protocols should be available in all sites of contact with pregnant women including accident and emergency department and staff should have regular review of guidelines and protocols. Regular drills on managing collapsed obstetric patients should be conducted.

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•

Clear protocols on how to contact radiology and other clinical staff should be available. Women should be counselled and given information necessary to enable them to understand and share in informed choices with regards to confirmatory tests and treatment options. The use of thrombolytic therapy during pregnancy should be reserved for women with severe PTE with haemodynamic compromise. If a woman is not suitable for thrombolytic treatment, a discussion with a cardiothoracic surgeon with a view to urgent thoracotomy should be undertaken.

Management in Low-Resource Settings Venous thromboembolism is responsible for 2% of maternal deaths during pregnancy in developing

Deep-Vein Thrombosis and Pulmonary Embolism

countries. VTE may be under-reported or undiagnosed and treatment is likely to be substandard. This is particularly true in those settings where multiple risk factors are more common than in developed countries: • Grand-multiparity • Prolonged labour • Dehydration • Higher incidence of comorbidities, e.g. anaemia, sickle cell anaemia, thalassaemia, haemolytic anaemia and chronic HIV • Postpartum: higher incidence of postpartum haemorrhage, hypertension and dehydration

Risk Reduction •

•

•

Dissemination of information to increase women’s and public awareness about VTE and its consequences Developing local protocols and guidelines in delivery units and sharing with those who care for women throughout pregnancy, childbirth and in the postpartum period Focus strategies to avoid dehydration during labour and proactively manage anaemia during antenatal periods

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References 1. Scottish Intercollegiate Guidelines Network (SIGN). Prevention and Management of Venous Thromboembolism: A National Clinical Guideline. NHS Quality Improvement Scotland, 2010. Update October 2014. 2. Royal College of Obstetricians and Gynaecologists. Reducing the Risk of Venous Thrombo-embolism During Pregnancy and the Puerperium. Green-top Guideline No. 37a. London: RCOG, 2015. 3. Royal College of Obstetricians and Gynaecologists. Thrombosis and Embolism During Pregnancy and the Puerperium: Acute Management. Green-top Guideline No. 37b. London: RCOG, 2015. 4. Royal College of Obstetricians and Gynaecologists. Providing Quality Care for Women Framework for Maternity Services Standard. London: RCOG, 2016. 5. Cathy Nelson-Piercy on behalf of the MBRRACEUK Thrombosis and Thromboembolism chapter writing group. Prevention and treatment of thrombosis and thromboembolism. In Knight M, Tuffnell D, Kenyon S, Shakespeare J, Gray R, Kurinczuk JJ (eds) on behalf of MBRRACE-UK. Saving Lives, Improving Mothers’ Care: Surveillance of Maternal Deaths in the UK 2011–13 and Lessons Learned to Inform Maternity Care from the UK and Ireland Confidential Enquiries into Maternal Deaths and Morbidity 2009–13. Oxford: National Perinatal Epidemiology Unit, University of Oxford 2015;42–52. 6. Mahmood T, Owen P, Arulkumaran S, Dhillon C (eds). Models of Care in Maternity Services. London: RCOG, 2010.

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Chapter

4

Management of Severe Preeclampsia and Eclampsia Antepartum, Intrapartum and Postpartum Peter von Dadelszen and Laura A. Magee

Key Facts Severe preeclampsia and eclampsia represent the severe end of a spectrum of hypertensive disorders of pregnancy and are associated with a large proportion of the global burden of maternal and perinatal morbidity and mortality [1, 2]. Of these associated adverse events, more than 99% occur in less-developed countries [3]; more than half occur in three countries alone: India, Pakistan and Nigeria. Definitions • Preeclampsia is broadly defined by the onset of

hypertension (systolic blood pressure (BP) ≥140 mm Hg and/or diastolic BP ≥90 mm Hg) and features of end-organ involvement first diagnosed at ≥20+0 weeks of pregnancy [4, 5]. Features of target organ damage may be expanded to include placental damage, as inferred by abnormal angiogenic balance, either reduced pro-angiogenic factors (e.g., placental growth factor [PlGF]) or an abnormal ratio of anti- to pro-angiogenic factors (e.g., soluble fms-like tyrosine kinase-1 [sFlt-1]:PlGF ratio) [6–9]. • Eclampsia is consistently defined as new onset

and otherwise unexplained seizures in the setting of preeclampsia [10].

Key Practice Points •

•

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A broad definition of preeclampsia to include not only women with significant proteinuria offers increased safety to pregnant women. The broad definition usefully includes an anti-angiogenic factor imbalance. Blood pressure devices should be validated for use in pregnancy and preeclampsia. If using https://www.cambridge.org/core. 21 May 2021 at 20:20:26,

• •

unvalidated devices, they can be used for monitoring trends but should not guide decisions around therapeutics. Pulse oximetry is a useful adjunct to care. Collaboration and standardised management protocols optimise maternal and perinatal outcomes. Such women should be cared for in regional centres of excellence.

Key Actions: Accurate Measurement of Vital Signs Measurement Errors in Aneroid and Automated BP Machines BP measurement techniques are the same both during and outside pregnancy, including positioning and correct cuff size [11]. About half of aneroid devices give inaccurate BP readings >10 mm Hg as a result of institutional failures to maintain 6-monthly device calibration with resultant calibration drift; in contrast, the same error occurs in only 10% of mercury devices [12]. In addition, many automated devices, especially those used in critical care and high-dependency settings, are inaccurate in pregnancy [13] and most are inaccurate in preeclampsia, generally under-reading both systolic and diastolic values by 5 mm Hg, although there is considerable variation [13]. A list of validated devices is available and maintained online (www.dableducational.org/index.html); to date, few have been validated for use in pregnancy or preeclampsia specifically. In the care of intensively monitored women, it may be reasonable to use commonly used automated devices (e.g., Dinamap) to track trends in BP, with validation of

Management of Severe Preeclampsia and Eclampsia

BP readings by hourly confirmation with either a validated automated or a calibrated manual device.

on the tertiary centre to provide support and advice by phone or weblink.

Pulse Oximetry

Time-of-Disease Assessment

Pulse oximetry is widely available where care is provided to women with severe preeclampsia, especially in more developed countries. In addition to heart rate and SpO2 readings, many pulse oximetry devices can provide an estimate of respiratory rate through detection of sinus arrhythmia; respiratory rate is often the most poorly observed vital sign but is critical in the early detection of pulmonary oedema.

Collaborative Approach •

•

•

An important aspect of the care of women with severe preeclampsia is teamwork [14, 15]. Where women may be either severely or critically ill, an effective relationship and dialogue between obstetrics (including maternal-fetal medicine when available), obstetric internal medicine (again when available), obstetric anaesthesia, laboratory medicine, neonatology (when timing of delivery decisions need to be made around viability and transfer between institutions to ensure access to neonatal intensive care), midwifery/nursing and pharmacy are essential. Depending upon local availability of specialist and subspecialist care, if the woman is too unstable to be transferred, or if transfer is precluded (e.g., by weather conditions), some members of the team may need to be recruited and consulted by teleconference. Ideally, virtual support systems will be planned in advance of emergency events. In all settings, practicing the care of women with either severe preeclampsia or eclampsia through team drills will improve the quality of care received during actual events.

Place of Care Optimally, all women with severe preeclampsia should be admitted to a tertiary centre with experience looking after such women. Therefore, women in smaller and lower-level facilities should be transferred to regional centres of excellence. However, there will be occasions when such a transfer of care is ill advised because of the status of the patient (e.g., massive subcapsular hepatic haematoma) or other factors (e.g., weather); in such circumstances, it is incumbent at 20:20:26, .006

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Standardised Care Standardised care and teamwork are essential to optimise maternal and fetal outcomes. ‘Bundles’ of complex care have been introduced in some centres and include the management of severe hypertension [16]. The bundle goes beyond the ‘response’ of antihypertensive therapy and both escalation measures for those unresponsive to standard treatment and postpartum follow-up to reporting and systems learning, readiness and recognition and prevention.

Formal Time-of-Disease Risk Stratification/ Outcome Prediction Models The miniPIERS (Preeclampsia Integrated Estimate of Risk) is used when laboratory tests are not readily available. The demographics-, symptom- and sign-based miniPIERS model was developed and validated in referral centres located in Brazil, Fiji, Pakistan, South Africa and Uganda [17].The final miniPIERS model included parity (nulliparous versus multiparous), gestational age on admission, headache/visual disturbances, chest pain/dyspnoea, vaginal bleeding with abdominal pain, systolic blood pressure and dipstick proteinuria. A predicted probability ≥25% to define a ‘positive’ test classified women with 85.5% accuracy. The open-access online miniPIERS calculator is available at https://pre-empt.bcchr.ca/monitor ing/minipiers.

fullPIERS for When Laboratory Tests Are Readily Available The fullPIERS model includes demographics, symptoms, signs, and laboratory tests [18]. The fullPIERS was developed and internally validated in Australia, Canada, New Zealand and the United Kingdom [19, 20]. Following the same model development procedures as miniPIERS, independently informative predictors of adverse maternal outcomes include gestational age, chest pain or dyspnoea, oxygen saturation, platelet count and creatinine and aspartate transaminase (AST) concentrations (in the United Kingdom, alanine transaminase [ALT] can be substituted for AST). The

Algorithms for Management of the Top Five ‘Direct Killers’

fullPIERS model predicts adverse maternal outcomes within 48 hours of admission with preeclampsia (AUROC 0.88 [95% confidence interval [CI] 0.84– 0.92], and performed well (AUROC >0.7) up to 7 days after admission [19, 20]. The fullPIERS model has been externally and temporally validated in both less and more developed country settings, is superior to the PREP (Prediction models for Risks of complications in Early-onset Pre-eclampsia) model for predicting adverse outcomes in women with early-onset preeclampsia [21] and is recommended by the 2019 update of the UK National Institute for Health and Care Excellence guidelines for pregnancy hypertension. The open-access online fullPIERS calculator is available at: https://preempt.bcchr.ca/monitoring/fullpiers.

CIPHER for Women Receiving Critical Care The aim of the CIPHER (Collaborative Integrated Pregnancy High-dependency Estimate of Risk) model is to provide an internally validated multivariable prognostic model calibrated specifically for pregnant or recently delivered women admitted for critical care [22]. Predictors included in the final CIPHER model are maternal age, surgery in the preceding 24 hours, systolic blood pressure, Glasgow Coma Scale score, serum sodium, serum potassium, activated partial thromboplastin time, arterial blood gas (ABG) pH, serum creatinine and serum bilirubin. The CIPHER model is a pragmatic risk prediction tool, as it identifies critically ill pregnant women at highest risk for adverse outcomes, informs counselling of patients and their families about risk and facilitates benchmarking of outcomes between centres by adjusting for baseline risk. The open-access online CIPHER calculator is available at https://pre-empt.bcchr.ca/monitoring/ cipher.

Fetal Assessment Severe preeclampsia is often associated with significant fetal growth restriction (FGR). The computerised cardiotocograph/non-stress test (cCTG) reflects changes in fetal autonomic and chemoreceptor activity, as placental oxygenation deteriorates in women with FGR [23, 24]. Progression of the ductus venosus (DV) waveform to absent and reverse a-wave (atrial contraction) patterns is generally limited to severe and early-onset FGR [25, 26]. At ≥32 weeks, late decelerations and reduced variability noted on CTG almost invariably precede DV abnormalities [27], Downloaded from https://www.cambridge.org/core. 21 May 2021 at 20:20:26, https://www.cambridge.org/core/terms. https://doi.org 06

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while fetal hypoxaemia and acidaemia result in autonomic system–mediated decreased fetal heart rate variation (i.e., lower cCTG short-term variability [cCTG-STV]). Shallow late decelerations are indicative of both fetal acidaemia and its effect on myocardial tissue [28].

Key Management Timing and Route of Delivery Timing of Delivery Delivery is the only intervention that initiates resolution of preeclampsia; however, it should be remembered that it initiates and does not cure the condition. In women with severe preeclampsia, the woman’s clinical and laboratory state may well deteriorate for 24–72 hours before resolution of the condition begins. Using our definition of severe preeclampsia, all women with severe preeclampsia should be delivered immediately (either vaginally or by caesarean section), regardless of gestational age. The phrase ‘planned delivery on the best day in the best way’ reflects the myriad of considerations regarding timing (and mode) of delivery [26]. Timing of delivery will reflect evolving complications (Table 4.1). Consensus-derived indications for delivery are (1) term gestation, (2) development of severe maternal complication(s) (Table 4.1) (3) stillbirth or (4) fetal monitoring results that indicate delivery (see the section ‘Fetal Assessment’). Currently, no tool exists to guide balancing risks, benefits and the preferences of the woman and her family. The best treatment for the mother is always delivery, limiting her exposure to preeclampsia; therefore, expectant management is best considered when potential perinatal benefits are substantial, usually at early gestational ages. For women with non-severe preeclampsia complicated by HELLP (haemolysis, elevated liver enzymes, low platelet count) syndrome at 24+0–34+6 weeks gestation, it may be reasonable to delay delivery long enough to administer antenatal corticosteroids for acceleration of fetal pulmonary maturity, especially as there is often temporary improvement in maternal laboratory testing. Expectant management of preeclampsia refers to attempted pregnancy prolongation following a period of maternal and fetal observation and assessment and maternal stabilisation. Expectant management should

Management of Severe Preeclampsia and Eclampsia

Table 4.1 Definition of severe preeclampsia

Organ system affected

Adverse conditions (that increase the risk of severe preeclampsia)

Severe preeclampsia (complications that warrant delivery irrespective of gestational age)

CNS

Headache/visual symptoms

Eclampsia PRES Cortical blindness or retinal detachment Glasgow Coma Scale 50% have temporary improvement of HELLP which may enable regional anaesthesia or vaginal delivery. For late preterm preeclampsia (34+0–36+6 weeks), delaying delivery facilitates cervical ripening and vaginal delivery and reduces the risks of neonatal respiratory morbidity, but at a modest risk to mothers [32]. With term preeclampsia (37+0–42+0 weeks), labour induction is indicated to reduce poor maternal outcome (relative risk [RR] 0.61; 95% CI 0.45–0.82) [33].

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Algorithms for Management of the Top Five ‘Direct Killers’

Route of Delivery All women with preeclampsia should be considered for labour induction. Choosing the mode of delivery should take into consideration both gestational age and fetal status. In severe early-onset preeclampsia with clinical evidence of fetal compromise, caesarean delivery may be preferable. For labour induction, cervical ripening (even with an unfavourable cervix), increases the chance of vaginal delivery. With severe preeclampsia, this will take more time and be less successful compared with normotensive pregnancy. Neither FGR nor oligohydramnios are contraindications to induction. Rates of vaginal delivery after induction are 6.7%– 10% at 24–28 weeks (suggesting advisability of caesarean delivery with viable fetuses), 47.5% at 28–32 weeks, 68.8% at 32–34 weeks and 30% with birthweights 150 mL/minute). Loss of >30% of blood volume as assessed by visible blood loss (estimated blood loss or EBL expressed as the percentage of estimated blood volume = EBL/100 mL/kg).

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‘Rule of 30’ (Rise in pulse >30/minute, drop in systolic blood pressure by 30 mm Hg, increased respiratory rate >30/minute, a drop in haematocrit [packed cell volume] by 30%), which is suggestive of at least 30% loss of blood volume. Shock index (pulse rate/systolic blood pressure) 0.9. Normal shock index in pregnancy is between 0.7 and 0.9, as the pulse rate is less than systolic blood pressure. Tense, tender abdomen with evidence of intrauterine death (massive placental abruption).

Key Actions: Massive Obstetric Haemorrhage Prior to Delivery Placental Abruption Placental abruption refers to the premature separation of a normally situated placenta. Maternal consequences include haemorrhage secondary to accumulation of blood in the retro-placental space after separation of placenta as well as, in severe cases, bleeding into the uterine myometrium, leading to the ‘couvelaire uterus’.

Postpartum Uterine Atonic uterus, ruptured uterus, uterine cavity and within the myometrial fibres. Activation of the extrinsic pathway of coagulation results in disseminated intravascular coagulation. Fetal complications include hypoxic cerebral injury and intrauterine death.

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Algorithms for Management of the Top Five ‘Direct Killers’

Predisposing Factors

Placenta Praevia

• •

Placenta praevia refers to the extension of the placenta wholly or partially to the lower uterine segment. Massive obstetric haemorrhage ensues as the progressive uptake of the lower segment with advancing gestation that leads to separation of the placenta, resulting from bleeding from the placental attachment. Such bleeding is therefore maternal with no direct effect on the fetus. Iatrogenic preterm delivery in the ‘maternal interest’ as well as effects of prolonged maternal hypotension may result in detrimental effects on the fetus. Paucity of muscle fibres and hence the inability of the lower segment to contract and retract after birth increases the risk of atonic postpartum haemorrhage.

• • •

Preeclampsia Placental ischaemia secondary to vasculopathy (e.g. systemic lupus erythematosus [SLE], chronic inversion, broad ligament tears with resultant haematoma. renal disease) Multiparity Abdominal trauma (road traffic accidents, domestic violence) Substance use (e.g. cocaine)

Clinical Presentation Vaginal bleeding that is associated with abdominal pain or discomfort (‘revealed’ bleeding). Sometimes, blood can accumulate behind the separated placenta and hence no bleeding may be noted (concealed haemorrhage). Rarely, it may be ‘mixed’ (a combination of these). On examination, the patient may be pale and may be in constant pain. Abdominal examination may confirm a very tense, tender ‘woody hard’ uterus (especially in a concealed haemorrhage). In severe cases of placental abruption, the fetal heart rate may be absent and the patient may show signs of coagulopathy. Observed blood loss may be out of proportion to the clinical condition and this may point to a ‘mixed’ haemorrhage.

Management Immediate management involves active resuscitation to ensure a patent airway and breathing and maintaining circulation with intravenous fluids, blood and blood products as well as correction of coagulopathy. The role of ‘left lateral tilt’ and administration of highflow oxygen (15 L/minute) at the outset cannot be overemphasised. A multidisciplinary input involving haematologists and anaesthetists is essential. Delivery should be planned once the patient is deemed haemodynamically stable. Emergency caesarean section may be considered for fetal reasons (i.e. evidence of fetal compromise). If intrauterine death is diagnosed, delivery should be expedited by performing artificial rupture of membranes (ARM) and commencement of oxytocin infusion. Postpartum haemorrhage should be anticipated due to coagulopathy as well as Couvelaire uterus (presence of blood within the myometrial fibres results in their disruption, leading to uterine apoplexy).

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Clinical Features ‘Painless, causeless and recurrent’ vaginal bleeding is typical of placenta praevia. The ‘non-engaged’ presenting part or abnormal lie or presentation with a soft non-tender uterus may help clinch the diagnosis. Uterine tenderness may be rarely present, as placenta praevia may be associated with co-existing abruption in 10% of cases. Ultrasound examination will help confirm the diagnosis and a digital vaginal examination should be avoided in all cases of massive antepartum haemorrhage prior to excluding the diagnosis of placenta praevia.

Management Initial management involves active resuscitation (as previously explained). Vaginal birth is not possible in major degree placenta praevia. Hence, emergency caesarean section should be performed by an experienced operator, once the woman is stabilised. Postpartum haemorrhage should be anticipated and managed effectively (the lower uterine segment has fewer muscle fibres and hence is not effective in controlling bleeding from the placental site).

Massive Obstetric Haemorrhage: Postpartum As massive atonic postpartum haemorrhage is a major cause of maternal morbidity worldwide, we have discussed the management algorithm ‘HAEMOSTASIS’ in detail.

Management of Massive Obstetric Haemorrhage

H: Ask for Help and Hands on the Abdomen (Uterine Massage) The first step should be to alert all members of the team (including the haematologist and the hospital porter) and activate the hospital emergency protocols (e.g. ‘Code Blue’ protocol). A multidisciplinary approach would optimise the monitoring and management of fluids, electrolytes and coagulation parameters apart from providing input when necessary. Uterine compression should be commenced early, as 80% of postpartum haemorrhages occur secondary to uterine atony.

A: Assess (Vital Parameters, Blood Loss) and Resuscitate The woman should be positioned flat and resuscitation should begin with administration of high-flow oxygen (10–15 L/minute) via a face mask regardless of her oxygen saturation. Body temperature should be maintained. Two large-bore cannulae (preferably 14-gauge) should be inserted in either arm and Hartmann’s or normal saline infusion should be commenced. Up to 2 L of crystalloids may be infused rapidly over 1–2 hours for initial stabilisation. Colloids such as gelatin (Haemacel) or hydroxyethyl starch (1–2 L) may also be needed to achieve haemodynamic stability. Pulse, blood pressure and respiration should be recorded every 15 minutes. Additional monitoring includes pulse oximetry and indwelling urinary catheter for hourly urine output. A central venous pressure (CVP) and an arterial line should be considered in cases of severe PPH.

E: Establish Aetiology; Ensure Availability of Blood, Ecbolics (Bolus of Oxytocin, Syntometrine, Ergometrine) The cause of massive postpartum haemorrhage (4 T’s: tone, tissue, trauma and thrombin) should be identified. The uterus should be examined for contraction and retraction; it may also be worthwhile to check for ‘free fluid’ in the abdomen, if the history suggests trauma (previous caesarean section, difficult instrumental delivery) or if the patient’s condition is worse than what would be expected based on the estimated blood loss. It is important to exclude any trauma to the genital tract and to ensure completeness of the placenta and membranes. at 20:20:28, .007

39

Ecbolics Once atonic uterus has been identified as the cause of PPH, measures should be taken to ensure uterine contraction and retraction. Syntocinon (5 units) should be administered intramuscularly and if bleeding persists, Syntometrine (combination of oxytocin 5 U and ergometrine 0.5 mg) or ergometrine (0.5 mg) should be administered (with caution in severe preeclampsia).

Ensure Availability of Blood and Blood Products Replacement of the circulating blood volume with crystalloids and colloids should be followed by restoration of the oxygen-carrying capacity of the blood and correction of any derangements in coagulation. The aim of blood and fluids should be to replenish the previous loss in the first hour followed by maintenance fluids to replace continuing loss and maintain normal vital parameters. If coagulopathy is suspected, the haematologist should be involved and fresh frozen plasma (FFP), cryoprecipitate and platelets administered as required. In massive obstetric blood loss, rapid infusion of FFP may be required to replace clotting factors other than platelets. It is recommended that with every 6 units of blood transfusion, 1 L of FFP should be administered. It is important to maintain the platelet count above 50 000 by infusing platelet concentrates when indicated. Cryoprecipitate may also be needed if the patient develops disseminated intravascular coagulation (DIC) and her fibrinogen drops to less than 1 g/dL (10 g/L).

M: Massage/ Compression of the Uterus Uterine massage helps stimulate uterine contraction and retraction and should be commenced very early. It may act synergistically with the uterotonic drugs. Compression of the aorta may be used to gain temporary control of bleeding by applying the fist directly in the midline, just above the umbilicus and the uterus with the heel of the hand pressing down on the aorta. In a low-resource setting, anti-shock garments may also be used if available, during transfer to operating theatre or to another referral centre. Uterine compression continuously for 8–10 minutes may help to arrest the bleeding.

O: Oxytocin Infusion/Prostaglandins Syntocinon 40 units can be added to 500 mL of normal saline and infused at a rate of 125 mL/hour [4]. It

Algorithms for Management of the Top Five ‘Direct Killers’

is important to avoid fluid overload, as fatal pulmonary and cerebral oedema with convulsions may occur secondary to dilutional hyponatraemia. An indwelling transurethral catheter is a requisite in these cases. In addition to monitoring urine output, it also helps to keep the bladder empty and promote uterine contractions. Prostaglandins such as Hemabate (15-methyl prostaglandin 2 alpha) 250 mcg can be administered intramuscularly, once every 15 minutes for a maximum of eight doses (2 mg). Intramyometrial injection of Hemabate has been tried, but serious complications, including severe hypotension and cardiac arrest, have been reported. Sublingual misoprostol (800 mcg) may be tried, especially if oxytocin infusion was not used earlier. This is a valuable option in developing countries because of its low cost and relatively easier storage without the need for a cold chain. Tranexamic acid (starting dose of 1 g followed by 1 g 30 minutes later or should there be a rebleed within 24 hours) may be considered for PPH if administration of uterotonics has failed to stop the bleeding, or it is thought that the bleeding may be partly due to trauma.

S: Shift to Theatre If the patient continues to bleed despite initial management (i.e. ‘HAEMO’) it is best to transfer her to the theatre (for ‘STASIS’). Theatre provides an environment suitable for continuous monitoring and resuscitation and facilitates an examination to exclude any retained placental tissue or membranes or tears. A bimanual compression can be carried out to ‘compress’ the uterus between the abdominal and vaginal hands.

T: Tamponade Balloon Uterine tamponade with a balloon is easy to perform and takes only a few minutes. It arrests the bleeding and may prevent coagulopathy due to massive blood loss and the need for further surgical procedures. Although a Sengstaken–Blakemore oesophageal catheter (SBOC) is most commonly used, the Rusch urological hydrostatic balloon and the ‘Bakri SOS’ balloon may also be used. Usually a volume of about 300 to 400 mL may be required to exert the desired counter-pressure to stop bleeding from the uterine sinuses. If the tamponade arrests the bleeding (i.e. .007

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positive), the chances of the patient requiring any further surgical intervention are remote. Such a ‘tamponade test’ has a positive predictive value of 87% for the successful management of PPH [5].

A: Apply Compression Sutures Failure of the tamponade test to arrest haemorrhage warrants an immediate laparotomy. Amount of blood loss, continuing bleeding, haemodynamic status and the patient’s parity should be considered prior to attempting conservative surgical measures. This will help avoid ‘too little being done too late’. It is prudent to discuss with the anaesthetist regarding the ability to withstand continued bleeding, while conservative surgical measures are attempted. This is vital in developing countries, where the patient might have lost a significant amount of blood by the time she reaches the referral centre. In such situations, radical measures such as total or subtotal hysterectomy to save the patient’s life should be considered at the first instance. Conservative surgical measures include compression sutures which include classical B-Lynch or vertical or horizontal brace sutures using a delayed absorbable suture material [6].

S: Systematic Pelvic Devascularisation If the compression sutures fail, ligation of blood vessels supplying the uterus should be tried. These include ligation of both uterine arteries, followed by tubal branches of both ovarian arteries proximal to the ovarian ligament (called the ‘quadruple ligation’). Uterine artery ligation is straightforward once the uterovesical fold of peritoneum is incised and the bladder is reflected down. A window is made in the broad ligament just lateral to the uterine vessels and the needle is passed through this opening. Medially, the needle is passed through the lower uterine myometrium, about 2 cm from the lateral margin, and then the sutures are tied. The same procedure is repeated on the other side. Internal iliac artery ligation is an option if bleeding persists. This requires an experienced surgeon who is familiar with the anatomy of the lateral pelvic wall. Bilateral internal iliac artery ligation has been found to reduce the pulse pressure by up to 85% in arteries distal to the ligation. This translates to an acute reduction in the blood flow by about 50% in the distal vessels.

Management of Massive Obstetric Haemorrhage

The reported success rate of this procedure has been between 40% and 75% and it is invaluable for avoiding a hysterectomy. Potential complications include haematoma formation in the lateral pelvic wall, injury to the ureters, laceration of the iliac vein and accidental ligation of the external iliac artery. Ligation of the main trunk of the internal iliac artery may result in intermittent claudication of the gluteal muscles due to ischaemia. Examining the femoral pulse prior to completely ligating the internal iliac artery is vital.

I: Interventional Radiology

Postoperative Care Women with massive obstetric haemorrhage often need multi-organ support. Hence, transfer to an intensive care unit or high-dependency unit should be considered for monitoring. Thromboprophylaxis should be considered once the coagulation parameters return to normal.

Complete the ‘3 E’s’ After Every Obstetric Emergency Examine – for heart rate, blood pressure, uterine contractility and vaginal bleeding and monitor urine output. Replenish lost fluid, blood and blood products adequately. Explain the delivery events, possible reasons, complications and future plan of care to the patient (i.e. debrief). Escalate – complete the Incident Reporting Form and inform senior colleagues as well as to the team to identify learning points to continuously improve patient care.

In women who are not acutely compromised or bleeding severely, interventional radiology can be considered. The success rates may be as high as 85%– 95% [7] and the entire procedure may take about 1 hour. Uterine artery embolisation helps to avoid radical procedures and preserve future fertility. Complications include vessel perforation, haematoma, infection and tissue necrosis.

S: Subtotal or Total Abdominal Hysterectomy If the bleeding is predominantly from the lower segment (as in PPH following a major degree placenta praevia), a total abdominal hysterectomy is warranted. A subtotal hysterectomy may be performed if the bleeding is mainly from the upper segment and the cause is ‘unresponsive’ uterine atony. Subtotal hysterectomy has lower morbidity and mortality rates and requires less time to perform. Because of the anatomical changes of pregnancy, it is important to exercise utmost care to prevent visceral trauma, especially of the bladder and ureters. It is also important to clamp the ovarian ligament medially to avoid nonintentional or inadvertent oophorectomy [8].

Key Pitfalls • •

Failure to accurately estimate blood loss ‘Too little done too late’ – ‘too little’ estimation of blood loss, ‘too little’ fluid replacement, ‘too little’ ecbolics, ‘too little’ replacement of blood and clotting factors, ‘too late’ referral or involvement of multidisciplinary team and ‘too late’ laparotomy and surgical haemostasis

Key Pearls Young fit women may maintain their blood pressure until significant blood loss occurs (Table 5.2).

Table 5.2 Symptoms and signs observed with massive obstetric haemorrhage [3]

Class I

Class II

Class III

Class IV

Per cent blood loss

15

15–30

30–40

>40

Amount of blood loss (mL)

1000

1500

2000

>2500

Respiration rate

14–20

20–30

30–40

>40

Pulse

140

Systolic blood pressure

Normal

Normal

Decreased

Decreased

Diastolic blood pressure

Normal

Increased

Decreased

Decreased

Mental state

Anxious

Anxious and confused

Confused and agitated

Lethargic

Urine output (mL/hour)

>30

20–30

5–15

Negligible

at 20:20:28,

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Algorithms for Management of the Top Five ‘Direct Killers’

Systematic management of massive obstetric haemorrhage with the use of algorithms (Figure 5.1 and Table 5.1) will save lives. Use of ‘Shock index’ and ‘Rule of 30’ may help in estimating actual blood loss, when the vital signs are maintained despite significant blood loss.

References 1. MBRRACE- UK. Saving lives, improving mother’s care: surveillance of maternal deaths in the UK 2012–2014 and lessons learned to inform maternity care from the UK and Ireland Confidential Enquiries into Maternal Deaths and Morbidity. 2009–2014. 2. Chandraharan E, Arulkumaran S. Management algorithm for atonic postpartum haemorrhage. J Paediatr Obstet Gynaecol. 2005; June:106–12.

