Ian Donald’S Practical Obstetrics Problems [8 ed.] 9789389859300

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Ian Donald’s

Practical Obstetric Problems Eighth Edition

Ian Donald’s

Practical Obstetric Problems Eighth Edition

Editor Renu Misra, MBBS, MS Senior Consultant & Head IVF Department of Obstetrics & Gynaecology Sitaram Bhartia Institute of Science and Research New Delhi Head Miracles Fertility and IVF Clinic Gurugram Formerly Additional Professor Department of Obstetrics and Gynaecology All India Institute of Medical Sciences New Delhi

Senior Publishing Manager: P Sangeetha Development Editor (Consultant): Dr Vallika Devi Katragadda Commissioning Editor: Gagandeep Kaur Production Editor: Megha Saini Assistant Manager-Manufacturing: Sumit Johry Copyright © 2020 by Wolters Kluwer Health (India) 10th Floor, Tower C, Building No. 10, Phase – II, DLF Cyber City Gurugram, Haryana – 122002 All rights reserved. This product, consisting of the printed book, is protected by copyright. No part of this book may be reproduced in any form or by any means, including photocopying, or utilized by any information storage and retrieval system without written permission from the copyright owner. The publisher is not responsible (as a matter of product liability, negligence, or otherwise) for any injury resulting from any material contained herein. This publication contains information relating to obstetrics and gynecology that should not be construed as specific instructions for individual patients. Manufacturers’ product information and package inserts should be reviewed for current information, including contraindications, dosages, and precautions. All products/brands/names/processes cited in this book are the properties of their respective owners. Reference herein to any specific commercial products, processes, or services by trade name, trademark, manufacturer, or otherwise is purely for academic purposes and does not constitute or imply endorsement, recommendation, or favoring by the publisher. The views and opinions of authors expressed herein do not necessarily state or reflect those of the publisher, and shall not be used for advertising or product endorsement purposes. Care has been taken to confirm the accuracy of the information presented and to describe generally accepted practices. However, the authors, editors, and publishers are not responsible for errors or omissions or for any consequences from application of the information in this book and make no warranty, expressed or implied, with respect to the currency, completeness, or accuracy of the contents of the publication. Application of this information in a particular situation remains the professional responsibility of the practitioner. Readers are urged to confirm that the information, especially with regard to drug dose/usage, complies with current legislation and standards of practice. Please consult full prescribing information before issuing prescription for any product mentioned in the publication. The publishers have made every effort to trace copyright holders for borrowed material. If they have inadvertently overlooked any, they will be pleased to make the necessary arrangements at the first opportunity. Eighth Edition, 2020 ISBN: 978–93–89859–30–0 Published by Wolters Kluwer (India) Pvt. Ltd., New Delhi Compositor: Mapsystems, Bangalore

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Preface The thought that came to my mind when I started working on this edition was, “Do we really still need a book? Why would someone want to read a book when all kind of scientific material is available freely on the internet?” But, after pondering on these questions a bit more, the answer was apparent. The very nature of information on the internet is what makes this book invaluable in this day and age. With a deluge of information on the internet—from sources both authentic and inauthentic— it is hard for students and especially for busy practitioners to filter out meaningful and trustworthy information. That is the void that this book aims to fill, providing comprehensive, vetted information and up-todate clinical practices. With medical science rapidly evolving, almost all chapters have something new to offer. Guidelines have changed, theories and practices have changed and newer treatment modalities are emerging. A welcome change in pregnancy is moving from invasive techniques to more conservative management strategies. Fetal cells can be identified in maternal blood for genetic analysis, and ultrasound is providing much more detailed and reliable information to diagnose and monitor intrauterine fetal problems. The age old labor norms have changed, recognizing that the pregnant population is now very different, with women being older, heavier and increasingly sedentary. And so, the chapter on labor has seen a major revision after a long time. With the ever-increasing incidence of cesarean births raising serious concerns worldwide, the issue has been addressed head-on and the strategies to reduce cesarean deliveries are discussed. To reiterate what I have always believed, and as the name of the book suggests, my focus has been on practical issues, and how to use our scientific knowledge to provide what is best for the patient. Knowing all the theories in the world is pointless if one does not know how to treat a patient. And above all, I have strived to reinforce that pregnancy is a physiological condition, and that at times, doing nothing may be the best intervention. I would like to thank my authors and co-authors who have put in great effort despite their busy clinical schedules. I also take this opportunity to thank the Wolters Kluwer India (WKI) team, particularly Vallika Katragadda, Consultant, who has supported me throughout this journey. She has painfully read every word of the book, made corrections, given constructive suggestions, and most of all has been patient with me. I must also put on record my appreciation and gratitude for Megha Saini, Production Editor. There are a number of other people, friends, and family, who have constantly helped me, I would like to say thank you all. I dedicate this book to All Those Who Have Craving For Knowledge. 

Renu Misra

List of Contributors Alka Kriplani, MBBS, MD, FRCS (Honorary) Director & Head Center for Minimally Invasive Gynecology, Obstetrics & ART Paras Hospitals, Gurugram Ex-Professor and Head All India Institute of Medical Sciences, New Delhi Amita Suneja,MD, FICMCH, FICOG Director Professor & Head              Department of Obstetrics & Gynecology University College of Medical Sciences & Guru Teg Bahadur Hospital, Delhi Anjan Trikha, MD, DA, FAMS, FICA, FAOA Professor  Department of Anesthesiology, Pain Medicine and Critical Care All India Institute of Medical Sciences, New Delhi Anju Singh, MBBS, MD Assistant Professor Department of Obstetrics & Gynecology All India Institute of Medical Sciences, New Delhi

Ashok Khurana, MBBS, MD Consultant Reproductive Ultrasound The Ultrasound Lab C584, Defence Colony, New Delhi Bindiya Gupta, MD, MAMS, FICOG Associate Professor Department of Obstetrics & Gynecology University College of Medical Sciences & Guru Teg Bahadur Hospital, Delhi Govind K Makharia, MBBS, MD, DM, DNB Professor Department of Gastroenterology and Human Nutrition All India Institute of Medical Sciences, New Delhi Jitender Nagpal, MBBS, MD Senior Consultant & Head Department of Pediatrics Sitaram Bhartia Institute of Science & Research New Delhi

Anubhuti Rana, MBBS, MD, Fellow MFM Assistant Professor Department of Obstetrics & Gynecology All India Institute of Medical Sciences, New Delhi

Kiran Guleria, MD, DNB, MNAMS, FICOG, FICMCH Director-Professor Department of Obstetrics & Gynecology University College of Medical Sciences & Guru Teg Bahadur Hospital, Delhi

K. Aparna Sharma, MBBS, MD Additional Professor Department of Obstetrics & Gynecology All India Institute of Medical Sciences, New Delhi

Madhavi Mathur Gupta, MBBS, MS Professor Department of Obstetrics & Gynecology  Maulana Azad Medical College, New Delhi

Asha Rijhsinghani, MD, FACOG Professor Maternal Fetal Medicine Department of Obstetrics and Gynecology Albany Medical Center Albany, NY, USA

Manju Khemani, MBBS, MD, FICOG Director Professor and Head Department of Obstetrics & Gynecology  Max Smart Super Specialty Hospital, New Delhi Ex-Professor Lady Hardinge Medical College, New Delhi

viii  Ian Donald’s Practical Obstetric Problems Manju Puri, MBBS, MD Director Professor and Head Department of Obstetrics & Gynecology Lady Hardinge Medical College, New Delhi Matthys H. Botha, MBChB, MMed, FCOG, PhD Associate Professor Department of Obstetrics and Gynecology Stellenbosch University, South Africa Mayank Priyadarshi, MBBS, MD, DM Consultant, WHO Project Department of Pediatrics All India Institute of Medical Sciences, New Delhi Neerja Bhatla, MBBS, MD Professor Department of Obstetrics & Gynecology All India Institute of Medical Sciences, New Delhi Nutan Agarwal, MD, MNAMS, FICOG, FICMCH, FIMSA, FGSI Senior consultant & Head, Fetal Medicine Department of Obstetrics & Gynecology Artemis hospital, Gurugram Ex-Professor All India Institute of Medical Sciences, New Delhi Preet Mohinder Singh, MBBS, MD  Assistant Professor  Department of Anesthesia, Division of Obstetric Anesthesiology Washington University in Saint Louis, MO Rakesh Yadav, MBBS, MD, DM Professor Department of Cardiology All India Institute of Medical Sciences, New Delhi Ramesh Agarwal, MBBS, MD, DM Professor Department of Pediatrics All India Institute of Medical Sciences, New Delhi Reeta Mahey, MBBS, MD, DNB Additional Professor Department of Obstetrics & Gynecology All India Institute of Medical Sciences, New Delhi

Renu Misra, MBBS, MS, MNAMS Senior Consultant & Head, IVF Department of Obstetrics & Gynecology Sitaram Bhartia Institute of Science & Research New Delhi Head, Miracles Fertility & IVF Clinic, Gurugram Ex-Additional Professor, All India Institute of Medical Sciences, New Delhi Richa Agarwal, MD, DNB Associate Professor                          Department of Obstetrics & Gynecology University College of Medical Sciences & Guru Teg Bahadur Hospital, Delhi Shalini Rajaram, MBBS, MD, FAMS, FICOG Director Professor & Unit Head Department of Obstetrics & Gynecology  University College of Medical Sciences & Guru Teg Bahadur Hospital, Delhi Suman Lal, MBBS, MD, FIMSA, FICMCH Senior Consultant Department of Obstetrics and Gynecology Max Healthcare Hospital, Gurugram Sumana Gurunath, MBBS, MD, DNB Consultant Infertility and Reproductive Medicine Cloudnine Hospitals, Bangalore Swati Sinha, MBBS, MD Senior Consultant Department of Obstetrics & Gynecology Sitaram Bhartia Institute of Science & Research New Delhi Vandana Mohan, MBBS, MS Senior Resident  Department of Obstetrics & Gynecology University College of Medical Sciences & Guru Teg Bahadur Hospital, Delhi Vatsla Dadhwal, MBBS, MD, FICOG, FIMSA Professor Division of Maternal Fetal Medicine Department of Obstetrics & Gynecology All India Institute of Medical Sciences New Delhi

Contents Prefacev List of Contributors 1. Antenatal care Renu Misra

vii 1

2. Miscarriage: Complications and management  Renu Misra

18

3. Prenatal screening and diagnosis of birth defects Asha Rijhsinghani

41

4. Ultrasound in obstetric practice Ashok Khurana

61

5. The high-risk gravida Renu Misra

87

15. Genital tract abnormalities: Congenital and acquired Nutan Agarwal

333

16. Premalignant and malignant conditions348 Shalini Rajaram, Matthys H. Botha 17. Antepartum haemorrhage Bindiya Gupta

357

18. Fetal growth restriction Neerja Bhatla, Reeta Mahey

381

19. Multiple pregnancy Manju Khemani

398

6. Common ailments in pregnancy Sumana Gurunath, Renu Misra

102

20. Polyhydramnios and oligohydramnios424 Renu Misra

126

21. Rhesus alloimmunization Alka Kriplani, K. Aparna Sharma

435

7. Anaemia Neerja Bhatla, Reeta Mahey

152

22. Preterm birth Sumana Gurunath, Renu Misra

454

8. Diabetes Renu Misra 9. Hypertensive disorders Renu Misra, K. Aparna Sharma

176

10. Cardiac disease Neerja Bhatla, Reeta Mahey, Rakesh Yadav, K. Aparna Sharma

211

24. Monitoring the fetus in pregnancy and labour Renu Misra

11. Renal disease Renu Misra

233

25. Normal labour Renu Misra

515

12. Liver disorders Suman Lal, Govind K. Makharia

245

26. Abnormal labour Renu Misra

530

13. Other systemic disorders Renu Misra, Madhavi Mathur Gupta

258

27. Analgesia and anaesthesia Anjan Trikha, P. M. Singh

563

14. Infections Vatsla Dadhwal, Anubhuti Rana

293

28. Induced labour Renu Misra

578

23. Prolonged pregnancy and stillbirth477 Renu Misra, Swati Sinha 489

x  Ian Donald’s Practical Obstetric Problems 29. Operative vaginal birth Sumana Gurunath, Renu Misra

596

35. Examination of the newborn Jitender Nagpal

717

30. Caesarean birth Renu Misra

615

36. Neonatal resuscitation 731 Mayank Priyadarshi, Ramesh Agarwal

31. Intrapartum maternal injuries Manju Puri, Vandana Mohan

641

32. Postpartum haemorrhage Amita Suneja, Richa Aggarwal

659

1. Normal laboratory values in pregnancy743

33. Postpartum collapse Renu Misra

683

2. Vaccination during pregnancy

744

3. Drugs in pregnancy and lactation

747

34. Puerperium Kiran Guleria, Anju Singh

695

Appendix

Index757

1

CHAPTER

Antenatal care Renu Misra

1 History

2 Maternal mortality 2.1 Measures of maternal mortality 2.2 Causes of maternal deaths 2.3 ‘Near miss’ 3 Perinatal and neonatal mortality 4 High-risk pregnancy 5 Pre-pregnancy care 6 Antenatal care

7

Booking visit 7.1 History-taking 7.2 Booking examination 7.3 Investigations at booking

8 Subsequent visits 8.1 Ultrasound

With the ever-increasing expectation of a perfect outcome of pregnancy and that ‘nothing should go wrong with the mother or the baby’, the obstetrician’s stress is leading to increasing medicalization of normal pregnancy. The calendar of pregnancy and labour is marked by advice on diet, lifestyle, blood tests, ultrasound scans and fetal monitoring. The population profile of the pregnant women has also changed in recent times. It now includes women that are older, obese, sedentary and with pre-existing medical and surgical conditions, factors which increase their risk during pregnancy and labour. This is a common urban or the metro scenario. India being a land of extremes in social demography, the problems in the rural and less resourceful society are different from those in the affluent settings. The obstetrician here still battles with anaemia, undiagnosed heart conditions, maternal infections, besides poor infrastructure



8.2 Screening for Down syndrome 8.3 Haemoglobin estimation 8.4 Screening for gestational diabetes 8.5 Routine antenatal anti-D prophylaxis for RhD-negative women 8.6 Tetanus immunization 8.7 Pelvic assessment 8.8 Imaging during pregnancy 8.9 Weight gain during pregnancy 8.10 Diet and supplements 8.11 Work 8.12 Exercise 8.13 Rest 8.14 Smoking 8.15 Alcohol 8.16 Travel 8.17 Sexual intercourse 8.18 Dental hygiene

to deal with emergencies and facilities to transport to higher centres. Nevertheless, the thrust in the last decade on better antenatal care facilities at primary and secondary care levels and institutional deliveries by the Government of India, coupled with general awareness in the population has contributed to a significant decline in maternal mortality in various parts of the country. While the hazards of pregnancy and labour to the mother continue to recede, those to the fetus during its intrauterine existence have come to be recognized more explicitly. The first 38 weeks of human life spent in the presumably protected environment of the amniotic sac are medically more eventful and fraught with danger and accident than the next 38 years of life. The scope of antenatal care is, therefore, widening rapidly. Much has been achieved over the last century and a brief look into the history shows how far we have come.

2  Ian Donald’s Practical Obstetric Problems

1  History Antenatal care began as a social service in Paris in 1788 for women who had committed the double offense of being both pregnant and destitute. These pitiable creatures were housed, sometimes two or three to a bed, in the Hôtel Dieu and Hôpital Salpetrière from the 36th week of pregnancy onwards. It was in Edinburgh at the very end of the 19th century that the first effective medical and scientific interest was shown in the antenatal patient. In 1902, the first antenatal bed was endowed for the purpose. Admittedly Ballantyne’s original concern was fetal deformity and stillbirth, but this soon came to embrace a wider interest in maternal wellbeing, which on more general adoption by the end of World War I had swamped concern for the unborn child. In fact until the period following World War II it was thoughtlessly assumed that antenatal care that was good enough for the mother was good enough to cover the needs of the baby as well. A few heretics talked about ‘antenatal paediatrics’ but they were not taken very seriously. This complacency was shaken first by the recognition of the possible effects of certain viruses upon the baby following Gregg’s observations in 1941 in Australia on the association between maternal rubella in early pregnancy and cataract1 and secondly by Dr. Alice Stewart’s enquiry in 1956 into the harmful effects of X-rays upon the fetus, increasing the hazard of leukaemia in later childhood,2 and finally at the end of 1961, came the terrible tragedy of thalidomide-­ deformed babies3–6 after the association between this drug and limb and intestinal deformities was first suspected in Western Germany. The firm supplying thalidomide very rightly withdrew the drug from sale at the first suggestion of responsibility, but even so it was estimated that not less than 800 babies in the UK alone were likely to have been damaged. This epidemiological investigation provided much food for thought. If such a catastrophe could follow the taking, in early pregnancy, of so apparently harmless a sedative and anti-emetic as thalidomide, then what of the possible effects of all sorts of other agents, drugs, poisons, radiations, metabolic diseases, even psychosomatic and stress disorders? Old wives’ tales have long told of how important it was that the mother should be in a happy frame of mind to ensure a healthy and

happy baby. It has now been confirmed using multiple regression analysis that alcohol intake in pregnancy, gestational depression, low educational level and the occurrence of negative life events during pregnancy are associated with low neuro-developmental scores subsequently.7 We are now all aware of the intrauterine vulnerability of the baby. Advances in diagnostic modalities and intrauterine therapy mean that congenital abnormalities can no longer be accepted with fatalism. And so the wheel has turned full circle and Ballantyne’s original teratological interest is revived. Technological advancements that facilitate antenatal detection of fetal birth defects and fetal compromise like ultrasonography, maternal serum markers, biochemical tests for metabolic defects, fetal karyotyping and Doppler ultrasound have become an integral part of our current obstetric practice. Increased awareness on the part of patients has meant an increase in their role in d ­ ecision making regarding management strategies during pregnancy and the mode of delivery. Newer developments like the practice of evidence-based medicine, the mapping of the human genome and the emphasis on outcomes-based research will further change the face of future obstetrics, hopefully working in synergy, to fulfil the primary aim of antenatal care, which is to reduce maternal and perinatal morbidity and mortality.

2   Maternal mortality Maternal mortality is defined by World Health Organization (WHO) as the death of a woman while pregnant or within 42 days of termination of pregnancy, irrespective of the duration and site of pregnancy, from any cause related or aggravated by the pregnancy but not from accidental or incidental causes. Direct obstetric deaths.  They are those resulting from obstetric complications during pregnancy, delivery and postpartum. Deaths due to, for example haemorrhage, pre-eclampsia/eclampsia, complications of anaesthesia or caesarean section are classified as direct obstetric deaths. Indirect obstetric deaths.  They are those resulting from previous existing disease, or diseases developing during pregnancy, not due to direct obstetric causes but aggravated by physiological

Antenatal care  3

effects of pregnancy. For example, deaths due to aggravation of an existing cardiac or renal disease are indirect obstetric deaths. An amendment made to ICD-10 (International Classification of Diseases) in 2010 now includes indirect maternal deaths due to HIV in maternal mortality. The scope of maternal mortality has been widened in the ICD-10 to include pregnancy-related death, which is defined as any death during pregnancy, childbirth, or the postpartum period even if it is due to accidental or incidental causes. Complications of pregnancy can sometimes lead to death after the six weeks postpartum period; these are now categorized as late maternal deaths. Late maternal death is defined as death of a woman from direct or indirect obstetric causes, more than 42 days but less than one year after the termination of pregnancy.

2.1 Measures of maternal mortality yy Maternal mortality ratio (MMR). It is the number of maternal deaths during a given time period per 100,000 births during the same time period. yy Maternal mortality rate. It is the number of maternal deaths during a period per 100,000 women of reproductive age during the same time period. yy Adult lifetime risk of maternal death is the probability of dying from a maternal cause during a woman’s reproductive lifespan. Although maternal mortality worldwide has dropped by 44% between 1990 and 2015, it is still unacceptably high. Approximately 830 women

die every day due to causes related to pregnancy and childbirth, 99% of these deaths occur in developing countries. The risk is greater in rural and low socioeconomic population, and in young adolescents.8 National Rural Health Mission (NHRM), now under National Health Mission, was launched in 2005 by the Government of India. One of the key initiatives of NHRM was Janani Suraksha Yojna, which promoted institutional delivery with the aim to provide safe delivery and emergency obstetric care in rural areas. As a result, India shown a remarkable decline in MMR by 77%, from 556 per 100,000 live births in 1990 to 130 per 100,000 live births in 2016. Under millennium development goal 5 (MDG 5), the goal was to reduce the maternal mortality by 75% between 1990 and 2015. Though it was not achieved by 2015, India’s present MMR is below MDG target and the country is now committed to achieve the United Nations Sustainable Development Goal (SDG) target of an MMR below 70 by 2030.9 Table 1.1 shows estimates of MMR and lifetime risk in different United Nations Millennium Development Goal (MDG) regions, 201510 and Table 1.2 shows MMR, maternal mortality rate and lifetime risk in different states of India as reported by Sample Registration System, Office of Registrar General India 2014–16.11 The MMR in India has declined by 68.7% between 1990 and 2015. The National Health Policy 2017 target was to achieve an MMR of 100 per 100,000 live births by 2020, which has been achieved by 11 states ahead of time. The next SDG target 3.1 given by WHO calls for a reduction in the global MMR to less than 70 per 100,000 by 2030.

Table 1.1  Estimates of maternal mortality ratio (MMR) and lifetime risk in different Millennium Development Goal (MDG) regions, 201510 MDG regions

World

MMR

Lower estimate

Upper estimate

Lifetime risk of maternal death 1 in

216

207

249

180

Developed regions

12

11

14

4900

Developing regions

239

229

275

150

70

56

92

450

546

511

652

36 2300

Northern Africa Sub-Saharan Africa

27

23

33

Southern Asia

Eastern Asia

176

153

216

210

South Eastern Asia

110

95

142

380

Western Asia

91

73

125

360

Central Asia

33

27

45

1100

4  Ian Donald’s Practical Obstetric Problems Table 1.2  Maternal mortality ratio (MMR), maternal mortality rate and lifetime risk of death in India and its states (SRS 2014–16)11 MMR

Maternal mortality rate

Lifetime risk %

INDIA TOTAL

130

8.8

0.3

Assam

237

16.2

0.6

Bihar/Jharkhand

165

15.8

0.6

MP/Chhattisgarh

173

15.7

0.5

Odisha

180

12.3

0.4

Rajasthan

199

18.3

0.6

UP/Uttarakhand

201

17.1

0.6

Andhra Pradesh

74

3.6

0.1

Telangana

81

4.2

0.1

Karnataka

108

8.4

0.3

Kerala

46

2.1

0.1

Tamil Nadu

66

5.2

0.2

Gujarat

91

6.4

0.2

Haryana

101

8.2

0.3

61

3.7

0.1

Punjab

Maharashtra

122

6.9

0.2

West Bengal

101

5.5

0.2

2.2  Causes of maternal deaths The major complications that account for nearly 75% of all maternal deaths are: yy Haemorrhage (mostly postpartum haemorrhage) yy Infection yy Pre-eclampsia and eclampsia yy Obstructed labour and other complications of delivery yy Embolism yy Unsafe abortion The remaining are caused by diseases such as malaria, anaemia and HIV/AIDS during pregnancy.

2.3  ‘Near miss’ It is defined by the WHO as the near death of a woman from a complication during pregnancy, childbirth or within 42 days after the termination of pregnancy.12 Investigating near misses provides an opportunity to understand factors contributing to maternal mortality and how it

can be prevented, particularly where MMR is low, and the event of maternal death is rare.

3  Perinatal and neonatal mortality Nearly three million babies are stillborn every year worldwide with a global stillbirth rate of 18.4/1000 births.13 The WHO’s goal of Every Newborn: An Action Plan To End Preventable Deaths aims to reduce the stillbirth rate to 12 or less per 1000 births by 2030 in every country, and for countries already meeting this target to reduce equity gaps. There is currently no systematic reporting for the causes of stillbirths. The WHO has therefore included International Statistical Classification of Diseases and Related Health Problems-Perinatal Mortality (ICD-PM) as part of ICD to improve reporting of causes of stillbirth and neonatal mortality.14,15 According to WHO, the perinatal period commences at 22 completed weeks (154 days) of gestation and ends seven completed days after birth. The causes of perinatal mortality (PM) are listed in Table 1.3.

Antenatal care  5

Table 1.3  Causes of stillbirths and early neonatal deaths in low- and middle-income countries19 Late stillbirth n=416 n (%)

Early neonatal deaths n=271 n (%)

Hypertensive disorders

98 (23.6)

22 (8.1)

Antepartum haemorrhage

68 (16.3)

20 (7.4)

Intrapartum asphyxia

66 (15.9)

106 (39.1)

Cause

Fetal abnormality

12 (2.9)

12 (4.4)

Infections

7 (1.7)

1 (0.4)

Maternal disease

6 (1.4)

1 (0.4)

Spontaneous preterm births

5(1.2)

104 (38.4)

Intrauterine growth restriction

4 (1.0)

Trauma

0.7

Miscellaneous

0.7

Unexplained intrauterine death

The neonatal period begins with birth and ends 28 complete days after birth. Neonatal deaths may be subdivided into: yy Early neonatal deaths, occurring during the first seven days of life (0–6 days). yy Late neonatal deaths, occurring after the seventh day but before the 28th day of life (7–27 days). The first 28 days after birth are the most critical days for survival for a newborn with a global neonatal mortality of 18/1000 live births in 2017. 2.5 million babies die globally in a year in the first month of life, about one million dying on the first day and another one million in the next six days of the first week. (UNICEF 2018).16 The common causes of neonatal death are congenital malformations, prematurity, intrauterine hypoxia during pregnancy and delivery, and infection. It is now clear that agents which do not harm the mother can damage rapidly growing tissues of the fetus. The damaging effects of X-rays and rubella virus are among the few that are well known. Thalidomide disaster is a classic example of a seemingly harmless drug used in early pregnancy for relief of morning sickness. In spite of an intensive witch-hunt for possibly teratogenic drugs in addition to thalidomide, remarkably little has so far been sub‑ stantiated. There are two reasons for this – firstly, the natural incidence of fetal abnormality (2–3% of all babies, alive or dead) for which no

0

34.6

­ xplanation can be found. Secondly, the species e difference, which invalidates the observations made on experimental animals to some extent, as they may not necessarily apply to the human fetus. According to the report of Ministry of Family Welfare, Government of India 2017, the overall PNMR in India declined from 37/1000 births (live births + stillbirths) in 2006 to 23/1000 in 2015; the rural perinatal mortality rate (PNMR) was 26 and urban was 15/1000. The stillbirth rate over the same period declined from 9/1000 to 4/1000.17 For comparison, the extended PNMR (stillbirths + neonatal deaths) of UK in 2017 was 5.64 per 1000 total births, comprising of 3.93 stillbirths per 1000 total births and 1.72 neonatal deaths per 1000 live births.18

4   High-risk pregnancy One of the responsibilities of an obstetrician is to identify women at high risk for pregnancy, labour and delivery. This helps the obstetric team, the patient and her family to plan and prepare for the extra care that a woman may require to achieve a normal pregnancy outcome. It does not necessarily mean that there will be a problem with the mother or the baby, if the necessary precautions are taken. Table 1.4 gives a list of high-risk factors. This list is by no

6  Ian Donald’s Practical Obstetric Problems Table 1.4  High-risk factors in pregnancy Category

Pre-existing medical conditions

Condition

• • • • • • • • • •

Hypertension PCOS Diabetes Heart disease Respiratory disease Chronic kidney disease Autoimmune disease Thyroid disease Obesity History of deep vein thrombosis • HIV positive status

Age

• Teenage 35 years

Pregnancy complications

• • • • • • • •

Multiple gestation Gestational diabetes Pre-eclampsia/eclampsia Antepartum haemorrhage Previous preterm birth Fetal growth 4000 g.35 Low maternal weight gain (20 mm on transvaginal scan Rarely, a pregnancy considered blighted may show evidence of growth, when re-examined a week later and may subsequently culminate in the birth of a healthy normal baby. This is of course extremely rare with the high-resolution ultrasound machines in use today. However, since there is no harm in waiting, it is prudent to offer the patient a follow-up study after 7–10 days to exclude error before pronouncing the diagnosis.

24  Ian Donald’s Practical Obstetric Problems The ultimate fate of these cases is spontaneous miscarriage, when the tissue that is frequently not recognized or not recognizable is passed to the accompaniment of bleeding, sometimes not much more than a period. If the material is fresh enough, it can be submitted for chromosomal analysis. It is estimated that 65% of these first trimester miscarriages have embryos with abnormal karyotype.19 The incidence increases with maternal age, the rate of chromosomal abnormality was found to be 57.2% in women younger than 35 years, and 82.5% in those 35 years or older.20 Although tragic, when the pregnancy is a wanted one, more so in women in whom this condition tends to be recurrent, it is nature’s way of reducing the burden of handicap. Fetal abnormalities which go through to term are simply the tip of this iceberg.

4  Differential diagnosis 4.1  Ectopic gestation The most important differential diagnosis is that of ectopic gestation, in which the clinical findings are by no means always characteristic. Typically, the onset of pain tends to precede bleeding, the latter usually dark in colour. There may be a history of fainting attack. The patient’s symptoms and general condition may be out of proportion to the amount of perceived blood A prolonged clinical lifetime has not, however, reduced the number of mistakes that I (and incidentally my colleagues) make from time to time, resulting either in a missed diagnosis or occasionally in an unnecessary laparotomy. Cases frequently present in altogether atypical fashion. Commonly, a persistently positive immunological urine test could lead one to treat a case of continuing mild vaginal bleeding as one of threatened miscarriage, with only vague clinical signs within the pelvis. Ultimate curettage in such a case shows only decidua and no villi, which should immediately alert one to the diagnosis of a pregnancy elsewhere. Even a negative urine test does not eliminate the possibility of a tubal mole with continuing invasive properties. Such a mistake once resulted in a massive haemoperitoneum some days after I had discharged the patient from hospital. – Ian Donald

loss. On vaginal examination, tenderness and pain on moving the cervix can be usually elicited, a boggy indefinite tender mass may be felt either behind the uterus or to one side of it. Abdominal rigidity is very rare. ‘When in doubt, do it’ was indeed standard teaching in the management of ectopic pregnancy until the development and easy availability of serum β-hCG testing, transvaginal ultrasound and laparoscopy. With highly sensitive urine pregnancy tests, if the test is positive and the uterus is empty on ultrasound, a diagnosis of ectopic pregnancy should be made unless proved otherwise. Because of the ready availability of both pregnancy test and the ultrasound, a number of ectopic pregnancies are now diagnosed even before any symptoms occur or at a very early stage with mild bleeding and discomfort and stable haemodynamic condition. This has opened up the possibility of treating ectopic pregnancies medically without the need for surgery. Serum β-hCG level is of great help in such situations to decide the management. Expectant management can also be offered in stable patients, when serum β-hCG level is less than 1000 IU/l and the size of the ectopic is less than 3 cm. When the levels are higher, it is preferable to administer a single intramuscular injection of methotrexate (50 mg/m2) and repeat serum β-hCG levels on day 4 and 7. Serum β-hCG level of more than 10,000 IU/l and/or the presence of cardiac activity are relative contraindications for medical management, although successful treatment has been reported. A 15% fall in the β-hCG level between day 4 and 7 is considered satisfactory and further monitoring continued, although the risk of tubal rupture and the need for surgery cannot be ruled out completely. If the levels plateau or rise, another injection may be given on day 7. An initial rise on day 4 is not significant as it may occur due to release of the hormone from the trophoblastic tissue. Medical treatment is successful in nearly 90% of cases. However, the hCG levels need to be followed up weekly till they are negative both in expectant as well as medical management. Surgery may be indicated, when the criteria for non-surgical management are not met, or there are symptoms suggestive of impending rupture or rupture of the ectopic sac. Laparoscopy is the preferred surgical access provided

Miscarriage: Complications and management   25

there is availability of appropriate equipment as well as surgical expertise, and the patient is not in shock. A salpingostomy or salpingectomy may be performed as deemed appropriate. Monitoring of serum β-hCG levels is essential, when the tube is preserved as described for non-surgical management. For more details of management and follow-up, a standard textbook of gynaecology should be referred.

4.2 Dysfunctional uterine bleeding All types of dysfunctional uterine bleeding may simulate miscarriage, particularly in cases of anovulatory bleeding, in which a period of amenorrhoea may have preceded the onset of bleeding. Pain is usually not a feature of such bleeding, although it may occur at times due to passage of large clots.

4.3 Fibroids Fibroids, likewise, may produce bleeding, together with signs of uterine enlargement, and occasionally there is associated pain due either to the attempt on the part of the uterus to extrude a fibroid polyp or, occasionally, due to acute degeneration in the fibroid, but fibroids never produce amenorrhoea.

4.4 Benign and malignant growths of cervix Other pelvic lesions that can simulate a miscarriage may be benign growths of the cervix. The most common is a cervical polyp; rare lesions are cervical tuberculosis. Premalignant and malignant growths may present with vaginal bleeding during pregnancy and mimic an abortion.

4.5  Hydatidiform mole It is a condition which arises from defective fertilization. It can be complete or partial. Complete hydatidiform moles are androgenetic with two sets of paternal haploid genes and none from the mother, probably due to duplication of the haploid sperm, or two haploid sperms fertilizing an empty ovum. There is no sign of fetus or fetal tissues in this variety. Partial moles are triploid with an extra set of haploid genes from the father, with evidence of fetus or fetal red blood cells. The usual presentation is with bleeding and early pregnancy failure. Early diagnosis with ultrasound has dramatically

changed the clinical pattern of the condition, with complications like hyperemesis, pre-eclampsia and hyperthyroidism becoming extremely rare. The typical history of passage of grape-like vesicles is seldom obtained nowadays. If diagnosed later in first trimester or second trimester, the uterus can be appreciated to be larger in size than the period of gestation. The classical snowstorm appearance on ultrasound can be seen in cases of complete mole, although a number of histologically proven complete moles are diagnosed as delayed or missed miscarriage or anembryonic pregnancy. All products of evacuation should be, therefore, sent for histological examination. Ultrasound picture in case of partial mole is much more variable and complex. Cystic changes may be seen in the placenta, but the diagnosis is usually confirmed on histopathology. Surgical treatment using suction curettage is the method of choice. Medical termination of complete molar pregnancies is not recommended as there are theoretical concerns of dissemination of trophoblastic tissue through the venous system. Medical methods of uterine evacuation have been reported to be associated with increased rates of chemotherapy.21 Use of oxytocics should be however avoided until after evacuation of the uterus for this reason, unless there is significant haemorrhage and the clinical condition dictates their use. Prostaglandins can be used for ripening the cervix before evacuation.

5  Management 5.1  Threatened abortion Patient should be advised to avoid strenuous activity and sexual intercourse, but strict bed rest is not necessary.22 If bleeding persists, ultrasound should be done to assess fetal viability and exclude ectopic pregnancy. If the uterine size is greater than the period of gestation, twins and molar pregnancy should be excluded. Medical treatment with estrogens or progesterone, and tocolytics is ineffective and not recommended.23 Sometimes apparently successfully treated threatened miscarriages with progestogens are later found to be missed, the amenorrhoea continuing because of the artificial progesterone support. One must bear in mind that in a normally implanted ovum, confirmed on ultrasonography to be alive and

26  Ian Donald’s Practical Obstetric Problems growing, and where there is no cervical incompetence, the chances of pregnancy continuing successfully on its own are very high. Ultrasonography should be repeated after 1–2 weeks to ensure all is well with the fetus. Speculum examination may be required in case bleeding continues beyond a few days to rule out any lesion in the lower genital tract. If blood loss is sufficient to cause anaemia or hypovolaemia, chances of pregnancy continuing successfully are remote.

5.3 Inevitable and incomplete miscarriage When the miscarriage is inevitable or incomplete, surgical evacuation, medical or expectant management are all reasonable options depending on the amount of bleeding, haemodynamic status and the patient’s choice. The objective is to encourage the uterus to complete the process and convert an inevitable or incomplete miscarriage into a complete one.

5.2  Complete miscarriage

General resuscitation measures should be implemented while the woman is being prepared for the procedure. Some cases are already so exsanguinated and shocked that immediate attention must first be given to their resuscitation. Blood transfusion is the most important single measure but crystalloid infusion should be started immediately with a wide bore intravenous canula to correct hypovolaemia, till blood is available. Dextran infusions may provoke clotting defects, therefore, should be used with caution. The continuous administration of oxygen by mask is helpful in addition to other general measures, such as judicious warmth and the raising of the foot of the bed.

In the case of a miscarriage that is deemed complete by inspection of the POC that have been passed or an ultrasound confirmation that the cavity is empty, no local treatment is indicated. However, if the patient continues to bleed, a check curettage may be performed. However, curettage is not justified as a routine procedure after miscarriage, as it increases the immediate risks of perforation and infection, and uterine rupture in a subsequent pregnancy. Routine administration of ergometrine after complete miscarriage is neither required nor desirable.

yy Expectant management It can be tried in a patient with minimal bleeding, but if expulsion does not occur in reasonable time, one needs to proceed with medical or surgical management. yy Medical management If the patient is stable with minimal bleeding, medical management can be tried. See Table 2.1 for medical management protocols. If it fails, surgical management should be undertaken. yy Surgical evacuation If the bleeding is significant, evacuation is the best option. If

Even though threatened miscarriage may be successfully treated, the pregnancy continues at a greater risk than normal. There is a significantly increased risk of placenta praevia, antepartum haemorrhage of unknown origin, low birth weight and perinatal mortality in women who have bleeding in early pregnancy.24,25 The evidence that threatened miscarriage increases the incidence of subsequent fetal abnormality is less clear. Fetal abnormality is far less likely to be the result of threatened miscarriage than the cause of miscarriage itself.

Table 2.1  Medical management for inevitable and incomplete abortion (WHO)22 Type of miscarriage

12–14 weeks

Inevitable miscarriage

Misoprostol 800 μg can be given vaginally or sublingual every 3–12 hours for a maximum of three doses

Misoprostol 400 μg vaginal or sublingual every 3 hours for maximum five doses OR Oxytocin 40 units in 1 l can be given IV at 40 drops per minute

Incomplete miscarriage

Misoprostol 400 μg sublingual or 600 μg by mouth is given for one dose

Misoprostol 200 μg by vagina every 4 hours (maximum 800 μg) OR Oxytocin 40 units in 1 l IV at 40 drops per minute

Miscarriage: Complications and management   27

the products are visible in the os or in the vagina, they can be removed with a sponge forceps. If the products are not visible, suction evacuation should be carried out. If the uterus is perforated in the course of this operation, a laparoscopy should be performed and haemostasis achieved. The evacuation, if incomplete, may also be completed under laparoscopic guidance. However, at times, the first warning of perforation may be the prolapse of omentum or bowel into the vagina or outside, the only safe measure in such circumstances is immediate laparotomy, repair of the rent and evaluation of the bowel. It will, therefore, be appreciated that evacuation of the pregnant uterus demands the availability of proper theatre facilities.

5.4  Missed miscarriage Clinically, the uterus fails to increase in size over a period, and indeed may regress in size. This course of action however is rarely required nowadays because an ultrasound exam would promptly and definitely make a diagnosis of missed miscarriage by the absence of cardiac activity in the fetus. An exception to this is a case of very early pregnancy or mistaken dates, where non-­visualisation of cardiac activity at an early gestation may be misinterpreted as absence of cardiac activity. A repeat ultrasound in 10–14 days would reveal fetal heart activity, if the pregnancy is viable. Management is either medical, surgical or expectant. About 50% women with anembryonic pregnancy and 35% with missed miscarriage will abort completely within 14 days, when followed expectantly.26 For medical management, misoprostol 800 μg vaginal or 600 μg sublingual can be given every three hours for two doses for first trimester miscarriage. To abort a second trimester missed pregnancy, 200 mg vaginal or sublingual (in case of vaginal bleeding) can be given every 4–6 hours till the patient aborts or maximum of four doses.27 Mifepristone is not recommended for the medical treatment of missed or incomplete miscarriage.28 The incidence of adverse effects like pain, diarrhoea and fever are greater with sublingual as compared to vaginal route.29 Oral misoprostol is also effective although the

time taken for expulsion of products is longer than with the vaginal route.30 With the availability of extremely effective prostaglandins, the oxytocin drip in escalating dosage is almost a thing of the past for the treatment of missed miscarriage in the second trimester. Although rare, there is a potential danger of serious coagulation defects developing, if a dead fetus is retained in utero for more than 4–6 weeks, but this is more likely in the case of a second trimester fetal death. The cornerstone of the treatment is to eliminate the underlying cause, that is, to evacuate the uterus of the dead fetus, together with other supportive therapy. Replacement of blood components like packed red cells, platelet concentrates, fresh frozen plasma and cryoprecipitate is done as indicated by the ­laboratory tests.

5.5 Anti-D prophylaxis for Rh-negative women Fetal–maternal transfusion has been demonstrated as early as 5–6 weeks of gestation.31 The mean volume of fetal–maternal transfusion at eight weeks has been calculated to be 0.33 ml. The amount of blood needed to cause isoimmunization has been estimated to be 0.25 ml. Therefore, theoretically, there is a possibility of isoimmunization in miscarriages after eight weeks of gestation, if not treated by prophylactic anti-D immunoglobulin (Ig). The question, however, is not completely resolved whether fetal red cells can express RhD antigen in early pregnancy. Bergstrom in 1967 demonstrated that fetal RBCs express the antigen as early as 52 days from the last menstrual period (over seven weeks of pregnancy),32 but there is no recent evidence to substantiate these early findings. Another controversial issue is that the evidence to support the use of anti-D immunoglobulin (lg) in the first trimester is based on studies assessing fetomaternal haemorrhage by Kleihauer-Betke (KB) test and not on detection of RhD antibodies. This severely limits the validity of the data estimating the incidence of Rh isoimmunization in the first trimester, more so because the correlation between KB test to assess fetomaternal haemorrhage and the subsequent seroconversion as demonstrated by Indirect Coombs test is poor.