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3. Chandraharan E, Arulkumaran S. Massive postpartum haemorrhage and management of coagulopathy. Obstet Gynaecol Reprod Med. 2007;17:119–22. 4. Royal College of Obstetricians and Gynaecologists. Prevention and Management of Postpartum Haemorrhage. Green-top Guideline No. 52. London: RCOG, 2016. 5. Condous GS, Arulkumaran S, Symonds I, et al. The tamponade test for massive postpartum haemorrhage. Obstet Gynecol. 2003;104:767–72. 6. Chandraharan E, Arulkumaran S. Surgical aspects of postpartum haemorrhage. Best Pract Res Clin Obstet Gynaecol. 2008;22(6):1089–102. 7. Ratnam LA, Gibson M, Sandhu C, et al. Transcatheter pelvic arterial embolisation for control of obstetric and gynaecological haemorrhage. J Obstet Gynaecol. 2008;28 (6):573–9. 8. Pinas A, Chandraharan E. Postpartum haemorrhage and haematological management. Obstet Gynaecol Reprod Med. 2014;24:291–5.

Chapter

6

Management of Septicaemia and Septic Shock Antepartum, Intrapartum and Postpartum Karin Leslie and Sarah Hammond

Key Facts Sepsis remains an important cause of maternal morbidity and mortality. Delays in diagnosis and treatment are often identified as contributory factors in maternal death due to sepsis [1]. Women with sepsis need • Early diagnosis • Rapid antibiotics • Review by senior doctors and midwives Sepsis remains as one of the leading causes of maternal deaths in the United Kingdom, and approximately 50% of cases may have been avoidable by a different care.Prompt action and effective teamwork can make the difference between survival and death. The Third International Consensus Definitions for Sepsis and Septic Shock (Sepsis-3) Sepsis Life-threatening organ dysfunction caused by a dysregulated host response to an infection Septic shock Septic shock is a subset of sepsis in which underlying circulatory and cellular/metabolic abnormalities are profound enough to substantially increase mortality. The consensus reached by the taskforce in 2016, ‘Sepsis 3’, has significantly changed the way we define sepsis. The definitions of sepsis, septic shock and organ dysfunction had remained largely unchanged for more than two decades prior to this. There has been a move away from earlier definitions that focused on a host’s systemic inflammatory response syndrome (SIRS), as SIRS criteria did not correlate with outcomes. Septic shock is defined as the need for vasopressors to maintain mean arterial pressure >65 mm Hg after an adequate fluid bolus and a lactate >2 mmol/ L. A pragmatic clinical definition outside critical care is a systolic blood pressure 40 from normal) • Heart rate >130 beats per minute • Respiratory rate ≥25 breaths per minute • Needs oxygen to keep SpO2 ≥92% • Non-blanching rash, mottled/ashen/cyanotic • Not passed urine in past 18 hours • Urine output less than 0.5 mL/kg/hour

Management of Septicaemia and Septic Shock

Lactate ≥2 mmol/L (lactate may be raised as a response to labour and delivery) Red Flag Sepsis criteria were developed by the UK Sepsis Trust in collaboration with NHS England and the Royal Colleges for use at the bedside. They can be rapidly assessed and if present suggest the woman has a degree of organ dysfunction, but they do not replace a formal ‘diagnosis’ of sepsis. •

Key Actions • • •

Remember: prompt treatment saves lives. Use the Sepsis 6 bundle within 1 hour (Table 6.2). Consider declaring sepsis as an emergency to the team. • ‘This could be sepsis, let’s start Sepsis 6’. Take a thorough history with the aim of identifying the source of infection. Consider other differential diagnoses for acute illness including VTE; haemorrhage; and cardiac, respiratory and neurological causes.

Clinical Examination Use an ABCDE approach to assess all systems. Antepartum and intrapartum, assess for signs chorioamnionitis. Is there a fetal tachycardia? The urinary tract is a common source; check previous microbiology results, dip and send the urine, check for renal tenderness and consider imaging. In the postpartum woman examine breasts (mastitis, breast abscess), legs/groin (thrombus), wounds (surgical site infection), perineum and vaginal exam (open cervix, offensive lochia, retained products, foreign body, e.g. swab). Do you have a ‘Sepsis Box’ (Table 6.3) to aid systematic an approach to management? In addition to blood cultures consider urine, throat, wound and vaginal swabs.

Remember the baby – are they well, do they need neonatal review? Go back and review (involve your obstetric anaesthetist): Is there a response to treatment? What is the MEOWS score (Modified Early Obstetric Warning System)? Review results including lactate. Any evidence of acute kidney injury? Has the patient improved? Do you need to escalate and involve critical care? Call critical care for input if after delivering Sepsis 6: • Systolic blood pressure remains 25 breaths per minute • Lactate level not decreasing • Other features suggesting critical illness

Antibiotics The Golden Hour – give IV broad spectrum antibiotics within 1 hour. Time to administration is a predictor of mortality in sepsis; with each hour of delay from diagnosis the risk of mortality increases by 8%.

Antimicrobial Stewardship Start Smart • • • •

Initiate prompt treatment with broad-spectrum IV antibiotic. Follow local antimicrobial guidance (this will help you to choose the RIGHT drug). Remember to check drug allergies. Prescribe only with clear clinical justification. Table 6.3 Maternal sepsis box: possible contents Laminated maternal sepsis risk assessment tool Laminated Sepsis 6 pathway

Table 6.2 The Sepsis 6 bundle

Oxygen mask and tubing

Three things in . . . .

Blood bottles and forms

1

Give O2 to keep saturations above 94%

Blood gas syringe

2

Give IV fluids

Blood culture bottles

3

Give IV antibiotics within 1 hour

Microbiology swabs

Three things out . . . . 4 5 6 at 20:20:26,

Check lactate (venous or arterial) Take blood cultures (ideally prior to IVAB) Measure urine output .008

IV cannulae Crystalloid fluid with IV giving sets Broad spectrum IV antibiotics Catheter and urometre

45

Algorithms for Management of the Top Five ‘Direct Killers’

•

Document prescribing decision in the medical notes.

Then Focus • • • •

Clinical review and decision at 48–72 hours STOP, change or continue Revise antibiotics in line with culture results IV to oral switch if possible Remember – women from outside the United Kingdom are more likely to be infected with resistant organisms.

Key Pitfalls Escalate and treat promptly. ‘Too little, too late’ is a common theme in mortality and morbidity enquiries. Sepsis may present in atypical ways; not all women will have a fever. Confusion is NOT an early warning sign but a sign of significant established disease. Go back and review; on a busy on call shift it is easy to think ‘antibiotics in’ and move on to the next case but women may rapidly deteriorate. Is there a positive response to treatment? Has the patient

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improved? Do you need to escalate and involve critical care?

Key Pearls Prompt treatment and effective teamwork with ‘Sepsis 6’ saves lives.

Online Resources https://sepsistrust.org/professional-resources/educa tion-resources/ Maternal sepsis e learning package: www.scottishma ternity.org/maternal-elearning.htm

References 1. NICE. Guideline NG51. Sepsis: Recognition, Diagnosis and Early Management, updated April 2019. 2. MBRRACE-UK. Saving lives, improving mother’s care: Lessons learned to inform maternity care from the UK and Ireland Confidential Enquiries into Maternal Deaths and Morbidity 2014–16. 3. Acosta CD, Kurinczuk JJ, Lucas DN, Tuffnell DJ, Sellers S, Knight M, United Kingdom Obstetric Surveillance System. Severe maternal sepsis in the UK, 2011–2012: a national case-control study. PLoS Med. 2014;11(7):e1001672.

Chapter

7

Management of Amniotic Fluid Embolism Derek Tuffnell, James Tibbott and Hlupekile Chipeta

Key Facts Definition Amniotic fluid embolus (AFE) is a rare obstetric condition that is characterised by one or more of the following features, in the absence of any other clear cause: Acute fetal compromise Cardiac arrhythmias or arrest Coagulopathy Convulsion Hypotension Maternal haemorrhage Premonitory symptoms, e.g. restlessness, numbness, agitation, tingling Shortness of breath Excluding women with maternal haemorrhage as the first presenting feature in whom there was no evidence of early coagulopathy or cardiorespiratory compromise [1] Histological amniotic fluid embolus is the presence of fetal squames or hair in maternal lungs at postmortem [1]. Incidence There has been no change in incidence since 2010. It is approximately 2.0 per 100 000 deliveries (95% confidence interval [CI] 1.5–2.5) in the United Kingdom [2]. Similar incidences are found elsewhere, for example, 3.3 per 100 000 deliveries in Australia [3] and 6.0 per 100 000 singleton deliveries in Canada [4].

Morbidity and Mortality Amniotic fluid embolus is the eighth most common cause of all maternal deaths, down one place from the previous edition of this book [2, 5]. At 0.35 per 100 000 maternities (95% CI 0.15–1.39) it has declined from the fourth to the fifth leading cause of direct ,

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maternal deaths in the United Kingdom. Maternal case fatality rates are between 11% and 32% in the United Kingdom, Australia and the United States [9, 4, ref surveillance]. There is a fall in case mortality rates which is probably due to high-level supportive care and diagnosis of milder cases [6]. Women who died or who had permanent neurological injury were more likely to present with cardiac arrest (83% vs. 33%, P < 0.001), be from ethnicminority groups (adjusted odds ratio [AOR] 2.85; 95% CI 1.02–8.00), to have had a hysterectomy (OR 2.49; 95% CI 1.02–6.06) and were less likely to receive cryoprecipitate (OR 0.30; 95% CI 0.11–0.80) [1].

Key Implications Maternal Pulmonary oedema, acute respiratory distress syndrome, disseminated intravascular coagulopathy (DIC), pulmonary embolus, haemorrhage, right and then left cardiac failure, cerebrovascular events, cardiorespiratory arrest, death Fetal Fetal distress, hypoxic ischaemic encephalopathy (HIE), learning difficulties, cerebral palsy, intrauterine and neonatal death

Key Pointers International variations exist in the definition of AFE [7], which may account for differences in incidence. Amniotic fluid embolus is sometimes considered in two phases. The first phase is characterised by an almost anaphylactoid reaction with hypotension and dyspnoea with or without cardiac arrest. The second phase is marked by haemorrhage and coagulopathy. The following risk factors have been identified: Maternal age greater than 35 years, (OR 9.85; 95% CI, 3.57–27.2)

47

Algorithms for Management of the Top Five ‘Direct Killers’

Induction of labour (OR 3.86; 95% CI 2.04–7.31) Multiple pregnancy (OR 10.9; 95% CI 2.81–42.7) Caesarean delivery (OR 8.84; 95% CI 3.70–21.1) Ethnic minority groups (OR 11.8; 95% CI 1.40–99.5) Hyperstimulation remains heavily linked to AFE. In the last MBRRACE report of the nine women who died from an AFE, five were induced, among whom four deaths followed hyperstimulation [2].

Key Symptoms and Signs Maternal Symptoms: dyspnoea, loss of consciousness, cough, wheeze, headache, chest pain Signs: cyanosis, hypoxia, hypotension, transient hypertension, cardiac arrhythmia, cardiopulmonary arrest, seizure, signs of pulmonary oedema Fetal Fetal distress, neonate with severe hypoxic ischaemic encephalopathy

Key Actions Suspect a diagnosis of AFE in any woman during labour, after delivery or following surgical evacuation of the uterus with the following features [6]: maternal haemorrhage; hypotension; shortness of breath and new-onset respiratory symptoms; coagulopathy; premonitory symptoms such as restlessness, agitation, numbness, tingling; acute fetal compromise; cardiac arrest and/or arrhythmia; seizures. A significant number of women present with maternal collapse. Therefore, management will consider this presentation foremost.

First-Line Management: Resuscitation Call for Help – Early Senior multidisciplinary involvement is important for a positive prognosis. The team should include obstetricians, anaesthetists, intensivists, haematologists and neonatologists.

Airway Pregnant women are at risk of a compromised airway due to depressed level of consciousness following

AFE. Maintain potency. Give high flow oxygen 15 L through a face mask with reserve bag. Attach a pulse oximeter. Consider intubation if the woman is still pregnant or experiencing respiratory distress or cardiopulmonary collapse. Place the patient into left lateral tilt.

Breathing Pregnant women with AFE are at risk of compromised breathing due to pulmonary oedema. Assess breathing (including respiratory rate) and ventilate if there is evidence of respiratory distress. Positive end expiratory pressures may be necessary to maintain adequate oxygen saturation.

Circulation Pregnant women with AFE are at risk of cardiac arrhythmias, cardiac arrest, massive haemorrhage and pulmonary embolus due to sudden fluid shifts and disseminated intravascular coagulation (DIC). • Assess circulation and blood pressure. • Start CPR and deliver fetus if cardiac arrest occurs. • Insert two large-bore intravenous cannulae. • Consider central monitoring especially if pulmonary oedema, haemodynamic instability or peripheral shutdown is present. • Send venous blood samples urgently for FBC, clotting and cross match. • Consider massive obstetric haemorrhage protocol. • Perform arterial blood gas measurements to exclude metabolic acidosis • Order a chest x-ray.

Correct Hypotension and Coagulopathy • •

•

Deliver the Fetus The main aim of early delivery is to facilitate and improve the outcome of maternal resuscitation. The fetus remains at significant risk of morbidity and demise even with prompt delivery. Outcome statistics

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Replace intravascular volume with clear fluids and blood. Liase early with haematologist to treat DIC with fresh frozen plasma, cryoprecipitate, platelets or red blood cells. Liase with intensivists and anaesthetists to maintain blood pressure with inotropic support.

Management of Amniotic Fluid Embolism

of fetuses and neonates are unlikely to be accurate due to the small numbers in UK case series but suggest a 50% survival if born to a dead woman, with 77% surviving if born to a live woman. Either way, infants are at significant risk of long-term neurological deficits [7]. If maternal cardiac arrest occurs immediate delivery of the fetus should be undertaken. The CAPS (Cardiac Arrest in Pregnancy and Perimortem Caesarean Section) study demonstrated that in women who survived cardiac arrest (all causes) the time from collapse to perimortem caesarean section was significantly shorter (median interval 3 versus 12 minutes, P = 0.001) [8]. Following delivery, beware of uterine haemorrhage due to DIC. • Consider medical treatments for atony including oxytocics, ergometrine, carboprost and misoprostol. • Consider mechanical measures including bimanual compression, intrauterine tamponading balloons and brace techniques. • Consider interventional radiology and uterine artery embolization. • Consider surgical options including internal iliac artery ligation and hysterectomy.

Second-Line Management: Diagnosis and Supportive Care Ascertain the Diagnosis With mortality from AFE falling, diagnosis is increasingly clinical. The long list of differential diagnoses reflects the breadth of symptoms and signs women present with. These must be excluded before a diagnosis is made but treatment of the acutely ill woman must not be delayed in the quest to find a diagnosis. Box 7.1 outlines a list of differential diagnoses. Various investigations should be performed in an effort to investigate the aforementioned differential diagnoses. Blood tests to perform include clotting, liver and renal function tests, arterial blood gases. An ECG (with or without an echocardiogram) may be helpful in showing myocardial problems. A ventilation/perfusion (V/Q) scan may reveal a perfusion defect. A computerised tomography pulmonary angiography (CTPA) scan would diagnose intrapulmonary abnormalities. ,

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Box 7.1 Differential diagnosis of women with suspected amniotic fluid embolism [5] Postpartum haemorrhage Placental abruption Uterine rupture Preeclampsia/HELLP (haemolysis, elevated liver enzymes, low platelet count) syndrome Septic shock Thrombotic embolus Air embolus Acute myocardial infarction Peripartum cardiomyopathy Local anaesthetic toxicity Anaphylaxis Transfusion reaction Aspiration of gastric contents

Zinc coproporphyrin and tryptase levels are not used routinely in the diagnosis of AFE.

Transfer to Intensive Care Unit The mainstay of management of AFE remains supportive. Rigorous, early supportive therapy saves mothers’ lives. The purpose of admitting a patient to the ICU is to monitor observations, maintain haemodynamic instability and reduce iatrogenic and disease complications. Options of treatment include diuretics, inotropes and steroids. Plasma exchange, haemofiltration and extracorporeal membrane oxygenation have been used in treatment.

Disclosure and Documentation At a local level, clear, chronological and contemporaneous documentation is essential preferably on a high-dependency chart. Incident reporting is important, for example, for transfer to the ICU, major postpartum haemorrhage, unexpectedly low cord pH and neonatal admission to the NICU.

Key Pitfalls • •

Failure to suspect AFE in a collapsed or unwell peripartum woman Failure to seek early input from intensivists, anaesthetists and haematologists

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Algorithms for Management of the Top Five ‘Direct Killers’

• • • • •

Failure to ensure ABC’s (Airway, Breathing and Circulation) Failure to consider early delivery of the fetus to aid maternal resuscitation Failure to correct coagulopathy, stop haemorrhage and control fluid balance Failure to keep adequate records Failure to report to the national register

Key Pearls •

•

All staff providing intrapartum care should attend annual skills and drills for management of maternal collapse. Regular skills drills on the labour ward can ensure that a robust system is in place for the acute management of AFE.

References 1. Knight M, Tuffnell D, Brocklehurst P, Spark P, Kurinczuk JJ, on behalf of the UK Obstetric Surveillance System. Incidence and risk factors for amniotic fluid embolism. Obstet Gynecol. 2010;115:910–17. 2. Knight M, Nair M, Tuffnell D, Shakespeare J, Kenyon S, Kurinczuk JJ (eds) on behalf of MBRRACE-UK. Saving Lives, Improving Mothers’ Care: Lessons Learned to Inform Maternity Care from the UK and Ireland Confidential Enquiries into Maternal Deaths and Morbidity 2013–15. Oxford: National Perinatal Epidemiology Unit, University of Oxford, 2017.

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3. Roberts C, Algert C, Knight M, Morris J. Amniotic fluid embolism in an Australian population-based cohort. Br J Obstet Gynaecol. 2010;117:1417–21. 4. Kramer MS, Rouleau J, Baskett TF, Joseph KS; Maternal Health Study Group of the Canadian Perinatal Surveillance System. Amniotic-fluid embolism and medical induction of labour: a retrospective, population-based cohort study. Lancet. 2006;368:1444–8. 5. Centre for Maternal and Child Enquiries (CMACE). Saving mothers’ lives: Report on Confidential Enquiries into Maternal Deaths in the United Kingdom. Br J Obstet Gynaecol. 2011;118 (Suppl. 1):1–208. 6. Howell C, Grady K, Cox C. Managing Obstetric Emergencies and Trauma: The MOET Course Manual, 2nd ed. London: RCOG, 2007. 7. Conde-Agudelo A, Romero R. Amniotic fluid embolism: an evidence-based review. Am J Obstet Gynecol, 2009;201(5):445.e1–13. Erratum in Am J Obstet Gynecol. 2010;202(1):92. 8. Tuffnell D, Knight M, Plaat F. Amniotic fluid embolism: An update. Anaesthesia. 2011;66(1):3–6. 9. Tuffnell DJ. United Kingdom amniotic fluid embolism register. Br J Obstet Gynaecol. 2005;112:1625–9. 10. Beckett VA, Knight M, Sharpe P. The CAPS Study: incidence, management and outcomes of cardiac arrest in pregnancy in the UK: a prospective, descriptive study. BJOG. 2017;124(9):1374–81.

Section 3

Intrapartum Emergencies

Chapter

Uterine Rupture

8

Caroline Reis Gonçalves and Edwin Chandraharan

Table 8.1 Risk factors for uterine rupture

Key Facts

General Obstructed labour, especially in low-resource settings Antepartum fetal death Previous first-trimester miscarriages Maternal age ≥35 years Parity ≥3 Malposition/malpresentation Birthweight ≥4000 g Sequential use of prostaglandins and oxytocin (odds ratio [OR] 48 without caesarean section scar and OR 16.1 for caesarean section scar) Intrauterine manipulation (internal podalic version and breech extraction, use of high forceps and ‘Kristellar’ manoeuvre )

Definition • Complete uterine rupture: consists in complete disruption of uterine layers with extrusion of fetus, placenta or both into the abdominal cavity. • Incomplete uterine rupture (uterine dehiscence): partial uterine disruption with uterine muscle compromise and sparing of visceral peritoneum [1]. • The final differentiation between this classification can be made during laparotomy.

Specific to the presence of a uterine scar Upper segment scar (10% vs. 0.5% for lower segment scar) Induction or augmentation of labour (two- to three-fold) Inter-pregnancy interval of 20 milliunits/minute) during VBAC augmentation increases the risk of uterine rupture by four-fold or greater [5].

Key Pointers Induction with or without Augmentation of Labour Using Prostaglandins or Oxytocin •

•

,

Sequential induction with prostaglandins and oxytocin has been reported to be associated with the highest OR for complete uterine ruptures in women either with or without a previous caesarean delivery. In women without caesarean delivery (CD) the adjusted OR was 48.0, whereas women with a previous CD had an OR of 16.1 [3]. Induction or augmentation of vaginal birth after caesarean section (VBAC), also called trial of labour after caesarean section (TOLAC), is

Obstetric Manipulation •

Obstetric manoeuvres: Breech extraction had a high correlation with uterine rupture (AOR 42.6) [3]. Other obstetric manoeuvres include Internal podalic version and breech extraction for the delivery of the second twin, manual removal of the placenta, fetal surgery, shoulder dystocia and surgical termination of pregnancy. Unfortunately, some outdated obstetric procedures, such as ‘Kristeller’ manoeuvre (i.e. application of fundal pressure in second stage of labour) are still performed in some centres where competency in

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Section 3

Intrapartum Emergencies

Chapter

Uterine Rupture

8

Caroline Reis Gonçalves and Edwin Chandraharan

Table 8.1 Risk factors for uterine rupture

Key Facts

General Obstructed labour, especially in low-resource settings Antepartum fetal death Previous first-trimester miscarriages Maternal age ≥35 years Parity ≥3 Malposition/malpresentation Birthweight ≥4000 g Sequential use of prostaglandins and oxytocin (odds ratio [OR] 48 without caesarean section scar and OR 16.1 for caesarean section scar) Intrauterine manipulation (internal podalic version and breech extraction, use of high forceps and ‘Kristellar’ manoeuvre )

Definition • Complete uterine rupture: consists in complete disruption of uterine layers with extrusion of fetus, placenta or both into the abdominal cavity. • Incomplete uterine rupture (uterine dehiscence): partial uterine disruption with uterine muscle compromise and sparing of visceral peritoneum [1]. • The final differentiation between this classification can be made during laparotomy.

Specific to the presence of a uterine scar Upper segment scar (10% vs. 0.5% for lower segment scar) Induction or augmentation of labour (two- to three-fold) Inter-pregnancy interval of 20 milliunits/minute) during VBAC augmentation increases the risk of uterine rupture by four-fold or greater [5].

Key Pointers Induction with or without Augmentation of Labour Using Prostaglandins or Oxytocin •

•

Sequential induction with prostaglandins and oxytocin has been reported to be associated with the highest OR for complete uterine ruptures in women either with or without a previous caesarean delivery. In women without caesarean delivery (CD) the adjusted OR was 48.0, whereas women with a previous CD had an OR of 16.1 [3]. Induction or augmentation of vaginal birth after caesarean section (VBAC), also called trial of labour after caesarean section (TOLAC), is

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Obstetric Manipulation •

Obstetric manoeuvres: Breech extraction had a high correlation with uterine rupture (AOR 42.6) [3]. Other obstetric manoeuvres include Internal podalic version and breech extraction for the delivery of the second twin, manual removal of the placenta, fetal surgery, shoulder dystocia and surgical termination of pregnancy. Unfortunately, some outdated obstetric procedures, such as ‘Kristeller’ manoeuvre (i.e. application of fundal pressure in second stage of labour) are still performed in some centres where competency in

51

Intrapartum Emergencies

• • •

Key Implications Maternal • • • •

Haemorrhage leading to hypovolaemic shock and need for blood transfusion Bladder and ureteric injury Peripartum hysterectomy and loss of future fertility Maternal death – less common in a well-resourced setting; however, it can account for around 1%–15% of obstetric deaths in low-resource settings [2, 10].

Uterine Scar

Neonatal

•

•

•

•

•

•

•

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operative vaginal births is lacking, and this manoeuvre has been reported to be associated with uterine rupture. High rotational forceps delivery [2] Forceps delivery carried out in an unsuitable patient by an inexperienced obstetrician [2] External cephalic version can be safely performed in women with a previous caesarean delivery scar. A systematic review of adverse outcomes of external cephalic version (ECV) and persisting breech presentation at term did not find any case of described uterine rupture after ECV [6].

Upper segment caesarean section scar has a higher (approximately 20-fold) risk of uterine rupture compared with lower segment scar [1]. Current scientific evidence appears to suggest that there is no significant difference in the rates of uterine rupture in VBAC with two or more previous caesarean births (92 per 10,000) compared with a single previous caesarean birth (68 per 10,000) [7]. An inter-pregnancy interval of less than 6 months between the previous caesarean section and subsequent VBAC was reported to be associated with an increased risk of uterine rupture (OR 2.66) and significant morbidity (AOR 1.95) [8]. A meta-analysis showed that single- and doublelayer closure of a caesarean uterine incision are associated with similar incidence of uterine scar defects, as well as uterine dehiscence and uterine rupture in the subsequent pregnancy. The doublelayer closure was associated with a significant increase in the residual myometrial thickness (RMT) on ultrasound compared with single-layer closure, which is of unclear clinical significance, as it was not associated with an increased incidence of uterine scar dehiscence or uterine rupture [9]. Risk of uterine rupture following myomectomy is significantly increased if the endometrial cavity has been opened during the procedure. Laparoscopic myomectomy, if performed by an expert, does not appear to carry any increased risk of subsequent uterine rupture compared with myomectomy via laparotomy. Uterine perforation during intrauterine procedures could also lead to a uterine rupture during subsequent pregnancies. https://www.cambridge.org/core. 21 May 2021 at 20:20:27,

Neonates born after uterine rupture were graded lower Apgar scores and had an increased risk of perinatal mortality compared with controls. [10]

Medico-legal •

•

•

Clinical negligence claims are especially likely in cases of uterine rupture following induction and augmentation of labour. To avoid this situation, one should promote informed consent and shared decision-making in women undergoing VBAC. In addition, use of continuous electronic fetal heart rate monitoring using a cardiotocograph (CTG) should be recommended for timely diagnosis of uterine rupture. As soon as possible, clear and accurate documentation of time of the uterine rupture, underlying predisposing factors, the decision to delivery interval (DDI), as well as a description of the rupture along with the type of surgery undertaken should be carried out. The whole sequence of events should be discussed with the patient by an experienced obstetrician or the obstetrician who performed the definitive surgery.

Key Diagnostic Signs •

Scar dehiscence could be asymptomatic while a complete rupture could lead to hypovolaemic shock, collapse, fetal demise and even maternal death.

Early Signs •

Intense and painful uterine contractions.

Uterine Rupture

•

• •

Bandl’s sign – infraumbilical ring of uterine myometrium – suggesting an imminent separation between the upper and lower uterine segments Frommel sign – uterine inclination due to stretching of round ligaments Gross haematuria (may occur even after a successful vaginal delivery)

•

•

◦ Abnormalities on the CTG trace (repetitive atypical variable or late decelerations or an increased in baseline variability) suggestive of uterine scar dehiscence

Late Signs o Intense abdominal pain followed by sudden relief o Cessation of uterine contractions o ‘Receding sign’ – Sudden elevation of fetal presenting part in the maternal birth passage o Clark’s sign – crepitation on the abdominal palpation due to the presence of air inside the abdomen o Fetal parts easily palpable in the abdomen o Persistent fetal bradycardia, loss of baseline variability or absent fetal heart sounds (separation of the placenta from the myometrium, as the fetus enters the abdomen through the site of rupture)

•

•

Key Actions •

•

•

•

•

As with any medical emergency, vital signs (‘ABC’) and supportive treatment should be initiated. The specific management of haemorrhagic shock and immediate maternal resuscitation may be necessary. Ensure an immediate availability of crossmatched red cells, in cases of maternal collapse secondary to hypovolemic shock. Perform an immediate laparotomy to deliver the fetus and to promote adequate haemostasis and repair of uterine rupture. The fetus and placenta can be delivered through the rupture (they may be already inside the abdominal cavity, in the cases of complete uterine rupture). Exteriorising the uterus out of the pelvis may help reduce bleeding and facilitate the view of the posterior uterine wall and the broad ligaments. In addition, it helps identify uterine lacerations.

at 20:20:27, .010

53

•

•

Haemostasis should be immediately achieved by rapid application of Green––Armytage Haemostatic Clamps to the bleeding vessels in the area of uterine rupture, ligation of uterine arteries or temporary haemostasis with the application of an Esmarch bandage or a tourniquet to the lower uterine segment, until senior obstetric help is available. Uterine artery ligation (responsible for 90% of uterine blood supply): Feel for pulsations of the uterine artery near the junction of the uterus and cervix. Using 0 chromic catgut (or polyglycolic) suture on a large needle, pass the needle around the artery and through 2–3 cm of myometrium at the level where a transverse lower uterine segment incision would be made. Tie the suture securely. Place the sutures as close to the uterus as possible, as the ureter is generally only 1 cm lateral to the uterine artery. Repeat on the other side [11]. Utero-ovarian artery ligation (9% of uterine blood supply): Make a ligation just below the point where the ovarian suspensory ligament joins the uterus An Esmarch bandage is applied with uterine compression sutures. Two wraps of external uterine elastic bandage (EUEB) can be placed from the uterine fundus towards the cervix. Two laparotomy pads can be placed in front of and behind the uterus and fixed with a gauze bandage before applying the EUEB. Esmarch’s bandage is easy to use, inexpensive and reusable. Cessation of bleeding is immediate, and EUEB can be maintained for 6 hours, time enough to achieve adequate haematological replacement in most obstetric centres [12]. A cervical tourniquet can be useful when there is a simple laceration of the fundal region of the upper segment of the uterus. Position a Foley catheter or Penrose drain (or any flexible rubber sterile tube such as intravenous infusion set) around the lower uterine segment through two openings on the broad ligament and tighten the sides of the tube. Manual internal aortic compression is a technique used to ensure a transient reduction of bleeding in which the operator compresses the aorta for a maximum time of 90 minutes using both hands against the aorta until it is possible to notice spinal resistance. This applied force accounts for a mass of approximately 45 kg. which is required to overcome the aortic blood flow. Compression can

Intrapartum Emergencies

•

•

•

• •

• •

•

be performed until other measures are adopted to arrest bleeding. Sometimes a simple repair of the laceration with continuous suture with 1-0 Vycril in double layers will be appropriate. Remember that lateral extensions of lacerations, if unseen, can lead to haematoma into the broad ligament. In cases of extensive laceration, it may be necessary to perform a subtotal hysterectomy. However, if the cervix and paracolpos are involved or if there is evidence of sepsis, a total hysterectomy should be performed. Remember to check the integrity of the urinary bladder, mainly if there is a lower segment rupture. A bladder laceration should be sutured in two layers in continuous running sutures using 3-0 Vicryl or equivalent. Insert a drain if deemed necessary. Administer peri-operative antibiotics and ensure dilutional and consumption coagulopathy secondary to massive obstetric haemorrhage is corrected. Thromboprophylaxis should be considered in all cases, once the coagulation profile is normal. In the cases in which the uterus is preserved, and tubal ligation was not performed, it is imperative to counsel the woman about avoiding a future pregnancy for 2 years. Any subsequent pregnancies should be monitored closely, and an elective caesarean section should be considered at 39 weeks of gestation in cases of a lower segment uterine rupture and earlier if there was an upper segment uterine rupture. In women with a history of uterine rupture, the reported rate of repeat rupture ranges from 4% to 32%, with higher quality, more modern studies reporting a rate of 4%–15%. The risk of repeat rupture increases with an upper uterine segment scar. Given the high risk of repeat rupture in the setting of labour, women with a history of uterine rupture are not candidates for vaginal delivery. There is no definitive determination for the timing of interruption; nevertheless, a planned caesarean delivery at 36–37 weeks of gestation seems optimal to balance maternal and neonatal risks. Location of a previous scar and timing of rupture should also be considered. If delivery is planned before 37 weeks of gestation, antenatal corticosteroids

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should be administered to reduce the risk of neonatal respiratory morbidity [13].