28  Ian Donald’s Practical Obstetric Problems Overall the available evidence suggests that the chances of significant fetomaternal haemorrhage in the first trimester is very low unless there is instrumentation33 or miscarriage is induced medically, which is likely to be associated with stronger uterine contractions. The British Committee for Standards in Haematology has given guidelines for anti-D Ig prophylaxis in Rh-negative women not previously sensitised.34 It recommends administration of 250 IU of anti-D within 72 hours in the following conditions: yy Ectopic pregnancy regardless of the mode of management (surgical or medical) yy Molar pregnancy yy Therapeutic termination of pregnancy (surgical or medical) yy Pregnancy associated with repeated heavy bleeding or associated with pain In cases of spontaneous miscarriage with mild painless vaginal bleeding which stops before 12 weeks, and in pregnancy that continues with fetal viability documented on ultrasound, the risk of fetomaternal haemorrhage is negligible. Hence administration of anti-D is not required. Rh-negative women with continuous bleeding between 12 and 20 weeks should be given 250 IU of anti-D every 6 weeks. A test for fetomaternal haemorrhage is not required in pregnancies before 20 weeks.

dysfunction associated with a higher risk of mortality.35 The basic principles of treatment of septic miscarriage include the removal of the infected POC and intravenous administration of broad-spectrum antibiotics. Cultures, both aerobic and anaerobic, should be obtained before any antibiotics are administered, but pending the return of sensitivity reports from the bacteriologists, broad-spectrum antibiotics should be administered in appropriate dosage. Though there is a danger of disseminating infection by surgical interference like curettage, it is also important to remove the septic focus so that the antibiotics can bring infection under control. Uterine evacuation is, therefore, planned 6–12 hours after initiation of antibiotic therapy. The hazards of surgical evacuation of the uterus are greatly increased in septic miscarriage because the uterus is very soft and may be very easily perforated. One standard antibiotic regimen for severe pelvic sepsis is as follows36: Penicillin 5 million units IV every 6 hours or ampicillin 2 g IV every 6 hours PLUS Gentamicin 2 mg/kg loading dose, followed by 1.5 mg/kg every 8 hours OR 5 mg/kg every 24 hours depending on blood levels and renal status PLUS

6   Septic miscarriage Septic miscarriage is any miscarriage, spontaneous or induced, complicated by infection of the uterus or its contents or both. Septic-induced miscarriages resulting from criminal interference far outnumber the spontaneous ones, although the principles of management of spontaneous miscarriages complicated by infection are no different. Sepsis is now defined, as per the Third International Consensus Definitions for Sepsis and Septic Shock 2016 (Sepsis-3), as life-threatening organ dysfunction caused by a dysregulated host response to infection. Septic shock is a subset of sepsis with circulatory and cellular/metabolic

Clindamycin 900 mg IV every 8 hours OR metronidazole 15 mg/kg initially followed by 7.5 mg/kg every 8 hours. Infection can be localised to the uterus, or it may extend to the parametrium producing adnexal masses and a localised peritonitis or, in unfortunate circumstances, even generalised peritonitis. Continuing tachycardia and rigors are suggestive of disseminated infection and blood cultures should be obtained in all such cases. Failure to respond within 36–48 hours suggests either the development of a pelvic abscess or some undiagnosed complication, such as uterine perforation or bowel injury in criminally induced cases. Laparotomy may be necessary in such a case, and hysterectomy may

Miscarriage: Complications and management   29

be warranted in a critically ill women with severe post-abortal sepsis. Infection in criminally induced cases is frequently polymicrobial and varying combinations of Gram-negative and Gram-positive aerobic and anaerobic organisms have been implicated. Most often the causative organism is Escherischia coli. Other organisms seen include group A β-haemolytic streptococci, Bacteroides species, peptostreptococci, Pseudomonas aeruginosa, Staphylococcus aureus, Clostridia, Enterococcus faecalis, Haemophilus influenzae and Campylobacter fetus and jejuni. This vast spectrum is the natural consequence of the rich microflora of the vagina and perianal area and common contaminants of instruments used to perform the procedure. Tissue ischaemia, devitalised tissue, extravasated body fluids and foreign bodies, all encountered in cases of criminal miscarriage, provide a fertile environment for the anaerobes to grow. Clostridium perfringens (earlier known as C welchii) infection which causes gas gangrene is rarely seen nowadays. Gas gangrene is characterised by rapidly spreading tissue edema, necrosis, myositis, gas production, profound toxaemia and thin, often haemorrhagic exudates, which may manifest as a brownish vaginal discharge. It is frequently complicated by intravascular haemolysis and oliguria. It should be noted, however, that gas formation and its clinical correlate, crepitus, are not limited to clostridial infection only. Infection with other organisms like Escherichia, Enterobacter and mixed anaerobic growth can also result in gas formation in the tissues. The patient has a subnormal temperature, a rapid, thready pulse, hypotension and oliguria. Increasingly refractory hypotension, haemorrhage and a characteristic bronzing of skin (due to haemolysis secondary to α toxin) may develop. Consciousness is retained till the end, and X-rays may show the presence of gas. Laboratory studies in patients with clostridial septicaemia reveal increased leucocyte counts and occasionally pink, haemoglobin-tinged plasma. Anaemia is proportionate to the degree of haemolysis, the haematocrit may be extremely low and platelets may be decreased. However, there is a pronounced lack of inflammatory cells (polymorphonuclear cells). Once there is clinical suspicion of clostridial infection in septic miscarriage, treatment should be prompt. There

is no substitute for thorough cleansing of any cervical or vaginal injuries. Penicillin G 20 million units a day has been the traditional agent of choice for clostridial infections. In cases with severe sepsis, metronidazole and aminoglycosides are used with high-dose penicillin. For patients sensitive to penicillin, alternative agents like clindamycin, chloramphenicol and third-generation cephalosporins can be used. Ileus is treated by continuous nasogastric suction and intravenous fluids, and carefully matched blood should be given judiciously. Once gas gangrene (myonecrosis) supervenes, surgery is the mainstay of treatment. Lastly, the patient’s immunization status for tetanus must always be assessed and appropriately managed.

6.1  Septic shock Bacteraemia and septicaemic shock are not confined by any means to septic miscarriage. Other causes related to pregnancy are pyelonephritis, chorioamnionitis, puerperal sepsis and necrotising fasciitis. Shock is a condition caused by acute circulatory failure with inadequate or inappropriately distributed tissue perfusion resulting in generalised cellular hypoxia. Septic shock can be defined as severe sepsis with hypotension (systolic BP 40 mmHg from baseline) in the absence of other causes for hypotension and despite adequate fluid resuscitation. Sometimes patients receiving inotropic or vasopressor agents may not be hypotensive, when perfusion abnormalities are documented.

6.1.1 Pathophysiology Septic shock results from the spread of an initially localized infection into the bloodstream. Most cases of septic shock are caused by endotoxin-producing Gram-negative bacilli, hence the alternative name, endotoxic shock. E. coli is the organism most commonly implicated. Endotoxins are bacterial lipopolysaccharides, which are released when bacterial cell walls are degraded. Lipopolysaccharides consist of a toxic fatty acid core (lipid A) and a complex polysaccharide antigenic coat unique to each bacterial species. Lipopoly­saccharides bind as a complex with lipopolysaccharide binding proteins to CD 14 molecules on leucocytes (mainly monocytes), macrophages, endothelial cells and other cell types. This initiates a cytokine cascade and

30  Ian Donald’s Practical Obstetric Problems releases chemical mediators that activate complement, kinins and the coagulation system. These include tumour necrosis factor α, the interleukins IL-1, IL-6 and IL-8, platelet activating factor, prostaglandins, vasoactive kinins and complement components. Nitric oxide (NO) has emerged as an important chemical mediator, and the resulting prolonged increase in NO formation is believed to be an important cause for sustained vasodilatation, hypotension and reduced reactivity to adrenergic agonists that characterises septic shock. Gram-positive organisms like group A β-haemolytic Streptococcus and Staphylococcus aureus produce exotoxins which are antigenic, and can therefore generate all the features of septic shock by triggering the inflammatory cascade. Vascular endothelial injury causes leakage of fluid from capillaries, which accumulates in the interstitial space. Leucocyte and platelet aggregation occur which result in capillary plugging, while vasoactive mediators cause selective vasodilation leading to unequal distribution of blood flow. In severe systemic inflammation as in septic shock, redox imbalances caused by increased production of free radicals can cause damage to cell membranes, increased capillary permeability, impaired mitochondrial respiration, DNA strand breakage and apoptosis. Haemodynamically, septic shock is characterised by vasodilation and low systemic vascular resistance. Cardiac output is maintained initially by increased heart rate and stroke volume, but once hypovolaemia and myocardial depression supervene, the cardiac output decreases and increased sympathetic activity causes vasoconstriction.

6.1.2  Clinical features The clinical features of septicaemic shock are sudden collapse with rigors and pyrexia. The association of hypotension and rigors helps to distinguish endotoxic shock from the other two types, namely cardiogenic and hypovolaemic. In early stages, the peripheries are warm and the pulse is rapid and bounding, but with fulminant sepsis, the patient looks toxic, she is cold and clammy and hyperventilating, with a systolic blood pressure often 60 mmHg or less. She may become delirious and lapse into coma. Acute respiratory distress syndrome (ARDS), renal failure and disseminated intravascular coagulation (DIC)

are other life-threatening complications, which may supervene. Some patients may have a skin rash as in staphylococcal shock syndrome or streptococcal infection. Striking individual variations may however be seen. There will be some patients with sepsis who may have normal temperature, respiratory rate and pulse. One-third may have a normal WBC count. In early sepsis, there is leucocytosis, but leucopaenia may develop later. WBC counts greater than 50,000 or less than 3000/ml are associated with a high mortality rate. Neutrophils in septicaemia contain toxic granulations and Döhle bodies. The platelet count may show an initial rise but falls with persistent sepsis. As the septic response accelerates, thrombocytopenia worsens and hyperbilirubinaemia and azotaemia become more prominent. Active haemolysis as exemplified by microangiopathic changes on the peripheral blood smear (‘helmet’ cells, ‘burr’ cells, schistocytes) suggests clostridial sepsis or the onset of DIC. Early in sepsis, patient hyperventilates inducing respiratory alkalosis. Later, when respiratory muscle fatigue and lactate accumulation supervene, metabolic acidosis occurs. Evaluation of arterial blood gases reveals hypoxaemia, which is initially correctable with supplemental oxygen but later refractoriness to 100% oxygen inhalation indicates right to left shunting. As septicaemia continues, serum lipid levels are elevated while those of serum albumin decline. DIC is associated with a constellation of hypofibrinogenaemia, thrombocytopenia, elevated fibrin degradation products (of which D-dimer is the most sensitive) and prolonged prothrombin time. Prolonged partial thromboplastin time and microangiopathic haemolytic anaemia are present in only a fraction of patients. Samples for blood and urine cultures should be taken before starting antibiotics. A Gram stain and culture from the local site of infection may be invaluable, for example, a high vaginal or an endocervical swab taken with care using a speculum. A chest X-ray should be done to exclude pneumonia or ARDS which gives rise to bilateral diffuse infiltrates. Plain X-ray abdomen will help to diagnose bowel injury which produces free gas under the diaphragm. An ultrasound is warranted, when

Miscarriage: Complications and management   31

there is suspicion of intra-abdominal or pelvic abscess; CT scan is the imaging modality of choice in case ultrasound is inconclusive.

6.1.3 Management If resources are available, these patients should be managed in an intensive care unit under the guidance of an intensivist. Promptness in instituting therapy, choice of appropriate antibiotics and careful monitoring makes the difference between life and death for these patients. The major goals of treatment of septic shock are to maintain oxygenation and circulation, treat infection and prevent multi-organ failure. Oxygen should be administered to all patients. If there is evidence of respiratory distress and arterial blood gases and acid–base balance is severely deranged, endotracheal intubation should be undertaken to maintain adequate oxygenation. Resuscitation.  Both treatment and resuscitation should begin immediately. During initial resuscitation from sepsis - induced hypoperfusion, at least 30 ml/kg IV crystalloids should be given in the first three hours. Further fluids should be administered depending on the response to fluids and haemodynamic status.37 Hydroxyethyl starches are not recommended for fluid resuscitation in treating sepsis. Placement of a central venous pressure line is therefore highly desirable. The goals of resuscitation in the first six hours should be to achieve the following: 1. Mean arterial pressure ≥65 mmHg 2. Systolic BP >90 mmHg 3. CVP 8–12 cm H2O 4. PCWP 14–18 cm H2O 5. Urine output ≥0.5 ml/kg/h 6. Central venous oxygen saturation (SCVO2) ≥70% If SCVO2 ≥70% is not maintained with fluid resuscitation in the first 6 hours, then transfusion of packed red blood cells should be given to achieve a haematocrit of ≥30% and/or administration of a dobutamine infusion (up to a maximum of 20 μg/kg/min) to achieve this goal. Vasopressors.  If the patient does not respond to fluid replacement and hypotension persists, vasopressors are required to maintain adequate

tissue perfusion. Norepinephrine should be the first choice in vasopressor agents. If given before adequate fluid replacement, it can cause profound tachycardia. Epinephrine is added or substituted as the first alternative agent in septic shock, when blood pressure is poorly responsive to norepinephrine. In patients requiring vasopressors, insert an arterial catheter as soon as practical. Dopamine is no longer routinely recommended due to increased risk of arrhythmia. Ionotropic therapy.  Dobutamine is the first choice inotrope for patients with measured or suspected low cardiac output in the presence of adequate fluid replacement. Antibiotic therapy.  Meanwhile the infection must be vigorously countered. Every hospital must have an antibiotic policy framed in collaboration with the microbiologists based on locally prevalent organisms and their sensitivity. Intravenous broad-spectrum antibiotics should be started empirically as soon as possible to cover the most likely pathogens, including Grampositive, Gram-negative and anaerobic bacteria. Appropriate cultures should be taken from all potential sites of infection before giving antibiotics, but this should not lead to unnecessary delay in their administration. For immunocompetent adults, the most commonly used regimen comprises a third-generation cephalosporin, aminoglycoside (gentamicin or amikacin) and metronidazole. Rarely, the patient may be allergic to the cephalosporins in which case she may be started on vancomycin or ofloxacin. The antibiotics may need to be modified depending on the response of the patient and bacteriological reports. Other antibiotics that are useful in resistant cases include ticarcillin-clavulanate, piperacillin-tazobactam and imipinem-cilastatin. Blood product administration. Red blood cells should be given when Hb is less than 7 g%. Erythropoietin is not advised for treating sepsis-induced anaemia. Platelets should be administered, when platelet count is: yy 10 minutes or a flat trace with poor beat-to-beat variability, tenderness over the scar, maternal tachycardia and formation of Bandl’s ring which is rising may all be warning signs of an impending rupture.

1.5 Consequences of uterine rupture The consequences of uterine rupture depend on the time elapsed from the rupture to the institution of definitive treatment. For the foetus, it may vary from sudden fetal death to hypoxia and acidosis. Maternal mortality ranges from 0 to 30% whereas perinatal mortality can vary from 10 to 80%. Causes of maternal mortality include hypovolaemic shock due to massive blood loss, disseminated intravascular coagulopathy (DIC) and sepsis. Serious maternal morbidity includes DIC, vesicovaginal and ureteric fistulae, anaemia, puerperal sepsis and renal failure. Other morbidities include wound sepsis and wound dehiscence.

1.6 Management Timely diagnosis and early intervention are the key to prevention of serious morbidity and mortality. Resuscitation and laparotomy should be undertaken as soon as possible with adequate arrangement of blood and blood components. Having opened the abdomen, three courses of action can be considered, namely hysterectomy, repair of the rupture and repair with sterilization of the patient. The decision depends on the following factors: yy yy yy yy

Type of rupture Extent of rupture General condition of the patient Desire for future childbearing

Hysterectomy may be the best course in cases of extensive rupture or if it is potentially infected. However, in a young woman, there may be strong desire for preserving the uterus for future fertility. Uterine repair may, therefore, be appropriate, provided the patient is in good condition and there is no evidence of coagulopathy. If there is an intractable bleeding with multiple or difficult to repair rents, hysterectomy may be preferred. Repair and sterilization are perhaps most suitable for young patients not desiring future fertility. The main advantages are avoiding the potential complications of hysterectomy, and the possible harmful impact on ovarian function. Hypogastric artery ligation may be a useful adjunct in some cases to reduce uterine vascularity and bleeding. While repairing a uterine rupture, it is customary to freshen up the edges of the wound. The uterus should be repaired with interrupted sutures in layers, starting with one traction suture at the upper most end of the rent and then working from bottom upwards. In this way, it is possible to examine the lowest and therefore the most difficult parts of the repair with the finger passed inside the uterus through the rent before it is finally closed. Great care must be taken not to include the ureter in any of the stitches, especially when the rupture extends to the sides of the lower segment. Antibiotics should be given in all cases. Before proceeding to hysterectomy, one should be fully satisfied that the main source of haemorrhage is not a vaginal vault laceration, if a tragic and irrelevant mistake is to be avoided. There have been occasions where vaginal bleeding continues even after hysterectomy and the source is later identified as a vaginal laceration.

1.7 Prevention Prevention includes identifying pregnant women at risk of uterine rupture and facilitate a hospital delivery for them. Proper selection of women for trial of labour after caesarean, appropriate use of oxytocic agents, monitoring of labour using partograph for early diagnosis of prolonged labour and careful monitoring of women with previous caesarean section in labour can prevent many cases of uterine rupture.

646  Ian Donald’s Practical Obstetric Problems

(a)

(b)

(c)

Figure 31.2  Stages of inversion (a) First degree (b) Second degree (c) Third degree.

With the increasing use of ultrasound in obstetrics, several studies have tried to correlate the sonographic measurement of scar thickness in women with previous caesarean section with the risk of rupture in subsequent labour. Different cut-offs have been proposed for the prediction of an increased risk of rupture from 1.5 to 2.3 mm.12 However, because of the heterogeneity of the studies analyzed, no ideal cut-off value can be recommended to be used for routine clinical practice.

2   Inversion of uterus Puerperal inversion of the uterus is a rare but potentially life-threatening complication occurring during the third stage of labour. The incidence of uterine inversion is approximately 1/8000–1/28,000 deliveries. It can be classified based on the severity of uterine inversion (Fig. 31.2): yy First degree: The fundus is just depressed. yy Second degree: The inverted fundus protrudes through the cervix. yy Third degree: The whole uterus, including the cervix, is inverted. It may drag the vagina and appear outside the vulva (Fig. 31.3). Uterine inversion can also be classified based on the timing of the event: 1. Acute: Within 24 hours of delivery 2. Subacute: After 24 hours but within 4 weeks of delivery 3. Chronic: After 4 weeks of delivery

Figure 31.3  Complete (third-degree) inversion of the uterus.

In a literature review of 241 cases over 20 years from 1975 to 1995, 83.4% inversions occurred as acute, 2.62 % subacute and 13.9% as chronic cases.13

2.1  Causes of Inversion Most common cause of puerperal inversion is mismanaged third stage of labour, when excessive cord traction is given along with fundal pressure on a relaxed uterus for delivery of the placenta. The various risk factors which predispose to puerperal inversion of the uterus are fundal insertion of placenta, morbidly adherent placenta, short cord and use of uterine relaxants for manual removal of retained placenta.

Intrapartum maternal injuries  647

Inversion of uterus is much more common at caesarean section though not reported because minor degrees of inversion are promptly and easily corrected. Rarely a major degree of inversion occurs bringing out the entire uterus out of the uterine incision. Haemorrhage and shock in such cases may be significant. An intravenous tocolytic or deepening of the anaesthesia to achieve relaxation of uterus may be helpful in reducing the inversion in a haemodynamically stable patient. Although it is a standard recommendation that the placenta should not be delivered before correcting the inversion, this may not hold true for inversion at caesarean section because the bulk of the uterus and the placenta may prevent reduction of the uterus through the incision. Oxytocic should be administered promptly after the inversion is corrected to prevent re-inversion.

2.2 Diagnosis The classic triad of symptoms: Haemorrhage, shock and severe pelvic pain are the hallmark of this condition. Shock is due to traction on the ligaments supporting the uterus causing parasympathetic stimulation (neurogenic) or due to hypovolaemia as a result of acute blood loss. The first step to arriving at a diagnosis is to palpate the uterine fundus and to note any cupping, dimpling or irregularity of the surface contour. In severe cases, the uterus is not palpable since it has turned itself inside out into the vagina. Abdominal palpation alone is not enough, since even when the patient is thin, the abdominal signs of cupping of the fundus may not be obvious. A bimanual examination should, therefore, be carried out to appreciate the cupped or the missing fundus. The diagnosis can be made more readily, if the fundus is routinely palpated for uterine contraction while conducting the third stage, which immediately alerts the obstetrician to the altered anatomy. Vaginally, there is a fleshy reddish mass seen outside the vulva in third-degree inversion.

2.3 Prevention Proper training of all skilled birth attendants in the correct management of third stage of labour is essential to prevent this complication. Early diagnosis, and immediate reposition without

removal of placenta if attached are important to reduce the associated morbidity and mortality.

2.4 Management Immediate resuscitation must be started simultaneously with the efforts to reduce inversion. Intravenous fluids must be infused with a wide bore cannula pending the arrival of crossmatched blood for transfusion. Oxygen is given by mask and an indwelling catheter is sited. The patient should be kept warm, and on no account should ergometrine or oxytocin be given, as these will only aggravate matters and make reduction or replacement of the uterus more difficult. The treatment is immediate replacement without attempting to remove the placenta from the inverted fundus, which can be delivered later. In many of these cases, the placenta is morbidly adherent, and, in any event, removal exposes the maternal sinuses, which are intensely engorged, to infection. Moreover, bleeding is likely to be very severe and will aggravate the already developing shock. Moreover, removing the placenta from the inverted uterus, predisposes to injury to the uterine wall that can be easily torn and perforated. There are only two indications for removing the placenta before replacement of the uterus. The first is when all but a portion of the placenta is already separated and second during caesarean section when there is difficulty in reducing the bulk of the uterus through the incision. If immediate replacement at the time of delivery is not feasible, shock supervenes so quickly that further attempts are no longer safe until the shock is first treated. Unfortunately, in several cases, acute inversion occurs in the absence of skilled assistants, so that when first seen the patient is already unstable and in shock. In these circumstances, or where it is not possible to correct the inversion immediately, the first thing to be done is to convert a third-degree inversion into second degree and to raise the foot of the bed to maintain the inverted mass within the vagina instead of hanging outside. This reduces shock to some extent and, to a lesser extent, the risk of infection. Attempts at replacement in the presence of shock may prove fatal and should only be made either before shock has developed or after it has been treated.