Key Pitfalls •

•

• •

• •

•

Not suspecting scar rupture if there is vaginal bleeding in a woman undergoing trial of labour after caesarean (TOLAC or VBAC) Injudicious use of oxytocin or prostaglandins, especially in cases of a scarred uterus or multiparous woman Ignoring gross haematuria even if it is after a successful vaginal delivery Not noticing a lateral extension of the rupture into the broad ligament or an extension of the rupture into the cervix or vagina during a laparotomy Failing to identify bladder damage during the repair of a uterine rupture Failing to appreciate that a uterine rupture could co-exist with or be mistaken for placental abruption in a scarred uterus Leaving unattended a woman complaining of persistent and increasing scar pain or tenderness

Key Pearls •

•

•

The anticipation of uterine rupture and early diagnosis is the key to good perinatal and maternal outcomes. Recognition of cephalopelvic disproportion or malposition is essential before augmentation of labour in all women, especially with secondary inertia or prolongation of the second stage of labour. Continuous electronic fetal heart monitoring is indicated for women undergoing VBACS or trial of labour with a scarred uterus.

References 1. Rameez MFM, Goonewardene M. Uterine rupture. In Chandraharan E, Arulkumaran S (eds), Obstetric and Intrapartum Emergencies: A Practical Guide to Management, Cambridge: Cambridge University Press; 2012, 52–8. 2. Turner MJ. Uterine rupture. Best Pract Res Clin Obstet Gynaecol. 2002;16(1):69–79. DOI: 10.1053/ beog.2001.0256. 3. Al-Zirqi I, Kjersti Daltveit A, Forsén L, Stray-Pedersen B, Vangen S. Risk factors for complete uterine rupture. Am J Obstet Gynecol. 2017;216:165.e1-8.

Uterine Rupture

4. Royal College of Obstetricians and Gynaecologists. Birth After Previous Caesarean Birth. Green-top Guideline No. 45, October 2015. London: RCOG. 5. Cahill AG, Stamilio DM, Odibo AO, Peipert JF, Stevens EJ, Macones GA. Does a maximum dose of oxytocin affect risk for uterine rupture in candidates for vaginal birth after cesarean delivery? Am J Obstet Gynecol. 2007;197:495.e1–5. 6. Nassar N, Roberts CL, Barratt A, Bell JC, Olive EC, Peat B. Systematic review of adverse outcomes of external cephalic version and persisting breech presentation at term. Paediatr Perinat Epidemiol. 2006;20(2):163–71. DOI: 10.1111/j.13653016.2006.00702.x. 7. Landon MB, Spong CY, Thom E, Hauth JC, Bloom SL, Varner MW, et al. National Institute of Child Health and Human Development Maternal-Fetal Medicine Units Network. Risk of uterine rupture with a trial of labor in women with multiple and single prior cesarean delivery. Obstet Gynecol. 2006;108:12–20. 8. Stamilio DM, DeFranco E, Paré E, Odibo AO, Peipert JF, Allsworth JE, Macones GA. Short interpregnancy interval: risk of uterine rupture and complications of vaginal birth after cesarean delivery.

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Obstet Anesth Dig. 2008;28(2):91, DOI: 10.1097/01. aoa.0000319805.82200.c5. 9. Di Spiezio Sardo A, Saccone G, McCurdy R, Bujold E, Bifulco G, Berghella V. Risk of Cesarean scar defect following single- vs double-layer uterine closure: systematic review and meta-analysis of randomized controlled trials. Ultrasound Obstet Gynecol. 2017;50 (5):578–83. DOI: 10.1002/uog.17401. 10. Ofir K, Sheiner E, Levy A, Katz M, Mazor M. Uterine rupture: risk factors and pregnancy outcome. Am J Obstet Gynecol. 2003;189(4):1042–6. DOI: 10.1067/ s0002-9378(03)01052-4. 11. Organização Pan-Americana da Saúde Assistential. Assistance recommendations for prevention, diagnosis and treatment of obstetric hemorrhage. Brasília: OPAS; 2018. 12. Palacios-Jaraquemada J, Fiorillo A. Conservative approach in heavy postpartum hemorrhage associated with coagulopathy. Acta Obstet Gynecol Scand. 2010;89(9):1222–5. DOI: 10.3109/ 00016349.2010.491524. 13. Larrea NA, Metz TD. Pregnancy after uterine rupture. Obstet Gynecol. 2017. DOI: 10.1097/ aog.0000000000002373.

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Chapter

9

Breech Delivery Enaya Mirza and Edwin Chandraharan

Table 9.1 Predisposing factors for breech presentation

Key Facts

Power • Uterine malformation (e.g. bicornuate or septate uterus) • Uterine fibroids • Lax uterus (grand multiparty) • Polyhydramnios (alters the pyriform shape of the uterus)

Definition • Breech presentation refers to a situation in which the buttocks, feet or knee of the fetus are positioned in the pelvis to be delivered first. • The torso and head of the fetus in relation to the breech are in a longitudinal lie.

Passenger • Prematurity • Multiple pregnancy • Previous breech presentation • Fetal malformation (e.g. hydrocephalus, anencephaly)

Incidence • At term the incidence of breech presentation is 3%– 4% [1]. • The incidence is higher in preterm gestations and can be up to 20% in extreme prematurity at 28 weeks’ gestation [2]. • The incidence is higher in primiparous women, and recurrence rates in subsequent pregnancies are significant. Types of Breech Presentation • Breech presentations can be classified as extended, flexed (both terms referring to the orientation of the knee) or footling (Figure 9.1). • Extended breech: The knees are both extended with the hips flexed and feet above the buttocks. This is the most common breech presentation, with an incidence of 65% [2]. • Flexed breech: The knees are both flexed and above the buttocks. • Footling breech: One or both feet or knee is below the buttocks and presenting.

Predisposing Factors •

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Factors that make a diagnosis of breech presentation more likely can be maternal or fetal (Table 9.1). https://www.cambridge.org/core. 21 May 2021 at 20:20:26,

Passage • Placenta previa or cornual placental position • Fibroids in the lower uterine segment • Pelvic masses (e.g. ovarian cysts, pelvic kidney) • Abnormalities in the bony pelvis (congenital and acquired)

Key Implications •

•

Breech presentation at term is associated with worse neonatal outcomes when compared to cephalic presentation irrespective of the mode of delivery. This may reflect the fact that breech presentation is more likely in extreme prematurity and congenital malformation, both independently linked with worse neonatal outcomes. Meta-analysis of retrospective observational studies suggests that elective caesarean section for breech reduced the perinatal morbidity and mortality two- to four-fold when compared with vaginal birth. This could reflect that caesarean section avoids labour and shortens the pregnancy, which otherwise may progress past term. Both labour and prolonged pregnancy are independent risks to perinatal mortality and morbidity. The excess risk of a breech presentation alone may be as small as 1 per 1000 [1].

Breech Delivery

(a)

(b)

(c)

(d)

Figure 9.1 Types of breech. (a) Complete breech – flexion at hip and knee joints (elbows flexed too). (b) Extended breech – flexion at the hip but extension at the knee joint. (c) Footling breech – extension at both hip and knee joints. (d) Knee presentation. at 20:20:26,

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Intrapartum Emergencies

•

Table 9.3 Contraindications to assisted vaginal breech delivery

The term breech trial published in 2000 led to a widespread reduction in attempted vaginal breech birth and an increase in the use of elective caesarean for breech delivery. This has over the years led to a reduction in operator experience in vaginal breech birth and therefore a reduction in skilled operators confident in performing an assisted vaginal breech birth. The presence of a skilled operator is essential for a safe and successful vaginal breech delivery. A recent retrospective study of more than 15 000 women found no difference in long-term childhood outcomes including cerebral palsy, infant mortality and developmental delay later in childhood when comparing planned vaginal and planned caesarean breech birth [3]. The primary concern during a breech vaginal delivery is possible trauma and difficulty in delivering the after coming head, which tends to be the largest circumferential part of a baby. This may translate to mortality or morbidity for the baby.

•

•

Key Pointers •

A thorough antenatal assessment should be performed to identify factors that may decrease the chance of a successful breech vaginal delivery and increase the risk. Contraindications to an attempted vaginal breech delivery are detailed in Table 9.2. Based on the antenatal assessment women may be offered external cephalic version (ECV), elective caesarean section or a planned assisted vaginal breech delivery. There should be a documented discussion with the mother on the benefits and risks to her and the baby for each appropriate option. A summary of these can be found in Table 9.3. Appropriate case selection, operator skill and correct intrapartum management are determinants of a safe vaginal breech delivery. Mode of delivery for an undiagnosed breech attending in labour should be individualised.

•

•

•

• • • • • • • •

•

•

External cephalic version Spontaneous breech delivery Assisted vaginal breech delivery Total breech extraction Elective caesarean section

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Dilatation, contraindications to normal vaginal delivery, presence of an operator skilled in vaginal breech delivery, signs of fetal compromise and maternal choice should all be considered before making a decision. Oxytocin may be used in the first stage if contractions are inadequate and there are no signs otherwise of a feto-pelvic disproportion. The decision to start Syntocinon should be made by a senior clinician. If progress is still slow despite a short trial of Syntocinon, then a caesarean section is recommended. Oxytocin should be used with extreme caution in the second stage and only if contractions are genuinely suboptimal (fewer than 3–4 every 10 minutes, or short lasting) with no evidence of a mechanical cause. If the breech has not descended within 2 hours of a passive phase while the contractions have been adequate, then a caesarean section should be considered.

Key Actions General Principles for an Assisted Breech Delivery •

Table 9.2 Options for management of breech presentation

• • • • •

Any pre-existing contraindications to vaginal birth (e.g. placenta praevia, compromised fetal condition, uterine malformations) Inadequate pelvis (on clinical examination or prior radiological evidence, e.g. road traffic accident with pelvic fractures) Footling or kneeling breech presentation (Figure 9.1c, d) Large baby (usually defined as larger than 3800 g) Growth-restricted baby (usually defined as smaller than 2000 g) ‘Star-gazing’ appearance – hyperextended fetal neck in labour (diagnosed with ultrasound or X-ray where ultrasound is not available) Unavailability of a clinician trained in vaginal breech delivery, at the time of birth Previous caesarean section (relative contraindication)

•

A skilled multidisciplinary team should be available. This includes a senior obstetrician, senior midwives who have the skill and expertise in assisted vaginal breech birth, as well as an anaesthetist and the neonatal team. Confirm type and position of the breech, preferably using ultrasound. Identify the position

Breech Delivery

•

• •

•

of the descending sacrum as anterior or posterior and note the laterality. Although it may be possible to deliver the breech in a sacro-lateral position, assisted breech delivery should aim to keep the sacrum anterior to avoid the risks of deflexion and entrapment of the ‘after-coming’ fetal head. The delivery itself should be in a centre with skilled and experienced staff. It is not essential to conduct the delivery in operating theatres, though some clinicians may prefer this in case an emergency caesarean is required. Active pushing should not be commenced until the breech becomes visible at the perineum. The use of episiotomy during the delivery should be selective and based on how distensible the perineum is for the delivery. Routine use of episiotomy may not be required, for example, in a multiparous woman or a preterm baby. Continuous fetal monitoring should be employed throughout a breech labour as well as during delivery.

clockwise or anti-clockwise to bring the sacrum anteriorly (Figure 9.2). In the case of an extended breech, once the baby has been delivered up to the point of the umbilicus, the Pinard’s manoeuvre can be employed to safely deliver the legs. It should be noted that the knee joints are usually just at the introitus or just above when this manoeuvre would become appropriate to attempt safely, and the sacrum is kept anterior throughout. The Pinard’s manoeuvre uses one or two fingers to apply gentle pressure at the popliteal fossae in order to flex the knee, and then deliver the leg by abduction of the hip (Figure 9.3). Once the legs are delivered it is important to try and keep tactile stimulation of the baby or cord to a minimum and consider placing a towel over the baby to avoid cold

Conducting the Assisted Vaginal Breech Delivery The technique for delivering in this circumstance can be considered in three stages: • Delivery of legs and buttocks • Delivery of the trunk, arms and shoulders • Delivery of the ‘after-coming’ head

Delivery of the Legs and Buttocks Early, unnecessary intervention leads to poorer outcomes, and therefore lithotomy position should be avoided until the breech is clearly visible at the perineum without any retraction in between contractions [4]. The delivery of the buttocks and legs should occur as a result of good contractions and maternal effort with little or no hands on assistance required. The circumstance under which manual assistance will be needed is to keep the sacrum anterior, to help deliver the legs in the case of an extended breech or to perform an episiotomy if required. It is obvious that in cases of abnormalities noted on the fetal heart rate, an urgent action is needed to expedite birth. To minimise trauma the baby should be handled only over its bony parts (at the hip joint), and pressure or handling of the fetal abdomen should be avoided. To keep the sacrum anterior the hips can gently be held at the bony prominences of the iliac crests and the breech guided at 20:20:26,

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Figure 9.2 Holding the fetus at the hips to avoid soft tissue trauma (hepatic or splenic rupture).

Figure 9.3 The Pinard manoeuvre to deliver the limbs in an extended breech. Note the finger gently pressing on the popliteal fossa to enable flexion at the knee joint, followed by abduction and external rotation of the thigh to deliver the fetal lower limb.

59

Intrapartum Emergencies

stimulation. Any stimulation of the baby may result in a reflex extension of the head, which could later make the delivery of the after coming head more difficult. In addition, excessive stimulation of the skin by cold air may precipitate an in utero gasping reflex.

Delivery of the Trunk and Shoulders If the fetal monitoring suggests that the baby is not compromised, and continued progress with each subsequent contraction was observed, the fetus should be allowed to deliver using the hands-off approach to deliver the trunk and shoulders. Wait for the scapulae to become visible as the fetus is delivered. If the arms do not follow spontaneously and are palpable and flexed on examination, they can be hooked down with a finger at the elbow, sweeping the forearm across the fetus’ chest and delivering the arm. The sacrum should be kept anterior throughout. If the scapulae do not become obviously visible, consider that the arms may be nuchal, or extended. The extended arms will not be easily palpable, as they would be placed higher up in the pelvis. Lovset’s manoeuvre can be used to deliver the nuchal arms. This requires holding the baby with both thumbs on the sacrum and one index finger on each anterior superior iliac spine. The fetus can then be rotated anticlockwise 90 degrees to bring the right arm and shoulder to the symphysis pubis. One finger is used to sweep in front of the now visible shoulder and used to flex the arm at the elbow. Delivery of the forearm can then occur by sweeping it across the face and chest of the baby. The fetus should be held again by the sacrum and the anterior superior iliac spines in order to rotate the breech clockwise 180 degrees, bringing the left shoulder to the symphysis pubis. The same sequence described should be used to deliver the left arm before the baby is again rotated back to the starting sacrum anterior position (Figure 9.4). Once the trunk and shoulders are delivered the body should be gently supported, usually by being draped over the operator’s forearm, while awaiting the descent of the head. Signs of fetal compromise on fetal monitoring, poor fetal tone or colour during the delivery or a delay in progressive delivery of the trunk and shoulders should all prompt early assistance [1].

Delivery of the ‘After-Coming’ Fetal Head Once the trunk and shoulders are delivered, await the appearance of the nape of the fetal neck. On examination .011

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Figure 9.4 The Lovset manoeuvre to deliver the nuchal arms. Initial rotation of the shoulders 90° anticlockwise to bring the anterior shoulder under the symphysis pubis.

the chin will be facing the sacrum and occiput will be just below the symphysis pubis. At this point it becomes appropriate to employ manoeuvres to aide in the delivery of the head. The head should be delivered in the most controlled manner possible to avoid intracranial haemorrhage that are associated with sudden compression and decompression of the fetal head at delivery, leading to the rupture of the intracranial veins. The head will need to be kept in the flexed position for the easiest and least traumatic delivery and can be achieved by using either the Mauriceau–Smellie–Veit (MSV) manoeuvre or a forceps. A third manoeuvre, the Burns–Marshall technique, can also be used to deliver the fetal head but it is the least favourable option. This is because of concern over fetal trauma that may be caused by inadvertently hyperextending the fetal spine and neck [1]. The decision to use one particular method over another should be based on operator skill, and the availability of an assistant in the case of forceps and the individual clinical situation. There is currently no evidence base that supports one method in particular. The MSV manoeuvre involves the fetus being draped over one arm (usually the left), with the index and middle fingers of the same arm providing

Breech Delivery

Figure 9.5 The Mauriceau–Smellie–Veit manoeuvre to flex the head to facilitate the delivery of the ‘after-coming’ head. Flexion of the head by applying ‘forward’ pressure on the occiput and ‘backward’ pressure on malar eminences, while resting the fetal trunk on the accoucher’s forearms.

gentle pressure on either side of the fetal nose (the malar eminences of the maxilla). The operator’s other hand is used to further flex the fetal head at the occiput using one or two fingers. The head is therefore delivered with flexion and minimal traction (Figure 9.5). When using forceps to deliver the fetal head an assistant will be needed to support the body of the baby draped over her arm while the operator has her hands free to deliver the head. Any forceps with a long shank and handle may be used; Wrigley’s forceps are therefore not appropriate, as they are a short outlet forceps [5]. The forceps are applied from below the supported body of the baby, and the head delivered with flexion and minimal traction. A mediolateral episiotomy is strongly advised, as with any other forceps delivery, to avoid serious maternal perineal or anal sphincter trauma (Figure 9.6). The Burns–Marshall technique requires the body of the baby being swung over onto the maternal abdomen (similar to an arc of a circle) from a starting back anterior position. The baby is held by the feet and supported as it is gently swung towards the maternal abdomen until the mouth and nose become visible at the perineum; the head is then expected to follow. Although there is no evidence in the literature regarding trauma to the fetus as a result of using this method, it is theoretically plausible and more so than the other methods of head delivery described. The current RCOG guidelines do not support its use. at 20:20:26,

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Figure 9.6 Application of the forceps to deliver the after-coming head.

Managing Complications Complications associated with the conduct of assisted vaginal breech delivery are listed in Table 9.4. The delay in delivery of the after coming head is an obstetric emergency. The head should be delivered no more than 3 minutes after the umbilicus, or 5 minutes from the buttocks and legs avoid fetal hypoxia and ischaemic injury [1]. Any such delay encountered should prompt the use of additional manoeuvres to expedite and aid delivery. The delay could be either because of the nuchal arms that fail to deliver with Lovset’s manoeuvre, or the delay of the head after shoulders and arms are already delivered. However, there is an increased risk of umbilical cord compression between the maternal bony pelvis and the hard fetal head (Figure 9.7).

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Intrapartum Emergencies

Table 9.4 Potential complications of assisted vaginal breech delivery

• • • • • • •

Hypoxic–ischaemic injury due to umbilical cord compression or cord prolapse Prolonged labour (ineffective cervical dilatation by the ‘soft’ breech) Intracranial haemorrhage Injury to ‘intra-abdominal’ abdominal organs Fracture of the bones (humerus, clavicle, femur and neck) Nerve injuries (cervical plexus, brachial plexus, spinal cord) Dislocation of the jaw (mal-conducted MSV manoeuvre by placing the fingers inside the mouth instead of on the malar eminences)

If Lovset’s manoeuvre in unsuccessful in delivering the arms it may be possible to attempt to reach in to grab the elbow on either side and force to correct the extension of the shoulder, with the fetal back kept anterior or as a last resort force the arm across the face to deliver. These additional steps may be traumatic and result in clavicular or humeral fractures and should be used only when there is a real impending risk of hypoxic brain injury [5].

Entrapped Fetal Head If the fetal head is entrapped and the described methods do not work to deliver it, the McRoberts position or suprapubic pressure can be tried as next steps. If the cervix is not fully dilated, for example in a preterm delivery, consider a cervical incision at 4 and 8 o’clock landmarks [5]. Last resort steps to deliver an entrapped head would include a symphysiotomy if the operator is skilled in doing this, or a rapid caesarean section after the baby is pushed back up into the pelvis from below [5]. The use of a specially designed forceps for breech delivery, Piper’s forceps, may be useful in avoiding or managing an entrapped fetal head (Figure 9.8).

Umbilical Cord Prolapse

Figure 9.7 The risk of umbilical cord compression at the pelvic brim when the fetal head enters the maternal pelvis.

Finally, cord prolapse is a complication that can occur at any point during the delivery of a breech presentation, or even prior to delivery if the membranes rupture. A vaginal examination should be performed at any time should the membranes rupture to check for a prolapsed cord. This occurs most commonly with a footling presentation (10%–25%), where there is plenty of room around the presenting part for the cord to slip down [2]. A cord prolapse is usually an indication for an emergency caesarean section if it occurs with evidence of fetal compromise and/or delivery is not eminent, except in cases of the second twin, where a safe breech extraction may be performed. If delivery is eminent, the quickest and safest way to deliver may be vaginally, by a breech extraction.

Figure 9.8 Piper’s forceps specially designed for the delivery of the ‘aftercoming’ fetal head.

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Breech Delivery

Breech Delivery and Twins In the case of twins, if the presenting twin is breech the current evidence suggests that a planned caesarean by 37 weeks’ gestation is the safest mode of delivery [1]. If the woman attends in labour prior to her planned caesarean section then the safest delivery option may not be a caesarean section, and the decision on mode of delivery needs to be individualised, taking into account dilatation and other maternal and fetal risk factors or compromise. The case in which the presenting twin is cephalic and second twin is either breech or transverse (as is the case in up to 40% of twins), a vaginal delivery can be offered as a safe alternative to a planned caesarean section [6]. There is no compelling evidence at present that a planned caesarean is significantly better than a planned vaginal delivery in this situation, although women should be advised that even with a planned vaginal delivery the risk of requiring an emergency caesarean section is high. A total breech extraction can be performed to expedite delivery where the second twin exhibits evidence of fetal compromise after twin 1 has already been delivered. A breech extraction can also follow an internal podalic version (where the second twin is transverse) in similar circumstances or be performed at caesarean section for a transverse lie. In a total breech extraction one or both ankles are grasped and manual downward traction is applied (keeping the sacrum anterior) until both hips are delivered. The baby can then be grasped at the bony pelvis for further traction until scapulae become visible. The delivery can then be completed as described earlier with manoeuvres to deliver the arms and head. A total breech extraction is generally contraindicated in singleton vaginal breech delivery with evidence of fetal compromise when the fetus is at the higher station (above the ischial spines), because an emergency caesarean section is a much safer option, in this situation. However, if the breech is at the perineum, the decision to perform a breech extraction in a singleton vaginal breech delivery would depend on the skills and competency of the operator and the given clinical situation (e.g. an acute fetal compromise).

Breech Delivery at Caesarean Section Delivery of a breech baby at caesarean section employs the same principles described for an assisted vaginal delivery. The skin and uterine incisions should be generous enough to allow for manoeuvres

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that may be needed to aid a safe delivery. As the presenting part in this situation is much softer as opposed to when the presentation is cephalic, it can be easier to misjudge the required depth of the uterine incision. Injudicious uterine entry could result in laceration or fetal trauma. The breech or ankles should be grasped and delivered first, keeping the sacrum anterior. The delivery should then proceed as an assisted vaginal delivery with regards to delivery of the trunk, arms, and the ‘after-coming’ head. Gentle fundal pressure after the arms are delivered can help to flex the head and aid delivery of the head when used alongside MSM or forceps.

Key Pitfalls •

•

•

•

•

Generalising the current evidence with regards to vaginal breech delivery to the breech presenting in advanced labour, in a second twin, or at the thresholds of viability. In all of these circumstances, the ‘Term Breech Trial’, which assessed the maternal and perinatal outcomes between a planned vaginal birth and a planned elective caesarean section, at term, cannot be blindly applied. An emergency caesarean section may not be the optimal choice in these situations and may in fact increase the risk of neonatal or maternal morbidity. Failing to re-examine in theatre prior to spinal analgesia once a decision for emergency caesarean has been made may lead to an increase in maternal and fetal trauma, if the breech has descended significantly. If the breech is found to be at the perineum after the spinal analgesia has already been administered, maternal effort will be very limited and the delivery more challenging. Pulling or using traction during an assisted breech delivery. This could result in fetal trauma and extension of the fetal head. Handling of the fetus over the abdomen during delivery, resulting in trauma or more severely splenic or hepatic rupture. Failing to control the delivery of the after coming head to avoid sudden compression– decompression injury to intracranial veins.

Key Pearls •

Make an antenatal assessment to determine if an assisted vaginal breech delivery is suitable. Discuss all appropriate options with the woman including

Intrapartum Emergencies

•

•

risks and benefits, and clearly document this in the handheld notes. If the chosen management of the breech presentation is an elective caesarean section or ECV, discuss an agreed on plan to follow in the event of spontaneous labour or rupture of membranes prior to the date set for the procedure(s). Document this plan clearly in the handheld notes. Ensure skilled and competent staff are available to conduct or oversee the assisted vaginal breech

•

•

delivery, and that an emergency theatre and team is available during the delivery should you require them. The neonatal team should be present at the delivery. Use abdominal ultrasound to diagnose nuchal arms or an extended neck prior to active pushing. Handle the fetus only over the bony prominences to avoid soft tissue trauma.

Exclude Contraindications

Early Labour

CTG monitoring Adequate analgesia (an epidural is recommended) Ensure adequate progress Judicious use of oxytocin

Emergency caesarean section for suspected fetal compromise or failure to progress despite the judicious use of oxytocin

Advanced Second Stage (>+2)

Recommend assisted vaginal breech birth with continuous electronic fetal heart rate monitoring (CTG)

Ensure skilled and competent operator able to perform a breech extraction, Pinard’s, Lovset’s, MSV manoeuvres, or forceps delivery, if required. Emergency caesarean section only in exceptional circumstances Figure 9.9 Algorithm for intrapartum management of breech presentation. Downloaded from https://www.cambridge.org/core. 21 May 2021 at 20:20:26, https://www.cambridge.org/core/terms. https://doi.org 11

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Breech Delivery

•

Be vigilant for any delay during the delivery. Be prepared to promptly use additional manoeuvres for nuchal arms or a slow after coming head. Aim for no more than a 5- to 6-minute interval from the delivery of the breech to the after coming head. This is essential if a ‘physiological approach’ to breech birth is being used. • Bring a scribe to record events throughout the delivery as they happen so that you can later document with accuracy. Debrief the parents at the end. • Recent 10-year experience from large tertiary centre has suggested that with better training on internal podalic version (IPV) with breech extraction and improving the skills in cardiotocograph (CTG) interpretation, the rate of second stage caesarean section for the second twin presenting by breech can be reduced [7]. An algorithm for intrapartum management of breech presentation is shown in Figure 9.9.

References 1. Royal College of Obstetricians and Gynaecologists. Management of Breech Presentation. Green top guidelines No. 20b. London: RCOG; 2017. 2. Winter C, Crofts J, Laxton C, Barnfield S, Draycott T. PROMPT Course Manual, 2nd ed. Cambridge: Cambridge University Press; 2012, 179–91. 3. Bin YS, Ford JB, Nicholl M, Roberts C. Long-term childhood outcomes of breech presentation by intended mode of delivery: a population record linkage study. Acta Obstet Gynecol. 2017;96(3):342–51. 4. Edmonds K. Dewhurst’s Textbook of Obstetrics and Gynaecology, 8th ed. Chichester: Blackwell Science; 2012.

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5. Paterson-Brown S, Howell C. Managing Obstetric Emergencies and Trauma, 3rd ed. Cambridge: Cambridge University Press; 2016, 405–13. 6. Barrett JF, Hannah ME, Hutton EK, Willan AR, Allen AC, Armson BA, et al. Twin Birth Study Collaborative Group. A randomized trial of planned cesarean or vaginal delivery for twin pregnancy. N Engl J Med. 2013;369:1295–305. 7. Rzyska E, Ajay B, Chandraharan E. Safety of vaginal delivery among dichorionic diamniotic twins over 10 years in a UK teaching hospital. Int J Gynaecol Obstet. 2017;136(1):98–101.

Further Reading Azria E, Le Meaux JP, Khoshnood B. Factors associated with adverse perinatal outcomes for term breech fetuses with planned vaginal delivery. Am J Obstet Gynecol. 2012;207 (4):285.e1-9. Goffinet F, Carayol M, Foidart JM, Alexander S, Uzan S, Subtil D, et al. Is planned vaginal delivery for breech presentation at term still an option? Results of an observational prospective survey in France and Belgium. Am J Obstet Gynecol. 2006;194(4):1002–11. Fruscalzo A, Londero AP, Salvador S, Bertozzi S, Biasioli A, Della Martina M, et al. New and old predictive factors for breech presentation: our experience in 14 433 singleton pregnancies and a literature review. J Matern Fetal Neonatal Med. 2014;27(2):167–72. Londero AP, Salvador S, Fruscalzo A, et al. First trimester PAPP-A MoM values predictive for breech presentation at term of pregnancy. Gynaecol Endocrinol. 2013;29(5):503–7. Royal College of Obstetricians and Gynaecologists. Caesarean Section Consent Advice No.7. London: RCOG; 2009. Vistad I, Klungsoyr K, Albrechtsen S, Skieldestad F. Neonatal outcome of singleton breech deliveries in Norway from 1991 to 2011. Acta Obstet Gynecol Scand. 2015;94 (9):997–1004.

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Umbilical Cord Prolapse Malik Goonewardene

Key Facts Definition Descent of the umbilical cord through the cervix, in the presence of ruptured membranes [1].

Incidence Varies from 0.1% to 0.6% (1–6 per 1000) [2]. Cord presentation occurs if the cord is below the presenting part but membranes are intact (Figure 10.3).

Types Overt: If the cord is below the presenting part and in the vagina or outside vulval introitus (Figure 10.1). Occult: If the cord is lying alongside the presenting part (Figure 10.2).