648  Ian Donald’s Practical Obstetric Problems The patient is moved to the operating theatre. Prophylactic broad-spectrum antibiotics are administered intravenously. Uterine tocolytics can be administered before correction by administration of glyceryl trinitrate 600 μg sublingual or terbutaline 250 μg subcutaneous. If adequate relaxation is not achieved, administration of general anaesthesia with halothane or sevoflurane causes dose-dependent depression of myometrial contractility facilitating rapid repositioning of the uterus. There are many manoeuvres to replace the uterus and they are summarized below. Conservative methods such as manual replacement and the hydrostatic method should be tried first. If these measures fail to achieve success, surgical intervention is required.

2.4.1 Manual replacement (Johnson manoeuvre) Using the palm of the hand, the fundus of the uterus is pushed along the direction of vagina towards posterior fornix, the uterus is then lifted towards the umbilicus to return to its normal position. While carrying out this manipulation, the other hand should be placed over the abdomen for counter support otherwise the inverted uterus may be pushed high up into the abdomen with the vagina on the stretch rather than inversion being corrected. The part which has inverted last should be reduced first, in other words, the part nearest the cervix should be reposited first rather than the inverted fundus and trying to push extra thickness of uterine wall through the cervical ring. If this manoeuvre is successful in replacing the uterus, the hand should be kept within its cavity until oxytocin has been started and the uterus has contracted. This will reduce the likelihood of a recurrence.

2.4.2 Hydrostatic reduction (O’Sullivan technique) When manual reduction fails, the correction of uterine inversion can be tried by infusing warm saline into vagina. Uterine rupture should be excluded prior to this procedure. The patient is put in Trendelenburg’s position to assist gravity and reduce traction on infundibulopelvic ligament. Two bags of 1 litre of warm normal saline are placed at a height of 1 m above

the patient and connected by a Y-tubing (used for cystoscopy). The tube is placed near the posterior fornix with the hand in the vagina. A near water-tight seal should be obtained at the vaginal introitus by approximating the labia majora. Alternatively, a 6-cm or appropriate-size Silastic ventouse14 cup or a large-volume capacity balloon catheter like Rusch Balloon15 can be used to seal the vagina as well as infuse the saline.

2.4.3  Surgical procedures Repositioning of the uterus can be done by open laparotomy, via the vaginal route or laparoscopically. Open reduction can be attempted by many techniques. Huntington procedure and Haultain procedure are the most popular.

2.4.4  Abdominal procedures Huntington method.  Locate the cup of inversion and identify the round ligaments at laparotomy. Allis or babcock clamps are applied on the myometrium or the round ligaments in the cup 2 cm below the ring and gentle upward traction is given. New clamps are applied, 2 cm below the previous ones, repeating until complete replacement occurs. An assistant can facilitate correction by pushing the fundus upwards vaginally. If the above method fails, correction is done by the Haultain method. Haultain method.  If the cervical ring is too tight and the uterine fundus cannot be pulled out through it, the size of the ring can be increased by giving an incision posteriorly on the uterine wall over the ring (Haultain method) or anteriorly (Ocejo’s method). Replacement of uterus is done by gentle upward traction (as in Huntington method). The hysterotomy site is repaired after replacement. Posterior incision is preferred to prevent accidental injury to the bladder with anterior incision.

2.4.5  Vaginal procedures Of the vaginal procedures, the best known is that of Spinelli, in which, using the vaginal approach, the bladder is dissected upwards and pushed out of the way. The ring and the lower part of the inverted uterus, that is, that part of it nearest the cervix, is divided anteriorly, and the inversion is

Intrapartum maternal injuries  649

then replaced, following which the incision is closed with interrupted sutures. An alternative method is that of Kustner, in which the cervical ring is divided posteriorly. In long-standing cases, it is better to resort to surgery. When the uterus is gangrenous, it may be best to proceed with hysterectomy after repositioning.

2.5  Post-correction management It is important to prevent recurrence. Oxytocic agents are administered without removing the uterine hand. Once the uterus contracts, wait for spontaneous separation of placenta if still attached and remove the placenta while removing the hand from the uterus while stabilizing the uterus by the other hand abdominally. Mark the fundus per abdomen and avoid pressing on the uterus repeatedly to check for vaginal bleeding. Oxytocics may be continued for 24 hours to prevent recurrence and antibiotics are administered as per antibiotic policy.

an incompletely dilated cervix, manual dilatation of cervix and instrumental delivery. Previous cervical operations causing scarring and cervical cerclage are also associated with increased risk of cervical lacerations. Induction of labour is associated with a three-fold increase in cervical lacerations.16 The tears may be circular, longitudinal or cause complete annular detachment. They may involve only the vaginal portion of the cervix or extend into lower segment of the uterus. The lateral cervical tears at 3 and 9 o’clock is more common. There is brisk bleeding due to injury to the descending cervical artery. A cervical tear must be suspected and excluded in any case of persistent bleeding in the presence of a well-contracted uterus, particularly in case of an instrumental or precipitate delivery. The entire circumference of the cervix must be explored to identify the nature and extent of the cervical tear and to suture it appropriately. At times, the cervical tear to extend upwards into the lower uterine segment (Fig. 31.4).

2.6 Complications Most common cause of maternal death is hypovolaemic and or neurogenic shock. But with proper management, maternal mortality due to uterine inversion can be prevented. If untreated, it may cause infection, uterine sloughing and chronic inversion. After treatment for uterine inversion, there is an increased risk of placenta accreta and postpartum haemorrhage in subsequent pregnancies which needs to be discussed with the mother. Localization of placenta by ultrasound and elective caesarean may be advised if placenta is morbidly adherent in the next pregnancy to prevent morbidity and mortality.

3   Cervical lacerations In normal labour, the cervix gradually dilates to 10 cm diameter and allows the smooth passage of the fetus. At the end of second stage the cervix is congested, soft and loose hanging like a frill. After involution the external os change its shape from circular to a transverse slit. The conditions resulting in rapid and forceful dilatation of the cervix predispose to cervical tears. These include precipitate labour, premature bearing down with

Figure 31.4  Image of a rupture uterus in a multigravida with a hydrocephalic fetus in breech presentation. The patient collapsed soon after the delivery of the head following abdominal cephalocentesis. There was a cervical tear extending into the lower uterine segment. She underwent emergency hysterectomy.

650  Ian Donald’s Practical Obstetric Problems It is essential to have good light and adequate exposure for cervical exploration. The cervical suturing set must have long blade vaginal retractors for proper exposure, and at least three sponge holders (ring forceps). yy The first sponge holder is applied on the anterior lip of the cervix at 12 o’clock position. yy The second sponge holder is applied at 45 degrees from the first one and the area between them is inspected. yy A third sponge holder is placed at 45 degrees from the second one and the area between them is inspected. The second and the third sponge holders are advanced further along the circumference until the entire 360 degrees of the cervix has been visualized. Superficial tears, which are not bleeding, need not be sutured, but if the tear is deep and bleeding, suturing should be done.

3.1  Method of suturing

A damaged perineum means an ineffective pelvic floor. The condensations of pelvic fascia, which maintain the pelvic viscera in their normal anatomical positions, cannot afford to do so indefinitely without the active muscular support of the levator ani. Thus, after a latent period of many years, the supports of the uterus, bladder and bladder-neck yield, and with the added insult of menopausal atrophy, the patient can have uterovaginal prolapse, stress incontinence or both. In this respect, a stretched perineum may be almost as bad as a torn perineum, for both lose some of their functional capacity. The pelvic floor is comprised chiefly of the pubococcygeus-puborectalis complex or the pubovisceral muscle, which is a part of the levator ani. This muscle complex forms a V-shaped pelvic floor providing a hiatus in the centre where they encircle the urethra, vagina and rectum. The area of the levator hiatus in nulliparous women on Valsalva manoeuvre varies from 6 to 36 cm2, through which a fetal head with an area of 70–100 cm2 (in the plane of least dimensions)

Two ring forceps are placed on either side of the laceration, and the cervix is gently pulled in the opposite direction to expose the apex. Visualization can be facilitated by pressing on the uterus per abdomen. The suturing must start above the apex of the tear in order to include the retracted blood vessels. In case it is difficult to reach the apex of the tear, a stitch is taken as high as possible and the sutures left long. The suture is then given traction and another stitch placed above the previous one. The tear can be traced in this fashion till the apex is reached and a stitch is placed above it. It is repaired with absorbable suture like polyglactin no. 1-0 by interrupted stitches (Fig. 31.5).

4   Pelvic floor trauma Pelvic floor trauma due to childbirth has been studied extensively in the last three decades, and the mechanics of injury worked out to some extent. Pelvic floor morbidity is the result of a complex pattern of trauma involving nerve injury particularly to the pudendal nerve and its branches, pelvic floor muscles and the endopelvic fascia, and anal sphincter.

Figure 31.5  Left cervical tear at 3 o’clock position following a forceps delivery. Interrupted sutures are seen approximating the tear.

Intrapartum maternal injuries  651

must pass in the process of vaginal birth.17 Indeed the distensibility of pelvic floor muscles is amazing, but at the same time, it is not difficult to visualize the potential for increasing damage in case of a macrosomic fetus or forceps application, which would further increase the stretch on these muscle fibres. Several studies have investigated the effect of parturition on the pelvic floor using MRI and three-dimensional (3D) and four-dimensional (4D) ultrasound. Defects in levator ani, mostly in the pubovisceral portion, were identified in 20% of primiparous women as compared to none in nulliparous on MR imaging.18 Uses of forceps, anal sphincter rupture and episiotomy were associated with an increased risk of levator defects on MRI. The incidence of levator defects demonstrated on trans-labial or trans-perineal 3D/4D ultrasound is higher than that in MRI. Avulsion of the pubovisceral muscle off the pelvic side wall was identified in nearly one-third of the women who delivered vaginally, on ultrasound.19 Electromyography shows a significant reduction in maximum contraction of pelvic floor muscles after vaginal delivery. Pelvic floor damage can probably be reduced but not necessarily avoided by primary caesarean section. Unfortunately, antenatal prediction of major levator trauma is difficult and hence it is important to provide optimal obstetric care.

5  Perineal tears (lacerations) An intact perineum is one in which there is no tissue separation at any site following a vaginal delivery. Almost 85–90% women will sustain some amount of perineal trauma during vaginal delivery, more so in the primipara. Various interventions have been tried to minimize perineal

injury, by delivering in different positions, different pushing techniques and perineal support. Ritgen’s manoeuvre and its modifications have been described to allow guarded extension of the head while delivering to prevent perineal tear.

5.1 Classification of perineal tears Perineal lacerations have been categorized for a long time into three degrees. However, with increasing understanding of the mechanism of faecal continence, modification to this classification has been suggested to include sub-classes based on the involvement of external anal sphincter (EAS) and internal anal sphincter (IAS). The following classification has been adopted by the International Consultation on Incontinence and the RCOG (Table 31.2).20 Obstetric anal sphincter injuries (OASIs) is a term used to describe both third- and fourth-degree tears that involve the anal sphincter complex.

5.2 Risk factors for obstetric anal sphincter injury Several studies have identified risk factors associated with third-and fourth-degree perineal lacerations.21–23 These are as follows: yy yy yy yy yy yy yy yy yy

Nulliparity Increased maternal age Asian ethnicity Prolonged second stage of labour Shoulder dystocia Operative vaginal delivery Persistent occiput-posterior position Birth weight >4.0 kg Midline episiotomy

Table 31.2  Classification of perineal tears First degree

Injury to perineal skin and/or vaginal mucosa

Second degree

Injury to perineum involving perineal muscles but not involving the anal sphincter

Third degree

Injury to perineum involving the anal sphincter complex: 3a: Less than 50% of EAS thickness torn 3b: More than 50% of EAS thickness torn 3c: Both EAS and IAS torn

Fourth degree

Injury to perineum involving the anal sphincter complex (EAS and IAS) and anorectal mucosa.

EAS, external anal sphincter; IAS, internal anal sphincter.

652  Ian Donald’s Practical Obstetric Problems The risk factors however do not always accurately predict OASIs. Women who have had previous anal sphincter injury are at five times greater risk for subsequent sphincter lacerations.24

5.3 Complications Perineal lacerations have varying manifestations and consequences. Immediate short-term complications include blood loss, need for suturing and perineal pain. Protracted pain occurs in 20% cases, varying degree of functional impairment of sphincters is seen in a few women. Wound infection can also occur. Long-term consequences occur due to pelvic floor dysfunction leading to bowel, urinary and sexual function impairment. These include stress incontinence overactive bladder, anal incontinence and prolapse.

5.4  Prevention of perineal tears The following preventive measures help to reduce the incidence of pelvic floor trauma: yy Identifying women at risk and avoidance of unnecessary obstetric interventions yy Mediolateral episiotomy for instrumental deliveries. yy Warm compresses to the perineum during second stage yy Maintaining the women in left lateral position till active pushing yy Mother advised not to push when the head is crowning yy Supporting the perineum during crowning yy Controlled head delivery Episiotomy.  The evidence whether episiotomy prevents OASIs is controversial. However, there is evidence to suggest that a mediolateral episiotomy performed with instrumental deliveries reduces the risk of OASIs.20 Most mediolateral episiotomies performed at 45 degrees are found to be very close to the midline after delivery and do not provide the desired protection. For a true mediolateral episiotomy, the incision in the perineum must be given at 60 degrees from midline when the perineum is distended, which will finally result in a 45-degree episiotomy after

delivery.20 Nevertheless, there is insufficient objective evidence to recommend routine episiotomy, and clinical judgement should be used to decide the indication for performing an episiotomy.25

5.5 Repair of second-degree perineal tear The purpose of repairing perineal tears after delivery is to arrest bleeding, prevent infection and to promote healing of lacerations and /or tears by primary intention. If tears are not sutured, they heal by secondary intention by formation of granulation tissue, which contracts and results in scarring and dyspareunia.

5.5.1  Method of repair A good light is essential. Local anaesthesia 1% lignocaine should be injected in the subcutaneous plane as well as into the perineal muscles. Use of lignocaine with vasoconstrictor reduces the amount of local anaesthetic required. The maximum dose of xylocaine used is 3–5 mg/kg body weight. For a 50-kg woman it is 150–250 mg that is approximately 25 ml of a 1% solution. After identifying the apex of the tear, the vaginal mucosa is first sutured with continuous absorbable suture. The muscles are stitched in interrupted, and finally the skin with a subcuticular continuous stitch or interrupted stitches. The use of a rapidly absorbed synthetic suture, such as polyglactin 2-0, is associated with a significant reduction in perineal pain, analgesia, dehiscence and resuturing.26 The repair should be done approximating the tissues without any tension. Use minimum amount of suture and do not over-tighten the knots. Perform a rectal examination to ensure no suture has gone through the rectal mucosa. Explain perineal hygiene to the patient. It is a common mistake to sew up too tightly, which causes perineal pain, and can lead to dyspareunia later. The tissues of the vulva and vagina shrink during the process of involution, and it should be a rule to ensure that three fingers can be easily inserted simultaneously into the vagina at the end of the operation. Otherwise such a patient may need to be relieved of her distress subsequently by Fenton’s operation.

Intrapartum maternal injuries 653

I once saw such a patient who suffered this fate at the hands of an over-zealous practitioner and assured me that was the reason she had never been able to conceive again. I was skeptical about this but yielded to her repeated requests. To my surprise, she was as good as her word – she promptly became pregnant once healing was complete. – Ian Donald

5.5.2 Identification of anal sphincter injury On visual examination, absence of normal puckering around the anterior aspect of the anus may give a clue about anal sphincter injury. Insert a finger into the rectum and ask the woman to squeeze. In case of damage to EAS, deficiency of the sphincter can be felt on squeezing, and the torn ends can be seen to retract backwards. Epidural analgesia can affect the power of the muscle; therefore, the bulk of the muscle should also be palpated between the finger and thumb by a pin-rolling movement.

5.6 Obstetric anal sphincter injuries Anal sphincter complex consists of the IAS and the EAS (Fig. 31.6). The IAS is the lower most part of the circular smooth muscle layer of the rectum and lies between the anal mucosa and the EAS. It contributes to 70% of the resting

Bulbocavernosus muscle

Transverse perineal muscles External anal sphincter Internal anal sphincter

Rectal mucosa

Figure 31.6 Diagrammatic representation of perineal anatomy in a fourth-degree perineal tear.

anal sphincter complex tone. It is invariably torn in fourth-degree tears, although occult disruption of the sphincter can occur even with an intact rectal mucosa. The EAS in contrast is a skeletal muscle and is, therefore, under voluntary control. The reported prevalence of third-and fourth-degree tears varies very widely depending on the population studied, parity, rates of instrumental delivery, type of episiotomy and diagnosis or mis-diagnosis between 0.1 and 19.0%.27 In 1993, Sultan et al. showed for the first time that the incidence of occult sphincter injury in postpartum women was much higher when endoanal ultrasound was used for their detection.28 In a meta-analysis of studies using endoanal ultrasonography, the incidence of anal sphincter defects in primiparous women was found to be 26.9%, whereas new sphincter defects occurred in 8.2% of multiparous women. About 30% of these occult defects were symptomatic, although 3.4% women experienced postpartum faecal incontinence without a detectable anal sphincter defect.29

5.6.1 Method of repair Repair of third- and fourth-degree tears should be done in the operation theatre under regional or general anaesthesia, by an experienced operator. Repair of a fourth-degree perineal tear (Figs. 31.5 and 31.6) requires approximation of rectal mucosa, IAS and EAS. The first step is to repair the anal mucosa. It can be repaired either with continuous or interrupted technique using 3-0 polyglactin, starting from above and working downwards. It has been a teaching for a very long time that interrupted sutures should be taken in the anal mucosa with the knots lying within the rectal lumen. This was recommended when catgut was used, to minimize tissue reaction. However with the availability of sutures like polyglactin, this is no longer necessary.20 When IAS inju ry is identified, it should be repaired separately with interrupted sutures using delayed absorbable 3-0 polydioxanone (PDS) or 2-0 polyglactin. Having repaired the anal canal, the torn ends of the EAS must be found and held with Allis forceps as shown in Fig. 31.7. Repair of EAS can be done either by an overlapping or an end-to-end approximation technique with similar outcome;

654  Ian Donald’s Practical Obstetric Problems after anal sphincter repair, and the option of caesarean section should be given.

6   Neurological injury The incidence of postpartum lower extremity motor and sensory dysfunction after labour and delivery reported in studies from late 1980s was 0.7/10,000–18.9/10,000.30 More recent studies, however, report significantly higher incidence of nerve injuries after childbirth, from 0.5 to 0.92%.31 The symptoms usually resolve within few days to six months, and long-term sequelae are fortunately rare.

6.1  Risk factors

Figure 31.7  Fourth-degree tear showing the location of the external anal sphincters (held in Allis clamps).

overlapping is done only in case of full-thickness tear. The recommended suture for EAS repair is the same as IAS, either 3-0 PDS or 2-0 polyglactin. The knots should be buried beneath the superficial perineal muscles to minimize the risk of knot and suture migration to the skin. Figure of eight sutures should not be taken as they cause tissue ischaemia.

5.6.2  Postoperative care Broad-spectrum antibiotics should be given postoperatively to reduce the risk of wound infection and dehiscence. Laxatives such as lactulose should be given for 7–10 days to reduce the risk of dehiscence rather than bowel confinement, as was practiced earlier. Pelvic floor exercises should be advised for 6–12 weeks after anal sphincter repair. A proper follow-up of patients must be arranged to ensure optimum outcome.

5.7 Pregnancy after anal sphincter injury Patients should be counselled regarding the risk of developing anal incontinence or worsening of symptoms with subsequent vaginal delivery

Factors associated with nerve injury are nulliparity, prolonged second stage of labour, cephalopelvic disproportion, low forceps delivery, premature bearing down efforts with flexion and external rotation of thighs and prolonged pushing in the semi-Fowler-lithotomy position. Labour analgesia induces sensory blockade and patients may not appreciate symptoms of impending nerve injury, predisposing to risk. Some drugs like nitrofurantoin intake for urinary tract infection can lead to severe sensory neuropathy but it is reversible.32

6.2  Type of neurological injuries The commonly involved nerves in obstetric palsies are as follows: yy yy yy yy

Lateral femoral cutaneous nerve Femoral nerve Obturator nerve Common peroneal nerve

The injury could be due to transection, stretching or compression of the nerve or due to vascular injury supplying the nerve. Less severe injuries cause focal demyelination whereas severe injuries cause axon loss and nerve conduction block. Recovery depends on the axon loss and occurs within 72 hours to 6 months. The most common nerve injury is meralgia paraesthetica due to injury to lateral femoral cutaneous nerve. The nerve is entrapped or compressed by the inguinal ligament during maternal pushing in the thigh flexed position. McRoberts manoeuvre for dealing with shoulder

Intrapartum maternal injuries  655

dystocia, also predisposes to transient lateral femoral cutaneous neuropathy.33 Left gluteal pain and left anterior thigh dysesthesia are the symptoms in this condition. Second most common nerve injury is femoral neuropathy. It is caused by prolonged lithotomy position leading to stretching of inguinal ligament. Most common presentation is buckling of the knee (due to weakness of knee extensors) and numbness down the leg anteriorly. Obturator nerve is vulnerable to compression injury by fetal head in the pelvis or forceps delivery as it crosses the upper margin of obturator internus muscle. Haematoma during pudendal block can lead to entrapment neuropathy. Symptoms include pain in the groin and medial thigh radiating to knee and difficulty in adduction of leg on the affected side. Foot drop can occur secondary to injury at lumbosacral root, lumbosacral plexus, sciatic nerve or common peroneal nerve. Fetal macrosomia, occiput-posterior position, straight sacrum and wide posterior pelvis are risk factors for deliveryrelated foot drop. It is commonly due to external compression of peroneal nerve as a result of pressure caused by inappropriate leg positioning, prolonged squatting position and excessive prolonged knee holding during bearing down efforts. Other causes are due to compression of lumbosacralis trunk against sacral ala by the fetal head (lumbosacral plexopathy).