Figure 10.3 Cord presentation.

Figure 10.1 Overt cord prolapse.

Key Implications Cord prolapse is an obstetric emergency with a high risk of perinatal mortality (ca. 6%) [1, 2]. Perinatal hypoxia, resulting from prolonged compression and mechanical occlusion of the prolapsed cord (e.g. by the fetal head which is presenting) or by vasospasm due to the relatively cooler temperatures in the vagina and especially outside the vulval introitus, is the leading cause of perinatal death [3, 4]. Babies who survive may have cerebral palsy resulting from hypoxic ischaemic encephalopathy [5]. Cord prolapse occurring at home is associated with a higher risk of perinatal deaths [5].

Figure 10.2 Occult cord prolapse. Arrow on right points to loop of umbilical cord protruding lying alongside the fetal head that may be easily missed on vaginal examination and hence, it is called ‘occult’ cord prolapse. Arrow on left (centre) shows fetal head (presenting part) lying alongside the umbilical cord. .012

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Key Pointers Presenting part of the fetus not fitting into the maternal pelvic inlet (e.g. small preterm baby or

Umbilical Cord Prolapse

twin; especially the second twin, transverse lie, malpresentation such as footling or flexed breech, and polyhydramnios). Grande multiparity, maternal pelvic abnormalities, relatively long cord or low placental implantations and male fetuses [1–3]. Obstetric interventions such as amniotomy, stabilising induction, insertion of a supracervical balloon catheter for induction of labour, placement of internal monitoring devices, external cephalic version (ECV) and internal podalic version [6]. Intrapartum spontaneous rupture of membranes with advanced cervical dilation and high presenting part of fetus.

Key Diagnostic Signs Prediction Routine abdominal real-time colour Doppler ultrasound scan examination has not been shown to be effective in antenatal diagnosis of cord presentation and predicting the possibility of cord prolapse [7]. Selective transvaginal scanning in women with high-risk factors such as a transverse lie, malpresentation (e.g. footling or flexed breech) or high presenting part of fetus, may be useful [8].

Prevention Women with a transverse or oblique lie or breech presentation should be offered an ECV at 37 weeks’ gestation. Women with persistent breech presentation or transverse, oblique or unstable lie should be offered admission to hospital at 38 weeks’ gestation. If this advice is declined, women should be advised immediate admission with any signs of labour or prelabour (prolonged) rupture of membranes (PROM) [2, 3]. During labour the presence of the cord should be looked for, at each vaginal examination. Amniotomy is contraindicated if the cord is palpable below or by the side of the presenting part during vaginal examination. Upward pressure and dislodging the head from the pelvis should be avoided during amniotomy, and amniotomy should be avoided if the presenting part of the fetus is high and mobile [2, 3]. Women with unstable lies should be offered ripening of the cervix and stabilising induction of labour after 39 weeks’ gestation unless the cervix is favourable for induction by amniotomy and oxytocin at 20:20:26, .012

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infusion at that gestation. This involves external cephalic version (ECV) followed by an intravenous oxytocin infusion to stimulate uterine contractions that would stabilise the fetal head against the pelvic inlet, and then a careful controlled amniotomy after excluding a palpable cord. The same procedure could be adopted in cases of mild to moderate hydramnios. An assistant should steady the fetal head against the pelvic inlet during and after amniotomy. The amniotomy should be by minimal puncture and the fingers should be kept inside the vagina to carefully control the volume of liquor draining out. This will prevent the liquor gushing out and the fetal head floating away from the inlet, predisposing to cord prolapse.

Diagnosis The possibility of cord prolapse should always be kept in mind in a woman with a risk factor for cord prolapse because signs of fetal distress may not occur immediately after cord prolapse. Women with PROM should be offered a speculum examination irrespective of the period of gestation. A digital vaginal examination is best avoided if there is no cardiotocograph (CTG) abnormality or risk factors for cord prolapse [2]. A digital vaginal examination is indicated in the presence of PROM or preterm PROM (PPROM) with CTG abnormalities such as variable decelerations, prolonged decelerations and bradycardia and a suspicion of cord prolapse [3]. The cord may be visible outside the vulva or at the introitus or may be seen on speculum examination or felt on vaginal examination.

Key Actions Initial Management Additional help (obstetric colleagues, nurses and midwives) should be called for immediately, and the anaesthesiologist and neonatologist (and the fetomaternal specialist if the gestational period is 24–28 weeks) informed. The aim is to prevent or minimise fetal hypoxia, resulting from mechanical compression or vasospasm of the prolapsed cord, until the delivery is achieved. Establish whether the fetus is alive by palpating for cord pulsations or using the fetal (Pinard’s) stethoscope or hand-held Doppler fetal heart detector or CTG and ultrasound scan (USS), depending on the

Intrapartum Emergencies

Figure 10.4 Head low position.

Figure 10.5 Knee–chest position.

facilities available. If USS facilities are available, visualisation of the fetal heartbeat is a possibility even if the fetal heart sounds cannot be detected [9]. If the fetus is dead, delivery is not urgent and the safest mode of delivery for the mother should be adopted. If the fetus is alive the measures described in the text that follows should be adopted. The mother should be placed in a head low (Trendelenburg) position (Figure 10.4) or in the ‘knee–chest’ position (Figure 10.5). The mother should be counselled regarding the problem and the plan of action, and verbal consent obtained for further management including caesarean delivery [2, 3]. If the cervix is not fully dilated and an assisted or operative vaginal delivery is not feasible within the next 15 minutes or so, the following steps are indicated [2, 3, 10–12]. The fetal presenting part should be manually displaced away from the pelvic inlet to prevent the cord being compressed between the pelvic wall and the presenting part of the fetus. This could be achieved digitally through the vagina (especially if the cord Downloaded from https://www.cambridge.org/core. 21 May 2021 at 20:20:26, https://www.cambridge.org/core/terms. https://doi.org 12

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Figure 10.6 Displacement of the presenting part away from the pelvic inlet.

prolapse occurs during vaginal examination or amniotomy) and maintained abdominally by an assistant thereafter (Figures 10.6 and 10.7). The cord should be gently cradled in the hand and replaced within the vagina (Figure 10.8), and a gauze towel, vaginal pack or tampon soaked in warm saline should be inserted into the vagina below the cord, if it tends to come out of the introitus. Using a Foley catheter and an IV infusion set the bladder should be filled with 500–750 mL of normal saline, until it is visibly distended above the pubic symphysis, and then the catheter should be clamped (Figure 10.9). The full bladder will relieve the pressure on the cord by moving the presenting part away and may also inhibit uterine contractions. An assistant should insert a 14 or 16 G intravenous cannula if it is not already in place, obtain blood for group and save and full blood count (FBC), and commence a Ringer’s lactate or normal saline infusion. If the woman is on an intravenous oxytocin infusion it should be stopped.

Umbilical Cord Prolapse

Figure 10.7 Maintaining displacement of the presenting part away from the pelvic inlet.

Oxygen should be given by face mask, 8 L/minute. Tocolytics (terbutaline 0.25 mg subcutaneously) may be of value in cases with fetal bradycardia or pathological decelerations. Measures to relieve compression of the cord should be continued during transfer of the woman to the operating theatre but they should not unduly delay the transfer. If the cord prolapse occurs at home: The woman should adopt the knee–chest position (Figure 10.5) until an ambulance arrives. Medical assistants need to ensure that the presenting part is displaced away from the pelvic inlet, replace cord within the vagina and fill the bladder (Figures 10.6–10.9). The woman should be in a head low, left lateral position with pillow under pelvis during transfer (Figure 10.10).

Figure 10.8 Replacement of cord within the vagina. Figure 10.9 Filling the bladder.

Figure 10.10 Head low left lateral position for transfer to hospital.

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Definitive Management Reconfirmation that the fetus is alive [1, 2]. If suitable for an assisted breech delivery, breech extraction, vacuum or forceps delivery, it should be carried out urgently [2]. Emergency caesarean delivery would be indicated in most instances if the fetus is alive, as cord prolapse frequently occurs prior to full dilation of the cervix [10–12]. It has been suggested that a calm approach should be taken and intrauterine resuscitation with 100% oxygen, elevation of presenting part and maternal positioning with head low, left lateral position to enable spinal analgesia, is a suitable procedure and that the ‘emergency’ situation could be converted to an ‘urgent’ situation [13]. This could be the case if there is no acute, severe ‘fetal distress’. The bladder should be emptied by removing the clamp on the Foley catheter, prior to opening into the peritoneal cavity at caesarean delivery, ideally carried out within 30 minutes of diagnosis to improve perinatal outcome [2, 3]. Although diagnosis to delivery intervals (DDIs) of more than 60 minutes may be associated with adverse perinatal outcomes, it has been shown that the perinatal outcomes are poorly correlated with the cord pH of the neonates in women who are delivered within 30 minutes, even in wellresourced settings [2, 12]. This suggests that in addition to decreasing the DDI, in utero resuscitation may be needed to reduce the effects of cord compression and improve the perinatal outcome. Facilities for immediate resuscitation and intensive care should be ready prior to delivery. However, differed cord clamping can be considered if the neonate is not asphyxiated at birth. Paired umbilical arterial and venous cord blood samples should be obtained immediately after birth for blood gas assessments [2, 3].

Conservative Management: In Cases of Extreme Prematurity This may be considered with parental consent if the fetus is alive, has no gross fetal anomalies and PPROM with cord prolapse has occurred at the limits of gestational viability (ca. 24–26 weeks) [2, 3]. Decision depends on neonatal facilities available in the centre. An in-depth discussion involving the obstetrician, feto-maternal specialist, neonatologist, the woman and her partner is needed regarding chances of .012

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unexpected fetal demise, chances of survival if delivered earlier rather than later and the risks of long-term morbidity due to extreme prematurity. The cord should be gently cradled in the hand and replaced in the vagina, and the woman placed in the Trendelenburg position and managed as described in the section on initial management. In utero transfer to a centre with better neonatal facilities (the concern of cord spasm and fetal demise during the transfer should be explained) is recommended for all preterm breech presentations admitted in labour. If the woman is in advanced labour, then it is best to deliver, and then arrange an urgent ex utero transfer to a centre with appropriate neonatal facilities. A gauze towel or tampon soaked in warm saline should be inserted into the vagina if the cord tends to come out of the vulval introitus (especially during bowel motions with prolonged conservative management), to keep the cord warm and moist within the vagina and to prevent it going into spasm. The gauze/ tampon needs to be removed just prior to delivery. Antibiotics, tocolytics and corticosteroids can be administered as per PPROM management if it is decided to have prolonged conservative management [14]. In cases in which a prolonged conservative approach is adopted because of extreme prematurity, maternal wellbeing should have precedence over the fatal outcome. The mother and fetus need very close monitoring and labour should be induced in cases of fetal demise. A caesarean delivery will be needed if chorioamnionitis is suspected, fetal distress is detected or spontaneous labour is established.

Post Delivery Parents, especially the mother, may be greatly affected psychologically. Adequate debriefing and counselling of parents are needed. Cord prolapse needs to be documented, reported and discussed at the next risk-management meeting.

Suggested Management of Cord Prolapse in Low-Resource Settings In Nigerian women with cord prolapse, perinatal mortality rates of up to 68% have been reported, and

Umbilical Cord Prolapse

up to 76% of the associated fetal deaths have been reported to occur prior to admission to hospital. Inadequate prenatal care was reported to be a highrisk factor for the occurrence of cord prolapse in these women [15]. The following actions are suggested for the management of cord prolapse in low-resource settings. • Health education in the community and motivation of pregnant women to attend prenatal clinics • Education of all prenatal caregivers regarding the key risk factors for cord prolapse • Education of all maternity caregivers regarding the possible measures that could be taken to prevent cord prolapse • Education of women and any available caregivers in the community that women with PPROM, PROM or in labour should ideally lie flat, in left lateral position with a pillow under their hips (Figure 10.10) and be transported to hospital as soon as possible • On arrival in hospital, establishing the viability of the fetus and adapting the management algorithm in Figure 10.11 according to the resources available, and carrying out the most appropriate actions • Training all the staff involved in maternity care in the management of cord prolapse and conducting refresher training courses annually.

Key Pitfalls • •

• •

•

•

Failure to appreciate that fetal distress does not always occur immediately after cord prolapse. Failure to appreciate that the fetus may still be alive although the fetal heart sounds are not detectable. Failure to carry out a speculum examination in PROM and PPROM. Carrying out amniotomy with a high head or when the fetal head is not fitting the pelvic inlet or dislodging the head upwards during amniotomy. Failure to exclude cord presentation or occult cord prolapse during early intrapartum vaginal examination. Failure to relieve compressions and vasospasm of cord prior to emergency delivery. Multidisciplinary training has been shown to improve overall management and reduction of decision to delivery interval (DDI)[16].

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Key Pearls • • •

•

• •

Cord prolapse is a life-threatening situation for the fetus. Immediately call for help and also request that the anaesthesiologist and neonatologist be informed. Anticipating cord prolapse in women with presenting part away from the pelvic inlet and gently replacing the cord within the vagina are essential primary steps in the management. Bladder filling maintains displacement of fetal presenting part away from the pelvic inlet and prevents cord compression. Tocolysis may be useful. Emergency caesarean delivery is frequently needed but assisted or operative vaginal delivery may be possible if the cervix is fully dilated. Post delivery debriefing and counselling of parents and risk management discussions are needed. Immediate displacement of the fetal presenting part is needed. Regular multiprofessional training programmes on the management of cord prolapse need to be conducted.

Training and Assessment Courses have been designed to enable simulation training of the multiprofessional obstetric team to manage obstetric emergencies including cord prolapse [10, 11]. Training has been found to improve clinical knowledge and skills as well as team working and result in better outcomes

A Suggested Training Scenario A primigravida at 38 weeks’ gestation is admitted to the labour ward in advanced labour. The fetal head is three-fifths palpable abdominally, and the fetal heart rate is 125 bpm and regular. You proceed with a vaginal examination and find that the cervix is 6 cm dilated and the membranes are bulging. The membranes spontaneously rupture during your vaginal examination, and the cord prolapses out of the vagina. The following equipment will be available for the drill: Delivery bed Obstetric manikin with perineum, baby with cord Fetal (Pinard’s) stethoscope

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FETUS ALIVE

Cervix not fully dilated

Relieve compression and prevent vasospasm of cord 1. Head low (Trendelenburg) position Knee–chest position Head low, left lateral position with pelvis elevated 2. Oxygen by face mask 8 L/minute 3. Manual elevation of presenting part vaginally/abdominally 4. Replace cord within vagina 5. Fill bladder (500–750 mL normal saline) 6. Warm, wet gauze towel or tampon to keep cord inside vagina (– if needed)

Cervix fully dilated

• Vacuum delivery • Forceps delivery • Assisted breech delivery • Breech extraction

Transfer to OT, maintaining relief of cord compression

Reconfirm fetus alive (US scan if possible, if in doubt)

Emergency caesarean section - Empty bladder before entering peritoneal cavity - Neonatal resuscitation and intensive care ready

Documentation, debriefing and counselling parents

Incident reporting and risk management discussion

Regular multiprofessional simulation training in management of cord prolapse Figure 10.11 Algorithm for the management of umbilical cord prolapse.

Hand-held Doppler fetal heart detector, CTG machine, US scanner (depends on centre) Intravenous cannulae without needles, normal saline packs Blood transfusion set, Foley catheter .012

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Face mask and oxygen source, cushion Case notes, drug chart Terbutaline and salbutamol vials, ranitidine and metoclopramide vials, disposable syringes without needles

Umbilical Cord Prolapse

• Any high-risk factors for cord prolapse ? • Spontaneous labour with a high head and increased liquor?

Anticipate

• Every VE – palpate for and exclude cord presentation/prolapse • Careful amniotomy

• PROM or PPROM with risk factor for cord prolapse

Suspect

• PROM or PPROM with CTG abnormality

Speculum examination

Diagnose

Cord visible/seen with speculum/felt on VE

Call for help

Obstetric colleagues/nurses/midwives

Inform

-

Anaesthesiologist

-

Neonatologist

-

Feto-maternal specialist (24–26 weeks’ gestation)

• Fetus alive? (cord pulsations, fetal stethoscope,

Establish condition

hand-held Doppler, CTG, US scan) • Cervix fully dilated? • Confirmed by US scan if possible

Fetus alive

Fetus dead

• Mode of delivery safest for mother • Not urgent

Counsel woman and partner - Problem - Plan of action - Obtain verbal consent for further action including caesarean section Figure 10.11 (cont.)

The trainer will ask the trainee ‘What will you do?’ The expected responses and actions would be: Call for help. Relieve compression and prevent vasospasm of cord. Immediately elevate the fetal head digitally and disimpact it from the pelvic inlet. at 20:20:26,

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While maintaining the above, instruct an assistant to adjust the delivery bed to a head-low position and place the mother in the Trendelenburg position or place the woman in the knee–chest position. Instruct an assistant to abdominally ensure that the displacement of the fetal head is maintained. Cradle the cord gently in the palm and replace it within the vagina.

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Intrapartum Emergencies

Insert a Foley catheter and fill the bladder with 500– 750 mL of normal saline using an IV infusion set, until the bladder is palpable supra-pubically. During this time other members of the team should: Insert a 16 G intravenous cannula and obtain blood for group and save and FBC. Inform the operating theatre and the anaesthesiologist. Inform the neonatologist and the neonatal intensive care unit. Commence oxygen by face mask 8 L/min. Recheck the fetal condition: palpating for cord pulsations, fetal stethoscope, hand-held Doppler, fetal heart detector, CTG and/or US depending on the facilities available and confirm that the fetus is alive. Explain to the woman and her partner the problem, the state of the fetus and the proposed plan of action and obtain verbal consent for a caesarean delivery. Administer terbutaline 0.25 mg subcutaneously. Administer ranitidine 50 mg and metoclopramide 10 mg intravenously. Transfer to the operating theatre for emergency caesarean section, maintaining the woman’s head at a lower level than her pelvis. Chronologically document accurately all the preceding steps. The training programme should consist of a preliminary lecture based on the key facts, key implications, key pointers, key diagnostic signs, key actions, key pitfalls and key pearls. This should be followed by the case scenario and drill. At the end of the drill the participants should be requested to identify what they did well and what they think they should improve on. The trainer should then give them feedback as to what they did well and what they could improve on. The drill should be repeated after these inputs until the trainer is satisfied that the team could efficiently manage a cord prolapse. The team too should be confident about their ability to manage a cord prolapse in real life. An effective training programme will lead to the trainees performing the required clinical tasks in a coordinated manner, communicating with each other well and working as a team with a clear understanding of individual roles and responsibilities. Frequent rehearsals will need to be conducted until the multiprofessional team acquires adequate skills. This should be followed by annual refresher training sessions [2, 3]. Downloaded from https://www.cambridge.org/core. 21 May 2021 at 20:20:26, https://www.cambridge.org/core/terms. https://doi.org 12

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Acknowledgements Doctors Myuru Manawadu and D. V. Priyaranjana of the Department of Obstetrics and Gynaecology, University of Ruhuna, Sri Lanka contributed the figures.

References 1. Lin MG. Umbilical cord prolapse. Obstet Gynaecol Surv. 2006;61(4):269–77. 2. Royal College of Obstetricians and Gynaecologists. Umbilical Cord Prolapse. Green-top Guideline No. 50. London: RCOG, 2014. 3. Institute of Obstetricians and Gynaecologists, Royal College of Physicians of Ireland and the Clinical Strategy and Programmes Division, Health Service Executive. Clinical Practice Guideline Cord Prolapse. Guideline 35. 2015. 4. Gibbons C, O’Herlihy C, Murphy JF. Umbilical cord prolapse: changing patterns and improved outcomes. BJOG. 2014;121:1705–9. 5. Johnson KC, Daviss BA. Outcomes of planned home birth with certified professional midwives: large prospective study in North America. BMJ. 2005;330:1416–22. 6. Dilbaz B, Ozturkoglu E, Dilbaz S, Ozturk N, Akin Sivaslioglu A, Haberal A. Risk factors and perinatal outcomes associated with umbilical cord prolapse. Arch Gynaecol Obstet. 2006;274:104–7. 7. Ezra Y, Strasberg SR, Farine D. Does cord presentation on ultrasound predict cord prolapse? Gynaecol Obstet Invest. 2003;56:6–9. 8. Kinugasa M, Sato T, Tamura M, Suzuki H, Miyazaki Y, Imanaka M. Antepartum detection of cord presentation by transvaginal ultrasonography for term breech presentation: potential prediction and prevention of cord prolapse. J Obstet Gynaecol Res. 2007;33(5):612–18. 9. Driscoll JA, Sadan O, Van Geideren CJ, Holloway GA. Cord prolapse: can we save more babies? Br J Obstet Gynaecol. 1987;94:594–5. 10. Sowter M, Weaver E, Beaves M, eds. Practical Obstetric Multi-Professional Training (PROMPT) Course Manual. Australian and New Zealand Edition. Melbourne Australia: PROMPT Maternity Foundation and the Royal College of Obstetricians and Gynaecologists, London, Royal Australian and New Zealand College of Obstetricians and Gynaecologists; 2014, 117–24. 11. Paterson-Brown S, Howell C, eds. Managing Obstetric Emergencies and Trauma – the MOET Course Manual, 3rd ed. London: Cambridge University Press; 2017, 233–7.

Umbilical Cord Prolapse

12. Department of Health, Government of South Australia. South Australian Perinatal Practice Guidelines: Cord Presentation and Prolapse, 2014. 13. McKeen D, Geeorge RB, Shukla R. We ‘can do it’ does not mean we ‘should do it’: obesity, umbilical cord prolapse, and spinal anesthesia in the knee-chest position. Can J Anesthes. 2009;56:168–9. 14. Royal College of Obstetricians and Gynaecologists. Preterm Prelabour Rupture of Membranes. Green-top Guideline No. 44. London: RCOG, 2006.

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15. Enakpene CA, Odukogbe AT, Morhason-Bello IO, Omigbodun AO, Arowojulu AO. The influence of health-seeking behavior on the incidence and perinatal outcome of umbilical cord prolapse in Nigeria. Int J Womens Health. 2010;9(2):177–82. 16. Siassakos D, Hasafa Z, Sibanda T, Fox R, Donald F, Winter C, Draycott T. Retrospective cohort study of diagnosis-delivery interval with umbilical cord prolapse: the effect of team training. Br J Obstet Gynaecol. 2009;116:1089–96.

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11

Fetal Compromise Diagnosis and Management Anna Gracia Perez-Bonfils and Edwin Chandraharan

Key Facts • Increasing strength, frequency and duration of uterine contractions during labour may reduce oxygenation to the utero-placental bed, increasing the risk of intrapartum hypoxia. o Intrapartum hypoxia and subsequent metabolic acidosis may lead to short-term complications such as admission to neonatal unit, hypoxic ischaemic encephalopathy (HIE) and neonatal death or long-term implications such as learning difficulties or in the worst case scenario, cerebral palsy. There is a wide range of neurological damage, some of which may not be obvious at birth, but may manifest later as functional disabilities. • According to current scientific evidence, the vast majority of fetuses are damaged antenatally or postnatally. Intrapartum hypoxia accounts for up to 30% of all cases of cerebral palsy and long-term neurological sequelae. • Fetuses with chronic utero-placental insufficiency (intrauterine growth restriction), congenital or acquired infection (chorioamnionitis) or pre- or post-maturity may have less physiological reserves to deal with intrapartum hypoxic insults. • Intrapartum sentinel hypoxic events such as uterine scar dehiscence (or rupture), placental abruption or cord prolapse may cause acute hypoxic injury. • The main aim of fetal monitoring is to timely identify and hence salvage fetuses that are at risk of intrapartum hypoxic injury, while avoiding unnecessary operative intervention to fetuses who are normoxic or those who are mounting a good compensatory response. • As a test of intrapartum hypoxia, cardiotocograph (CTG) interpretation based purely on pattern recognition has a very high false positive rate (approximately >90%). There is a significant intraand inter-observer variation and the positive predictive value of abnormal features of a CTG for intrapartum hypoxia is less than 30% [1, 2]. Since

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its introduction into clinical practice in late 1960s there has been an increase in operative interventions during labour without any noticeable reduction in the rates of perinatal deaths or cerebral palsy. • Except in cases of acute hypoxia, management decisions should not be taken based on CTG patterns alone. Interventions should be based on understanding the wider clinical picture, fetal reserves and compensatory mechanisms. • According to a Cochrane systematic review in 2017 [3], compared with intermittent auscultation, continuous cardiotocography showed no significant improvement in overall perinatal death or cerebral palsy rates but was associated with halving neonatal seizure rates. There was an increase in caesarean sections and instrumental vaginal births. Intermittent auscultation therefore is appropriate for use in the low-risk setting.

Key Implications •

•

•

•

The cardiotocograph (CTG) has been used for fifty years to identify intrapartum hypoxia and when CTG was introduced into obstetric practice it was hoped that it would help reduce the cerebral palsy (CP) rate. Unfortunately, the incidence of CP has remained fairly stable over the last 50 years, whereas there has been a significant increase in the incidence of operative delivery since the introduction of CTG [3]. The 4th Confidential Enquiries into Stillbirths and Deaths in Infancy (CESDI) report in 1997 [4] concluded that issues with interpretation and failure to act when a CTG abnormality was detected may have contributed to more than half of all intrapartum related deaths. Lack of knowledge to interpret CTG traces, failure to incorporate the wider clinical picture (meconium staining of amniotic fluid, intrapartum bleeding, maternal pyrexia, pre- and

Fetal Compromise: Diagnosis and Management

Temperature Drugs

Human factors Birth trauma

Mechanical compression

Hypoxia

Vagal stimulation

Type Fetal reserve

Fetal compensatory mechanisms CTG changes

Maturity

Delays Communication Lack of knowledge

Rapidity of onset

Inflammation Perinatal outcome

Meconium

Duration

Figure 11.1 The CTG complexogram. Source: Ref. [5].

•

•

•

•

post-maturity), failures in communication and team working as well as delay in action contribute to intrapartum injury [5] (see Figure 11.1). CTG interpretation based on ‘pattern recognition’ leads to unnecessary interventions as well as lack of action, as all the CTG patterns of fetal neurological injury are not currently known. Moreover, the ‘specific’ CTG patterns are not consistently present in all cases. It is therefore essential to understand the pathophysiology of intrapartum fetal hypoxia to improve outcomes and to reduce unnecessary interventions, rather than reacting to ‘CTG patterns’ [6]. The STAN (ST Analyser) is a technology developed to assess the oxygenation of the fetal heart that notifies the switch to anaerobic metabolism in the myocardium secondary to an ongoing hypoxia. A recent meta-analysis including six randomised controlled trials (26,446 women) concluded that there was a 36% reduction in the rate of neonatal metabolic acidosis when using STAN. In addition, there was a statistically significant reduction in operative vaginal delivery rate and the use of fetal blood sampling [7]. Two randomised controlled trials have recently been conducted to determine whether the use of a decision support software to assist the interpretation of CTG improves perinatal or maternal outcomes. The INFANT (INtelligent Fetal AssessmeNT) trial included 46,042 women and the results did not support the hypothesis. The FM alert trial (a

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randomised clinical trial of intrapartum fetal monitoring with computer analysis and alerts versus previously available monitoring) included 7730 women and access to computer analysis of CTGs resulted in the lowest incidence of newborn metabolic acidosis ever reported in randomised controlled trials, but the difference was not statistically significant. Therefore, current scientific evidence does not support the use of computerised CTG interpretation during labour [8, 9].

Key Pointers • •

•

•

Recognition of the fetus that is at an increased risk of intrapartum hypoxic insult: Prematurity and postmaturity, intrauterine growth restriction, maternal disorders (severe preeclampsia, diabetes mellitus, immunological disorders such as systemic lupus erythematosus), maternal infections including pyrexia with or without clinical chorioamnionitis. Recognition of markers of sentinel hypoxic events during labour: fresh thick meconium, intrapartum bleeding, prolonged or sudden cessation of uterine contractions. Erroneous monitoring maternal heart rate is sadly not an uncommon error. High index of suspicion must be exercised to avoid this pitfall. A sudden improvement of the CTG trace with disappearance of decelerations as well as presence of accelerations, especially during the second stage of labour, should raise an alarm.

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Key Diagnostic Signs Intrapartum hypoxia should be suspected when there are changes in the baseline heart rate (i.e. below 110 beats/minute or above 160 beats/minute) and/or presence of decelerations (on auscultation for 1 minute after a uterine contraction) on intermittent auscultation. Similarly, if any of the following risk factors are present (Table 11.1), continuous electronic fetal monitoring (CEFM) using a CTG should be commenced.

CTG Interpretation Commencing CTG Monitoring: Getting the Basics Right The Machine and the Trace The patient’s details and maternal pulse should be recorded at the beginning of the trace. Table 11.1 Indications for continuous electronic fetal heart rate monitoring in labour

Maternal problems Any condition that increases the risk of utero-placental insufficiency, including: Induced labour Diabetes Prolonged rupture of membranes (>24 hours) Antepartum haemorrhage (placental abruption) Previous caesarean section (scar dehiscence) Preeclampsia (placental insufficiency) Post-term pregnancy (>42 weeks) Other maternal medical disease (systemic lupus erythematosus, renal disease)

Fetal problems Any condition that reduces fetal blood flow or compromises fetal response to hypoxic insults: Prematurity Oligohydramnios (possible cord compression/utero-placental insufficiency) Fetal growth restriction Abnormal Doppler artery velocimetry Multiple pregnancy Meconium-stained liquor Intrauterine infection

Intrapartum risk factors Events that occur in labour and rapidly reduces fetal oxygenation: Vaginal bleeding in labour (abruption, vasa praevia) Oxytocin augmentation (hyperstimulation) Epidural analgesia (maternal hypotension) Maternal pyrexia (fetal inflammatory damage) Fresh meconium-stained liquor (meconium aspiration syndrome) Any deceleration or abnormal baseline on intermittent monitoring Downloaded from https://www.cambridge.org/core. 21 May 2021 at 20:20:26, https://www.cambridge.org/core/terms. https://doi.org 13

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Moreover, the date and time on the CTG trace should be checked to ensure it is correct. It is very important to set the paper speed at the correct rate. In most countries, including the United Kingdom, the paper speed is set at 1 cm/minute, while in the United States is set at 3 cm/minute. If the paper speed is incorrectly set the appearance of the CTG may change. For example, increase in the speed from 1 cm/ minute to 3 cm/minute may create an erroneous impression that the variability is reduced. This may result in an incorrect classification and unnecessary intervention. It is also important to record vaginal examinations, applications of scalp electrode, administration of oxytocin, and so forth so as to optimise interpretation. If there is any doubt that the machine is recording the maternal pulse instead of the fetal heart rate (e.g. repeated accelerations with increased amplitude and duration of uterine contractions), it is recommended to check maternal pulse to exclude the misinterpretation of maternal heart rate as fetal heart rate .