6.3  Diagnosis of nerve injuries Diagnosis is made on clinical examination and electrophysiological studies. MRI is now emerging as an important diagnostic tool in diagnosing nerve damage as it can differentiate nerve injury from normal nerves and can also be used to follow regeneration.34

6.4 Prevention Preventive measures must be taken to avoid nerve injuries as far as possible. Women should be encouraged to change position frequently during labour and avoid lying or pushing continuously in a position. Care should also be taken to avoid prolonged lithotomy position and pressure from metallic parts of operating table.

7   Injuries to urinary tract Urinary tract invariably suffers some damage during pregnancy and childbirth which can give rise to postpartum urinary symptoms.

7.1 Postpartum stress urinary incontinence The stretching of pelvic floor muscles during pregnancy and more so during childbirth weakens the support to bladder neck and urethra, which can result in stress urinary incontinence (SUI). The reported incidence of SUI is 5–18% following caesarean section and 20–30% following vaginal delivery.35 Predisposing factors include elderly primipara, obesity, chronic constipation and cough. Obstetric risk factors include reduced pelvic floor muscle strength, prior SUI and birth weight >3 kg. The risk of developing postpartum SUI can be reduced by postnatal pelvic floor exercises during pregnancy and postpartum. A formal training on how to perform pelvic floor exercises should be given in antenatal classes which helps in achieving better contraction pressures.

7.2  Postpartum urine retention Incidence of postpartum urinary retention (PUR) varies from 0.4 to 0.7%.36 Risk factors include prolonged first and second stage of labour, instrumental delivery, perineal laceration, nulliparity and epidural analgesia. The risk of PUR is greater after caesarean section than after vaginal delivery, and more so when epidural analgesia with morphine is used.37 PUR may be overt when the woman is unable to void spontaneously within six hours after delivery, or covert when a post-void residual bladder volume on ultrasound is >150 ml. Treatment begins with supportive measures to enhance spontaneous micturition like ambulation, privacy, running water and warm bath. If the above measures fail, catheterization should be done. A catheter sample for culture and sensitivity should be sent. If the urine drained is 150–700 ml, the indwelling catheter is left for 24 hours, but if it is >700 ml, catheter should be left longer and a trial of voiding given after 72 hours.

656  Ian Donald’s Practical Obstetric Problems Unrecognized urinary retention and mismanagement may lead to recurrent UTI, upper urinary tract damage and permanent voiding difficulties.

7.3  Vesicovaginal fistula An obstetric fistula is a devastating yet often neglected injury that occurs as a result of prolonged or obstructed labour. In an obstructed labour, the soft tissues of the vagina, bladder and rectum are compressed between the fetal head and maternal pelvic bones. This impairs the blood supply to the tissues resulting in ischaemic injury. A few days later, the necrotic tissues slough resulting in a fistula between the vagina and the bladder, or the vagina and the rectum, or both. Vesicovaginal fistula (VVF) is an abnormal opening between the bladder and vagina resulting in continuous and unremitting urinary incontinence. Other causes of VVF are direct laceration with instruments and symphysiotomy. According to the WHO, this devastating condition affects more than two million women worldwide and an estimated 50,000–100,000 are added each year.38 Most of the victims are young women. Fistulae occur in areas where access to care at childbirth is limited, or of poor quality, mainly in sub-Saharan Africa and parts of southern Asia. In 2003, the United Nations Population Fund along with the WHO and other partners

launched a global campaign for the elimination of fistula.39 The diagnosis is not difficult. The larger fistulae can either be seen, or felt with the finger, but the instillation of methylene blue into the bladder may help to reveal very small lesions and the three-swab test helps to distinguish the site of the fistula, whether involving the ureter, bladder or the urethra. The fistula is usually situated on the anterior vaginal wall, but occasionally it may open into the anterior fornix or even into the cervix or uterus. At LSCS, failure to displace the bladder downwards before incising the uterus, or careless suturing later, may damage the bladder wall and cause a vesicouterine fistula. Damage to the bladder at the time of the operation is usually demonstrated by blood-stained urine. Symptoms usually develop within 7–10 days after delivery. If the woman presents within 4–6 weeks of delivery, continuous bladder drainage with an indwelling catheter can allow spontaneous closure of small fistula (150 ml. yy If the woman presents within 4–6 weeks of delivery, continuous bladder drainage with an indwelling catheter may allow spontaneous closure of small fistula (15% of total blood volume, or 10% decline in haematocrit levels.5 PPH can be further subdivided into thirdstage haemorrhage when bleeding occurs before the expulsion of the placenta, and true postpartum haemorrhage, which occurs after the expulsion of the placenta. Primary ­postpartum haemorrhage occurs within the first 24 hours after delivery. Secondary postpartum haemorrhage is defined as abnormal or

660  Ian Donald’s Practical Obstetric Problems ­ xcessive bleeding from the birth canal between e 24 hours and 12 weeks postnatally. PPH can be major (500–1000 ml) or minor (>1000 ml). Major can be further subdivided into moderate (1001–2000 ml) and severe (>2000 ml).6 In women with lower body mass (e.g. 1 has been shown to predict the need for blood transfusion and is therefore a useful adjunct in estimating blood loss.

5  The ‘Golden First Hour’ and the ‘Rule of 30’ The ‘Golden First Hour’ is the time at which effective resuscitation must occur to achieve maximum survival and prevent metabolic acidosis. The Rule of 30 is used to measure the severity of shock. It states that if there is a fall in SBP of 30 mmHg or more, an increase in heart rate by at least 30 beats/min, a respiratory rate >30 breaths/min, a fall in the haemoglobin or haematocrit of 30% and/or a reduction in urinary output to 4 g/dL or acute loss requiring transfusion of >4 units of packed cell transfusion, or any haemorrhage associated with haemodynamic instability. Blood transfusion is of course the first immediate necessity. Fresh blood naturally is ideal but usually not available. When a patient requires massive transfusion, generalised bleeding may occur. This is because banked blood is deficient in viable platelets and to some extent in factors V and VIII. These have to be replaced either by fresh blood or by FFP.21 Special blood filters should not be used, as they slow infusions.12 Each hospital/institution catering to obstetric emergencies must have a massive transfusion protocol (MTP) in the labour ward and the following arrangements. yy Have a minimum of 4 units of O-negative PRBC. yy Provision to obtain 6 units PRBC and 4 units FFP (compatible or type specific). yy Provision to obtain platelets and additional blood products in a timely fashion. Massive Transfusion Protocol as suggested by the ACOG is as follows in the order 1–4: 1. Patient bleeding and at risk of uncontrolled bleeding a. Activate helpline or mobilise help b. Take blood sample for type and crossmatch, haemoglobin and platelet count, PT (international normalized ratio), PTT, fibrinogen and ABG (as needed) 2.  Immediate need for transfusion (typed crossmatched not available) a. Give 2–4 units of O-negative PRBC

3. Anticipate ongoing blood loss needs a.  Administer massive transfusion pack (MTP) (4–6 units of PRBC, 4 units FFP, 1 apheresis pack of platelets) 4. Initial lab results a. Normal i. Bleeding ongoing – repeat MTP ii.  Bleeding controlled – deactivate MTP b. Abnormal i. Repeat MTP ii. Consider cryoprecipitate iii.  Consultation for other coagulant agents Recent studies suggest that increasing the initial transfusion ratio for packed red cells:FFP:platelets in the range of 1:1:1 mimics replacement of whole blood and improves survival. Also, more patients in the 1:1:1 group were reported to achieve ‘anatomic’ haemostasis (objective assessment by the surgeon indicating that bleeding within the surgical field was controlled and no further haemostatic interventions were anticipated), and better survival.66 Earlier protocols which suggested a ratio of 4:4:1 or 6:4:1 were related to how a unit of platelet is defined. Rapid blood product selection may benefit from the use of a thromboelastograph, a pointof-care device that examines clot formation and dissolution in whole blood and provides faster results than laboratory testing and its availability in labour rooms can significantly improve PPH management.

14  Thromboprophylaxis There is a global consensus to recommend thromboprophylaxis following a blood loss of greater than 1000 ml, or after transfusion and surgery. Twelve to 24 hours after bleeding has been controlled, pharmacologic thromboprophylaxis should be added, provided coagulation tests are normal or close to normal, as there is a high risk of thrombosis. Alternatively, anti-embolism stockings, foot impulse devices or intermittent pneumatic compression devices can be used if chemical thromboprophylaxis is contraindicated, for example, in cases of thrombocytopenia.67

678  Ian Donald’s Practical Obstetric Problems

15  Prevention and treatment of PPH in low-resource settings yy Correction of anaemia during the antenatal period. yy Skilled attendants at delivery. yy Oxytocin/Misoprostol. If oxytocin is not available or administration is not feasible, single dose of 800 μg of misoprostol given sublingually yy External aortic compression yy Non-pneumatic anti-shock garment (NASG) and the pneumatic military anti-shock trousers: NASG is a lightweight, reusable lower-body compression garment made of neoprene and Velcro.68 It increases blood pressure by decreasing the vascular volume and increasing vascular resistance by compressing the lower half of the body, but not as much as to cause tissue ischaemia. The NASG reverses shock by returning blood to heart, lungs and brain. This restores the woman’s consciousness, pulse and blood pressure. Additionally, the NASG decreases bleeding from the parts of the body compressed under it. It has been designed to allow perineal access so that examinations and vaginal procedures can be performed without it being removed69 (Fig. 32.9). The use of this reusable and lightweight device for stabilizing and transporting

Figure 32.9 Non-pneumatic anti-shock garment.

women in low-resource settings needs further exploration as a step towards decreasing maternal mortality and morbidity in developing countries. It is easy to use and does not require trained personnel. The relatively low cost together with the possibility of reuse makes this device an attractive option. However, it is not a definitive treatment and the need for substantive PPH treatment remains. Application: Place NASG under the woman. Close segments 1 tightly around the ankles; Close segments 2 tightly around each calf and segments 3 tightly around each thigh, leaving knees free. Segment 4 is closed around pelvis and segment 5 with pressure ball over the umbilicus. Finish closing the NASG using segment 6. Segments 1,2,3 can be applied by two persons, however, segments 4,5,6 should be applied by only one person. NASG is removed when the source of bleeding is treated, the woman has been haemodynamically stable for at least 2 hours and blood loss is less than 50 ml/h. Removal begins at the ankles and proceeds slowly, waiting 15 minutes between opening each segment.

16   Secondary haemorrhage When bleeding occurs after an interval of 24 hours or more following delivery, the most likely aetiologies include endometritis, retained products, subinvolution of the placental implantation site and, occasionally, a large blood clot or a submucous fibroid. Most secondary PPH reveal themselves within the first 7–10 days of the puerperium, but sometimes much later, and are often preceded by an advance warning in the form of increased red lochial loss with or without lowgrade puerperal pyrexia. The management of women presenting with secondary PPH should include an assessment of their haemodynamic status, and an assessment of the blood loss. Investigations should include an assessment of vaginal microbiology (endocervical swabs) and appropriate use of antimicrobial therapy should be initiated when endometritis is suspected. A pelvic ultrasound may help to exclude the presence of retained products of conception. Surgical evacuation of retained placental tissue should be undertaken or supervised by an experienced clinician.

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17  Sequelae of postpartum haemorrhage Maternal complications of PPH vary from none to hypovolemic shock, DIC intravascular coagulation, renal failure, hepatic failure, adult respiratory distress syndrome and maternal death. Many patients, who do not have any serious immediate complication, develop chronic anaemia and general ill health and become more vulnerable to puerperal sepsis. If the SBP remains below 80 mmHg, renal filtration ceases. Acute tubular necrosis may occur as a result of ischaemia leading to total renal shut down and anuria. Renal failure is usually self-limiting and recovers completely, dialysis may be however required to allow time for recovery. After severe PPH, lactation may be poor and chronic subinvolution may undermine the woman’s gynaecological health for years to come. Anterior pituitary necrosis (Sheehan syndrome) is an uncommon but serious complication in a patient who remains shocked for a prolonged period. The most common presenting symptoms are failure to lactate and resume

menstruation. Acute onset severe hypopituitarism may present with circulatory collapse, severe hyponatraemia, diabetes insipidus, hypoglycaemia, congestive cardiac failure or psychosis. Most women however have mild disease which often goes unnoticed and untreated. Partial or complete panhypopituitarism may occur. The growth hormone and prolactin secretion are most commonly affected in 90–100% patients, while deficiencies in cortisol secretion, gonadotrophin and thyroid stimulating hormone occur in 50–100%.70 Treatment is as for hypopituitarism with the aim to replace deficient hormones. Thromboembolism. Pregnant women are at increased risk of venous thrombosis and embolic events. Venous stasis due to shock and immobility also contribute, and caregivers should maintain a high index of clinical awareness. Other complications include secondary infertility, uterine perforation, uterine synechiae (Asherman syndrome), urinary tract injury and genitourinary fistula, bowel injury and genitointestinal fistula, vascular injury, pelvic hematoma and sepsis.

Key points yy Postpartum haemorrhage (PPH) is defined as the loss of more than 500 ml of blood from the genital tract at vaginal delivery, or 1000 ml at caesarean section. yy Prevention of PPH starts in the third stage by giving uterotonic agents. yy Oxytocin is the preferred first-line uterotonic agent, ergometrine can be used as second line. yy Misoprostol should be given, if other uterotonics or trained personnel to offer

active management of the third stage are not available. yy When medical management fails, mechanical methods like uterine tamponade can be tried in case of uterine atony. yy Conservative surgical methods like arterial embolisation, stepwise devascularization and compression sutures may be helpful in preserving the uterus. yy Hysterectomy is indicated when conservative measures fail, but it should not be delayed to the point of haemodynamic decompensation

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3. Say L, Chou D, Gemmill A, et al. Global causes of maternal death: a WHO systematic analysis. Lancet Glob Health 2014;2(6):e323–33. 4. Mousa HA, Alfirevic Z. Treatment for primary postpartum haemorrhage. Cochrane Database Syst Rev 2007;(1):CD003249.

680  Ian Donald’s Practical Obstetric Problems 5. Drife J. Management of primary postpartum haemorrhage. Br J Obstet Gynaecol 1997;104:275–7.

in the third stage of labour. Cochrane Database Syst Rev 2011;(11):CD007412.

6. Knight M, Tuffnell D, Kenyon S, Shakespeare J, Gray R, Kurinczuk JJ, editors, 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.

18. World Health Organization. WHO recommendations: uterotonics for the prevention of postpartum haemorrhage. 2018.

7. Ramnathan G, Arulkumaran S. Postpartum hemorrhage. J Obstet Gynaecol Can 2006;28(11):967–73. 8. Leduc D, Senikas V, Lalonde AB. No. 235-Active Management of the Third Stage of Labour: Prevention and Treatment of Postpartum Hemorrhage. J Obstet Gynaecol Can 2018;40(12):e841-e855. 9. Kramer MS, Berg C, Abenhaim H, et al. Incidence, risk factors, and temporal trends in severe postpartum hemorrhage. Am J Obstet Gynecol 2013;209(5):449.e1–7. 10. Schorn MN. Measurement of blood loss: review of the literature. J Midwifery Womens Health 2010;55(1):20–7. 11. Toledo P, McCarthy RJ, Hewlett BJ, Fitzgerald PC, Wong CA. The accuracy of blood loss estimation after simulated vaginal delivery. Anesth Analg 2007;105(6):1736–40. 12. Mavrides E, Allard S, Chandraharan E, et al. Prevention and management of postpartum haemorrhage. Green-top guidelines no. 52. BJOG 2016;124:e106–49. 13. Le Bas A, Chandraharan E, Addei A, Arulkumaran S. Use of the “obstetric shock index” as an adjunct in identifying significant blood loss in patients with massive postpartum hemorrhage. Int J Gynaecol Obstet 2014;124:253e5. 14. Ghosh M, Chandraharan E. Management of postpartum hemorrhage. Obstet Gynaecol Reprod Med 2017;27(8):239–44. 15. Begley CM, Gyte GM, Devane D, McGuire W, Weeks A, Biesty LM. Active versus expectant management for women in the third stage of labour. Cochrane Database Syst Rev 2019;2:CD007412. 16. International Confederation of Midwives, International Federation of Gynaecologists and Obstetricians. Joint statement: management of the third stage of labour to prevent post-partum haemorrhage. J Midwifery Womens Health 2004;49:76–7. 17. Begley CM, Gyte GM, Devane D, McGuire W, Weeks A. Active versus expectant management for women

19. WHO recommendations for the prevention and treatment of postpartum haemorrhage. 2012. 20. Varatharajan L, Chandraharan E, Sutton J, Lowe V, Arulkumaran S. Outcome of the management of massive postpartum hemorrhage using the algorithm “HEMOSTASIS”. Int J Gynaecol Obstet 2011;113:152–4. 21. Committee on Practice Bulletins—Obstetrics. Practice bulletin no. 183: postpartum hemorrhage. Obstet Gynecol 2017;130(4):e168–86. 22. Hunt BJ, Allard S, Keeling D, et al. A practical guideline for the haematological management of major haemorrhage. Br J Haematol 2015;170:788–803. 23. Weeks AD, Alia G, Vernon G, et al. Umbilical vein oxytocin for the treatment of retained placenta (release study): a double-blind, randomised controlled trial. Lancet 2010;375(9709):141–7. 24. World Health Organization. Managing complications in pregnancy and childbirth. 2017. p. S-29–45. 25. Cunningham FG, Leveno KJ, Bloom SL, Hauth JC, Rouse DJ, Spong CY. Obstetrical hemorrhage. In: Williams obstetrics. 23rd ed. New York: McGrawHill; 2010. p. 760. 26. Blum J, Winikoff B, Raghavan S, et al. Treatment of post-partum haemorrhage with sublingual misoprostol versus oxytocin in women receiving prophylactic oxytocin: a double-blind, randomised, noninferiority trial. Lancet 2010;375(9710):217–23. 27. Winikoff B, Dabash R, Durocher J, et al. Treatment of post-partum haemorrhage with sublingual misoprostol versus oxytocin in women not exposed to oxytocin during labour: a doubleblind, randomised, non-inferiority trial. Lancet 2010;375(9710):210–6. 28. WOMAN Trial Collaborators. Effect of early tranexamic acid administration on mortality, hysterectomy, and other morbidities in women with post-partum haemorrhage (WOMAN): an international, randomised, double-blind, placebo-controlled trial. Lancet 2017;389:2105–16. 29. Franchini M, Lippi G, Franchi M. The use of recombinant activated factor VII in obstetric and gynaecological haemorrhage. BJOG 2007;114:8–15. 30. Bagga R, Jain V, Kalra J, Chopra S, Gopalan S. Uterovaginal packing with rolled gauze in postpartum hemorrhage. MedGenMed 2004;6(1):50.

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partum hemorrhage and review of published cases. Int J Fertil Womens Med 2005;50(4):148–63.

31. Nwagha UI, Okaro JM, Nwagha TU. Intraoperative uterine packing with mops: an effective, but under utilized method of controlling postpartum haemorrhage—experience from South Eastern Nigeria. Niger J Med 2005;14(3):279–82.

45. Wohlmuth CT, Gumbs J, Quebral-Ivie J. B-Lynch suture: a case series. Int J Fertil Womens Med 2005;50(4):164–73.

32. Ge J, Liao H, Duan L, Wei Q, Zeng W. Uterine packing during cesarean section in the management of intractable hemorrhage in central placenta previa. Arch Gynecol Obstet 2012;285(2):285–9.

46. Hayman RG, Arulkumaran S, Steer PJ. Uterine compression sutures: surgical management of postpartum haemorrhage. Obstet Gynecol 2002;99:502–6.

33. Lo A, St Marie P, Yadav P, Belisle E, Markenson G. The impact of Bakri balloon tamponade on the rate of postpartum hysterectomy for uterine atony. J Matern Fetal Neonatal Med 20176;30(10):1163–66.

47. Cho JH, Jun HS, Lee CN. Haemostatic suturing technique for uterine bleeding during caesarean delivery. Obstet Gynaecol 2000;96:129–31.

34. Tindell K, Garfinkel R, Abu-Haydar E, et al. Uterine balloon tamponade for the treatment of postpartum haemorrhage in resource-poor settings: a systematic review. BJOG 2013;120(1):5–14. 35. Aggarwal N. The “tamponade test” in the management of massive postpartum hemorrhage. Obstet Gynecol 2003;102(3):641 [author reply 641–2]. 36. Bakri YN, Amri A, Abdul Jabbar F. Tamponadeballoon for obstetrical bleeding. Int J Gynaecol Obstet 2001;74(2):139–42. 37. Dildy GA, Belfort MA, Adair CD, et al. Initial experience with a dual-balloon catheter for the management of postpartum hemorrhage. Am J Obstet Gynecol 2014;210(2):136.e1–6. 38. Akhter S, Begum MR, Kabir Z, Rashid M, Laila TR, Zabeen F. Use of a condom to control massive postpartum hemorrhage. MedGenMed 2003;5(3):38. 39. Salvat J, Schmidt MH, Guilbert M, Martino A. Vascular ligation for severe obstetrical haemorrhage: review of the literature. J Gynecol Obstet Biol Reprod 2002;31:629–39. 40. AbdRabbo SA. Stepwise uterine devascularization: a novel technique for management of uncontrolled postpartum hemorrhage with preservation of the uterus. Am J Obstet Gynecol 1994;171(3):694–700. 41. Morel O, Malartic C, Muhlstein J, et al. Pelvic arterial ligations for severe post-partum hemorrhage. Indications and techniques. J Visc Surg 2011;148(2):e95–102. 42. Matsubara S, Yano H, Ohkuchi A, Kuwata T, Usui R, Suzuki M. Uterine compression sutures for postpartum hemorrhage: an overview. Acta Obstet Gynecol Scand 2013;92(4):378–85. 43. Zhang ZW, Liu CY, Yu N, Guo W. Removable uterine compression sutures for postpartum haemorrhage. BJOG 2015;122(3):429–33. 44. Price N, B-Lynch C. Technical description of the B-Lynch trace suture for treatment of massive post-

48. Dildy III GA. The pelvic pressure pack and the uterovaginal balloon system. In: Arulkumaran S, Karoshi M, Keith LG, Lalonde AB, B-Lynch C, editors. A comprehensive textbook of postpartum hemorrhage. 2nd ed. London: Sapiens Publishing; 2012. 49. Boulleret C, Chahid T, Gallot D, et al. Hypogastric arterial selective and superselective embolization for severe postpartum hemorrhage: a retrospective review of 36 cases. Cardiovasc Intervent Radiol 2004;27(4):344–8. 50. Ojala K, Perala J, Kariniemi J, Ranta P, Raudaskoski T, Tekay A. Arterial embolization and prophylactic catheterization for the treatment for severe obstetric hemorrhage. Acta Obstet Gynecol Scand 2005;84(11):1075–80. 51. Likis Fe, Sathe NA, Morgans AK, et al. Management of postpartum hemorrhage. Comparative effectiveness. Review no. 15. AHRQ publication no. 15-EHC013-EF. Rockville, MD: Agency for Healthcare Research and Quality; 2015. 52. Chen C, Lee SM, Kim JW, Shin JH. Recent update of embolization of postpartum hemorrhage. Korean J Radiol 2018;19(4):585–96. 53. Stensaeth KH, Sovik E, Haig IN, Skomedal E, Jorgensen A. Fluoroscopy-free resuscitative endovascular balloon occlusion of the aorta (REBOA) for controlling life threatening postpartum hemorrhage. PLoS One 2017;12(3):e0174520. 54. McCandlish R, Bowler U, van Asten H, et al. A randomised controlled trial of care of the perineum during second stage of normal labour. Br J Obstet Gynaecol 1998;105:1262–72. 55. Combs CA, Murphy EL, Laros Jr RK. Factors associated with postpartum hemorrhage with vaginal birth. Obstet Gynecol 1991;77:69–76. 56. Charbit B, Mandelbrot L, Samain E, et al. The decrease of fibrinogen is an early predictor of severity of postpartum haemorrhage. J Thromb Haemost 2007;5(2):266–73.

682  Ian Donald’s Practical Obstetric Problems 57. Jansen AJ, van Rhenen DJ, Steegers EA, Duvekot JJ. Postpartum hemorrhage and transfusion of blood and blood components. Obstet Gynecol Surv 2005;60(10):663–71.

64. Davis AK. When more is less efficacious: fibrinogen concentrate in complex cardiac surgery. Br J Anaesth 2016;117(4):415–7.

58. Royal College of Obstetricians and Gynaecologists. Blood transfusion in obstetrics. Green-top guideline no. 47. May 2015.

65. Robinson S, Harris A, Atkinson S, et al. The administration of blood components: a British Society for Haematology guideline. Transfus Med 2018;28(1):3-21.

59. National Institute for Health and Clinical Excellence. Intraoperative blood cell salvage in obstetrics. NICE interventional procedure guidance 144. 2005.

66. Treml AB, Gorlin JB, Dutton RP, Scavone BM. Massive transfusion protocols: a survey of academic medical centers in the United States. Anesth Analg 2017;124(1):277–81.

60. Centre for Maternal and Child Enquiries (CMACE). Saving mothers’ lives: reviewing maternal deaths to make motherhood safer: 2006–08. The eighth report on confidential enquiries into maternal deaths in the United Kingdom. BJOG 2011;118 Suppl 1:1–203. 61. Walker ID, Walker JJ, Colvin BT, Letsky EA, Rivers R, Stevens R. Investigation and management of haemorrhagic disorders in pregnancy. J Clin Pathol 1994;47:100–8. 62. Tanaka H, Matsunaga S, Yamashita T, et al. A systematic review of massive transfusion protocol in obstetrics. Taiwan J Obstet Gynecol 2017;56(6):715–8. 63. Wikkelsoe AJ, Edwards HM, Afshari A, et al. Pre-emptive treatment with fibrinogen concentrate for postpartum haemorrhage: randomized controlled trial. Br J Anaesth 2015;114:623–33.

67. Royal College of Obstetricians and Gynaecologists. Reducing the risk of venous thromboembolism during pregnancy and the puerperium. Green-top guideline no. 37a. 2015. 68. Miller S, Fathalla MM, Ojengbede OA, et al. Obstetric hemorrhage and shock management: using the low technology non-pneumatic anti-shock garment in Nigerian and Egyptian tertiary care facilities. BMC Pregnancy Childbirth 2010;10:64. 69. Lester F, Stenson A, Meyer C, Morris J, Vargas J, Miller S. Impact of the nonpneumatic antishock garment on pelvic blood flow in healthy postpartum women. Am J Obstet Gynecol 2011;204(5): 409.e1–5. 70. Shivaprasad C. Sheehan’s syndrome: newer advances. Indian J Endocrinol Metab 2011;15 Suppl 3:S203–7.

Renu Misra

1 Pathophysiology of non-haemorrhagic shock 2 Causes 2.1 Acute inversion 2.2 Amniotic fluid embolism 2.3 Pulmonary thromboembolism 2.4 Air embolism 2.5 Cardiac arrest 2.6 Rupture uterus 2.7 Sepsis

33

CHAPTER

Postpartum collapse

2.8 Drug toxicity and overdose 2.9 Intracranial haemorrhage 2.10 Anaphylaxis 2.11 Mendelson syndrome 3 Cardiopulmonary resuscitation of the pregnant patient 3.1 Basic life support 3.2 Advanced life support 4 Perimortem caesarean delivery

Postpartum maternal collapse is a frightening obstetric complication. The incidence of maternal collapse has increased due to the demographic changes in the pregnant population. These factors include increased average maternal age and body mass index, increased caesarean delivery rate and increased incidence of serious underlying co-morbidities in pregnant women.

noticeable features may be bulging of the flanks, dullness to percussion and the patient’s clear dislike of lying down flat which allows the blood to run up and irritate the diaphragm. Many haemorrhages into the retroperitoneal tissue spaces and between the layers of the broad ligament are overlooked, if not large, but they add to the patient’s shock.

Majority of these cases occur as a result of haemorrhage, which is revealed. However, if the patient has lost no more than 0.5–0.75 litre of blood and yet has collapsed, either she is losing blood internally or other shock-producing factors are operative. In the first instance, the most likely sites of bleeding are within the body of the uterus itself, the peritoneal cavity and the retroperitoneal spaces.

Only a small minority of cases of collapse after delivery occur without obvious vaginal bleeding, but these are the ones that pose a greater challenge for diagnosis and management. The management of postpartum haemorrhage has already been discussed in detail in Chapter 32, Postpartum Haemorrhage the pathophysiology and aetiology of non-haemorrhagic shock will be addressed here.

A uterus, which is slowly filling with blood, would often be fairly hard and the impression of size on palpation is more important than the actual height of fundus. Quite large quantities of blood can lie in the peritoneal cavity without producing significant physical signs locally, although general signs of shock are obvious. Pain is often much less than would be expected, and abdominal rigidity is usually absent in a postpartum case due to immunosuppression of pregnancy. Tenderness may not be significant, and the most

1  Pathophysiology of nonhaemorrhagic shock Blood flow is greatly reduced in a shocked patient due to vasoconstriction, although the brain and its vital centres are spared as far as possible. Blood flow to the skin is significantly reduced, hence the impression of pallor and coldness. Muscle blood flow and all visceral blood flow are also reduced.

684  Ian Donald’s Practical Obstetric Problems Kidneys.  All renal filtration usually ceases at systolic blood pressures of less than 80 mmHg, resulting in anuria. The duration of uncorrected shock will largely determine the recovery of renal function. Heart.  The heart is operating under grave handicap, the venous return is reduced and atrial filling is poor, so that cardiac output falls, and even acceleration of the heart cannot compensate for the poor stroke volume. These effects, namely vasoconstriction and tachycardia, are the result of sympathetic activity, and are highly protective in cases of haemorrhage by preventing further blood loss and maintaining blood supply to the vital centres, but where shock without blood loss occurs, this mechanism may be harmful by embarrassing the heart action through poor venous return and thus precipitating cardiac failure. Initially, there is a fall in pulse pressure because the diastolic pressure is increased due to vasoconstriction and the systolic pressure is maintained for some time. As the condition worsens, vasoconstriction begins to fail, the heart meanwhile becoming more inefficient, and both systolic and diastolic pressures fall together. The awareness of pain is for some unknown reason dulled. Other autonomic effects observed are dilatation of the stomach, the ascending colon and the proximal half of the transverse colon, corresponding to the predominant sympathetic nerve supply of the intestinal tract. The anterior lobe of the pituitary is very susceptible to damage during pregnancy. Necrosis to a greater or lesser degree may occur following postpartum haemorrhage or shock resulting in hypothyroidism, adrenal failure, hypogonadism, prolactin and growth hormone deficiency.1 This is called Sheehan syndrome. The immediate effects are less noticeable and serious than the remote complications. Failure to lactate and resume menses after delivery is the most common presenting symptom. The signs of hypopituitarism manifest later with genital atrophy and infertility. Although acute severe hypopituitarism may occur in a few patients, most have a mild disease that may go untreated for many years. Treatment includes hormone replacement with physiologic doses of glucocorticoids, levothyroxine and sex steroids, with appropriate increase in glucocorticoid doses during periods of stress.

2  Causes The most common cause of maternal collapse is vasovagal syncope and postural hypotension.2 Other common causes without associated haemorrhage are eclampsia, uterine rupture, vasovagal syncope, pulmonary embolism (amniotic fluid, air or thrombus), septic shock and uterine inversion. The causes can be divided in the following categories: yy Head: Eclampsia, epilepsy, cerebrovascular accident, vasovagal syncope yy Heart: Myocardial infarction, arrhythmias, peripartum cardiomyopathy, congenital heart disease, dissection of thoracic aorta yy Hypoxia: Pulmonary embolism, pulmonary edema, anaphylaxis yy General systemic disorders: Hypoglycaemia, amniotic fluid embolism (AFE), septicaemia, trauma, complications of anaesthesia, drug toxicity Some of the causes will be discussed in greater detail.

2.1  Acute inversion Acute inversion after delivery can be a cause of neurogenic shock. It should be quickly excluded or treated and should be one of the first possibilities to cross the obstetrician’s mind. It may occur due to improper conduct of third stage, by pulling on the cord before placental separation, but it is well to remember that about 15% of cases of acute inversion occur spontaneously and for no apparent reason. Complete inversion or the third degree is the rarest variety, and it is with the lesser degrees of inversion that such a cause of collapse may be overlooked. Abdominal palpation should be made at once to determine the location and shape of the uterine fundus, and if there is any doubt, for example, in case of gross obesity, a vaginal examination may have to be made. This is dealt with fully in the chapter on maternal injuries (see Chapter 31, Intrapartum Maternal Injuries).

2.2  Amniotic fluid embolism Amniotic fluid embolism (AFE) is a rare obstetric emergency in which amniotic fluid, fetal cells,

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hair or other debris enter the maternal circulation, causing cardiorespiratory collapse. It is defined by the Delphi consensus as an acute cardio-respiratory collapse within six hours after labour, delivery or ruptured membranes, with no other identifiable cause, followed by acute coagulopathy in those women who survive the initial event.3 AFE was first described in 1926,4 but its real significance as a killer disease was probably recognized in 1941 when Steiner and Lushbaugh5 published an autopsy series of eight pregnant women who died of sudden shock during labour. Fetal mucin and squamous cells were found in the pulmonary vessels of these women, and the authors believed that AFE was the most common cause of obstetric death during labour or in the first 10 hours after delivery. The mortality have since fallen due to better supportive care. The reported incidence in a recent population-based cohort is between 0.8 and 1.8 per 100,000 births, and 30–41% of these either died or had permanent neurological injury.6 Women who died or had permanent neurological injury were more likely to present with cardiac arrest.7 The associated perinatal mortality rate is 9–44%.8 Neurologic status of the infant is directly related to the time elapsed between maternal arrest and delivery.

2.2.1  Risk factors Older maternal age and induction of labour are the most consistently associated risk factors for AFE. Risk of AFE was increased when labour was induced with prostaglandins, and not with oxytocin. Other risk factors include multiple pregnancy, polyhydramnios, placenta praevia, placental abruption, operative deliveries, eclampsia, polyhydramnios, cervical lacerations and uterine rupture.4,5

2.2.2 Pathogenesis The pathogenesis of the condition is not clear. Amniotic fluid probably enters the maternal venous circulation through a breach in the barrier between the maternal vasculature and the amniotic fluid, most likely from the placental site or at the site of a uterine trauma, after the membranes have ruptured. These emboli containing particulate constituents of liquor amnii such as

epithelial squames, fat, lanugo hairs and meconium, provoke immunological and humoral reactions in the mother. This results in an inflammatory cascade, which leads to multi-organ failure and disseminated coagulopathy. The maternal response to amniotic fluid in many ways resembles an anaphylactic reaction. Moreover, fetal tissue or amniotic fluid components are not universally found in women who present with signs and symptoms of AFE. It was, therefore, suggested that the condition should be renamed as the “anaphylactoid disease of pregnancy” Whatever is the trigger, it initiates a massive anaphylactic reaction, activation of the complement cascade or both.9 In the early phase, pulmonary artery vasospasm and elevated right ventricular pressure causes hypoxia resulting in myocardial and pulmonary capillary damage. This leads to left heart failure and acute respiratory distress. The haemorrhagic phase follows characterized by massive haemorrhage with uterine atony and disseminated intravascular coagulation (DIC).

2.2.3 Diagnosis There are four diagnostic criteria, all of which should be met.10 1. Sudden onset of cardiorespiratory arrest, or both hypotension (systolic blood pressure 20 weeks pregnant should be put into a left lateral position to relieve aortocaval compression. yy If chest compressions are required in a patient with cardiac arrest, patient should be in supine position with the uterus displaced to left side manually. yy If resuscitation is not effective in four minutes, the fetus should be delivered immediately by caesarean section, preferably within five minutes of cardiac arrest. yy Perimortem caesarean should be performed even if the fetus is non-viable, if maternal resuscitation fails with uterine displacement and uterus is above umbilicus.

Postpartum collapse  693

References 1. Dokmetas HS, Kilicli F, Korkmaz S, Yonem O. Characteristic features of 20 patients with Sheehan’s syndrome. Gynecol Endocrinol 2006;22(5):279–83. 2. Government of South Australia. Perinatal practice guideline. Collapse (maternal). SA Health Safety & Quality Strategic Governance Committee. March 1, 2017. 3. Schaap T, Bloemenkamp K, Deneux-Tharaux C, et al. Defining definitions: a Delphi study to develop a core outcome set for conditions of severe maternal morbidity. BJOG 2019;126(3):394–401. 4. Meyer JR. Embolia pulmonar amnio caseosa. Bras Med 1926;2:301–3. 5. Steiner PE, Lushbaugh C. Maternal pulmonary embolism by amniotic fluid as a cause of obstetric shock and unexpected deaths in obstetrics. J Am Med Assoc 1941;117:1245–54, 1340–5. 6. Fitzpatrick KE, van den Akker T, Bloemenkamp KWM, et al. Risk factors, management, and outcomes of amniotic fluid embolism: a multicountry, population-based cohort and nested case– control study. PLoS Med 2019;16(11):e1002962. 7. Fitzpatrick KE, Tuffnell D, Kurinczuk JJ, Knight M. Incidence, risk factors, management and outcomes of amniotic-fluid embolism: a population-based cohort and nested case–control study. BJOG 2016;123(1):100–9.

13. Kaneko Y, Ogihara T, Tajima H, Mochimaru F. Continuous hemodiafiltration for disseminated intravascular coagulation and shock due to amniotic fluid embolism: report of a dramatic response. Intern Med 2001;40(9):945–7. 14. Centre for Maternal and Child Enquiries (CMACE). Saving mothers’ lives. Reviewing maternal deaths to make motherhood safer 2006–2008. BJOG 2011;118 Suppl 1:1–203. 15. Bates SM, Greer IA, Hirsh J, Ginsberg JS. Use of antithrombotic agents during pregnancy. The seventh ACCP conference on antithrombotic and thrombolytic therapy. Chest 2004;126:627S–44S. 16. Kim CS, Liu J, Kwon JY, Shin SK, Kim KJ. Venous air embolism during surgery, especially cesarean delivery. J Korean Med Sci 2008;23(5):753–61. 17. Younker D, Rodriguez V, Kavanagh J. Massive air embolism during cesarean section. Anesthesiology 1986;65(1):77–9. 18. Rodgers L, Dangel-Palmer MC, Berner N. Acute circulatory and respiratory collapse in obstetrical patients: a case report and review of the literature. AANA J 2000;68(5):444–50. 19. Maternal collapse in pregnancy and the puerperium. Green-top guideline no. 56. January 2011. p. 1–24.

8. Conde-Agudelo A, Romero R. Amniotic fluid embolism: an evidence-based review. Am J Obstet Gynecol 2009;201(5):445.e1–13.

20. Mhyre JM, Tsen LC, Einav S, Kuklina EV, Leffert LR, Bateman BT. Cardiac arrest during hospitalization for delivery in the United States, 1998–2011. Anesthesiology 2014;120:810–8.

9. Benson MD. Current concepts of immunology and diagnosis in amniotic fluid embolism. Clin Dev Immunol 2012;2012:946576.

21. ACOG practice bulletin no. 212: Pregnancy and heart disease. Obstet Gynecol 2019;133:e320–56.

10. Bonnet MP, Zlotnik D, Saucedo M, et al. Maternal death due to amniotic fluid embolism: a national study in France. Anesth Analg 2018;126(1):175–82. 11. Levy R, Furman B, Hagay ZJ. Fetal bradycardia and disseminated coagulopathy: atypical presentation of amniotic fluid emboli. Acta Anaesthesiol Scand 2004;48(9):1214–5. 12. Kobayashi H, Ooi H, Hiroshi H, et al. Histological diagnosis of amniotic fluid embolism by monoclonal antibody TKH-2 that recognizes NeuAC [alpha]2-6GaINAc epitope. Hum Pathol 1997;28:428–33.

22. Chu J, Johnston TA, Geoghegan J; Royal College of Obstetricians and Gynaecologists. Maternal Collapse in Pregnancy and the Puerperium: Green-top Guideline No. 56. BJOG 2020;127(5):e14e52. 23. Ok SH, Hong JM, Lee SH, Sohn JT. Lipid emulsion for treating local anesthetic systemic toxicity. Int J Med Sci 2018;15(7):713–22. 24. Tacquard C, Chassard D, Malinovsky JM, et al. Anaphylaxis-related mortality in the obstetrical setting: analysis of the French National Confidential Enquiry into Maternal Deaths from 2001 to 2012. Br J Anaesth 2019;123(1):e151–3.

694  Ian Donald’s Practical Obstetric Problems 25. McCall SJ, Bunch KJ, Brocklehurst P, et al. The incidence, characteristics, management and outcomes of anaphylaxis in pregnancy: a population-based descriptive study. BJOG 2018;125(8):965–71. 26. Mendleson CL. The aspiration of stomach contents into the lungs during obstetric anesthesia. Am J Obstet Gynecol 1946;52:191–205. 27. Salik I, Doherty TM. Mendelson syndrome. In: StatPearls. Treasure Island, FL: StatPearls Publishing; 2020. 28. Whitty J. Maternal cardiac arrest in pregnancy. Clin Obstet Gynecol 2002;45(2):377–92. 29. Jeejeebhoy FM, Zelop CM, Lipman S, et al. Cardiac arrest in pregnancy: a scientific statement from the American Heart Association. Circulation 2015;132(18):1747–73. 30. Panchal AR, Berg KM, Hirsch KG, et al. 2019 American Heart Association focused update on advanced

cardiovascular life support: use of advanced airways, vasopressors, and extracorporeal cardiopulmonary resuscitation during cardiac arrest: an update to the American Heart Association guidelines for cardiopulmonary resuscitation and emergency cardiovascular care. Circulation 2019;140(24):e881–94. 31. Vanden Hoek TL, Morrison LJ, Shuster M, et al. Part 12: cardiac arrest in special situations: 2010 American Heart Association guidelines for cardiopulmonary resuscitation and emergency cardiovascular care. Circulation 2010;122 Suppl 3:S829–61 [published correction appears in Circulation 2011;123:e239; Circulation 2011;124:e405]. 32. Dijkman A, Huisman CM, Smit M, et al. Cardiac arrest in pregnancy: increasing use of perimortem caesarean section due to emergency skills training? BJOG 2010;117:282–7.