Interpreting the CTG Trace When analysing a CTG trace, the one should start from the beginning of the trace, when the fetus is in general less exposed to stress, checking if the baseline is appropriate for gestational age [10]. From there, scrutinise all the progression looking for an increase of the fetal heart rate (FHR), among other changes. Consider the following five features of a CTG trace prior to classification of CTG.

Baseline Fetal Heart Rate Baseline FHR is the mean FHR rounded to increases of 5 beats per minute (bpm) during a period of 10 minutes. In a term fetus an FHR is considered normal between 110 and 160 bpm. An increase in the baseline FHR above 160 bpm is called tachycardia and may be physiological in preterm fetus due to the immaturity of the parasympathetic system [11]. In term fetuses it might be secondary to maternal pyrexia or dehydration or rarely due to medications (e.g. betamimetics). Moreover, it can be seen as a fetus attempts to compensate for the ongoing hypoxic stress, as a result of a surge in catecholamines. Therefore, it is mandatory to consider the trend of the baseline FHR over time (and compare it to the FHR recorded at the beginning of the CTG) as well to the absolute number of baseline FHR.

Fetal Compromise: Diagnosis and Management

Prior to starting the CTG

STEP 1: Maternal history

STEP 2: Current status

Parity Antenatal history (IUGR, drugs...) Check previous CTG

STEP 3: Anticipate the expected CTG features

Clinical situation Indication for CTG

Before starting, think of the acceptable limits for this fetus When prolonged SROM with potential chorioamnionitis exclude baseline higher than expected for GA and/or absence of cycling If vaginal bleeding is noted exclude Atypical sinusoidal pattern/late decelerations. Start the CTG

Preliminary check Document:

Check: Date & time Paper speed/ Paper orientation

Name, DOB, hospital number Maternal BP, T° and observations

STEP 4: Exclude Chronic hypoxia Chronic hipoxia checklist Baseline FHR appropriate for GA Confirm normal variability and cycling

Is Chronic hypoxia suspected?

Confirm presence of accelerations (if not in labour/early labour)

Yes

Needs safest & quickest mode of birth

No Exclude shallow/late decelerations Continue observation

CTG interpretation, consideration of WIDER clinical picture abd timely & appropriate action

Consider the wider clinical picture

Always consider the wider clinical picture MOTHERS: Meconium, Oxytocin, Temperature, Hyperstimulation/haemorrhage, Epidural, Rate of progress, Scar

STEP 5: Initial assessment Contractions: minimum inter-contraction interval should be of >90 seconds Fetus: Check the next 4 features: 1

3

Baseline FHR: The most important feature. Is it appropriate for GA? An increase of >10% should raise concerns. An increase in the baseline without preceding decelerations suggest a non-hypoxic cause (chorioamnionitis, cardiac arrhythmias..)

2 Variability and cycling: Cycling is a hallmark of fetal wellbeing, which reflects fetal active & quite sleep cycles. Reduced variability preceded by a rise in FHR indicates CNS depression and needs an urgent & appropriate management* 4

Accelerations: Considered to be a reassuring feature Starts from and returns to the baseline. In the 2nd stage of labour, when coinciding with contractions, exclude maternal heart rate.

Decelerations: Repetitive chemoreceptor-mediated decelerations imply uteroplacental insufficiency. Needs an immediate management to reduce fetal compromise*

*Intrauterine resuscitation -Stop Oxytocin / remove prostaglandins -Stop active maternal pushing

-Consider tocolysis -Change maternal position

STEP 6: Carefully scrutinize the CTG trace to exclude 3 types of intrapartum hypoxia: If there is an evidence of intrapartum hypoxia take immediate measures to improve oxygenation*, if this is not possible expedite delivery.

TYPES OF INTRAPARTUM HYPOXIA ACUTE HYPOXIA: Prolonged deceleration (>3’) Rate of fall in pH: 0.01/min Observe the previous trace and the first 3’ of the deceleration

SUBACUTE HYPOXIA: More time spent decelerating than at the baseline. Rate of fall in pH: 0.01/2-3min

A

1st stage of labour

B

Always consider the clinical picture GRADUALLY EVOLVING HYPOXIA: Starts with the onset of decelerations and progresses as follows: ABCDE 1. Accelerations disappear 2. Baseline FHR increases 3. Compensated stress 4. Decompensation (loss of variability,

2nd stage of labour

unstable baseline, ZigZag pattern)

5. End stage: Step-ladder pattern to death

A

Preceded by reduced variability/lack of cycling, or reduced variability within the first 3’ of deceleration

B

Preceded by normal variability & cycling and normal variability within the first 3’ of deceleration Apply the 'Rule of 3'

No

Is it possible to exclude the 3 major intrapartum accidents? Yes

Apply Intrauterine resuscitation*

Stop maternal pushing and commence intrauterine resuscitation*

Compensated Variability is maintained despite ongoing decelerations and a rise in FHR

If no improvement is seen within 15’

If no improvement is noted consider an operative vaginal delivery

Careful observation. Commence intrauterine resuscitation*

Needs urgent intervention to improve oxygenation*

Most likely will recover, if decompensation, follow

If no improvement or Step-ladder pattern to death is detected

Correct reversible causes If no improvement is detected by 9’

Decompensated From reduced/increase d variability to Step-ladder pattern to death

Expedite delivery

Figure 11.2 Suggested algorithm for physiological CTG interpretation.

Baseline bradycardia is defined as FHR below 110 bpm lasting for more than 10 minutes. Similarly, at 20:20:26,

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a post-term fetus can physiologically have a lower baseline due to parasympathetic overdrive. Attention

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Intrapartum Emergencies

should be taken to ensure that the heart rate recorded is not the maternal one.

Accelerations (Transient Increase in the Baseline Heart Rate)

Baseline Heart Rate Variability (‘The bandwidth’ 5–25 bpm)

A transient increase in the FHR >15 beats from the baseline rate and lasting for >15 seconds but less than 10 minutes. Accelerations appear to reflect the integrity of the somatic nervous system, as they are almost always associated with fetal movements and are not present in the absence of fetal movements due to hypoxia, infection or cerebral haemorrhage.

The ‘bandwidth’ or the variation of the heart rate above and below the baseline on the CTG trace is called baseline fetal heart variability. This reflects oxygenation of the central nervous system (CNS) centres (the sympathetic and parasympathetic) that are responsible for the control of the FHR. The normal baseline variability of 5–25 beats per minute (bpm) implies that cerebral hypoxia is unlikely. Reduced baseline variability of 0–5 bpm may represent a quiet sleep phase or may indicate depression of the CNS due to causes such as pharmacological agents (CNS depressants), fetal CNS infections, fetal strokes or hypoxia. An increase in the baseline variability (more than 25 bpm during more than 30 minutes in the absence of decelerations) is termed ‘saltatory pattern’ and should be viewed with caution. This may reflect a rapidly developing intrapartum hypoxic insult that may cause instability to the fetal autonomic nervous system [12, 13]. The sinusoidal pattern (also called typical sinusoidal pattern) is defined as a regular sine-wave oscillation with an amplitude of 5–15 bpm and a reduced or absent baseline variability and deficiency of accelerations, lasting for longer than 30 minutes. It can be seen in a physiological situation such as fetal thumb sucking or pathologically, in association with severe fetal anaemia. A pattern similar to the sinusoidal but with a more jagged ‘saw-tooth’ appearance has been called ‘atypical sinusoidal pattern’ or ‘Poole shark teeth pattern’ and can be secondary to acute feto-maternal haemorrhage in ruptured vasa praevia [14]. If suspected, efforts should be made in delivering in the safest and quickest manner. ‘Pseudo-sinusoidal pattern’ is the term used by some authorities to describe undulatory waveforms alternating with episodes of normal baseline variability with the presence of accelerations. It is of unknown significance.

A healthy fetus at term will demonstrate active and quite sleep cycles approximately once every 50 minutes. This important physiological phenomenon called ‘cycling’ should be considered while interpreting the CTG. Absence of cycling might occur during hypoxic and none hypoxic causes such chorioamnionitis [15]. .013

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Decelerations (Any Decrease in the Heart Rate Below the Baseline) A transient decrease of the FHR below the baseline heart rate (15 bpm and lasting for more than 15 seconds) is termed ‘deceleration’. Decelerations are considered to be a reflex response to an ongoing hypoxia or mechanical stress to protect the myocardial workload and maintain aerobic metabolism. The decelerations can be classified in relation to the uterine contractions as early, late and variable. They occur due to the type of receptor that is stimulated by the underlying pathophysiological process, which stimulates the parasympathetic nervous system (PNS) to mediate a drop in the FHR. The PNS will attempt to reduce the FHR in order to maintain a positive energy balance in the heart in response to any hypoxic stress, and this will be shown in the CTG as a ‘sharp drop and quick recovery’ (i.e. baroreceptor mediated) or a gradual recovery to the baseline (i.e. chemoreceptor-mediated decelerations). It is important to appreciate that labour is a complex process with several patho-physiological processes occurring at any given time. Hence, it is possible to have decelerations that combine characteristics from the types described in the text that follows. Types of Decelerations According to Uterine Contractions Early Decelerations These appear as ‘mirror-images’ of accelerations (i.e. approximately a drop of 15 bpm lasting for 15 seconds.) They commence with the onset of uterine contractions, reach the nadir with the peak of contractions and return to the baseline at the end of the contraction. They are believed to be caused by head compression. Hence, early decelerations are observed during the late first stage or second stage of labour. The presence of early decelerations at these stages does not imply fetal hypoxia/acidosis [12].

Fetal Compromise: Diagnosis and Management

Late Decelerations Late decelerations are so termed because, in relation to uterine contractions, they occur ‘late’: both the onset of deceleration as well as the subsequent recovery to the baseline occur after the beginning and after the end of a uterine contraction, respectively. The nadir of these decelerations is seen after the peak of uterine contraction and they return to baseline at least 20 seconds after the contraction wanes off. The presence of late decelerations indicates uteroplacental insufficiency, mediated through the fetal chemoreceptor mechanism secondary to fetal hypoxaemia, hypercarbia and acidosis. If late decelerations are observed, interventions aimed at enhancing utero-placental circulation should be implemented, such as changing maternal position, reducing or stopping oxytocin administration, use of tocolytics or infusion of intravenous fluids, depending on the underlying pathology. Variable Decelerations These are the most common decelerations occurring during labour (>80%). Variable decelerations are due to umbilical cord compression and they indicate a baroreceptor-mediated ‘reflex’ response to slow down the heart rate in view of an increase in arterial pressure. They are so termed because they vary in shape, form and timing in relation to the uterine contractions. A ‘typical’ or ‘uncomplicated’ variable deceleration consists of a V-shaped deceleration that lasts for less than 60 seconds and has a slight rise in the FHR (called ‘shouldering’) both before and after the deceleration. ‘Atypical’ or ‘complicated’ variable decelerations: Any variable deceleration that does not conform to the typical features as described earlier are termed ‘atypical’ or ‘complicated’ variable deceleration. These may last for more than 60 seconds and may lose their shouldering, have a slow recovery, have an ‘overshoot’ or may be combined with a late deceleration. They may have ‘U’, V’, or ‘W’ patterns or total loss of variability during a deceleration. Unlike ‘typical’ variable decelerations, ‘atypical’ variable decelerations are not due to a transient umbilical cord compression alone. They may signify co-existing utero-placental insufficiency or a sustained umbilical cord compression. Prolonged Decelerations These refer to decelerations lasting for more than 3 minutes. It is considered that they are mediated by chemoreceptors and are commonly associated with hypoxia/acidosis and therefore demand an urgent intervention (improve oxygenation or expedite delivery). at 20:20:26,

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Types of Decelerations Postulated Mechanisms Baroreceptors These are stretch receptors located in the carotid sinus and aortic arch. With the onset of uterine contractions the fetal head and the umbilical cord may experience repeated compression. When the umbilical cord is squeezed, there may be a sudden and abrupt increase in the fetal systemic blood pressure that stimulates the baroreceptors. These send impulses to the cardiac inhibitory centre in the brain stem, that in turn, inhibits the sinoatrial node and activates the atrioventricular node (via the vagus nerve). The result is a slowdown of the FHR that will be observed as a deceleration on the CTG trace with a sharp fall and a sharp rise, thus features of ‘typical’ variable decelerations. As these ‘typical’ variable decelerations are secondary to a mechanical stimulus and they do not represent acidosis, in the absence of other anomalies on the CTG trace (i.e. if the detus continues to show a stable baseline FHR and a reassuring variability), it has been suggested they do not require any intervention other than close observation [16]. Chemoreceptors Located in the aortic and carotid bodies and centrally in the brain, chemoreceptors are stimulated by changes in the biochemical composition of the blood (such as hydrogen ion, carbon dioxide and oxygen). These receptors take longer to get stimulated, they in turn will activate the PNS that will slowly decrease the FHR. Only when fresh oxygenated blood reaches the maternal venous sinuses and washes out the accumulated metabolites, a progressive recovery to the baseline will be seen on the CTG trace. These ‘late decelerations’ are frequently associated with fetal metabolic acidosis and require intervention to improve fetal oxygenation. Decelerations mediated by baroreceptors are secondary to compression of the umbilical cord and will show a sharp drop and ascent. The total duration of the entire ‘typical’ variable deceleration lasts less than 60 seconds. They do not expose the fetus to any hypoxic injury. On the contrary, decelerations secondary to chemoreceptor stimulation are due to metabolic acidosis and will show a more gradual fall and recover from the original baseline FHR. Thus, they will be seen as ‘late decelerations’ and require intervention.

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Contractions Contractions are a transient increase in the uterine activity signal. With the tocodynamometer, only the frequency of contractions can be reliably evaluated [17]; the intensity and duration should be assessed by manual palpation. Contractions occurring repeatedly at intervals of less than 2.3 minutes are likely to result in progressive cerebral desaturation when oxytocin is used [18]. Tachysystole: Presence of 5 or more contractions during a period of 10 minutes, repeated in 2 consecutive periods, or as an average over a period of 30 minutes. Hyperstimulation refers to any increased uterine activity (frequency, duration or strength) that causes fetal CTG changes.

Types of Intrapartum Hypoxia When exposed to hypoxia, the fetus will show different mechanisms to adapt. Based on the pace of onset, intrapartum hypoxia is classified into the following four types.

Acute Hypoxia Acute hypoxia is a prolonged deceleration with a drop in baseline FHR at 90%) and a low positive predictive value for intrapartum hypoxia (30 Estimated fetal weight >4000 g or clinically big baby Occipito-posterior position Mid-cavity delivery or when one-fifth of the fetal head is palpable per abdomen. The procedure must be abandoned if there is no evidence of progressive descent with each pull or where delivery is not imminent following three pulls in spite of correct application by an experienced operator. Paired cord blood samples should always be processed at the time of delivery for acid–base analysis. Ventouse delivery causes an elevated circular soft tissue swelling called chignon on the fetal scalp. This soft tissue swelling settles in the next 2–3 days and it is important to reassure parents about this after the delivery. Appropriate postpartum bladder care and thromboprophylaxis should be instituted as per the hospital protocol.

Ultrasound Assessment of the Fetal Head Position Before Instrumental Vaginal Delivery

Complications of Instrumental Delivery

A number of studies have been conducted to assess the utility of ultrasound to assess fetal head position in the second stage of labour prior to conducting an

Maternal complications are higher with forceps while neonatal complications are more common with the use of ventouse.

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instrumental vaginal delivery. Clinical determination of fetal head position can be subjective and ultrasonographic determination of the fetal occiput position should provide better accuracy and reproducibility. The ultrasound technique involves placing the ultrasound probe horizontally on the maternal abdomen to obtain a transverse view of the fetal trunk at the level of the fetal upper abdomen. The position of the fetal spine is then determined. The ultrasound transducer is further moved downwards until the maternal suprapubic region is reached, visualising the fetal head. The landmarks depicting fetal occiput position are the midline cerebral echo, fetal thalami and cerebellum for OT and OA positions and the fetal orbits for OP position. The orbits are directly under the symphysis in the case of direct OP position, towards the upper portion of the right inferior ramus of the pubis in left OP position, and towards the upper portion of the left inferior ramus of the pubis in right OP position. Although there is insufficient evidence to recommend routine use of ultrasound to determine fetal head position prior to operative vaginal delivery, ultrasound can be utilised if suitable equipment as well as expertise is available and there is no urgency to deliver the fetus (such as acute fetal or maternal compromise). A multicentre randomized controlled study determined whether the use of ultrasound can reduce the incidence of incorrect diagnosis of the fetal head position at instrumental delivery and subsequent morbidity in comparison to standard care [5]. A cohort of 514 nulliparous women at term (37 weeks of gestation) with singleton cephalic pregnancies, aiming to deliver vaginally were recruited prior to an induction of labour or in early labour. The incidence of incorrect diagnosis was significantly lower in the ultrasound group than the standard care group (4 of 257, 1.6%, vs. 52 of 257, 20.2%; odds ratio 0.06; 95% confidence interval 0.02– 0.19; p < 0.001). The decision to delivery interval (DDI) was similar in both groups. The incidences of maternal and neonatal complications after failed instrumental delivery and caesarean section were not significantly different between the two groups [5].

Instrumental Vaginal Delivery

Maternal: Vaginal/cervical lacerations, third- or fourth-degree tears, postpartum haemorrhage Fetal: Superficial bruising and abrasions of scalp and face, transient facial nerve palsy, neonatal jaundice, cephalhaematoma. Rarely subgaleal haemorrhage with lethal hypovolaemia after ventouse delivery, retinal haemorrhage, subdural and cerebral haemorrhages, serious cranial injury such as depressed skull fracture

Key Pitfalls • • • • • •

Failure to anticipate difficult delivery and involve senior clinicians Failure to call for help/communicate in difficult situation Failure to avoid excessive or inappropriate traction Failure to abandon the procedure in time and proceed to caesarean section Failure to anticipate shoulder dystocia and postpartum haemorrhage Failure to document appropriately

Key Pearls •

•

•

In most cases it will be clear that the head is in a low or outlet position and that assisted delivery will be accomplished with ease. However, in those cases in which the fetal head is arrested in between spines to+1 station it is often prudent to declare ‘a trial of instrumental delivery’. This should be performed in an operating theatre with facilities and personnel available to perform a caesarean section. If difficulties are encountered during the delivery the obstetrician can immediately abandon the procedure and proceed to caesarean section. This takes away the pressure from the obstetrician to persist with an attempt at vaginal delivery and minimises risks to both mother and fetus [6]. During ventouse delivery it is important not to change the direction of pull sooner than necessary or else it often results in cup detachment. It is wise to wait until the vacuum cup and the biparietal diameter are beyond the vulval outlet, prior to applying traction upwards. Recognising potential difficulties and making the timely decision to abandon any further attempts at vaginal delivery form an important part of learning the art of an instrumental delivery.

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•

•

All staff performing instrumental vaginal deliveries should undergo annual skills and drills training involving use of ventouse and forceps for assisted vaginal delivery. Learning points emerging from adverse incidents related to use of ventouse or forceps should be discussed at an appropriate risk management forum and disseminated amongst the entire labour ward team to facilitate continued learning.

Management in Low-Resource Settings In developing countries, caesarean section may not be universally available due to lack of resources. It is important for practising obstetricians and midwives to be familiar with common operative procedures applicable in their set-up to improve maternal and fetal outcome. At all instrumental vaginal deliveries, someone in attendance should be capable of performing neonatal resuscitation. Although instrumental delivery is a service provided in both basic and comprehensive essential (or emergency) obstetric care, it is under-used in low-resource settings [7]. There is a definite need for instrumental vaginal deliveries to be made widely available. This in turn will require specific interventions to increase the availability of both the necessary equipment and the operators skilled in its use. Political will and increasing international advocacy will play a major role in implementation of country-specific interventions to ensure provision of equipment and trained operators to areas where they are currently unavailable.

Training and Assessment Training is central to patient safety. There are increased levels of neonatal trauma associated with initial unsuccessful attempts at operative vaginal delivery by inexperienced operators. The Royal College of Obstetricians and Gynaecologists (RCOG) recommends that obstetricians should achieve experience in spontaneous vertex delivery before commencing training in operative vaginal delivery. Competency in instrumental deliveries under supervision should be achieved before conducting unsupervised deliveries and should be monitored regularly thereafter. An experienced operator, competent at mid-cavity deliveries, should be present from the outset for all attempts at rotational or mid-cavity operative vaginal delivery [8]. The RCOG also recommends dedicated consultant sessions on the labour ward to facilitate

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2. Howell C, Grady K, Cox C. Managing Obstetric Emergencies and Trauma: The MOET Course Manual, 2nd ed. London: RCOG, 2007.

better training and supervision of trainees. Assessment of clinical competence should be carried out using the Objective Structured Assessment of Technical Skills (OSATS) form designed for operative vaginal delivery (www.rcog.org.uk/en/careers-training/aboutspecialty-training-in-og/assessment-and-progressionthrough-training/workplace-based-assessments/osats/). Local and specialist courses in labour ward management can contribute to the development and maintenance of operative delivery expertise. In general, the supervising obstetrician should make a full assessment as to whether the indication for instrumental delivery is appropriate and choice of instrument correct. During traction he or she should confirm that the descent is occurring and not wait until three pulls have been completed, as this will lead to abandoning of any further attempt and also risk use of excessive force. After delivery, an adequate review of overall conduct of the delivery, perineal repair and postpartum care should follow.

6. Baskett TF, Arulkumaran S (eds). Assisted vaginal delivery. In Intrapartum Care for the MRCOG and Beyond. London: RCOG; 2002, 63–74.

References

7. Ameh C, Weeks A. The role of instrumental vaginal delivery in low resource settings. Br J Obstet Gynaecol. 2009;116(Suppl. 1):22–5.

1. American College of Obstetricians and Gynecologists. ACOG Practice Bulletin No. 17: Operative Vaginal Delivery. Washington, DC: ACOG, 2000.

8. Royal College of Obstetricians and Gynaecologists. Operative Vaginal Delivery. Green-top Guideline No. 26. London: RCOG; 2011.

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3. Baskett TF, Calder AA, Arulkumaran S. Assisted vaginal delivery. In Munro Kerr’s Operative Obstetrics, 11th ed. Edinburgh: Elsevier; 2007, 91–125. 4. Chandraharan E, Arulkumaran S. Operative delivery, shoulder dystocia and episiotomy. In Arulkumaran S, Penna LK, Bhasker Rao K (eds), The Management of Labour, 2nd ed. Orient Longman (India); 2006, 137–62. 5. Ramphul M, Ooi PV, Burke G, Kennelly MM, Said SAT, Montgomery AA, et al. Instrumental delivery and ultrasound: a multicentre randomised controlled trial of ultrasound assessment of the fetal head position versus standard care as an approach to prevent morbidity at instrumental delivery. BJOG. 2014;121:1029–38.

Chapter

15

‘Crash’ Caesarean Section Leonie Penna

Key Facts Definition A caesarean section (CS) is an operation in which a laparotomy (abdominal incision) is undertaken to allow a uterine incision to deliver one or more fetuses, alive or dead after viability (usually 24 weeks’ gestation). Depending on the urgency, caesarean sections are categorised as follows [1]: ○ Grade 1: For indications that are an immediate threat to the life of the mother or fetus (about 16% of all). In this subgroup of CSs the time taken to achieve delivery will have implications for the risk of fetal morbidity (hypoxic brain injury and possible multi-organ failure in the early neonatal period) and mortality (with a risk of intrapartum demise and stillbirth or death after birth due to the severity of the hypoxic insult). In any situation in which there is a persistent fetal bradycardia or a terminal fetal heart rate pattern (usually swinging deep decelerations with very reduced variability and a slowly falling baseline) the term ‘crash’ caesarean should be used to denote that within Category 1 this is one of the most urgent, in which the whole team needs to pull together, so as to shave valuable minutes off the time it may take to achieve delivery. The underlying pathologies in these situations are usually sudden catastrophic events such as a massive abruption, uterine rupture or a cord occlusion accident such as cord prolapse with pressure on the cord from fetal parts. Perimortem CS done for a woman with cardiac arrest not responding to resuscitation falls within this category, and although not normally described as ‘crash’ also needs to be performed with speed to try to improve outcome. Within this category there are also cases in which there is a high suspicion of established and worsening fetal hypoxia such as pathological (but nonterminal) fetal heart rate patterns or abnormal results from fetal blood sampling or for maternal at 20:20:27,

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wellbeing, with the main indication being ongoing antepartum haemorrhage due to placenta praevia where there is concern that ongoing resuscitation is not able to keep pace with the blood loss. ○ Grade 2: For indications other than maternal or fetal compromise that was not immediately life threatening but where urgent delivery is required (about 32% of all), for example, slow progress in the first stage of labour with a reassuring fetal heart pattern. ○ Grade 3: For indications where there is a need for early delivery for a fetal or maternal reason but there was no acute compromise (about 18% of all), for example, planned next day delivery for a 34week fetus with growth restriction and deteriorating Doppler scans. These CSs are often described as ‘semi-planned’. ○ Grade 4: For non-urgent indications where delivery is timed to suit the mother and the healthcare provider (about 31% of all), for example, prelabour delivery at 39 weeks for two previous caesarean sections. These CSs are also called ‘elective’ or planned. There are few recommendations made on time scales for different grades, as even within the grades the exact urgency of the indication is variable. The Royal College of Obstetricians and Gynaecologists (RCOG) advises that the urgency of CS should be considered as a ‘continuum of risk, pointing out that while in some grade 1 indications decision to delivery intervals (DDIs) of as little as 15 minutes can be achieved, studies have shown that this is not invariably the case and also that evidence shows that a DDI of up to 75 minutes is not associated with an increased risk of neonatal compromise compared to shorter a DDI [1]. It also points out that in some cases even delivery within 30 minutes cannot prevent a poor neonatal outcome, adding an argument for the need to treat each case individually. Overall, they conclude that the

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urgency of CS should be individualised based on the risk to the fetus and the safety of the mother. They recommend that in cases of acute fetal compromise a target DDI of 30 minutes is used but with the caveat that in some cases delivery needs to be undertaken even more rapidly to try to reduce the risk of a poor outcome. The term ‘crash’ caesarean should be reserved for those cases as described that are truly time critical where all efforts need to be made so that the DDI will be as quick as possible without compromising maternal safety. Incidence The World Health Organisation longstanding recommendation is that the total CS rates (combination of elective and emergency procedures) should be 10%–15%, commenting that on a population basis higher rates of CS do not appear to be associated with reduction in maternal and neonatal mortality rates. They also acknowledge that these rates are not being achieved, with most developed countries reporting CS rates well in excess of these levels and have recommended the use of the Robson classification system in order to allow CS rates to be compared globally over time [2]. There is no global evidence on the rates of emergency versus elective type CS and what optimal rates might be expected. Of note, the indications for ‘crash’ CS are almost never open to dispute such that the expected rates of CS within this category should depend only on the incidence of these conditions and the availability of a healthcare system to undertake the operation. There are no prospective studies that have assessed what the optimal rate of CS should be, but it would seem reasonable to assume that it would vary significantly depending on population demographics. However, a number of recent studies have reviewed data on global CS rates and used mathematical modelling to assess the association between CS rates and maternal, neonatal and infant mortality/morbidity; a systematic review of these ecologic type studies concluded that CS rates above a threshold of 9%–16% are not associated with decreases in mortality even where adjustments for socio-economic factors are made [3]. A retrospective analysis of mode of delivery data for 2010 from 31 European countries showed wide variation in CS rates, with the highest total rate seen in Cyprus (52.2% due to a 38.8% rate of planned CS) and the lowest 14.8% in Iceland; the lowest rate of emergency CS was seen in Sweden, where only 8.6% of women required delivery by emergency CS. The rate of emergency CS in all four countries of the United Kingdom was similar at about 15%, with an elective rate showing more variability, 9.9% (England) to14.6% (Northern Ireland), resulting in an overall CS rate of 24.6% (England) to 29.9% (Northern Ireland) [4].

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Key Implications Benefits ○ To prevent threat to the mother’s long-term health or life. This benefit is rarely in doubt, as the clinical signs allow a firm diagnosis of a situation with serious risk. ○ To prevent intrauterine fetal demise or damage usually due to hypoxia. It is not always possible to confirm that a fetus is at risk and so this benefit may be based on a situation with a high likelihood of risk.

Maternal Risks Emergency CS has risks for both the mother and the baby. The risks are greater than those associated with planned CS (24% vs. 16%) [5]. Maternal morbidity: • Operative and postpartum haemorrhage • Infection and wound problems ○ Wound, urinary tract, endometritis, chest (if general anaesthetic) ○ Wound dehiscence ○ Burst abdomen •

Visceral injury ○ Bladder and ureteric injury ○ Bowel injury

•

Thromboembolism ○ Deep vein thrombosis and pulmonary embolism

•

Anaesthetic risk ○ Major: total spinal or aspiration pneumonia ○ Minor: post spinal headaches

•

Long-term risks ○ Increased risk of future CS ○ Increased risk of complications during future abdominal surgery ○ Increased risk of placenta praevia and morbidly adherent placenta ○ Reduced future fertility ○ Small increase in the risk of stillbirth in future pregnancies ○ Development of adhesions and incisional hernias

All these risks are common to both elective and emergency CS but many of the typical indications for

‘Crash’ Caesarean Section

emergency CS further increase the risk of the possible complications associated with CS: • Infection is more likely in ruptured membranes and in cases of multiple repeated vaginal examinations. • Haemorrhage is more likely, as prolonged labour predisposes to uterine atony and greater risk of tears in the lower segment due to deeply engaged fetal head • Anaesthesia may be more complicated in emergency CS, as the woman is less well prepared especially in ‘crash’ CS when there may not be time to use regional anaesthesia so that general anaesthesia is used. • Thrombo-embolism is more likely in prolonged labour and pre-eclampsia • Surgical complications are more likely cases with deeply engaged (or even impacted) head and with CS in advanced rather than early labour (33% incidence of complication for CS at 9–10 cm versus 17% at 1 cm or less)[5]. The rapid delivery required in ‘crash’ CS delivery may increase the risk of surgical complications, especially in women with other risk factors (previous CS or other abdominal surgery) who need unexpected urgent delivery. • Both anaesthesia and surgery are more likely to be undertaken by a less experienced clinician than planned surgery, increasing the risk of blood loss, anaesthetic complications and surgical complications.

Mortality Although rare, the risk of maternal death is increased following CS. In the United Kingdom the risk of death for a woman during or following CS is three times that related to vaginal birth; however, this figure includes CS for all indications and in women with comorbidities. The true risk of CS will depend on the absolute indication, with the risk of certain operations being much greater than that of others. The absolute risk for a healthy woman for simple indications such as fetal distress has never been calculated but is lower and in all probability is not much higher than the risk of vaginal birth.