34

CHAPTER

Puerperium Kiran Guleria, Anju Singh

1 Physiological changes during puerperium 1.1 Genital tract 1.2 Abdominal wall 1.3 Hormonal changes 1.4 Haematological and coagulation factors 1.5 Cardiovascular system

2 Routine postpartum care 2.1 WHO recommendations for postpartum care 2.2 Postnatal care for the newborn

3 Lactation and breastfeeding 3.1 Advantages of breastfeeding 3.2 Contraindications to breastfeeding 3.3 Lactation suppression

The word puerperium is derived from Latin; puer-child and parus-bringing forth. Puerperium or postpartum period is defined as the period from delivery up to six weeks postpartum.1 Post-delivery period is a dynamic phase when the anatomical and physiological changes that occur during pregnancy revert back to near pre-pregnant state. It is also referred to as “fourth trimester of pregnancy.” Therefore, women need considerable medical attention and psychological support during this period for quick and complete recovery. A clear understanding of changes during puerperium is essential to appreciate the disease processes that can threaten the women during this period.

1  Physiological changes during puerperium 1.1  Genital tract Uterine involution.  It is the process which involves returning of the uterus from pregnant to



4 Postpartum contraception 4.1 Newer contraceptives 4.2 Emergency contraceptives



5 Puerperal fever 5.1 Puerperal sepsis 5.2 Persistent postpartum fever 6 Late infections



7 Differential diagnosis of puerperal sepsis/ puerperal fever 7.1 Breast infection 7.2 Urinary tract infections 7.3 Septic pelvic thrombophlebitis 7.4 Skin and soft tissue infections 8 Psychological disorders

non-pregnant state. It starts soon after delivery; the uterine fundus becomes firm and retracted immediately after delivery of placenta and can be palpated just below the umbilicus. Thereafter, the uterine height recedes at a rate of approximately 1cm/day on abdominal palpation. It becomes an intrapelvic organ by the 12th postpartum day and takes about 4–6 weeks for completing involution to non-pregnant state. It weighs nearly 1000 g immediate postpartum, 500 g at the end of first week, 300 g at second week and 50–100 g by the end of 4–6 weeks.2 Total number of myocytes do not decrease, rather myometrial retraction (brachystasis) is the unique characteristic of the uterine muscle that enables it to maintain its shortened length following successive contractions and is responsible for its involution. Clinically, women may experience cramping pain caused by involuntary contractions during the phase of uterine involution known as ‘afterpains’ which usually resolve by the end of first postpartum week. These are more common in multiparous women and are exaggerated during breastfeeding due to the release of oxytocin.

696  Ian Donald’s Practical Obstetric Problems The superficial endometrial layer sloughs contributing to the lochia. Basal layer is the source for regeneration of the new endometrial glands and stroma which begins in the first week, and by the third postpartum week, the entire endometrium is restored except at the placental site which takes about six weeks. Lochia.  It is the physiological postpartum vaginal discharge resulting from sloughing of decidua and consists of erythrocytes, shredded decidua, epithelial cells and bacteria. It is reddish in colour for the first three to four days after delivery because it contains more blood initially, and is therefore called lochia rubra. This changes to brownish colour and serous consistency, the lochia serosa, which persists for about a week and then becomes whitish turbid fluid, lochia alba. The total volume of postpartum lochial secretion is 200–500 ml, which is discharged over a mean duration of one month.3 Up to 15% of women continue to pass lochia for 6–8 weeks.4 The duration of lochia does not appear to be related to lactation or to the use of either estrogen-containing or progesterone-only contraceptives. However, women with bleeding diatheses may be prone to longer duration of discharge of lochia.5 Cervix.  After delivery, the cervix is soft and floppy. The cervix remains 2–3 cm dilated for the first few postpartum days, the lumen then reduces to less than 1 cm at one week forming the endocervical canal. The external os never resumes its pre-gravid shape; the small, smooth, regular circular opening of the nulliparous cervix becomes a large, transverse slit after childbirth. Small lacerations can be found at the margins of the external os. Histologically, the cervix does not return to baseline for up to 3–4 months after delivery. Vagina and vulva.  Vagina which distends during delivery involutes more slowly than the uterus. Normal rugosities of the vaginal wall reappear at about third week, but pre-pregnant size and elasticity of the tissues is never regained. Hymen is lacerated and represented by tags, known as caruncle myrtiformes.

1.2  Abdominal wall Abdominal wall becomes flabby and remains soft and poorly toned for many weeks postpartum. Postnatal exercises can play an important role in regaining the pre-pregnant tone of

abdominal muscles. Striae gravidarum or stretch marks are reddish linear lesions which often develop during pregnancy over the breasts, abdomen and thighs. After the pregnancy, they do not disappear completely but tend to become depigmented and lighter in colour in due course of time, known as striae albicantes. Sometimes they can cause itching or burning, but it is the physical appearance which is more distressing to women. The aetiological factors include stretching and damage to the elastic fibres in the skin, hormonal changes and perhaps the most important, a genetic predisposition. Younger women and those who gain more weight during pregnancy have a greater incidence of developing striae.6 However, regardless of the aetiology, the histological examination of the dermis shows atrophy and loss of rete ridges, similar to scar tissue.7 A number of creams and oils are marketed claiming reduction of stretch marks of pregnancy, but no medication has been found to be effective in prevention or treatment of the striae.

1.3  Hormonal changes Gonadotropins and sex steroids.  These are at low levels for the first 2–3 weeks postpartum. In addition, initial hyperprolactinemia also decreases GnRH and gonadotropin secretion. Ovulation.  It is suppressed for a variable period of time due to increased levels of prolactin stimulated by lactation resulting in low levels of gonadotropins. The average time to first ovulation is about 45 days (range 25–72) in non-breastfeeding and 189 days (range 34–256) in the breast-feeding mothers. In studies using urinary pregnanediol levels to measure ovulation in non-lactating women, the return to menstruation following delivery ranged from 45 to 64 days and the mean time to ovulation from 45 to 94 days, the earliest reported as 25 days postpartum.8 Approximately 40% women remain amenorroheic for at least six months if they breastfeed exclusively.9 Human chorionic gonadotropin (hCG) values typically return to normal non-pregnant levels 2–4 weeks after delivery. This return to normal level takes less time (median duration-12 days) if uterus is removed. This fall in serum beta-hCG level is clinically important as rising levels in

Puerperium  697

postpartum period may point towards development of gestational trophoblastic disease.

1.4 Haematological and coagulation factors Pregnancy-related hematologic changes return to baseline by 6–8 weeks after delivery.10 Plasma volume.  It decreases immediately after delivery with a rise again 2–5 days later because of a rise in aldosterone secretion. It then starts to decline with levels 10–15% above non-pregnant levels at three weeks postpartum and return to normal non-pregnant levels at six weeks postpartum. Physiologic anaemia.  Coinciding with return of normal plasma levels, physiologic anaemia of pregnancy also resolves by six weeks postpartum. Postpartum leucocytosis and neutrophilia. It is a normal physiological phenomenon. In a recently published data, the mean postpartum white blood cell (WBC) count was found to be 13.39 ± 0.24 × 109/L (range 1.20−37.30 × 109/L).11 It falls to the normal non-pregnant range by the sixth day postpartum. As a single parameter, postpartum leucocytosis should not prompt further work up. However, detailed evaluation is needed if it is associated with fever or a large number of immature WBC forms or blasts are seen on peripheral smear. Platelets.  For most pregnant women, the platelet count remains within the normal range during pregnancy and does not change postpartum. For individuals with gestational thrombocytopenia, mild thrombocytopenia begins to resolve soon after delivery and is no longer present at 3–4 weeks postpartum. Coagulation and fibrinolysis.  Postpartum normalization of coagulation parameters and return to baseline thromboembolic risk generally occurs by 6–8 weeks after delivery.10 So, it is advisable to delay thrombophilia testing until three months following delivery, if indicated.

1.5  Cardiovascular system Significant haemodynamic alterations start within the first 10 minutes following a term vaginal

­ elivery, which include increase in the cardiac outd put and stroke volume by 59 and 71%, respectively.12 At one hour postpartum, both the cardiac output and stroke volume remain increased by 49 and 67% respectively, heart rate decreases by 15% and blood pressure remains unchanged.13 This increase in stroke volume and cardiac output most likely results from raised cardiac preload from auto transfusion of utero-placental blood to the intravascular space. As the uterus decompresses following delivery, a reduction in the mechanical compression of the vena cava allows for further increases in cardiac preload. There is substantial reduction in left ventricular size and contractility as early as two weeks postpartum. These cardiovascular physiologic changes resolve slowly after delivery. These changes aggravate the risk of heart failure in a patient with underlying heart disease and severe anaemia. So, such patients must be monitored closely in the immediate postpartum Elevated glomerular filtration rate and renal plasma flow return to normal by six weeks. Dilatation of renal calyces, pelvis, and ureters resolve by 2–8 weeks postpartum. Because of the dilated collecting system, coupled with incomplete emptying and residual urine in traumatised bladder, symptomatic urinary tract infection (UTI) remains a concern in postpartum period.

2   Routine postpartum care Clinical assessment.  The period of 1–2 hours after delivery is also known as ‘fourth stage of labour’. This ‘Golden’ period is important to pick any complication particularly, postpartum haemorrhage (PPH) at an earlier stage since the likelihood of significant haemorrhage is greatest in immediate postpartum period. Blood pressure and pulse rate are measured every 15 minutes for 2 hours or more frequently if needed. Temperature is measured every four hours for first eight hours and then eight hourly. Uterine fundus is closely monitored for one hour to ensure that it is well contracted and the amount of vaginal bleeding is checked. Uterine fundal palpation may help to detect atonic PPH as blood can accumulate within the uterus without external bleeding. If regional or general anaesthesia is used, then monitoring should be done in a well-equipped and staffed recovery room.

698  Ian Donald’s Practical Obstetric Problems Laboratory testing.  Routine post-delivery haemoglobin for all the patients is not required. It should be done in women with pre-delivery anaemia or who have had PPH. Similarly, determination of the increased WBC count to predict impending infection is not required since leucocytosis as high as 15,000 cells/mm3 is normal in postpartum women.14,15 Leucocytosis needs further evaluation only if there is clinical suspicion of infection or presence of large number of blasts. Perineal care.  The woman should be advised to clean the perineum from anterior to posterior- from vulva to the anus. In the initial 24 hours after delivery, application of cool pack may help in reducing edema and pain if there is perineal laceration or episiotomy. After 24 hours, moist heat in the form of sitz bath can be advised to relieve local discomfort. Normally episiotomy heals by third week. Oral non-steroidal anti-inflammatory drugs (NSAIDs) can be prescribed to relieve pain, except in volume depleted cases like pre-eclampsia where acute kidney injury can be precipitated. However, severe perineal, vaginal or rectal pain or difficulty in passing urine always warrants careful local examination to rule out haematoma on day 1 and infection after day 3. Ambulation. Early ambulation within few hours after vaginal birth should be encouraged as it helps in early recovery, reduces bladder and bowel complications and reduces the risk of venous thromboembolism. An attendant should be present at least for the first few times woman gets out of the bed as she may feel dizzy. Diet.  There are no dietary restrictions after vaginal delivery. Lactating women require an additional 500 kcal and 25 g of proteins/day in addition to what is recommended for non-pregnant women. For non-lactating women, dietary requirements remain same as for non-pregnant. Iron and folic acid supplementation should be continued for at least three months. Bladder care.  In early puerperium, urinary retention and bladder overdistention is common. Oxytocin-induced or augmented labour (antidiuretic effect), perineal lacerations, operative vaginal delivery, prolonged labour etc. are some of the factors which may increase likelihood of decreased bladder sensation and

urinary retention. In postpartum period, first urine void should be ensured within six hours. If woman is not able to pass urine, she should be thoroughly examined to rule out any haematoma. After ruling out haematoma, she should be catheterized. It is best to leave the catheter in place for 24 hours even without a demonstrable cause. As it allows recovery of normal bladder sensation and tone and prevent any recurrence. Bowel care.  Constipation may occur in the early puerperium because of decreased tone of bowel during pregnancy, decreased food intake during labour, presence of episiotomy or perineal lacerations or painful haemorrhoids. Haemorrhoids often resolve spontaneously as the perineum recovers so only symptomatic relief with pain killers and laxatives is advocated. Support for breastfeeding.  The World Health Organization (WHO), the American Academy of Pediatrics (AAP), the American College of Obstetricians and Gynecologists (ACOG) and the Indian Obstetric and Paediatric societies, all recommend exclusive breastfeeding for the first six months of life.16–18 The WHO and UNICEF launched the Baby-friendly Hospital Initiative and recommend ‘Ten steps to successful breastfeeding’ to promote breastfeeding and should be adopted by all health facilities.19 These are as listed as follows: Ten steps to successful breastfeeding19

1a. Comply fully with the International Code of Marketing of Breast-milk Substitutes and relevant World Health Assembly resolutions. 1b.  Have a written infant feeding policy that is routinely communicated to staff and parents. 1c. Establish ongoing monitoring and datamanagement systems. 2.  Ensure that staff have sufficient knowledge, competence and skills to support breastfeeding. 3. Discuss the importance and management of breastfeeding with pregnant women and their families. 4. Facilitate immediate and uninterrupted skinto-skin contact and support mothers to initiate breastfeeding as soon as possible after birth. 5. Support mothers to initiate and maintain breastfeeding and manage common difficulties. Continued....

Puerperium  699

Continued.... 6. Do not provide breastfed newborns any food or fluids other than breast milk, unless medically indicated. 7. Enable mothers and their infants to remain together and to practise rooming-in 24 hours a day. 8. Support mothers to recognize and respond to their infants’ cues for feeding. 9.  Counsel mothers on the use and risks of feeding bottles, teats and pacifiers. 10. Coordinate discharge so that parents and their infants have timely access to ongoing support and care.

Mood and cognition.  It is common for some postpartum women to have depressed mood for few days which is termed as postpartum blues. This disorder is usually mild and persists for 2–10 days. If this persists for long, then thorough evaluation for depressive disorders should be done and treated accordingly. The ACOG, the AAP and the United States Preventive Service Task Force Recommendation Statement recommend screening of all postpartum women for depression.20–23 Resumption of coitus. There is no evidence-based data regarding resumption of coitus after delivery. After two weeks, coitus may be resumed based on desire and comfort. Due to postpartum hypoestrogenic state, vulvovaginal epithelium is thin and this state persists till ovulation is resumed. To relieve this, small amount of topical estrogen cream may be applied. Vaginal lubricants may be useful during coitus. Postpartum immunization. Ideally, women should be vaccinated against preventable diseases in their environment prior to conception. However, if not received both inactivated and live vaccines (except smallpox and yellow fever vaccine) may be administered to nursing mothers. Breastfeeding does not adversely affect success or safety of vaccination and vice versa.24,25 Measles, mumps, rubella, (MMR) and varicella vaccines are given postpartum to non-immune women, ideally prior to discharge.24 These can be given safely to lactating mothers also since the virus is not transmitted through breast milk or casual contact. Tdap should be given to postpartum women who have not received it during pregnancy.26 This reduces the risk of maternal pertussis, and thus transmission to the infant, in whom pertussis can be lethal or have significant

morbidity. However, the maternal immune response may not be sufficiently rapid to provide indirect protection to the infant until two weeks post-immunization. RhD-negative mothers of Rh(D)-positive infants should be given anti-D immunoglobulin as soon as possible after delivery, within 72 hours of birth. For RhD-negative women who have received anti-D Ig postpartum, MMR and/or varicella vaccine can still be administered immediately postpartum, if indicated. There are no known risks to the fetus from passive immunization of pregnant and postpartum women with immunoglobulin preparations. Postexposure prophylaxis for hepatitis A and B, rabies and tetanus is not altered by pregnancy or postpartum state. Advice on discharge.  At the time of discharge, women should be counselled regarding anticipated normal physiological changes, importance of breastfeeding, dietary advice, wound care if any, infant care and immunization, contraception and should be explained warning signs which warrant reporting immediately to health care facility. A postpartum follow-up visit between four and six weeks is recommended in all.

2.1 WHO recommendations for postpartum care According to the WHO, if birth is in a healthcare facility, mothers and newborns should receive postnatal care in the facility for at least 24 hours after birth. If birth is at home, the first postnatal contact should be as early as possible within 24 hours of birth. At least three additional postnatal contacts are recommended for all mothers and newborns, on day 3 (48–72 hours), between days 7 and 14 after birth and six weeks after birth. A summary of WHO recommendations for postnatal care27 is given in Table 34.1.

2.2  Postnatal care for the newborn Breastfeeding.  All babies should be exclusively breastfed from birth until six months of age. Mothers should be counselled and provided support for exclusive breastfeeding at each postnatal visit. Cord care.  Daily chlorhexidine (7.1% chlorhexidine digluconate aqueous solution or gel delivering 4% chlorhexidine) application to the

700  Ian Donald’s Practical Obstetric Problems Table 34.1  World Health Organization (WHO) recommendations for care of postnatal women During the first 24 hours of birth Monitor • General condition, temperature, pulse rate, blood pressure • Uterine contraction, fundal height • Vaginal bleeding • Urine void should be documented within six hours Beyond 24 hours Assess at each postnatal visit • Micturition and urinary incontinence, bowel function • Healing of any perineal wound, perineal pain and perineal hygiene • Headache, fatigue, back pain, breast pain, uterine tenderness and lochia • Breastfeeding progress • Emotional wellbeing At 10–14 days • Assess for resolution of postpartum depression • Observed for any risks, signs and symptoms of domestic abuse. • Ask about resumption of sexual intercourse and possible dyspareunia Counselling Encourage to • Mobilize as soon as appropriate following the birth. • Take gentle exercise and make time to rest during the postnatal period Advise regarding • Nutrition • Contraception • Hygiene, especially handwashing • Signs and symptoms of postpartum haemorrhage: Sudden and profuse blood loss or persistent increased blood loss, faintness, dizziness, palpitations/tachycardia. • Signs and symptoms of pre-eclampsia/eclampsia: Headaches, visual disturbances, nausea, vomiting, epigastric or hypochondrial pain, feeling faint, convulsions (in the first few days after birth) • Signs and symptoms of infection: Fever, shivering, abdominal pain and/or offensive vaginal loss. • Signs and symptoms of thromboembolism: Unilateral calf pain, redness or swelling of calves, shortness of breath or chest pain

Iron and folic acid supplementation: Should be provided for at least three months. Antibiotics: Give to women with vaginal delivery with third- or fourth-degree perineal tear.

umbilical cord stump during the first week of life is recommended for newborns who are born at home in settings with high neonatal mortality (30 or more neonatal deaths per 1000 live births). Clean, dry cord care is recommended for newborns born in health facilities and at home in low neonatal mortality settings. Use of chlorhexidine in these situations may be considered only to replace application of a harmful traditional substance, such as cow dung to the cord stump. Bathing.  Should be delayed until 24 hours after birth. If this is not possible due to cultural reasons, bathing should be delayed for at least

six hours. Appropriate clothing of the baby for ambient temperature is recommended. This means one to two layers of clothes more than adults, and use of hats/caps. Rooming-in.  The mother and baby should not be separated and should stay in the same room 24 hours a day. Communication  and playing with the newborn should be encouraged. Immunization  should be promoted as per existing guidelines. Preterm and low-birth-weight babies should be identified immediately after birth and should be provided special care.

Puerperium  701

Immediate contact to health facility/­ referral  for further evaluation if any of the signs is present: Stopped feeding well, history of convulsions, fast breathing (breathing rate ≥60/min), severe chest in-drawing, no spontaneous movement, fever (temperature ≥37.5 °C), low body temperature (temperature embryo-fetal risk • Effective for the reduction of maternal–fetal transmission of HIV-1. Can cause neonatal anaemia

Contraindicated

Beclomethasone

Compatible

Limited human data – probably compatible

Betamethasone

• Compatible–maternal benefit >> embryo-fetal risk. No reports of betamethasone and birth defects. • Studies on corticosteroids use in first trimester have shown association with orofacial clefts

No human data – probably compatible

Dexamethasone

• Compatible – maternal benefit >> fetal risk • Reports of orofacial clefts with use in first trimester

No human data – probably compatible

Esomeprazole

No human data. Animal data suggest low risk

Potential toxicity

Lansoprazole

Human data suggest low risk

No human data – potential toxicity

Omeprazole

Human data suggest low risk

Potential toxicity

Pantoprazole

Human data suggest low risk

Limited human data – probably compatible

Rabeprazole

Limited human data – animal data suggest low risk Avoid in first trimester

No human data – potential toxicity

Ranitidine

Compatible

Compatible

Corticosteroid

GI anti-secretory

Immunosuppressant Azathioprine

• Human data suggest risk in third trimester • Risk of neonatal immunosuppression in third trimester; dose modification may reduce this effect

Probably compatible

Cyclosporine

• Limited human data – animal data suggest low risk • Teratogenesis unlikely. Problems like FGR may be due to the disease for which it is prescribed

Limited human data – potential toxicity May interfere with cellular metabolism in the nursing infant

Tacrolimus

Human data suggest low risk Risk of congenital malformations low

Limited human data – probably compatible

Bisacodyl

No human data – probably compatible

No human data – probably compatible

Lactulose

No human data – probably compatible

No human data – probably compatible

Laxative

Continued....