Fetal Risks •

A scalp or buttock laceration (2%)

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• • •

•

Trauma ○ Skull, femoral or humeral fracture Increased risk of respiratory distress syndrome (RDS) and transient tachypnoea of the newborn (TTN) when compared to equivalent gestation infants delivered vaginally Iatrogenic prematurity with early delivery ○ Neonatal prematurity related complications

Key Pointers •

•

•

All unnecessary emergency CSs should be avoided to limit maternal risks [6]. Involvement of a senior obstetrician in the decision for all emergency CSs is strongly recommended. The indications for all CSs should be carefully considered, with any borderline indications reviewed using a full assessment of the risk and benefit. It is essential to avoid carer bias by remaining ‘open minded’ when taking care of women in labour and to not become overly focused on risk factors that are known to increase the risk of emergency CS but are not in themselves an indication to recommend emergency CS (examples include increased body mass index, increased maternal age, previous delivery by CS). These factors should be reviewed in the context of the usual obstetric indications for CS.

Indications for Emergency CS Category 1 CS ‘crash’ indications = DDI as short as can be achieved • All persistent fetal bradycardia or other preterminal fetal heart rate patterns • Suspected uterine rupture • Fetal blood sample showing pH 35) the dose of cephalosporin should be adjusted for weight and the option of continuing antibiotics into the postnatal period should be considered. This should also be considered when the intraoperative haemorrhage is more than 1000 mL, as the risk of infection is increased. Although intravenous antibiotics are often prescribed, these have no advantage over oral antibiotics for prophylaxis following the loading dose in a woman who is eating and drinking; in addition, oral administration avoids the need for prolonged cannulation. Thromboprophylaxis A risk assessment should be undertaken immediately after delivery in all women to decide on the duration of prophylactic measures. However, a group of universal precautions are recommended for all cases: • Perioperative pneumatic calf compression. • Ensuring early mobilisation and good hydration. • Low-molecular-weight heparin (LMWH): All women undergoing emergency CS should be prescribed a prophylactic dose of LMWH such as Enoxaparin 30–80 mg depending on their weight for the first 7 days after surgery. Very highrisk women should be prescribed LMWH for 6 weeks. Premedications Improving gastric emptying and reducing the acidity of stomach contents reduces the risk of aspiration and damage to lung parenchyma if it occurs. Women who are considered to be more likely to have delivery by emergency CS (such as poor progress between vaginal examinations in spite of oxytocin) should be prescribed premedication as a precaution (usually metoclopramide 10 mg and ranitidine 150 mg orally). If premedication has not been administered previously it should be prescribed as soon as the decision to perform CS is made, in this situation

‘Crash’ Caesarean Section

metoclopramide 10 mg and ranitidine 50 mg can be given intravenously. Sodium citrate 10–15 mL as a single oral dose oral should also be administered immediately prior to transfer to theatre. Catheterisation All women should have a catheter inserted in the bladder prior to the skin incision regardless of the need for rapid delivery. This is essential to reduce the risk of bladder injuries during entry to the uterus. Catheterisation at the time of vaginal examination with a decision for ‘crash’ CS without full aseptic precautions will reduce delay in theatre. Personal Protective Equipment (PPE) For all CSs it is good practice to wear visor masks to avoid splashes of body fluids. This is recommended as part of standard precautions that should be adopted for all surgical cases even if the woman is known to be at low risk for infections such at HIV or hepatitis B. Double gloving has not been shown to reduce the risk of needle stick injuries but does reduce the risk of skin contamination due to micro glove puncture. It is not recommended where high-quality gloves are in use but may be required where poor quality gloves are used. Cell Salvage : The evidence does not support the use of cell salvage in reducing the need for blood transfusion when used in all emergency CSs. However, if facilities are available it should be considered in any clinical situation in which blood loss may be above average (e.g. any situation where atonic postpartum haemorrhage is more likely such as long labours with prolonged oxytocic infusion) or where the woman is at greater risk if haemorrhage occurs (such as Jehovah’s Witnesses membership or significant anaemia). Many indications for ‘crash’ CS are associated with a higher risk of haemorrhage (specifically abruption and uterine rupture); however, the surgery should not be delayed by the desire to use cell salvage and local protocols should remind personnel that the operation can be commenced with cell salvage being set up after delivery of the fetus. Safely Speeding Up ‘Crash’ CS: ‘Crash’ type CSs are time critical for the fetus. The indication for these types of CS is suspicion of severe or rapidly developing hypoxia. In a persistent fetal bradycardia the fetal pH is known to fall at a rate of 0.01 per minute, so a fetus with a normal pH of 7.29 at onset of the bradycardia will be expected to be delivered with a pH of 6.99 in the DDI is 30 minutes. Neonatologists use an umbilical at 20:20:27,

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arterial pH of 1000 mL). A loss of more than 2000 mL of blood is often classed as massive postpartum haemorrhage and is often audited [2]. The causes of primary PPH can be remembered as ‘the 4 T’s’ – tone, trauma, tissue and thrombin. Secondary PPH occurs after 24 hours of delivery and is attributable mostly to retained products of conception (placental fragments) and endometritis.

Tone Atony, or a loss of tone due to a lack of uterine contractility, is the most common cause of PPH. It is important to assess the woman for antenatal and intrapartum risk factors (Table 19.1) in order to make adequate preparations for prompt management.

Trauma Vaginal, perineal and cervical trauma are commonly seen following vaginal deliveries and are particularly associated with instrumental deliveries. Haematomas, from a ruptured vessel during the course of delivery, or from unsecured haemostasis following perineal suturing, can form postpartum. This can be an immediate or late complication post-delivery. Uterine rupture typically presents intrapartum but can occasionally also present in the immediate postpartum period. Collapse in a patient with a scarred uterus following delivery, with or without associated bleeding and/or abdominal pain, should raise suspicion. Therefore, it is important to remember that visual estimation of blood loss does not always

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Table 19.1 Risk factors for uterine atony Antepartum

at 32–36 weeks to exclude placenta accreta spectrum [3].

High BMI/obesity Past history of PPH Multiple pregnancy Polyhydramnios Macrosomia Uterine fibroids Induction of labour Antepartum haemorrhage Intrapartum Induction or augmentation of labour Failure to progress in labour Prolonged labour Operative/instrumental delivery Chorio-amnionitis Use of general anaesthetic Postpartum Inappropriate third stage management

Thrombin Patients with inherited bleeding disorders or those who are on anticoagulants will be at an increased risk of PPH. Antenatal plans should be made with regards to the timing of their anticoagulation around the time of delivery, and availability made for blood products in those with bleeding disorders, with input from the haematologist if required. Preeclampsia may cause a reduced platelet count and coagulopathy that can predispose the mother to PPH. Disseminated intravascular coagulation (DIC) can also occur in women who have suffered a placental abruption, or those with severe sepsis or a massive haemorrhage. It is therefore important to gain an accurate and up-to-date clotting profile at the time of diagnosing these conditions in order to promptly identify DIC and liaise with the blood bank to prepare for necessary blood products.

Retained placenta/manual removal

Other Causes correlate with the actual volume lost and is often underestimated. Therefore, it is vital to assess the patient clinically. Due to the physiological changes of pregnancy, heart rate and blood pressure may not begin to show alterations unless the blood loss has exceeded 1000 mL [2].

Tissue Retained placental tissue can prevent uterine contractility and cause continued bleeding. In a primary PPH, it is essential to check that both the placenta and its membranes are complete. The increase in caesarean section rates has led to an increase in the prevalence of abnormally invasive placenta (placenta accreta spectrum). This can cause massive bleeding during planned caesarean sections, or if a woman laboured with an undiagnosed placenta accreta. Preparations to minimise bleeding should be made prior to such planned caesarean sections, such as availability of a skilled surgeon and anaesthesiologist, interventional radiology input, availability of blood products, and consent for hysterectomy [3]. In women with previous caesarean section and a low-lying anterior placenta, an assessment with ultrasound (and MRI if necessary) should be arranged .021

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Intra-abdominal bleeds can occur, more often following a caesarean section, but can also rarely take form in liver or splenic rupture, particularly associated with severe preeclampsia. Broad ligament haematomas have been reported following instrumental vaginal deliveries. The bleeding is concealed and the symptoms can be nonspecific, making diagnosis difficult. Clinical signs of shock, along with abdominal pain, uterine deviation, and a fall in haemoglobin, should raise the suspicion of an intra-abdominal bleed. Imaging such as CT or ultrasound can aid diagnosis but should not delay treatment if the patient’s condition is critical.

Eclampsia Most cases of eclamptic seizures postpartum occur within the first 24 hours but can occur up to 6 weeks postpartum. The diagnosis of a collapse due to eclampsia is usually obvious, particularly on the background of preeclampsia; however, the onset of this can occur suddenly and unexpectedly. Care should be taken to risk-assess each patient for disease severity and their need for anticonvulsants, which should be commenced without delay (if indicated) to prevent disease progression. Epilepsy should also be considered in patients who experience fits postnatally, especially in the absence of hypertension and proteinuria [4].

Sudden Postpartum Maternal Collapse

Amniotic Fluid Embolism Amniotic fluid embolism is a rare but catastrophic emergency and occurs in 2 of 100,000 maternities. Survival have increased to as high as 80% [4]; however, it is still a significant cause of maternal death, responsible for 8 deaths in the past triennium according to the UK Enquiries into Maternal Deaths and Morbidity report [1]. Postpartum collapse is typically seen within 30 minutes of delivery, but can occur as late as 48 hours after [4, 5]. Clinical signs include hypotension, hypoxia and respiratory distress, and in severe instances, seizures and cardiac arrest. Pulmonary hypertension develops as a result of pulmonary vasospasm, which can result in left ventricular failure, and is also often associated with DIC, predisposing these women to a PPH. Unfortunately, no identifying cause has been found, which deems it unpreventable [5], but early recognition and diagnosis can ensure prompt treatment and a better prognosis.

cardiac arrest [4]. Magnesium toxicity is more likely to occur in cases of renal impairment. High regional blocks can lead to sudden respiratory collapse and loss of consciousness and are easily recognisable following a spinal or epidural top-up.

Anaphylaxis Anaphylaxis can be a cause of collapse in any hospital setting and occurs in 3–10 of 1000 patients, with a mortality rate of 1% [4]. Causative factors are mostly drugs but can also include latex and food allergens. These reactions are characterised by a rapid onset of respiratory distress, cardiovascular collapse, angioedema and a skin or mucosal rash. It can mostly be quickly treated if diagnosed and managed in a timely manner, and serum tryptase levels may be helpful to confirm the anaphylaxis reaction once the reaction has settled [4].

Causes of Late Postpartum Collapse

Uterine Inversion

Pulmonary Embolism

The incidence of uterine inversion have been described to be 1 of 3737 deliveries [6], and can be seen during or immediately following the third stage of labour. The most common cause is premature cord traction or fundal pressure, but can also be associated with morbidly adherent placentas, uterine atony and connective tissue disorders [6]. This can be characterised by pain associated with or immediately following the delivery of the placenta, neurogenic shock due to stretching of the pelvic nerves and ligaments and PPH will often take place immediately following the event in 94% of cases [6]. Shock out of proportion to blood lost, inability to feel the uterine fundus transabdominally and a bulge into the vagina during examination should trigger recognition of a uterine inversion.

Despite improved practice and guidelines on thromboprophylaxis and venous thromboembolism (VTE) risk assessment, venous thrombosis remains the leading direct cause of maternal death according to the UK Enquiries into Maternal Deaths and Morbidity report [1]. Puerperium is the highest risk period, with a risk of VTE 20 times higher than in the non-pregnant population [7]. Massive pulmonary embolism leading to collapse is often associated with shock, hypoxia and possible right heart failure [7]. It can occur at any time during the pregnancy or puerperium and can be seen to occur in the immediate postpartum period. It is therefore important that all women are thoroughly assessed for their VTE risk and promptly prescribed thromboprophylaxis following delivery if indicated.

Non-obstetric Causes Drug Toxicity Drug overdose and toxicity, as well as recreational drug use, should always be considered in cases of maternal collapse. Drugs commonly used in labour that can lead to collapse are magnesium sulphate, lidocaine (if accidentally injected IV), and high regional block, all of which can cause maternal collapse. Symptoms can range from altered consciousness to convulsions and at 20:20:44,

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Sepsis Septic shock is defined as sustained tissue hypoperfusion due to systemic manifestations of infection, despite adequate fluid therapy, and, if associated with acute organ failure, has a mortality rate as high as 20%–40% [8]. Numerous sources of infections can occur postpartum, with genital tract sepsis being the most common. Signs and symptoms include pyrexia, tachycardia, increased respiratory rate, abdominal pain, offensive discharge, wound erythema, rash or other systemic symptoms depending on the source of infection.

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Genital Tract The most common source of sepsis leading to maternal death lies within the genital tract [1], due to an increasing prevalence of group A Streptococcus causing invasive infections [8]. Women may develop chorio-amnionitis during pregnancy or labour, particularly if there is prolonged rupture of membranes, which may continue to manifest into the immediate postpartum period. Later infections may occur as endometritis, presenting with abdominal pain, secondary PPH, offensive lochia and sepsis. Risk factors include pre-existing intrapartum infection, operative delivery, manual removal of placenta, retained parts of the placenta, retained swabs and incompletely treated chorio-amnionitis.

Urinary Tract Pregnant women are particularly susceptible to urinary tract infections due to the raised progesterone levels and anatomical changes, and are more at risk of ascending infections, leading to pyelonephritis. A positive urine dipstick, along with urinary symptoms and loin pain, should prompt the diagnosis of urinary tract infection.

Other Systems Skin and soft tissue (caesarean and perineal wound), mastitis and chest infections are commonly seen infections in the puerperium. Examinations should involve wound inspections and swabs if the area appears infected, breast examination and palpation for an abscess, which may require ultrasound guided drainage, and a full respiratory system examination and a chest radiograph to elicit the source of infection. Pain out of proportion to signs may be an indication of deep infection such as necrotising fasciitis [8]. Intra-abdominal sepsis can include surgical causes (appendicitis, bowel perforation, cholecystitis), or an infected collection following caesarean section. In these cases, CT imaging may be helpful to aid diagnosis, and a surgical opinion obtained if necessary. Tropical diseases should be considered if there has been recent foreign travel and the aforementioned sources of infection are excluded.

Non-obstetric Causes Cardiac Postpartum cardiomyopathy is the development of heart failure in the months post-delivery, without .021

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other establishing causes. Symptoms include palpitations, shortness of breath, orthopnoea and peripheral oedema, and these patients can develop congestive heart failure, arrhythmias and venous thrombosis. Diagnosis is based on echocardiographic evidence of an enlarged heart, with a reduced left ventricular ejection fraction of 1.5 times of normal range. If fibrinogen levels are 500 units/L; bilirubin >12 mg/L), raised liver transaminases (alanine transaminase >70 units/L) and low platelets (24 weeks)

Vascular disorders

Placental abruption Acute polyhydramnios Red degeneration of fibroid Torsion of pedunculated fibroid or an ovarian cyst

Abdominal aortic dissection

HELLP syndrome (haemolysis, elevated liver enzymes, and low platelets) (rarely bleeding into Glisson’s capsule or hepatic rupture)

Superior mesenteric artery syndrome Ruptured aneurysm (e.g. mesenteric artery)

Uterine rupture (previous uterine scar/ spontaneous) Chorioamnionitis Pelvic venous thrombosis

Rare (but, potentially lifethreatening) incidental causes

Symphysis pubis dysfunction (SPD)

Intestinal volvulus Abdominal trauma with intraperitoneal haemorrhage Diabetic ketoacidosis Acute intermittent porphyria Meckel’s diverticulitis

Table 24.3 Topographical guide to abdominal pain in pregnancy

Abdominal region where pain is experienced

Organs to consider

Causes to be excluded

Supra-pubic

Bladder, uterus

Cystitis, placental abruption, uterine scar rupture

Left iliac

Sigmoid colon, left Fallopian tube and ovary

Inflammatory bowel disease, ectopic pregnancy, tuboovarian abscess, ruptured ovarian cyst, ovarian torsion

Right iliac

Appendix, caecum, right Fallopian tube and ovary

Appendicitis, caecal diverticulitis, ectopic pregnancy, tubo-ovarian abscess, ruptured ovarian cyst, ovarian torsion

Left hypochondrial

Spleen, pancreas, splenic flexure of colon

Splenic infarction, rupture or haemorrhage, colitis

Epigastric

Stomach, pancreas, aorta, heart

Gastritis, acute pancreatitis, aortic dissection/rupture, myocarditis, infarction

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Abdominal Pain in Pregnancy

Table 24.3 (cont.)

Abdominal region where pain is experienced

Organs to consider

Causes to be excluded

Right hypochondrial

Liver, kidney, hepatic flexure of colon, gallbladder

Hepatitis, cholecystitis, hepatic rupture or haemorrhage, acute fatty liver of pregnancy, HELLP syndrome, imminent preeclampsia

Right lumbar

Right kidney, ascending colon

Pyelonephritis, renal/ureteric calculi, inflammatory bowel disease

Umbilical

Transverse colon, appendix (early ‘visceral pain’), uterus

Appendicitis (early), gastroenteritis, mesenteric lymphadenitis, acute pancreatitis, placental abruption, uterine scar dehiscence or rupture

Left lumbar

Left kidney, descending colon

Pyelonephritis, renal/ureteric calculi, inflammatory bowel disease

Arrive at a Provisional diagnosis based on: History Examination Possible underlying pathology

Consider appropriate Investigations based on the differential diagnosis (above)

Blood tests

Imaging

Others

Full blood count CRP Urea & electrolytes Renal function tests Liver function tests Serum amylase Serum tryptase Blood gases Coagulation profile Blood culture

Obstetric ultrasound Abdominal ultrasound MRI scan abdomen Chest X-ray Abdominal X-ray V/Q scan or CTPA Cardiac ECHO

High and low vaginal swabs Urine (MSU) for microscopy and culture ECG CT chest

Formulate definitive management plan Immediate resuscitation, if required, and senior input Supportive therapy, including pain control Correction of metabolic, biochemical and coagulation derangements Multidisciplinary care plan, if appropriate Obstetric management – is urgent delivery required after maternal stabilisation in the maternal or fetal interest? Does this woman require transfer to another unit or intensive treatment unit to optimise management?

Figure 24.3 Suggested algorithm for management of abdominal pain during pregnancy. at 20:20:44,

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Medical and Surgical Emergencies During Pregnancy

Rarely, peptic ulcer disease may present with generalised pain secondary to bleeding or perforation. Management is conservative with antacids except if gastric bleeding or perforation is diagnosed, which would necessitate a laparotomy and repair. A high degree of clinical suspicion should be exercised to diagnose both common as well as potentially life-threatening causes of acute abdominal pain during pregnancy (Table 24.2). •

•

•

Understanding the topographical location of internal organs and their pathways for referred pain may help improve the diagnosis (Table 24.3). Rare causes such as secondary abdominal pregnancy, placenta percreta, acute pancreatitis and hepatic or splenic rupture should also be considered, especially if there is a diagnostic dilemma. Use of a management algorithm (Figure 24.3) may help clinicians to optimise management.

References 1. American College of Obstetricians and Gynecologists. Guidelines for Diagnostic Imaging during Pregnancy. ACOG Committee Opinion 158. Washington, DC: ACOG, 1995. 2. Groen RS, Bae JY, Lim KJ. Fear of the unknown: ionizing radiation exposure during pregnancy. Am J Obstet Gynecol. 2012;206:456–62. 3. Masselli G, Derchi L, McHugo J, Rockall A, Vock P, Weston M, Spencer J, Subcommittee EFPI. Acute abdominal and pelvic pain in pregnancy: ESUR recommendations. Eur Radiol. 2013;23:3485–500. 4. Katz DS, Khalid M, Coronel EE, Mazzie JP. Computed tomography imaging of the acute pelvis in females. Can Assoc Radiol J. 2013;64:108–18. 5. Kennedy A. Assessment of acute abdominal pain in the pregnant patient. Semin Ultrasound CT MR. 2000;21:64–77. 6. Hurwitz LM, Yoshizumi T, Reiman RE, et al. Radiation dose to the fetus from body MDCT during early gestation. AJR Am J Roentgenol. 2006;186:871–6. 7. Forsted DH, Kalbhen CL. CT of pregnant women for urinary tract calculi, pulmonary thromboembolism, and acute appendicitis. AJR. 2002;178:1285. 8. Cook TS, Hilton S, Papanicolaou N. Perspectives on radiation dose in abdominal imaging. Abdom Imaging. 2013;38:1190–6. .026

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9. Moore W, Bonvento MJ, Lee D, Dunkin J, Bhattacharji P. Reduction of fetal dose in computed tomography using anterior shields. J Comput Assist Tomogr. 2015;39:298–300. 10. Baron KT, Arleo EK, Robinson C, Sanelli PC. Comparing the diagnostic performance of MRI versus CT in the evaluation of acute nontraumatic abdominal pain during pregnancy. Emerg Radiol. 2012;19:519–25. 11. Unal A, Sayharman SE, Ozel L, Unal E, Aka N, Titiz I, Kose G. Acute abdomen in pregnancy requiring surgical management: a 20-case series. Eur J Obstet Gynecol Reprod Biol. 2011;159:87–90. 12. Berlingieri P, Grudzinkas JG. Assessment of abdominal pain in pregnancy, BMJ Best Practice, Aug 2018. https://bestpractice.bmj.com/ topics/en-gb/ 13. Royal College of Obstetricians and Gynaecologists. Management of Early Pregnancy Loss. Green-top Guideline No. 25. London: RCOG, 2006. 14. Shur J, Bottomley C, Walton K, Patel JH. Imaging of acute abdominal pain in the third trimester of pregnancy. BMJ. 2018;361:k2511. 15. Schenker JG, Weinstein D. Ovarian hyperstimulation syndrome: a current survey. Fertil Steril. 1978;30:255–68. 16. Golan A, Ron-El R, Herman A, et al. Ovarian hyperstimulation syndrome: an update review. Obstet Gynecol Surv. 1989;44:430–40. 17. Devarajan S, Chandraharan E. Abdominal pain in pregnancy: a rational approach to management. Obstet Gynaecol Reprod Med. 2011; 21(7):198–206. 18. Centre for Maternal and Child Enquiries (CMACE). Saving mothers’ lives: reviewing maternal deaths to make motherhood safer: 2006–2008. The Eighth Report on Confidential Enquiries into Maternal Deaths in the United Kingdom. Br J Obstet Gynaecol. 2011;118(Suppl. 1):1–208. 19. Chandraharan E, Arulkumaran S. Acute abdomen and abdominal pain in pregnancy. Obstet Gynaecol Reprod Med. 2008;18(8):205–12. 20. Dellinger RP, Carlet JM, Masur H, et al. Surviving Sepsis Campaign guidelines for management of severe sepsis and septic shock. Crit Care Med. 2004;32:858–73. 21. Chandraharan E, Arulkumaran S. Painful uterine contractions. In Arulkumaran S (ed.), Emergencies in Obstetrics and Gynaecology. Oxford: Oxford University Press; 2006, 8–23. 22. Kammerer WS. Nonobstetric surgery during pregnancy. Med Clin North Am. 1979;63:1157–64.

Abdominal Pain in Pregnancy

23. Augustin G, Majerovic M. Non-obstetrical acute abdomen during pregnancy. Eur J Obstet Gynecol Reprod Biol. 2007;131:4–12. 24. Pedrosa I, Levine D, Eyvazzadeh AD, et al. MR imaging evaluation of acute appendicitis in pregnancy. Radiology. 2006;238(3):891–9.

at 20:20:44,

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25. Pearl JP, Price RR, Tonkin AE, Richardson WS, Stefanidis D. Guidelines for the Use of Laparoscopy During Pregnancy. Society of American Gastrointestinal and Endoscopic Surgeons (SAGES). May 2017.

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25

Blurring of Vision and Sudden Loss of Vision in Pregnancy Anomi Panditharatne and Edwin Chandraharan

Key Facts The ocular conditions in pregnancy can be broadly subdivided into three main categories: • Changes seen secondary to normal physiological changes observed during pregnancy [1] • Changes due to pathological conditions – both pregnancy-specific and non-specific • Changes due to preexisting ocular disease or its altered course during pregnancy

Visual Symptoms Due to Physiological Changes of Pregnancy Tear Film Changes The tear film consists of three layers: the outer lipid layer, the middle aqueous layer and the inner mucin layer. The stability of the tear film is dependent on all three layers functioning in an optimal, synergistic manner. The lipid layer is secreted by the Meibomian glands and the aqueous and the mucin layers by the lacrimal glands and goblet cells, respectively. In pregnancy, the tear film becomes unstable and alters in composition, causing it to break up quickly, resulting in irritation and discomfort to the patient (Figure 25.1). It is important to examine the eye under a slit lamp and exclude any other lid or corneal pathology, which could be contributing to these ocular symptoms.

Management If no other disease process to explain ocular irritation is found, the patient can be reassured. Initially, simple steps can be tried such as ocular hygiene (use of cotton buds and warm water to clean the upper and lower eyelids to remove any dust) and Downloaded from https://www.cambridge.org/core. 21 May 2021 at 20:20:45, https://www.cambridge.org/core/terms. https://doi.org 27

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Figure 25.1 Physiological changes during pregnancy: drooping of eyelids (ptosis); changes in corneal surface; reduction in intraocular pressure; changes in tear film – increased dryness and irritation.

creation of a more humid atmosphere at work or at home. The latter may include use of a humidifier and practical steps such as opening windows, having plants on the desk or around the home and keeping them watered. Smoke also irritates the eyes and patients should be advised to avoid smoking during pregnancy. When outdoors, ‘wrap-around’ sunglasses may help. Massaging the eyelids gently may encourage mucus to be pushed out of goblet cells. Despite these measures, if the symptoms are troublesome and are affecting everyday activities,

Blurring of Vision and Sudden Loss of Vision in Pregnancy

then preservative-free lubricants could be prescribed to alleviate discomfort and irritation.

Corneal Changes The cornea is the transparent structure located on the front of the eyeball that is important for clarity of vision. It consists of the following five layers: • Stratified squamous non-keratinised epithelium • Bowman’s membrane, which is acellular • Stroma consisting of regularly arranged collagen fibres with a ground substance of proteoglycans • Descemet’s membrane of thin collagen fibres • Single-layered endothelium The thickness of the cornea changes during pregnancy, and this could affect the clarity of vision. Changes in the shape and size of the eyeball secondary to physiological fluid retention and changes in blood pressure during pregnancy may result in minor changes in the refractive power of the eyes. In addition, contact lens wearers may feel they are intolerant of contact lenses during pregnancy and may find them ‘ill-fitting’.

Management It is important to exclude any other ocular pathology that may cause changes in vision by careful anterior and posterior segment examination. A refraction test may show slight changes in the power compared with the previous examination. If pathological causes have been excluded, the changes observed in vision should be explained to the patient and she should be reassured that these changes will subside following pregnancy and she need not change the prescription of her glasses or contact lenses [2]. However, contact lens wearers should be advised that if irritation and ‘ill-fitting’ contact lenses due to changes in the shape of the eyeball are a problem, changing to glasses during pregnancy may improve their symptoms. Patients contemplating corneal surgery should be advised that the corneal thickness is variable during pregnancy and may affect the final outcome. Hence, corneal surgery should be recommended 3 months after birth.

Visual Symptoms Due to Pathological Conditions During Pregnancy Blurring of vision and sudden loss of vision may occur due to pregnancy-specific pathological conditions as at 20:20:45, .027

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well as primary ocular or ocular manifestations of underlying systemic disorders that occur de novo during pregnancy.

Pregnancy-Specific Disorders: Severe Preeclampsia and Eclampsia Severe preeclampsia and eclampsia are potentially life-threatening conditions that are specific to the pregnant state. Although the exact aetiology is unknown, they are believed to be due to the widespread endothelial damage secondary to abnormal placentation and subsequent release of vasoactive factors. These result in systemic vasospasm, endothelial cellular damage (endotheliosis) and activation of the coagulation system resulting in disseminated intravascular coagulation. The diagnostic criteria for preeclampsia include blood pressure of >140/90 mm Hg in a pregnant woman after 20 weeks’ gestation with proteinuria >300 mg/24 hours. However, severe preeclampsia is diagnosed when the systolic blood pressure rises above 160 mm Hg and/or the diastolic blood pressure rises above 110 mm Hg with or without visual, hepatic or neurological symptoms. Onset of seizures is referred to as eclampsia. Preeclampsia is common in primigravidas and has an incidence of about 5%. Women with underlying chronic hypertension and renal disorders are at increased risk of developing ‘superimposed’ preeclampsia during pregnancy. In addition, women with underlying immunological disorders (e.g. systemic lupus erythematosus [SLE]) and thrombophilia (congenital and acquired) are also at increased risk of developing preeclampsia. Visual symptoms include blurred vision, double vision and photopsia, which are often associated with headaches and epigastric or right hypochondrial pain (hepatic involvement). Ocular manifestations of preeclampsia include features of optic neuropathy, which include papilloedema, optic neuropathy and optic atrophy. On examination, visual acuity may be reduced depending on the severity and the location of the disease process within the eye. Retinopathy seen in preeclampsia is similar to hypertensive changes and is characterised by nerve fibre layer infarcts, hard exudates, flame-shaped haemorrhages, retinal oedema and narrowing of arterioles. Swelling of the optic nerve head is a hallmark of malignant hypertension. Choroidal changes are less

Medical and Surgical Emergencies During Pregnancy

common in preeclampsia and would lead to Elschnig’s spots, which represent focal choroidal infarcts. There may also be bilateral exudative retinal detachments. There is a correlation between the severity of preeclampsia and the extent of retinal involvement. Retinal changes are more marked in patients who have pre-existing conditions such as renal disease and long- standing diabetes mellitus. In preeclampsia, serous retinal detachments may also occur due to choroidal non-perfusion and subretinal leaks. These usually present as bilateral bullous detachments and resolve in the postpartum period. Rarely, occipital infarcts and visual loss due possibly to cerebral oedema may occur in severe preeclampsia and these often resolve with the control of preeclampsia. History of sudden onset of blurred vision should be taken very seriously and preeclampsia needs to be excluded in all pregnant women. Ocular symptoms improve with treatment of hypertension and usually resolve after birth. Excluding any other coexisting pathology is paramount. Rarely, thrombotic thrombocytopenic purpura (TTP) may be confused with severe preeclampsia with HELLP (Haemolysis, Elevated Liver enzymes and Low Platelets) syndrome. Clinical presentation in TTP includes thrombosis of small vessels leading to thrombocytopenia, microangiopathic haemolytic anaemia associated with neurological and renal dysfunction. Patients are often febrile. Ocular manifestations in TTP occur due to narrowing of retinal artery, serous retinal detachment, retinal haemorrhage and oedema of the optic disc. Rarely, patients may complain of homonymous hemianopia.

Pregnancy ‘Non-specific’ Disorders (Primary Ocular or Systemic Illnesses): Benign Intracranial Hypertension Benign intracranial hypertension refers to the presence of raised intracranial pressure in the absence of an intracranial mass or hydrocephalus. This condition is usually common in obese females in the third trimester but may occur throughout pregnancy. Benign intracranial hypertension may cause sudden loss of vision and may occur due to papilloedema. Other associated symptoms include headaches, which are worse with postural changes and straining, transient visual obscuration lasting a few seconds and nausea and vomiting. Some patients may have drowsiness and horizontal diplopia. .027

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On examination of the fundus, in the early stages, hyperaemia and mild disc swelling may be seen. Once papilloedema is established, visual acuity may be normal or reduced and the optic disc margins may appear indistinct. Appearance of venous engorgement, parapapillary flame-shaped haemorrhages and cotton wool spots as well as hard exudate around the macular forms, macular fan and the enlargement of the blind spot are the associated ocular signs.

Management Regular ophthalmological examinations to observe optic nerve functions are essential. Serial visual field examinations are useful. Conservative measures include bed rest. Medications such as acetazolamide or steroids are best avoided in pregnancy in view of potential teratogenic effects. Intractable cases may benefit from lumbar puncture, optic nerve sheath decompression and lumbar peritoneal shunts to reduce the intracranial pressure.

Central Serous Retinopathy Central serous retinopathy (CSR) is typically a sporadic self-limiting disease that affects the young, reproductive age group. It is characterised by unilateral localised detachment of the sensory retina at the macula with or without pigment epithelial detachment [3].

Aetiology Central serous retinopathy is associated with hyperpermeability of the retinal pigment epithelium (RPE) or the choroidal vasculature.

Clinical Features Unilateral blurring of central vision with micropsia or metamorphopsia. Visual acuity is 6/9–6/12. On ocular examination, round or oval detachments of the sensory retina at the posterior pole are observed and the fluid may be turbid or clear.

Management Central serous retinopathy spontaneously resolves, usually in 1–6 months. Visual acuity returns to normal or near normal. Rarely, it may run a chronic course and persist for more than 12 months with progressive changes at the macula. Argon laser treatment to the RPE leak or detachment may speed recovery but has no effect on the final visual outcome.

Blurring of Vision and Sudden Loss of Vision in Pregnancy

Arteriovenous Occlusions Causing Sudden Loss of Vision Pregnancy is associated with changes in the vessel walls and vascular endothelium as well as in the coagulation system. Incidence of optic or retinal arterial and venous occlusions may be increased in pregnancy, which may be due to the hypercoagulable state that occurs due to changes in platelets, clotting factors and arterial–venous flow dynamics during pregnancy. Clinical features would depend on the location and severity of the occlusions and may range from sudden onset of loss or blurring of vision, usually in one eye but rarely both eyes may be affected. On examination, the visual acuity would be reduced. Fundoscopic examination in arterial occlusions would confirm a pale retina and there would be arterial attenuations. In venous occlusions, the retina would appear haemorrhagic with venous dilation and tortuosity with haemorrhages and exudates in the involved areas of the retina. Other features include macular oedema and disc swellings. In women with circulating anti-phospholipid antibodies, there may be features of vascular thrombosis of the retina with choroid, optic nerve and ocular motor involvement. Management of vascular occlusions in pregnancy is similar to that in the non-pregnant state. Regular monitoring of visual acuity, intraocular pressure, optic nerve functions and retinal vascularity is essential. Complications such as macular oedema and retinal neovascularisation could occur, and in this situation laser treatment may be needed.

Preexisting Systemic Diseases with Ocular Manifestations in Pregnancy: Diabetic Eye (Retinopathy) Diabetes mellitus is a complex condition associated with endocrine, metabolic, cardiovascular, renal and ophthalmological complications and is characterised by relative or absolute deficiency of insulin leading to sustained hyperglycaemia. There are two types of diabetes mellitus: type 1 and type 2. Diabetic retinopathy is a microangiopathy which affects arterioles, capillaries and post-capillary venules, although larger vessels may also be involved. Diabetic retinopathy does progress in pregnancy and such a progression depends on the extent of retinopathy prior to conception, duration and control of diabetes. at 20:20:45,

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Smoking, obesity, nephropathy and hyperlipidaemia are also associated risk factors for progression during pregnancy.

Non-proliferative Diabetic Retinopathy This consists of background retinal changes that include microaneurysms, hard exudates, retinal oedema and haemorrhages. Fifty per cent of nonproliferative retinopathy may worsen in early and mid pregnancy, but usually improves by term and during the postpartum period. These patients should have an ophthalmological examination in each trimester.

Clinical Features of Pre-proliferative Retinopathy Cotton wool spots occur, which are focal infarcts of the retinal nerve fibre layer due to occlusion of the precapillary arterioles and the build-up of transported material within axons. Intraretinal microvascular abnormalities (IRMA) represent shunts that run from the arteriole to the venule bypassing the capillary bed. These are seen in areas of capillary closure. There is also venous dilation, arteriolar narrowing and silver wiring with blot haemorrhages.

Proliferative Diabetic Retinopathy This is a more serious condition. Prior to frank proliferation there is pre-proliferation, which indicates progressive retinal ischaemia. The risk of preproliferation becoming proliferative retinopathy depends on the extent of ischaemia.

Clinical Features of Proliferative Diabetic Retinopathy Proliferative retinopathy affects 5%–10% of the diabetic population. Individuals with type 1 diabetes are at particular risk, with an incidence of 60% in 10 years. Neovascularisation is the hallmark of proliferative diabetic retinopathy. Neovascularisation can occur in the optic disc or elsewhere in the retina. It can lead to fibrosis that could lead to sight-threatening tractional retinal detachments.

Management Pan-retinal photocoagulation is the treatment of choice, as this causes involution of new vessels and prevents visual loss from vitreous haemorrhage and retinal detachment. The extent of the area of the retina lasered depends on the severity of the disease.

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Regular follow-up of patients who have received laser therapy is mandatory to detect involution of new vessels. In advanced disease, early vitreous surgery may be necessary, as there is a risk of vitreous haemorrhage and tractional retinal detachments. Approximately 45%–50% progress during pregnancy and if severe retinopathy is detected, early laser treatment has been found to be beneficial. Monthly ocular assessments are indicated in those with more advanced disease. Macular oedema associated with diabetes also can be exacerbated in pregnancy and may present with visual symptoms. Visual acuity assessment with detailed dilated funduscopy would give the clinicians an indication of the level of diabetic control and also may help detect any ocular changes that may require treatment.

Intracerebral Tumours The common tumours that increase in size in pregnancy are pituitary adenomas and meningiomas. Pituitary adenomas cause visual field defects due to the location of the optic nerve pathway and the pituitary gland. Non-secreting pituitary adenomas often present first to ophthalmologists whereas secreting adenomas may first present to endocrinologists.

Clinical Features Presenting symptoms include headaches, which are often non-specific. Visual symptoms are gradual in onset and examination of visual functions is useful. Visual field defects are another feature, especially bitemporal hemianopia due to compression of the optic chiasm by the enlarging pituitary adenoma. There may be evidence of colour desaturation across the vertical midline in early compressive lesions. Optic atrophy is a late finding due to compression of the optic pathway. The optic disc would appear pale with clear margins and poor visual functions in the late stages. Examination of visual functions such as visual acuity, colour vision, pupil response, fundus examination as well as visual fields testing, would help confirm the diagnosis. Brain imaging would indicate the relationship between the mass lesion and the optic chiasma and associated ‘endocrine work-up’ is also important. During pregnancy, ocular examinations and visual field testing are performed during every trimester and also at 6 weeks postpartum to detect any compressive signs. Pituitary adenomas tend to regress in size following pregnancy. If there are signs of compression of .027

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optic chiasma, medical treatment with bromocriptine or cabergoline for prolactinomas, steroids or transphenoidal surgery may be attempted. Radiotherapy is not recommended during pregnancy because of potential effects on the fetus, unless the tumour is rapidly enlarging and is life threatening. Pituitary apoplexy is a rare and sight-threatening condition due to sudden increase in the size of the gland secondary to haemorrhage [4]. Patients may complain of severe headaches, diplopia, visual loss and photophobia. Treatment with systemic steroids, and if unresponsive, urgent surgery may be needed to prevent blindness.

Meningiomas Intracranial meningiomas typically affect middleaged women but may also be seen during pregnancy. Visual field defects and clinical features depend on the location of the meningioma and its relationship to the intracranial centres. They commonly occur in the tuberculum sellae, sphenoidal ridge or in the olfactory groove. Meningiomas are generally slow-growing tumours and often regress following parturition. If there is compression on the optic nerve, surgical excision is the treatment of choice.

Thyroid (Graves’) Eye Disease This is an autoimmune disorder that usually presents in the third and fourth decades in women. The eye symptoms may increase in early pregnancy but usually settle down in the later stages of pregnancy. Thyroid eye disease affects the soft tissue around the eye and causes globe protrusion. In addition, it affects extraocular muscle movements and the eyelids as well as causing compressive optic neuropathy. Thyroid orbitopathy can be kept under observation by routine eye examination during pregnancy and by observing for signs of compressive optic neuropathy. Regular use of tear supplements can avoid corneal overexposure and dryness.

High Myopia Myopia refers to short-sightedness and is associated with an increased size of the globe that results in distant images formed in front of the retina. It was thought earlier that spontaneous vaginal deliveries were not suitable for patients who were ‘high myopic’ with or without previous retinal pathology or treatment. This was because there was a concern that an increase in the intraocular pressure that occurs during spontaneous

Blurring of Vision and Sudden Loss of Vision in Pregnancy

vaginal delivery would cause retinal tears or detachment. However, this has not been proved by scientific studies and recent evidence suggests that there may not be any significant increase in retinal detachment or tears in women with high myopia who attempt vaginal births. In patients who have high myopia, clinical examination of the retina with dilation is useful to determine whether there are any untreated retinal lesions [5]. If so, they could be treated with laser and the patients could be reassured. Assisted vaginal birth should be considered to avoid a prolonged second stage of labour with active pushing.

Key Pearls It is important to understand the normal changes in the eye during pregnancy [6, 7], to timely recognise ocular disorders. It is important to appreciate that some ocular signs [8] may be benign, but others may mask an underlying medical condition [9]. Although, few case repots

on the use of intravitreal injection of anti-VEGF (vascular endothelial growth factor) have been published in the medical literature [10], it is not routinely recommended in clinical practice due to concerns regarding maternal and fetal safety during pregnancy. A management algorithm of blurring of vision or sudden loss of vision is provided in Figure 25.2.

References 1. Wang C, Li AL, Pang Y, Lei YQ, Yu L. Changes in intraocular pressure and central corneal thickness during pregnancy: a systematic review and meta-analysis. Int J Ophthalmol. 2017;10(10):1573–9. 2. Yenerel NM, Küçümen RB. Pregnancy and the eye. Turkish J Ophthalmol. 2015;45(5):213–19. DOI:10.4274/ tjo.43815. 3. Landau D, Seelenfreund MH, Tadmor O, Silverstone BZ, Diamant Y. The effect of normal childbirth on eyes with abnormalities predisposing to rhegmatogenous retinal detachment. Graefes Arch Clin Exp Ophthalmol. 1995;233(9):598–600.

Check: Visual acuity, pupils, colour vision Funduscopy Visual field examination Cranial and orbital imaging

Figure 25.2 Management algorithm of blurring of vision or sudden loss of vision.

Systemic examination Blood pressure, cardiovascular and neurological examinations Investigations Full blood count Urea and electrolytes Clotting profile Liver function tests Blood sugar

Pregnancy specific Severe preeclampsia or eclampsia

Control blood pressure Control seizures Deliver

Pregnancy non-specific Benign intracranial hypertension Central serous retinopathy Arterial/venous occlusions Thrombotic thrombocytopenic purpura (TTP) Diabetic retinopathy (proliferative and nonproliferative) Thyroid eye disease (Grave’s) Intracranial tumours High myopia

Serial monitoring during pregnancy and treat specific underlying aetiology at 20:20:45,

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4. Pizzarello LD. Refractive changes in pregnancy. Graefes Arch Clin Exp Ophthalmol. 2003;241(6):484–8. 5. Kanski JJ (ed.) Clinical Ophthalmology: A Systematic Approach, 5th ed. Boston: Butterworth Heinemann. 6. Chandraharan E, Arulkumaran S. Pituitary and adrenal disorders in pregnancy. Curr Opin Obstet Gynecol. 2003;15:101–6. 7. Naderan M. Ocular changes during pregnancy. J Curr Ophthalmol. 2018;30(3):202–10. DOI: 10.1016/j. joco.2017.11.012.

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8. Mackensen F, Paulus WE, Max R, Ness T. Ocular changes during pregnancy. Dtsch Arztebl Int. 2014;111 (33–34):567–76. DOI: 10.3238/arztebl.2014.0567. 9. Roche, JC, Alarcia, R. Can ocular flutter be due to pregnancy? Acta Neurol Belg. (2019). https://doi.org/10 .1007/s13760-019-01080-z 10. Polizzi S, Mahajan VB . Intravitreal anti-VEGF injections in pregnancy: case series and review of literature. J Ocul Pharmacol Ther. 2015;31(10):605–10. DOI: 10.1089/jop.2015.0056.

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Psychiatric Emergencies Lorraine Cleghorn

Key Facts Definition Serious disturbances of behaviour, cognition and emotion requiring immediate management to prevent a risk to self or others that are not attributable to an underlying medical illness or alcohol and substance misuse. Types • Suicidal ideation – can present with any psychiatric disorder. • Deliberate self-harm – associated with depression, alcohol and substance misuse and personality disorder; increased risk of suicide subsequently. • Severe anxiety – associated with significant subjective distress with retained insight; usually self-limiting in the short term. • Severe depression – associated with significant subjective distress, high suicide risk and selfneglect; usually not self-limiting. • Acute psychosis – associated with abnormal experiences and beliefs that may be florid and frightening and drive abnormal behaviour that can present a risk to self or others. Incidence • Mild and transient psychiatric symptoms occur in up to 1 in 2 pregnancies. • Diagnosable psychiatric disorders are present in up to 1 in 5 pregnancies. • True psychiatric emergencies are relatively rare.

Key Pointers • • •

Maternal distress Concerned partner, relatives or friends. Already under the care of a specialist mental health service Past history of emergency psychiatric presentations

Key Diagnostic Signs •

• • • •

•

No impairment of consciousness. This would imply delirium with an underlying medical cause. Subjective complaints of severe anxiety or depression. Acts or thoughts of deliberate self-harm, or suicidal thinking. Self-neglect, withdrawal or mutism. Marked emotional lability, euphoria, excitability, irritation or hostility [1]. Delusional thinking: expressing rigid and unshakeable abnormal beliefs that are not understandable in the context of the patient’s cultural, educational or social background; for example, the belief that staff are evil and trying to harm the unborn baby. Hallucinations: perceptions in the absence of a stimulus; for example, hearing a voice commanding the patient to kill herself.

Key Actions Key Implications

Assess Any Immediate Risks

•

The safety of the patient, other members of the public, including any accompanying children, and staff is the paramount consideration [2]. While the very large majority of pregnant women presenting with a serious psychiatric problem are much more likely to be the victims of aggression and violence than they are to be the perpetrators, there are rare exceptions. If

•

Maternal: Suicide is a preventable cause of maternal mortality. Misdiagnosis of medical illness as psychiatric disorder contributes to maternal morbidity and mortality. Fetal: Untreated psychiatric disorder is associated with a range of adverse fetal outcomes, including intrauterine growth restriction and prematurity.

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the possibility of any risk is anticipated then appropriate precautions should be taken. It is better to be overprepared than caught off guard. Consider whether the patient presents any immediate risks to herself or others that will determine where and how the assessment should be conducted. Indicators of potential risk include aggression, disinhibition, fearfulness, hyper-arousal, paranoia and sudden, unprovoked outbursts of anger. Recent alcohol or substance misuse may be a compounding factor as a result of their disinhibiting effects. The risk is increased if the patient is previously unknown and presenting in crisis in the maternity department for the first time. If any risk is suspected, then assessment by more than one staff member in a safe and relatively quiet environment, such as a counselling room free of ultrasound machinery and other potentially hazardous clinical equipment, is preferred. If the assessment is being conducted by one staff member, then other staff should be aware of the situation and close at hand. The seating arrangements should allow the patient and clinician to be at the same level, in the order of at least two arm lengths apart, and at an angle where eye contact can be made or avoided without discomfort. Both staff and patient should have easy access to the door to avoid a frightened and paranoid patient feeling trapped and becoming more dangerous as a result. If the assessment is taking place at the patient’s home, then it is sensible to avoid assessing her in the kitchen or anywhere else where there are potential dangers should she become aroused and impulsive.

Obtain Background Information It is rarely possible or necessary to conduct a full psychiatric assessment in an emergency ‘triage’ situation. Details of family and personal history, beyond the immediately relevant, such as family or personal history of any psychiatric disorder, can usually wait. Unless she is presenting for the first time, however, a large amount of background information will already be available in the woman’s maternity record. If the patient is already under the care of specialist psychiatric services, then she is likely to have a care plan that includes a risk assessment and a risk and contingency management plan. This can be an invaluable guide to any emergency obstetric mental health assessment. Midwives and obstetricians booking women for maternity care who are under the care of specialist .028

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mental health services should have sought these plans in advance so that they can be available in the maternity record [3]. If the patient is under the care of specialist mental health services she is likely to have a mental health care coordinator, for example a community psychiatric nurse, and it should be possible to contact him or her by telephone during normal working hours in an emergency situation to obtain any missing information on risk assessment and risk and contingency management plan [4]. Once again, contact details for the care coordinator should ideally have been recorded at booking and feature prominently in the list of key emergency contacts in the maternity record. If a midwife specialising in mental health and/or a perinatal psychiatrist was involved at any previous stage of the pregnancy, then they may have provided further information in relation to perinatal risk and risk management.

Obtain Collateral Information Depending on the circumstances, including the ability of the patient to provide clear information herself, information should be obtained from any accompanying partner, relative or friend. This may be during the assessment of the patient herself if she chooses to remain accompanied throughout, but if she is assessed on her own in the first instance it is important to ask anyone accompanying her to wait so that they can be interviewed subsequently.

Obtain History If a patient is well enough to communicate without major difficulty, and not too distressed, then it is helpful to begin the assessment interview with one or two open questions. This has the advantage of putting the patient at her ease and emphasising that she is being listened to and that her concerns are being taken seriously. If she has any insight into the nature of her distress she may be very embarrassed and a calm, gentle and non-judgmental approach that allows her to explain her fears or concerns can be very therapeutic in itself. Many patients who go on to have specialist psychiatric assessment speak very positively about the experience of talking to a midwife or obstetrician who paid attention to their problems when they presented in crisis. Identification of the presenting complaint or concern will guide subsequent enquiry.

Psychiatric Emergencies

If the patient complains of low mood or depression then further questions about the impact of depression on functional ability; feelings of hopelessness and despair; energy levels; ability to experience enjoyment or interest; and sleep, appetite and weight disturbance will all be helpful and positive answers confirmatory. If the patient complains of fearfulness or severe anxiety, then further questions about potential antecedents (A = antecedents) or triggers that might have precipitated the fear, for example a recent investigation that might have triggered fears that the unborn baby is at risk; any behaviour (B = Behaviour) evoked by the fear such as excessive reassurance seeking or escaping from a fear-inducing situation, and any consequences (C = Consequences) of the fear, for example avoidance of any further investigations or fear-inducing situations, might give a clue as to the nature of the problem. Sometimes fear is free-floating without any obvious cognitive association, as might occur in a patient experiencing her first panic attack for example, but asking the patient what thoughts were going through her mind when she was frightened will often elicit a cognitive component. It is also helpful to ask about specific physical concomitants of fear, including markers of autonomic arousal such as racing heart rate, hyperventilation and sweating. If the patient presents as confused or perplexed, or if she describes abnormal beliefs or experiences, then it will be important to establish whether she is experiencing a psychotic illness such as schizophrenia. Delirium often has a very similar presentation and it is particularly important to consider the possibility in cases of suspected psychosis. If the patient presents as aroused, emotionally labile, excitable and uncharacteristically irritable and argumentative, then hypomania or mania may be a possibility. Once again, the possibility of delirium needs to be carefully considered. The presence of any suicidal ideation or intent should be sensitively explored in all patients presenting with a psychiatric problem in an emergency, and not just in patients with depression. It is also important to sensitively explore the possibility of any recent alcohol or substance misuse in all patients. Patients from minority groups who do not speak the same language as the assessing clinician are particularly vulnerable and should be assessed with the assistance of an interpreter whenever possible [5]. The at 20:20:45,

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use of a partner or relative is not an adequate substitute, although in an emergency situation with no access to an interpreter this may be necessary.

Mental State Examination A mental state examination, even if relatively brief, is a core component of any assessment of a psychiatric emergency. When the patient is uncooperative or uncommunicative, it will assume even more importance. The process of mental state examination is very simple and largely accomplished ‘automatically’ during the assessment interview itself. Key points follow: Appearance and behaviour: Any abnormalities of appearance or behaviour should be noted, as they might give important clues about the underlying problem. These might include evidence of distractibility, fearfulness, perplexity or preoccupation in a patient with a psychotic illness; overexcitability and overactivity in a patient with mania; agitation, withdrawal or neglect in a patient with a depressive illness; and tremulousness, restlessness or reassurance seeking in a patient with an anxiety disorder. Speech: Speech can be abnormal in flow, tempo, tone or volume. Subtle abnormalities can be difficult to spot, but in an emergency triage situation obvious problems such as loud verbosity, possibly suggesting mania; disorganised or muddled speech, possibly suggesting delirium or schizophrenia; and poverty of speech, possibly suggesting depression, should be noted. Mood: The presence of any subjective and objective anxiety, depression or perplexity should be recorded. If she has not been asked already, the patient should be asked if she is experiencing any active suicidal ideation. Beliefs and experiences: If psychosis is suspected, it is appropriate to ask whether the patient has experienced any ideas that others have considered unusual or paranoid, and specifically whether she has worried that something strange has been going on, like people spying on her or wishing her harm. ‘Normalisation’ is a very useful technique when trying to elicit any abnormal beliefs or experiences. For example, questions can be phrased in the following way: ‘Lots of people who have been under the kind of stress that you have been get so stressed out that they experience odd things, like paranoia or

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hearing voices when there is no one there. Has anything like that happened to you?’ Cognitive function: Any impairment of consciousness or disorientation should suggest delirium and an underlying medical cause requiring further investigation. Most people who are alert and oriented should be able to identify the time of day to the nearest half hour, and the day of the week and month, if not the exact date. In broad terms disorientation in time is the most sensitive marker of disorientation, followed by place and then person. Although there are specific tests for attention, concentration, immediate recall and recent memory, the patient’s performance at interview will give a great deal of information in the first instance. Additional tests of attention and concentration, such as naming the days of the week backwards, or recalling three items in 1 minute, can be used to confirm initial impressions. Insight: The degree of insight lies on a continuum. At one extreme a patient expressing floridly abnormal beliefs and behaving bizarrely may believe she is completely well. This would imply psychosis and the potential use of legal measures to enforce a safe assessment and subsequent treatment in hospital should the patient be a risk to herself or others. At the other end of the continuum, a very distressed patient may recognise that she is unwell and in need of immediate help.

Next Steps Severe anxiety and panic attacks can usually be managed in the maternity department without recourse to specialist psychiatric intervention. Reassurance and explanation, particularly in relation to the benign nature of any physical symptoms of anxiety that the patient might have misinterpreted as signs of an imminent life-threatening problem, such as racing heart beat or hyperventilation, may be all that is required. The hyperventilating patient should be instructed to take slow, even breaths. If she is experiencing physical symptoms of high pO2, such as perioral tingling, she can be instructed to re-breathe from a paper bag. All of the other psychiatric emergencies described imply high risk and the need for an urgent specialist psychiatric assessment. If admission is required, and the patient is more than 32 weeks pregnant, then this should ideally be to a specialist psychiatric mother and baby unit. Downloaded from https://www.cambridge.org/core. 21 May 2021 at 20:20:45, https://www.cambridge.org/core/terms. https://doi.org 28

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Specific Techniques Risk Assessment Suicide risk is by far the more likely risk in a psychiatric emergency presenting in pregnancy. Psychiatric textbooks rightly emphasise the importance of actuarial risk factors in any assessment of suicide risk, but in an emergency triage setting it is much more vital to elicit whether the patient has any active thoughts of harming or killing herself. Active thoughts indicate high risk and the need for specialist psychiatric assessment. Associated factors indicating heightened risk include feelings of hopelessness and pessimism about the future, which may have particular connotations in the context of pregnancy, social isolation and lack of support. Patients presenting with severe depression, mania or psychosis may be vulnerable to self-neglect, harm as a consequence of their abnormal beliefs and behaviours and exploitation by others. The possibility of domestic violence should always be considered in vulnerable women in pregnancy, and discreetly and sensitively enquired about. Any serious psychiatric illness presenting late in pregnancy has potential implications for the safety of the unborn baby following delivery, depending on the patient’s circumstances and supports. Harm might arise as a result of neglect, emotional harm or the direct consequence of any abnormal beliefs or behaviours. If there is a risk, then consultation with the relevant social care agency responsible for child safeguarding is indicated.

De-escalation If the patient should become very angry and aroused but does not present an immediate danger, de-escalation may be attempted. The assessing clinician(s) should remain outwardly calm and helpful and talk quietly and reassuringly. Reassurance may need to be repeated more than once if a preoccupied and distractible patient does not respond to it the first time. Staff should remain seated if it remains safe to do so, as this will appear less threatening. Eye contact should neither be sustained nor avoided altogether, as this can also appear threatening. Intermittent eye contact is usually perceived as more reassuring. Provocative, confrontational and threatening comments should be avoided and staff should never become visibly angry. It can be appropriate, however, to set clear boundaries

Psychiatric Emergencies

and tell patients when their behaviour is intimidating or frightening. De-escalation does not always work and departmental operational policies should include a protocol for the management of the very disturbed patient who becomes rapidly aggressive, identifying clear procedures for the rapid involvement of liaison psychiatry services and hospital security if required.

Restraint and Rapid Tranquillisation It is very rarely necessary to attempt restraint or rapid tranquillisation in the maternity department, and such an exigency should be avoided. In all but the least well-resourced settings specialist psychiatric advice can be quickly sought and the patient transferred to a psychiatric ward or facility where there is on-site nursing expertise in control and restraint techniques. The key principle of emergency restraint that applies to the pregnant patient is the avoidance of vena cava syndrome. She should not be restrained on her back or her right side, but to her left, ideally with the use of bean bags or similar for comfort and support. All hospitals should have rapid tranquillisation protocols that include consideration of the needs of a pregnant patient, and staff should be familiar with these [6]. The emergency use of a short-acting benzodiazepine, such as intramuscular lorazepam, is not contraindicated in a pregnant woman who requires rapid tranquillisation for her own safety and the safety of others.

Key Pitfalls • • • •

Failure to identify delirium; failure to identify suicide risk Failure to use an interpreter for a patient who does not speak the clinician’s language Failure to consider the safeguarding of needs of any children at home Failure to communicate any concerns and or mental health plan for ongoing monitoring to other health and/or social care services

Key Pearls • •

Psychiatric assessment is very straightforward if a few key principles are observed. While psychiatric disorders are common in pregnancy, true psychiatric emergencies are

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•

•

relatively rare and caused by a small number of conditions. Maternity units should have a midwife specialising in mental health and access to a specialist perinatal psychiatry service. Lessons learnt from adverse incidents due to psychiatric emergencies [7, 8] should be disseminated through the ‘maternity dashboards’ and clinical governance seminars.

Management in Low-Resource Settings In the absence of a specialist perinatal psychiatry service or hospital-based psychiatric liaison service the management of psychiatric emergencies is more complicated. All of the high-risk situations described in this chapter, with the exception of severe anxiety, imply the potential need for admission to a psychiatric hospital if the patient cannot be managed at home by a well-resourced, specialist psychiatric home treatment team. In such circumstances consideration should be given to admitting the patient to the maternity ward until a full psychiatric assessment can take place or transfer to a specialist psychiatric hospital arranged. If psychiatric medication has to be used before specialist psychiatric advice can be obtained, for example if a patient is manic or psychotic and difficult to manage safely on the maternity ward, then advice should be sought from a pharmacist regarding the safety of the medication. Opinions on the safety of medications in pregnancy are subject to change, although at the time of writing haloperidol and olanzapine are considered reasonably safe antipsychotic medications in pregnancy, depending on the balance of risks, if used at appropriate dosages.

References 1. Glick RL, Berlin JS, Fishkind AB, Zeller SL. Emergency Psychiatry. Principles and Practice. Philadelphia, PA: Lippincott Williams & Wilkins, 2008. 2. Puri BK, Treasaden IH. Emergencies in Psychiatry. Oxford: Oxford University Press, 2008. 3. NICE. Antenatal and Postnatal Mental Health. NICE Clinical Guideline 45. London: National Institute for Health and Clinical Excellence, 2007. 4. Kent A. Psychiatric disorders in pregnancy. Obstet Gynaecol Reprod Med. 2009;19:37–41.

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5. Centre for Maternal and Child Enquiries (CMACE). Saving Mothers’ Lives: Reviewing Maternal Deaths to Make Motherhood Safer – 2006–2008. The Eighth Report on Confidential Enquiries into Maternal Deaths in the United Kingdom. Br J Obstet Gynaecol. 2011; 118(Suppl. 1):1–208.

7. Knight M, Bunch K, Tuffnell D, et al. (eds.) on behalf of MBRRACE-UK. Saving Lives, Improving Mothers’ Care: Lessons Learned to Inform Maternity Care from the UK and Ireland Confidential Enquiries into Maternal Deaths and Morbidity 2014–16. Oxford: National Perinatal Epidemiology Unit, University of Oxford, 2018.

6. American College of Obstetricians and Gynecologists. Use of psychiatric medications during pregnancy and lactation. ACOG Practice Bulletin No. 92. Obstet Gynecol. 2008;111:1001–20.

8. Rodriguez-Cabezas L, Clark C. Psychiatric emergencies in pregnancy and postpartum. Clin Obstet Gynecol. 2018;61(3):615–27.

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Chapter

27

Drug Overdose in Pregnancy Lakshman Karalliedde

Key Facts

Key Diagnostic Signs

• Intentional overdoses (i.e. suicide rates due to drug overdose) are low and generally result in low toxicity to the mother. • The risk of overdose is highest during the first few weeks of pregnancy and the first pregnancy, low socioeconomic status and in those who abuse ethanol. • Antipyretics, analgesics and anti-rheumatics are the most common drugs ingested. • Adverse birth outcomes such as preterm labour and low birth weight have been reported in a very small number of patients. Most drug overdoses require only supportive care. However, a few drugs which may cause severe overdose are discussed in this chapter. Treat the poison if an antidote is available, as the ‘poison’ is bound to be more toxic than the antidote to the fetus. • Physiological changes in pregnancy may be associated with changes in pharmacokinetics and toxicokinetics following overdose. The delay in gastric emptying time of up to 50% would result in lower peak plasma concentrations. Similarly, the increase in plasma volume during pregnancy and the associated increase in the volume of distribution would also result in reduced peak plasma concentrations of the drug.

These depend on the class of drug/s ingested. Always suspect poisoning when the presenting physical signs are not commonly associated with known disease states. Some examples: • Anticholinergic signs: dilated pupils, sweating, warm and red peripheries – for example tricyclic antidepressant or belladonna alkaloid self-poisoning • Sympathomimetic signs: tachycardia, high blood pressure, sweating, dilated pupils – overdose of sympathomimetics, for example, amphetamines • Increased respiratory rate, sweating and tinnitus – salicylate self-poisoning • Bradycardia and hypotension – calcium channel blocker or beta-blocker self-poisoning • Depressed respiration, consciousness and small pupils – opioids (pinpoint pupils) or benzodiazepines self-poisoning • Hyperthermia and rigidity – selective serotonin reuptake inhibitors (SSRIs) • Hypoglycaemia – self-poisoning with antidiabetic medications

Key Actions Assess and Stabilise the Patient

Key Implications • • • •

Maternal: Some pharmaceutical agents may induce renal, liver and cardiac malfunction. Fetal: Effects on the fetus following overdose of the mother are sparse or non-existent at present. Often effects on the fetus are considered to be directly related to maternal outcome. Some drugs are known to be mutagenic and/or teratogenic. Others have the potential to be carcinogenic.

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Drug overdose should be treated as a medical emergency. Attend to the patient immediately and stabilise (maintain vital physiological parameters, e.g. oxygen saturation, blood pressure) the patient as a priority (Table 27.1).

Use Standard Advanced Cardiac Life Support •

Assess airway, breathing and circulation – use standard guidelines.

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Table 27.1 Clinical signs and management summary of some commonly ingested pharmaceutical agents

Drug class

Clinical effects

Toxic dose

Action

ACE inhibitors

Hypotension and tachycardia. Hyperkalaemia

Variable

Supportive care. Intravenous fluids

Amiodarone

Non-specific ECG changes, hypotension and bradycardia

Variable

AC and supportive care

Antihistamines

Nausea, vomiting, retention of urine, tachycardia

Cyclizine 5 mg/kg, Diphenhydramine >300 mg

Activated charcoal (AC) and supportive care

Antibiotics

Mainly gastrointestinal – variable signs depending on the agent

Anticoagulants (warfarin)

Bleeding tendency and prolonged international normalised ratio (INR)

Barbiturates

Nystagmus, ataxia, small pupils, respiratory depression and coma

Benzodiazepines

CNS and respiratory depression

Variable

Manage airway. AC

Bromocriptine

Nausea, vomiting and hypotension. Psychosis and hallucinations

50–75 mg

AC. IV fluids and supportive care

Clonidine

Drowsiness, coma, bradycardia Variable and hypotension. Hypertension

AC. Supportive care, IV fluids

Ergotamines

Cold cyanotic peripheries, abdominal pain

AC, glyceryl trinitrate, nitroprusside and nifedipine

Lithium (acute ingestions)

Nausea, vomiting, ataxia, myoclonic twitches, confusion and coma

Whole bowel irrigation if May induce congenital >4 g of sustained release malformations. is ingested. Do lithium Haemodialysis if coma, levels at 6 hours post convulsions and ingestion. respiratory failure or Observe for up to levels >7.5 mmol/L 24 hours. Manage airway and fluid balance

MAOI

Drowsiness, confusion, agitation, coma, hypertension, hyperthermia

Airway management, diazepam, fluids

Opioids

Drowsiness, respiratory depression, hypotension, pinpoint pupils, coma

AC, naloxone (0.4 mg IV, Observe for minimum of increased every 2–3 6 hours. In addicted minutes to a maximum patients, naloxone bolus dose of 2 mg – use may precipitate 2/3 the dose required as withdrawal a maintenance each hour), airway management

Non-steroidal anti-inflammatory drugs

Variable – no symptoms to CNS depression and acidosis in massive doses

SSRI

Nausea and vomiting.

AC. In serotonin syndrome –

Drowsiness and serotonin

cooling, IV fluids, sedate with

syndrome (hyperthermia, rigidity, rhabdomyolysis)

diazepam and cyproheptadine

Theophylline

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Nausea, vomiting, tachycardia, convulsions, hypokalaemia

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Variable

Comments

AC and supportive care

Some are teratogenic

AC and vitamin K for up to 10 days

If mother is on long-term warfarin, correction should be gradual to prevent thrombosis

Manage airway. AC

Variable

Variable

1g

Do not give flumazenil

Increases uterine tone, fetal hypoxia

Symptoms may occur 24 hours post-ingestion

AC, supportive care

Multiple dose AC

Observe 4 hours or up to 24 hours if sustainedrelease drug is ingested

Drug Overdose in Pregnancy

Assess airway – talk to the patient. If she responds, the airway is patent. If there is no response, carry out airway opening manoeuvres (head tilt and jaw thrust). • Assess breathing – look, feel and count respiratory rate – feel for air on palm. Cyanosis? • Assess circulation – presence of pulse, measure blood pressure. • Assess neurological disability – note score on Glasgow Coma Scale (GCS). • Connect the patient to an ECG monitor and pulse oximeter. Measure blood sugar and serum electrolytes. All patients who present with a ‘threatened airway’ (i.e. at risk of aspiration into the lungs) and low GCS score should have endotracheal intubation. •

Assess Risk • • •

• •

•

•

Ask for the name of the drug/s. Determine number of tablets, strength and preparation (ordinary release or slow release). Decide if the ingested dose is likely to cause toxicity. Examine to detect the presence of signs of toxicity. In the absence of signs of toxicity, assess the probability of subsequent development of toxicity. Observed for widened QRS (100 ms) complex on the ECG in patients with tricyclic antidepressant poisoning. Similarly, observe for bradycardia and heart blocks in patients with calcium channel blocker and beta-blocker poisoning. Observe for tachyarrhythmias in patients with tricyclic antidepressants (TCA), digoxin poisoning. Patients with beta-blockers poisoning are at increased risk of Prolonged QT interval. Similarly metabolic acidosis may occur in patients with metformin poisoning (lactic acidosis), and salicylate and iron poisoning.

• •

•

•

•

Administer activated charcoal 1 g/kg (50 g) if the patient presents within 1 hour post-ingestion. The patient should have a protected airway and a verbal or written consent should be obtained for this if the clinical situation (i.e. conscious level) permits Multiple doses of activated charcoal may be given in some cases of overdose with drugs such as carbamazepine and salicylates [1]. Whole bowel irrigation should be carried out following overdose with drugs such as slowrelease calcium channel blockers, lithium and iron. Method: Administer 1 L of oral polyethylene glycol hourly until the rectal effluent is clear.

Confirmation of Poisoning Serum drug assays – limited use but a necessity in some instances, for example, instances e.g. overdose with paracetamol, iron, salicylates, digoxin or lithium. Other indicators of toxicity, for example: • ECG: widened QRS (100 ms) complex in tricyclic antidepressant poisoning. Bradycardia and heart blocks in calcium channel blocker and betablocker poisoning. • Tachyarrhythmias in tricyclic antidepressants (TCA), digoxin poisoning. • Prolonged QT interval – beta-blockers poisoning. • Metabolic acidosis – metformin poisoning (lactic acidosis), salicylate and iron poisoning.

Give Antidotes Some drug overdoses should be treated using specific antidotes.

Paracetamol Mechanisms of Toxicity

Decontaminate •

•

Decontamination may be effective for longer periods than the usually recommended 1 hour post-ingestion. Gastric lavage is not routinely recommended for a pregnant patient with drug overdose. Use activated charcoal.

For ordinary-release medications in overdose: at 20:20:45,

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Paracetamol is largely metabolised in the liver to nontoxic glucuronide (60%) and sulphate (30%) conjugates, which are subsequently excreted in the urine. A small fraction is also converted (by cytochrome P450-dependent mixed function oxidase enzymes) to the toxic metabolite N-acetyl-p-benzoquinone imine (NAPQI). The toxic metabolite is inactivated by conjugation with hepatic glutathione and eventually excreted as cysteine and mercapturic acid conjugates.

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Medical and Surgical Emergencies During Pregnancy

Investigations

mg/L 200 190 Normal

180

Measure plasma paracetamol level 4 hours after ingestion. Obtain baseline values for INR, serum creatinine, aspartate transaminase (AST) and alanine transaminase (ALT). A specialist liver centre should be contacted if • The INR is >2 at 24 hours; >4 at 48 hours; >6 at 72 hours post-ingestion

High risk

170 160 150 140 130 120 110

•

100 90

• • •

80 70 60 50 40

OR if the patient has any of the following: An elevated plasma creatinine (>200 μmol/L). Hypotension (mean arterial pressure less than 60 mm Hg) following accepted methods of resuscitation. Encephalopathy.

30 20

•

10

Treatment

0

0

4

8 12 16 20 Hours post ingestion

24

28

Figure 27.1 Paracetamol normogram.

In overdose, there is accumulation of this toxic metabolite. In healthy women, a dose greater than 200 mg/kg or 10 g in total (whichever is less) may be hepatotoxic. In those considered as high-risk, that is, malnourished patients, patients on enzyme-inducing drugs (e.g. carbamazepine, phenytoin, rifampicin) or patients suffering from HIV, liver toxicity may occur at lower doses. The risk of liver damage is assessed using the paracetamol normogram (Figure 27.1) which plots the plasma paracetamol concentration in relation to the time of ingestion. Those on or above the treatment line will require treatment with N-acetylcysteine (NAC), without which severe liver damage could be expected in approximately 60% of patients. Where paracetamol has been taken chronically or in a staggered manner (e.g. >2 hours between doses), or where the time of ingestion is unknown, the plasma paracetamol concentration cannot accurately be interpreted using the normogram. If the total dose in 24 hours exceeds 200 mg/kg or 10 g, whichever is the smaller (> 100 mg/kg in high-risk patients), NAC should be administered. Downloaded from https://www.cambridge.org/core. 21 May 2021 at 20:20:45, https://www.cambridge.org/core/terms. https://doi.org 29

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OR The PT in seconds is greater than the number of hours since overdose

It is important to treat within 8 hours post-ingestion, as the recovery is almost 100% in this case. If a plasma paracetamol level could be obtained within 8 hours, start treatment after the plasma paracetamol level is available. If the level is unlikely to be available within 8 hours of ingestion, start treatment when the ingested dose is considered potentially toxic. Continue/discontinue treatment after receiving the plasma paracetamol level. NAC is the antidote and it should be administered as follows: • 150 mg/kg body weight in 200 mL of 5% dextrose by slow IV infusion over 15 minutes, followed by • 50 mg/kg by IV infusion in 500 mL of 5% dextrose over 4 hours and 100 mg/kg in 1 L of 5% dextrose over the next 16 hours. Two hours after completion of the infusion, repeat measurements of INR, serum creatinine and AST. If the INR is stable or declining, there is no need for further treatment with NAC. If the patient is symptomatic and has an elevated INR, the patient is likely to require further doses of NAC.

Sulphonylureas and Other Blood Sugar Lowering Agents Clinical features are due to the hypoglycaemic effect. Patients may be asymptomatic or present with low

Drug Overdose in Pregnancy

GCS score, nausea, vomiting, sweating, convulsions or even hemiparesis. Activated charcoal should be administered to all patients who present within 1 hour of ingestion of tablets. Measure blood glucose every 6 hours. Monitor serum potassium levels, as administration of dextrose may cause hypokalaemia. Occurrence of hypoglycaemia may be delayed if prophylactic dextrose has been given to patients with normal blood glucose levels or if the patient has had a recent meal. Hypoglycaemia may persist for days. Care must be taken to monitor for recurrent hypoglycaemia. Rebound hypoglycaemia may develop following cessation of dextrose therapy, as dextrose could cause increased and persistent release of insulin.

Management of Hypoglycaemia Dextrose Avoid intravenous administration of dextrose solutions prophylactically to patients with no clinical or laboratory evidence of hypoglycaemia, as this measure may delay the onset of hypoglycaemia. Oral glucose supplementation may be used as and when necessary. In symptomatic patients and patients with significant hypoglycaemia (blood glucose 2 ng/mL (2.56 nmol/L) are associated with a higher risk of toxicity but toxicity is not always related to plasma level. Patients with healthy hearts are likely to tolerate large doses up to 5 mg. Overdose usually leads to onset of symptoms within 6 hours. The early symptoms are associated mainly with the gastrointestinal system: anorexia, nausea and vomiting being the most common. CNS manifestations include headache, fatigue, lethargy, depression, confusion and hallucinations. Reversible visual disturbances, such as blurred vision, photophobia and alteration of colour perception, may also be observed. Biochemically, hyperkalaemia may be a prominent feature in acute toxicity. Different cardiac effects may be seen and occur within 6 hours. • Bradyarrhythmias such as AV conduction disturbances (first-degree heart block, seconddegree heart block and complete heart block). • Tachyarrhythmias are common. Ventricular tachycardia and fibrillation indicate severe toxicity. • Hypotension and cardiac arrest may also occur.

Treatment Gastric decontamination with activated charcoal should be carried out when a patient presents within 1 hour of ingestion. Observe the patient on a cardiac monitor for at least 6 hours following ingestion. If the

Drug Overdose in Pregnancy

patient develops signs of toxicity, continue observations until signs of toxicity abate. Hyperkalaemia should be treated aggressively with insulin/dextrose. Sodium bicarbonate or calcium resonium exchange resin may be used as an alternative if required. Calcium gluconate is contraindicated, as ventricular fibrillation may follow its administration. Bradycardias may respond transiently to intravenous boluses of atropine. Digibind is the antidote of choice and is indicated in the presence of any of the following: • Hyperkalaemia >5.5 mmol/L, or resistant to correction. • Bradyarrhythmias (e.g. high-grade AV block) unresponsive to atropine or associated with hypotension. • Tachyarrhythmias, especially if associated with hypotension. One of the following methods may be used to calculate the required dose of Digibind. ðaÞ Number of vials ¼ amount of digoxin ingested ðmgÞ  0:8 0:5 ðbÞ Number of vials ¼ serum digoxin concentration in ng=mL  weight in kg 100 If dose ingested or serum concentration is not known 20 vials of Digibind could be administered as a single dose. Alternatively, 10 vials may be administered initially and the remainder later if indicated.

preparation. Consequently, all individuals who have ingested SR preparations should be observed for at least 18 hours from the time of ingestion. As deterioration may occur suddenly, close monitoring is a necessity.

Clinical Features Hypotension is the most common feature to all the agents in this class of drugs. Some agents (verapamil and diltiazem) may produce varying degrees of conduction blocks including complete heart block. Nifedipine may cause a tachycardia.

Treatment These patients need close observation. Following ingestion of SR preparations, cardiac monitoring should be continued for at least 18 hours. Gastric decontamination may be attempted within 1 hour post-ingestion. In very severe overdoses, whole bowel irrigation can be attempted. All symptomatic patients should be managed in a facility for cardiac monitoring. Hypotension should initially be treated with intravenous fluids. If there is no response, intravenous calcium gluconate should be administered (3 g in a 10% solution, i.e. 30 mL repeated every 10–20 minutes for 3–4 doses). Severe overdoses may not respond to this therapy. In the absence of a response to fluids and calcium gluconate, patients should be treated with insulin and dextrose. Usually high doses of insulin are administered – initially 1–2 units/kg of soluble insulin as a bolus. Thereafter, an infusion of 0.5–1 unit/kg per hour in 10% dextrose should be administered. Measure blood sugar and serum potassium levels every 1–2 hours.

Calcium Channel Blocker Overdose The calcium channel blockers are used in the treatment of hypertension, angina and arrhythmias. There are three groups of calcium channel blockers: the dihydropyridines (e.g. nifedipine), benzothiazepine (diltiazem) and a phenylalkylamine (verapamil). All three groups do produce serious toxicity in overdose. In overdose, these drugs produce profound hypotension while some agents may cause bradyarrhythmias while others may cause tachyarrhythmias. Most of these agents are also available as sustained release (SR) preparations. Following ingestion of SR preparations, signs and symptoms may occur as late as 18 hours afterwards and therefore it is important to confirm whether the patient had ingested a SR at 20:20:45,

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Beta-blockers Beta-blockers are widely used antihypertensive and anti-angina agents. Poisoning with these drugs is not uncommon. They act by blocking the beta-adrenergic receptors. Consequently beta1 receptors regulate heart rate and blood pressure. Some beta-blockers, for example atenolol and bisoprolol are more ‘cardioselective’ than others, that is, they selectively block the beta1 receptors more than the beta2 receptors at therapeutic doses, resulting in fewer side effects. Some beta-blockers block fast sodium channels and thus cause myocardial depression while others are lipid soluble and hence cross the blood–brain barrier,

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causing central nervous system effects following an overdose. After ingestion, most patients develop symptoms within 2–4 hours. Hypotension is common and is mostly due to the negative inotropic effect on the heart. Bradycardia may also occur but this is less common with cardio-selective beta-blockers. ECG changes may include prolonged PR interval, first-degree AV block and bundle branch block. Severe toxicity may result in disappearance of P waves, total AV block, asystole and intraventricular conduction defects. Agents with membranestabilising activity may prolong the QRS interval. Cardiogenic shock and pulmonary oedema are possibilities, especially in patients with pre-existing cardiac disease. CNS effects such as drowsiness are more commonly seen in overdose with beta-blockers with membrane-stabilising activity.

Treatment Gastric decontamination with activated charcoal to patients presenting within 1 hour of ingestion. All patients require cardiac monitoring for at least 6 hours post-ingestion. If patients have ingested slowrelease preparations observe patients for at least 12 hours. Hypotension should initially be treated with IV fluids; this should be done cautiously in patients with pre-existing cardiac disease or in those at risk of serious poisoning. In such cases CVP (central venous pressure) monitoring is advisable. Glucagon is the drug of choice for patients who are haemodynamically unstable. An average patient should receive a 10 mg IV bolus of glucagon and repeated as required or a 1– 10 mg/hour IV infusion, depending on the response. Vomiting is a useful indicator that an adequate dose has been given.

Iron Overdose Iron tablets are easily accessible to pregnant mothers. Iron poisoning is dangerous to the mother. It causes mitochondrial damage, interfering with cellular respiration and resulting in cellular dysfunction, metabolic acidosis and, ultimately, cell death, particularly in the liver. Toxic doses of elemental iron are: 30 mg/kg – moderate toxicity >60 mg/kg – severe toxicity >150 mg/kg could be lethal The clinical course of iron poisoning may be divided into four phases; the time scale is variable. What is presented in the following is only a guide. • Phase 1: Predominantly vomiting, diarrhoea, abdominal pain occurring 30 minutes to 6 hours post-ingestion. The vomitus and stools may be dark or bloodstained and may have a metallic smell. Leukocytosis and hyperglycaemia may occur. In severe cases, drowsiness, lethargy, coma, convulsions, metabolic acidosis, shock and gastrointestinal haemorrhage may occur. • Phase 2: Apparently asymptomatic phase occurring 6–24 hours post-ingestion. Some patients would not proceed beyond this phase. • Phase 3: At about 12–48 hours post-ingestion relapse may occur with severe lethargy, coma, convulsions, gastrointestinal haemorrhage, shock, cardiovascular collapse, metabolic acidosis, liver failure with hypoglycaemia, coagulopathy, pulmonary oedema and renal failure. • Phase 4: At 2–5 weeks stricture formation, pyloric stenosis and small bowel obstruction.

Treatment Patients who ingest >30 mg/kg body weight elemental iron require assessment and treatment.

Radiological Assessment and Gut Decontamination An abdominal radiograph should be performed following ingestion of a potentially toxic dose to determine the need for gut decontamination [3]. As there are potential fetal risks, this examination should be done after discussion with the patient. Iron tablets are radiopaque and they may be visualised on a radiograph. If tablets are visible in the stomach, gastric lavage may be performed. If they are detected further down the gastrointestinal tract, whole bowel irrigation should be carried out. Some tablets may not be seen on a radiograph. Measure serum iron level 4 hours after ingestion. Patients with serum iron levels between 55 and 90 µmol/L require only observation and intravenous fluids. A concentration >90 µmol/L indicates severe toxicity and warrants treatment with desferrioxamine. A dose of 15 mg/kg per hour as a continuous infusion (in 0.9% saline or 5% dextrose) should be

Drug Overdose in Pregnancy

administered. The dose should be reduced as soon as the clinical situation permits, usually after 4–6 hours, to prevent exceeding a dose of 80 mg/kg in any 24hour period. Chelation therapy should be continued until there are no radiological abnormalities and all symptoms have resolved.

Extracorporeal Drug Removal Some drugs may be effectively removed by haemodialysis. It is not contraindicated in pregnancy and should be offered to all mothers when indicated.

Supportive Care Most drug overdoses require only supportive care. This includes management of the airway in drug overdoses that may lead to reduced consciousness. Antiepileptics and sedatives are the most common drugs in this group. Some drugs may cause stimulation of the sympathetic nervous system. Salbutamol and theophylline are known examples. These patients present with an elevated blood pressure and tachycardia. Fluid replacement and sedatives such as benzodiazepines should be administered to such patients. Some drugs may induce a serotonin syndrome (e.g. selective serotonin reuptake inhibitors). These patients develop high temperatures and muscle rigidity. Such patients require active cooling measures and liberal IV fluids. Most overdoses with ordinary-release drugs require monitoring for at least 6–8 hours. Signs and symptoms should appear by this time lag. However, sustained-release drugs may produce symptoms as late as 18–24 hours post-ingestion.

Recent Developments Recent pharmacogenetic study looking at multiple CYP3A and other betamethasone metabolic pathway single nucleotide polymorphisms (SNPs) and glucocorticoid pathway genes found that both maternal and fetal genotypes were associated with respiratory distress syndrome after betamethasone treatment when controlling for gestational age and a host of other sociodemographic factors. Some individuals possess many copies of theCYP2D6 gene and are either extensive metabolizers (EMs) or ultrarapid metabolizers (UMs). The presence of these SNPs can be particularly relevant depending on the woman’s SNPs in UGT. UGT

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facilitates the excretion of opioids from the body. The combination of CYP2D6 UM status of the mother and infants with aUGTB7*2 genotype, indicative of reduced activity, can lead to toxicity of morphine in breastfeeding. Because these findings have explained infant deaths, the US FDA issued a Public Health Advisory for women who are breastfeeding and taking narcotics. Nifedipine (calcium channel blocker used in obstetrics to stop contractions and delay birth), a tocolytic is metabolized by the CYP3A family. Recent studies have demonstrated that polymorphisms in CYP3A5 and the use of CYP3A inhibitors can impact the concentration of nifedipine in maternal blood.

References 1. McClure CK, Patrick TE, Katz KD, Kelsey SF, Weiss HB. Birth outcomes following self-inflicted poisoning during pregnancy, California, 2000 to 2004. J Obstet Gynecol Neonatal Nurs. 2011;40 (3):292–301. 2. Czeizel AE. Attempted suicide and pregnancy. J Inj Violence Res. 2011;3(1):45–54. 3. Dart RC (ed.). Medical Toxicology, 3rd ed. Philadelphia: Lippincott Williams & Wilkins, 2003.

Further Reading Haas DM, Lehmann AS, Skaar T, et al. The impact of drug metabolizing enzyme polymorphisms on outcomes after antenatal corticosteroid use. Am J Obstet Gynecol. 2012;206 (5):447.e417–447.e424. Haas DM, Quinney SK, Clay JM, et al. Nifedipine pharmacokinetics are influenced by CYP3A5 genotype when used as a preterm labor tocolytic. Am J Perinatol. 2013;30(4):275–81. Madadi P, Avard D, Koren G. Pharmacogenetics of opioids for the treatment of acute maternal pain during pregnancy and lactation. Curr Drug Metab. 2012;13(6):721–7. Madadi P, Ross CJ, Hayden MR, et al. Pharmacogenetics of neonatal opioid toxicity following maternal use of codeine during breastfeeding: a case-control study. Clin Pharmacol Ther. 2009;85(1):31–5. US FDA Public Health Advisory. Use of Codeine by Some Breastfeeding Mothers May Lead to Life-Threatening Side Effects in Nursing Babies. 2007. www.fda.gov/Drugs/Drug Safety/PostmarketDrugSafetyInformationforPatientsandPr oviders/DrugSafetyInformationforHeathcareProfessionals/ PublicHealthAdvisories/ucm054717.htm

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28

Diabetic Ketoacidosis in Pregnancy Dagmar Krueger and Ayona Wijemanne

Key Facts • Diabetic ketoacidosis (DKA) is an acute medical emergency. It increases the morbidity and mortality for both mother and fetus. This is increased by delay in recognition and errors in management [1]. • The occurrence of DKA in women with diabetes who become pregnant is rare 1%–3% [2]. Newer reports quote lower incidences of 0.2% [3]. • It is more commonly seen in patients with type 1 diabetes but can occur in the presence of type 2 and gestational diabetes [4]. It might also be the first presentation with diabetes in pregnancy. • Most presentations occur in the second and third trimester. • The risk of maternal mortality is low (0.17%) if DKA is recognised and treated promptly [5]. There were no deaths in the most recent UK confidential enquiry report due to DKA [6]. A review from 2014 reported fetal demise in 15.6%, preterm births in 46.3% and neonatal intensive care unit (NICU) admissions in 59% of pregnancies [7]. In another slightly older review fetal death occurs in 60% at the time or within a week of the DKA and 40% within 1–11 weeks after the event. The exact reason is not understood [4]. Information on the long-term effect of DKA on the surviving fetus is lacking (pmjbmj. com/content/79/934/454). Diabetic ketoacidosis sin pregnancy). • Prompt recognition and management of this medical emergency complicating pregnancy is essential in order to optimize perinatal outcome for both mother and fetus. Incidence and mortality are likely higher in developing countries [8].

b. Dehydration and decreased caloric intake (e.g. nausea or hyperemesis gravidarum) c. Decreased buffering capacity (compensated respiratory alkalosis of pregnancy with bicarbonates usually reduced to 18–20 mmol/L) d. Increased production of insulin antagonists (human placental lactogen, prolactin and cortisol) [9] e. Increased prevalence of obesity which increases insulin resistance 2. Precipitating risk factors for the development of DKA (as in non-pregnant patients) are a. Infection-related acute illness (viral/ bacterial) b. Failure to take insulin as prescribed (usually due to patient non-compliance)[10] c. Less common i. Insulin pump failure (rare with modern pumps equipped with alarms to alert the patient when there is a lack of insulin delivery, but as pumps run fast acting insulin only if they are blocked the patient is entirely deprived of insulin and at risk to develop DKA quickly) ii. Concurrent use of medications (e.g. steroids, β-adrenergic medications) iii. Diabetic gastroenteropathy iv. Physician management errors

Pathophysiology of DKA Key Pointers 1 Factors that predispose the pregnant patient to DKA a. Accelerated starvation (especially in the second and third trimester) .030

https://www.cambridge.org/core. 21 May 2021 at 20:20:46,

Insulin enables glucose to enter muscle, liver and adipose tissues to cover energy demands and lowers the serum glucose concentration. If there is a reduction in effective circulating insulin and/or an increase in counter-regulatory hormones such as glucagon, catecholamines, cortisol, growth hormone, prolactin

Diabetic Ketoacidosis in Pregnancy

or human placental lactogen, then this results in insulin-sensitive tissues not being able to utilise glucose and more remains in the circulation. The liver increases glucose production, gluconeogenesis and glycogenolysis. These mechanisms cause hyperglycaemia, glucosuria and osmotic diuresis and dehydration. The liver further starts the pathway to gain energy from ketogenesis. The accumulation of ketone bodies results in metabolic acidosis. The ketone bodies in DKA are predominantly 3-β-hydroxybutyrate. These can be measured in urine or serum. The adipose tissue undergoes lipolysis, which is exquisitely sensitive to inhibition by insulin. Its activity is increased by the counter-regulatory hormones (especially catecholamines and cortisol). This further increase acidosis. Fluid depletion occurs in DKA via the following mechanisms: a. Osmotic diuresis due to hyperglycaemia b. Vomiting – commonly associated with DKA c. Reduced level of consciousness leading to inability of adequate fluid intake Electrolyte shifts and depletion are in part related to the osmotic diuresis. Hyperkalaemia and hypokalaemia are of particular importance.

Key Symptoms and Signs 1. Maternal symptoms are attributed to three main features +/− possible signs of infection: a. Hyperglycaemia. i. Polyuria (at the initial stage) ii. Polydipsia. b. Acidosis i. Nausea/vomiting ii. Abdominal pain (can be mistaken for threatened preterm labour) iii. Generalised malaise iv. Distinct smell on the breath (‘pear drops’) v. Tachypnoea c. Dehydration (consequence of hyperosmolarity and polyuria) i. ii. iii. iv. at 20:20:46,

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Dry skin/mouth Blurred eyesight Oliguria Tachycardia

v. Drop of blood pressure, shock vi. Lethargy, confusion, coma (cerebral dehydration and possible hypoxia, late sign) d. +/− Infection/ sepsis i. Cough, shortness of breath, fever if chest infection ii. Dysuria and/or loin pain if urinary tract infection/pyelonephritis Ketoacidosis should always be considered when a pregnant woman with diabetes feels unwell. These women must be assessed by a medical or diabetes team in due course. 2. Fetal signs a. Acidosis (diabetic ketoacidosis, lactacidosis, hyperuraemia and hypoxaemia) are all toxic to the fetus. Cardiotocograph (CTG) monitoring is advisable if fetus is of a viable gestation >28 weeks. Below this gestation the use of CTG is controversial. CTG is likely to show abnormal features with reduced variability +/− shallow decelerations. The treatment is resuscitation of the mother, which will lead to potential reversal of CTG changes. Delivery is associated with greater maternal complications and high fetal mortality and not a priority unless considered for maternal treatment, that is chorioamnionitis. Discussion with the fetal medicine team were available should occur if the CTG remains abnormal >4–8 hours [11] after her improvement, to exclude other causes of fetal compromise.

Diagnosis of DKA in Pregnancy DKA is characterised by the biochemical triad of 1. Presence of diabetes of any kind Women with diabetes may have only very modest elevation of blood glucose with DKA and do not need to reach >11 mmol/L. 2. Ketosis: a. Urinary ketones >2+ on dipstick or b. Blood ketones >3.0 mmol/L (the risk of developing ketosis increases when the level rises above 1.5 mmol/L) 3. Acidosis:

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a. Venous blood gas (VBG) pH 4 mEq/L are mentioned in the literature as other helpful findings [12].

Severe DKA The definition is based upon clinical appearance, observations, comorbidities and laboratory markers. Oxygen saturation and pulse rate in the maternity early obstetric warning score (MEOWS) levels should be adapted for pregnancy. Call for help early and escalate faster if one of more of the following are present [13]: 1. Blood ketones >6 mmol/L 2. Bicarbonate level 5.5 mmol/L. Aim for keeping K+ between 4.0 and 5.5 mmol/L. If the serum potassium level is 7.3 units; bicarbonate >15.0 mmol/L; and blood ketone