Drugs in pregnancy and lactation  755

Table A-3  ....Continued Adverse effects

Drug

Pregnancy

Breastfeeding

Vitamin/nutrient Vitamin A

Compatible, contraindicated in doses above RDA (8000 IU/d)

Compatible

Vitamin B12

Compatible

Compatible

Vitamin C

Compatible

Compatible

Vitamin D

Compatible

Compatible

Vitamin E

Compatible

Compatible

Calcium carbonate (nutrient/antacid)

Compatible

Compatible

Cholecalciferol

Compatible

Calcitriol

Compatible Miscellaneous

Aminocaproic acid

Limited human data – no relevant animal data

Hold breastfeeding

Alprazolam

Human and animal data suggest risk. Neonatal withdrawal

Potential toxicity

Bromocriptine

Compatible

Contraindicated

Cabergoline

Human data suggest low risk

Contraindicated

Calcitonin (calcium regulating hormone)

Limited human data – probably compatible

No human data – probably compatible

Cholestyramine

• Human data suggest risk • Interferes with absorption of fat-soluble vitamins (A, D, E, K) resulting in deficiencies in mother and fetus • Ursodeoxycholic acid was more effective than cholestyramine for intrahepatic cholestasis

No human data – probably compatible

Clomiphene

Contraindicated. Each new course should be started only after excluding pregnancy

No human data – potential toxicity May reduce lactation in some patients

Cocaine

Contraindicated. Teratogenic. Risk of spontaneous abortions, premature delivery, abruptio placentae and fetal death

Contraindicated

Codeine

Human data suggest risk

Human data suggest potential toxicity

Dextromethorphan (anti-tussive)

Compatible

Compatible

Isotretinoin

Contraindicated – potent human teratogen

Potential toxicity

Levothyroxine

Compatible

Compatible

Lorazepam

Human data suggest risk in first and third trimesters

Limited human data – probably compatible Potential toxicity if combined with other CNS suppressants

Marijuana

Contraindicated

Contraindicated Continued....

756  Ian Donald’s Practical Obstetric Problems Table A-3  ....Continued Adverse effects

Drug

Pregnancy

Breastfeeding

Mifepristone

Contraindicated. Risk of embryotoxicity

Contraindicated

Misoprostol

Contraindicated in first trimester – association with congenital malformations

Potential toxicity. Potential for severe drug-induced diarrhoea

Montelukast

Limited human data – probably compatible

No human data – probably compatible

Ritodrine

Compatible in second and third trimesters. No data on first trimester use

Probably compatible

ACE, angiotensin-converting enzyme; CNS, central nervous system; CPM, Chlorpheniramine maleate; FGR, fetal growth restriction; G6PD, glucose-6-phosphate dehydrogenase; GI, gastrointestinal; HIV, human immunodeficiency virus; IUGR, intrauterine growth restriction; NSAID, non-steroidal anti-inflammatory drug; RDA, recommended daily allowance.

Sources of information 1. US Food and Drug Administration. Pregnancy and lactation labelling. 2. Breastfeeding and maternal medication. Recommendations for Drugs in the Eleventh WHO Model List of Essential Drugs. Department of Child and Adolescent Health and Development. World Health Organization, 2002.

3. Briggs GG, Freeman RK,Towers CV, Forinash AB. A reference guide to fetal and neonatal risk. Drugs in Pregnancy and Lactation, 11th edition. Wolters Kluwer, 2017.

Index Numbers in bold indicate major discussion

A Abdominal cerclage, 35, 36, 338, 362, 459, 461, 472 Abdominal circumference, 80, 169, 386, 387 Abortion, see Miscarriage Abruptio placentae, 113, 115, 370–74 aetiology, 370 grading, 372 management, 374 pathophysiology, 371 Acardiac twin, see TRAP Accidental haemorrhage, see Abruptio placentae Active management of labour, 526–27 Acute abdominal pain in pregnancy, 113–18 early pregnancy, 114 late pregnancy, 115 Acute appendicitis, 115–16 Acute fatty liver of pregnancy, 196, 242, 246, 253 Acute inversion, 646–49, 684 Acute kidney injury, 240–42 Acute liver failure in pregnancy, 106, 254–55 Acute pancreatitis, 117–18 Acute pulmonary edema, 198, 215, 224 Acute pyelonephritis, 112 Acute renal failure, 131, 182, 189, 196, 240–42 Acute rheumatic carditis, 223–24 Acute severe hypertension, 198–99 Advance life support, 691–92 Air embolism, 687–88 Alpha–fetoproteins, 48, 371 American College of Obstetricians and Gynecologists (ACOG), 71, 110, 163, 177, 381, 414, 437, 450, 477, 495, 527, 619, 688, 698, 718, 744 Amniocentesis, 43, 47, 50, 51 early, 52 Amnioinfusion, 431–32 Amnioreduction, 410 Amniotic fluid embolism, 590, 674, 684–85 Amniotic fluid index, 81, 410, 424–25, 429

Amniotic fluid volume, 81, 193, 388, 410, 424–25, 429–32 Anaemia, 10, 12, 126 aplastic, 143–44 definition, 126 haemoglobinopathies 144–49 haemolytic, 131 iron deficiency, 132 megaloblastic, 140–43 RBC indices haematocrit, 131, 320, 442, 444 mean corpuscular haemoglobin (MCH), 130 mean corpuscular haemoglobin concentration (MCHC), 130, 131, 146 mean corpuscular volume (MCV), 130, 146 Anaemia Mukt Bharat programme, 135 Anal sphincter injury, 653–54 identification, 653 postoperative care, 654 repair, 652–53 Anembryonic pregnancy, 22, 23, 25, 27 Aneuploidy, 54, 71, 168, 385, 405, 406, 426, 429 Antenatal care, 1–15 abdominal examination, 9 biochemical screening, 9, 168–69, 271, 406 blood pressure, 9 booking visit,7–8, 168, 270–71 checklist for uncomplicated singleton pregnancies, 14–15 diet in pregnancy, 11–12 examination, 7–8 exercise in pregnancy, 13 history–taking, 7 investigations, 8 subsequent visits, 8–14 travel in pregnancy, 13–14 urinalysis for protein, 9 weight, 9 weight gain during pregnancy, 11 work during pregnancy, 12

758  Ian Donald’s Practical Obstetric Problems Antepartum haemorrhage, 357–76 causes, 357 Anti–D prophylaxis, 10, 27–28 Anti–dsDNA titre, 237–38 Antihypertensive therapy, 193, 196–99 Anti–La antibodies, 237, 270, 271 Antiphospholipid syndrome, 34–35, 94, 185, 272–76 antepartum management, 275–76 antiphospholipid antibodies, 33, 182, 236–37, 273 diagnostic criteria, 273–74 maternal complications, 274–75 obstetric complications, 275 Anti–Ro antibodies, 237, 270, 271, 272 Antithrombin III, 19, 274, 287 Apgar score, 717–18 Arcuate uterus, 69, 334 Arrhythmias 213, 214–15, 501 Arterial embolisation, 670, 673 Artificial rupture of membranes (ARM), 375, 554, 579 Asphyxia, fetal, 500, 718, 729, 740 Asymptomatic bacteriuria, 111–12 Atosiban, 467 Autoimmune thyroid disease, 261

B B12 deficiency, 143 Bacterial vaginosis, 462–63 Bad obstetric history, 93–96, 542 Basic life support, 690–91 Beta agonists, 225, 465–67 ritodrine, 466 terbutaline, 466 Beta–thalassaemia, 144 Bicornuate uterus, 35, 335–37, 365 Bimanual uterine compression, 665, 668 Biochemical markers acetylcholinesterase, 50 alpha–fetoproteins, 48 amniotic fluid, 48 human chorionic gonadotrophin, 48–49 maternal serum, 48–49 pregnancy associated plasma protein A (PAPP–A), 49, 51,190 pregnancy specific beta–1 glycoprotein, 48 unconjugated estriol, 49, 169 Biochemical screening, see Biochemical markers Biophysical profile, 82, 93, 146, 169, 193, 219, 236, 276, 338, 388, 495–97

Bishop score, 170, 480, 580–81 Bladder injury, 95, 623, 630 Blighted ovum, see Anembryonic pregnancy Blood and blood products transfusion, 26, 31, 139, 249, 310, 321 Blood pressure, 96, 179–80 Korotkoff sounds, 179–80 technique of measurement, 179–80 variations in pregnancy, 180 Bloody tap, 589 Blunt abdominal trauma, 123, 642 B–lynch suture, 671–72 Breastfeeding, 171, 701–3 advantages, 702 contraindications, 702–3 Breast fever, 701 Breast infection, 709 Breech, 335, 338, 343, 536–48 aetiology, 538 Breech delivery, 542–48 assisted breech delivery, 542–46 spontaneous delivery, 542 total breech extraction, 542 Brow presentation, 516, 548, 550–51, 558, 605 Burns–Marshall technique, 544–45

C Caesarean hysterectomy, 363, 635–36 Caesarean myomectomy, 344, 636 Caesarean scar pregnancy, 366 Caesarean section, 615–37 anaesthesia, 619–20 classical, 617, 618 closure of abdominal wall, 626 closure of peritoneum, 625–26 complications, 629–32 enhanced recovery after surgery, 632, 633 fetal risks, 618 incidence, 616–17 indications, 618–19 Joel–Cohen skin incision, 621 low vertical skin incision, 621 Pfannenstiel incision, 620–21 prophylactic antibiotics, 628–29 repeat, 632 Robson’s classification, 617 safety, 636 suture of uterine incision, 624–26 technique, 620 uterine incision, 622 Calcium channel blockers, 197, 362, 467–68

Index  759

Caput succedaneum, 607, 723 Carcinoma thyroid, 265 Cardiac arrest, 688 Cardiac arrhythmias, 203, 251 Cardiac disease in pregnancy, 211 antenatal management, 218–19 balloon valvuloplasty, 224 causes of death, 215 congenital, 228–29 fetal prognosis, 230 induction of labour, 219 ischaemic heart disease, 226 maternal prognosis, 229–30 mortality, 215 open heart surgery, 223 pre–pregnancy counselling, 215–16 prosthetic valves, 226–28 termination of pregnancy, 218 Cardiac evaluation in pregnancy, 213 echocardiography, 214 electrocardiography, 214 imaging, 214 Cardiac failure, 215, 230 Cardiomyopathy, 225–26 hypertrophic, 226 peripartum, 225 Cardiopulmonary resuscitation in pregnancy, 690–92 Cardiotocography, antepartum, 491 Cardiotocography, computerised, 494 Cardiotocography, intrapartum, 500 baseline variability, 500, 501 early deceleration, 503 fetal bradycardia, 501 fetal tachycardia, 501 late deceleration, 503 sinusoidal, 503 variable deceleration, 506 Cardiovascular changes in pregnancy, 211–12 Centers for Disease Control and Prevention, The, 135, 248–249, 260, 302, 326, 373, 744 Cephalhaematoma, 611, 723 Cervical cerclage, 35, 36, 362, 461–62, 649 Cervical incompetence, 20, 26, 338, 457–458, 462 Cervical insufficiency, see Cervical incompetence Cervical lacerations, 649–50 Chickenpox, see Varicella–zoster Cholestasis obstetric, 245, 250–51 Cholestyramine, 250 Chorioamnionitis, 29, 115, 241, 305, 370, 471, 472

Choriodecidual haemorrhage, 22, 23, 67 Chorionicity, 70, 399–404, 406, 414 Chorionic villus sampling, 41, 52–54, 70, 78, 146, 250, 437 Cho sutures, 672 Chromosomal disorders, 70, 75–79 Chronic hypertension, 96, 156, 183–84 Chronic kidney disease, 234–40 effect on kidney, 236 effect on pregnancy, 235–36 management, 238 Combined spinal epidural analgesia, 570–71 Complicated breech delivery, 546 arrest of breech, 546 extended arms, 546–47 Lovset manoeuvre, 547 Pinard manoeuvre, 546 Compression uterine sutures, 671–73 B–lynch suture, 671–72 Cho sutures, 672 Hayman sutures, 672 Conisation, 35, 349, 351, 354 Congenital adrenal hyperplasia, 43 Congenital fetal anomalies, 5, 42, 74, 160, 295, 405, 415 Congenital fetal malformations, see Congenital fetal anomalies Congenital heart disease with pregnancy, 228–29 atrial septal defect, 229 coarctation of aorta, 229 cyanotic heart disease, 229 Eisenmenger syndrome, 228 ventricular septal defect, 229 Congenital rubella syndrome, 295 Congenital uterine abnormalities, 19, 333–38, 538 Congenital varicella syndrome, 301 Contraception, 148, 171, 205, 222, 703–5 Contraction stress test, 495 Controlled cord traction, 526, 663, 665 Cordocentesis, 51, 54, 264, 394, 442, 497 Cord prolapse, 415, 418, 429, 501, 506, 542, 548, 553–55 Corticosteroids, 161, 169, 170, 252, 268, 271, 330, 375, 412, 468–69 COVID–19, 329–31 Cryoprecipitate, 27, 472, 675, 687 Cystitis, 112 Cytokines, 456, 459, 687 Cytomegalovirus, 296–98, 482

760  Ian Donald’s Practical Obstetric Problems

D D–dimer, 30, 196, 284, 743 Dengue, 319–322 Denominator, fetal, 516, 549 Depot medroxy progesterone acetate, 148, 704 Diabetes mellitus, 152–72 classification, ADA, 153–54 diabetic nephropathy, 156 diabetic neuropathy, 156 diabetic retinopathy, 156 ketoacidosis, 157, 170 type 1 diabetes, 153 type 2 diabetes, 88, 94, 153–54, 160 Dialysis, 238–39 Diameter of engagement, 516, 549 Didelphys uterus, 335, 336, 341 DIPSI (Diabetes in Pregnancy Study Group India), 163 Disproportion, 92, 95, 503, 530, 532–34, 548, 588–89, 600, 609, 632 clinical assessment, 533 Disseminated intravascular coagulation (DIC), 30, 120, 182, 277, 278, 320, 368, 685 Doppler, fetal, see Fetal Doppler Down syndrome, 9–10, 42, 45–48, 50–51, 56, 75–76, 88 Duchenne muscular dystrophy, 43 Dysfunctional uterine bleeding, 25

E Ebola virus disease, 112 Echocardiography, fetal, 63, 74, 94, 169, 214, 228 Echocardiography, maternal, 181, 214, 222, 225–26, 284, 686 Eclampsia, 201–5 clinical features, 201 impending, 201 management, 203–205 prophylaxis, 202 Ectopic pregnancy, 21, 24–25, 68–69, 450 Effort syndrome, 213 Elderly primigravida, 87 Electrical injury, 123 Electronic fetal monitoring, 122, 148, 170, 469, 480, 500–501, 507–11 accelerations, 501 baseline fetal heart rate, 501 baseline variability, 501 bradycardia, 501 early decelerations, 503

late decelerations, 503 sinusoidal, 503 tachycardia, 501 variable decelerations, 506 Endocarditis, 220, 224 Endocarditis prophylaxis, 220, 229 Engagement, 516, 520, 528, 533, 549, 552 Entonox, 564, 566, 571 Epidural analgesia, 170, 195, 221, 415, 522, 542, 566–71, 598, 605, 653 combined spinal epidural, 570–71 complications, 468–70 postdural puncture headache, 469–70 regimens, 567 Episiotomy, 95, 139, 221, 469, 524, 526, 543, 571, 610, 652 Ergometrine, 26, 169, 195, 255, 417, 436, 526, 572, 647, 666, 667 Erythropoietin, 31, 140, 155, 238, 239 External cephalic version, 371, 415, 540–41 European League Against Rheumatism (EULAR), 237, 268

F Face presentation, 516, 531, 549–50, 606 Failed forceps, 610 Failed induction, 480, 588, 592 Fetal attitude, 516, 530, 534 Fetal blood sampling, 279, 310, 442, 506, 508, 509 Fetal electrocardiogram, 509, 510 Fetal growth restriction, 80–81, 194, 381–94, 412, 591 aetiology, 382–83 aspirin, 392 bed rest, 392 betamimetics, 411 diagnosis, 386–91 ductus venosus, 390 early onset, 383–84 fetal biometry, 386 late onset, 384–85 middle cerebral artery Doppler, 390 nutritional supplements, 392 pharmacological therapy, 392 steroids, 393–94 umbilical artery Doppler, 389 Fetal monitoring, 122, 193, 490–511 antepartum, 490–500 biophysical profile, 495–97 intrapartum, 500–11

Index  761

NICHD classification, 493, 507 non–stress test, 492–95 Fetal movement count, 448, 491–92 Fetal pneumonia, 589 Fetal pulse oximetry, 509–10 Fetal scalp lactate, 509 Fetal scalp pH, 509 Fetal scalp stimulation, 508 Fetal skull, 515, 516 Fetal station, 523 Fetal surveillance, see Fetal monitoring Fetal venous Doppler, 499 Fetoscopic laser photocoagulation, 410 Fever, 109–12 Fibrin degradation products (FDP), 30, 182, 188, 407 Fibrinogen concentrate, 676 Fibrinogen level, 675 Fibroid, 20, 25, 67, 115, 341–44 red degeneration in pregnancy, 342 Fibronectin, fetal, 411, 459 Folate deficiency, 129, 141, 142–43 Folic acid supplementation, 6, 12, 135, 238, 627 Bracht technique, 545 Forceps, 599–607 aftercoming head, 545, 606 analgesia, 601–2 classification, 598–99 face presentation, 606 face to pubis, 605–6 prerequisites, 600 technique of application, 602–5 trial of, 610 types, 559–60 Forchheimer spots, 294 Free erythrocyte protoporphyrin (FEP), 133 Fresh frozen plasma, 27, 32, 221, 228, 255, 366, 374, 675, 687 Functional cardiac assessment, 215, 216

G Gallstone disease, 116–17 Genetic counselling, 56, 218, 253 Gestational age assessment, 9, 79–80, 479, 720–21 Gestational diabetes mellitus, 162 contraception, 171 diagnosis, 163–64 fetal surveillance, 169 insulin, 165–66 intrapartum, 170

monitoring blood sugar level, 167 nutritional therapy, 165 obstetric management, 168–69 oral hypoglycaemic agents, 166 screening, 162 Gestational hypertension, 183, 205 Glomerular filtration rate, 182, 233, 697 Glucose homeostasis, 154–55 fetal, 155 maternal, 154–55 Glucose tolerance test (GTT), 90, 162–63, 427 Glycosylated haemoglobin A1C, 160 Grand multipara, 90–93

H Haemoglobinopathies, 144–48 sickle cell disease, 144–45 thalassaemia, 144 Haemolytic disease of the newborn, 435 Haemophilia, 43 Hayman sutures, 672 Heartburn, 106 HELLP syndrome, 195–96, 205, 251–53 Hepatitis viral, 246 hepatitis A virus, 247 hepatitis B virus, 247–49 hepatitis C virus, 249–50 hepatitis D virus, 250 hepatitis E virus, 250 Herpes simplex virus, 298 fetal and neonatal disease, 299–300 first–episode primary infection (type 1), 298–99 non–primary first episode (type 2), 299 reactivation disease, 299 Heterotopic pregnancy, 68 High head, 532, 552, 589 High–risk pregnancy, 5–6, 90, 254 Home uterine activity monitoring, 462 Human immunodeficiency virus, 305–310 Hydatidiform mole, 25, 69, 104, 450 Hydramnios, 106, 403, 425–29 causes, 426–27 evaluation, 427–28 fetal malformations, 427 management, 428 prostaglandin synthetase inhibitors, 428 Hyperstimulation, uterine, 205, 480, 495, 501, 508, 587 Hypertensive disorders, 91, 176–206 classification, 178

762  Ian Donald’s Practical Obstetric Problems definition, 176–78 investigations, 181–83 Hyperthyroidism, 263–65 Hypofibrinogenaemia, 30, 407 Hypothyroidism, 8, 34, 261–63 subclinical, 261 Hysteroscopic, 35 metroplasty, 35, 337 myomectomy, 20

I Immunoglobulins, intravenous, 247, 272, 280, 447 Impending eclampsia, 181, 193, 195, 199, 201 Induction of labour, 148, 168, 457, 478, 479, 485, 542, 579–80 contraindications, 591–92 failed, 588 indications, 590–91 mechanical, 581 methods, 580–87 pharmacological, 583–87 previous caesarean section, 591–92 risks, 587–90 surgical, 582–83 Infective endocarditis prophylaxis, 215, 220, 229 Influenza, 110, 147, 240, 745 Intermittent auscultation, 89, 170, 500, 507, 527, 585 Internal iliac artery ligation, 669, 670 Internal rotation, 520–21, 549 International Federation of Gynecology and Obstetrics, 190, 350, 351, 364 Intestinal obstruction, 104, 106, 113, 631 Intrapartum fetal monitoring, 305, 394, 431, 500, 542 Intrauterine fetal death, see Stillbirth Intrauterine growth restriction, see Fetal growth restriction Ischaemic heart disease, 157, 212, 213, 226 In vitro fertilization, 255 Iodine deficiency, 259–60 Iodine requirement in pregnancy, 259–60 Iron supplementation, 136–38, 140, 146 intramuscular, 137–38 intravenous, 138 oral, 136 total dose iron, 138

J Janani Suraksha Yojna, see National Rural Health Mission (NHRM) Jaundice in pregnancy, 110, 118, 130, 245 causes, 245–46 hepatitis A virus, 247 hepatitis B virus, 248–49 hepatitis C virus, 249–50 hepatitis D virus, 250 hepatitis E virus, 250 viral hepatitis, 246 Joel–Cohen skin incision, 621

K Kielland forceps, 599, 600, 604, 606–7 Kleihauer–Betke test, 121, 375, 437, 483, 589

L Labour, 549 management, 522–27 prolonged active phase, 556–57 prolonged latent phase, 555–56 second stage arrest, 557 stages, 521–22 Labour admission test, 506–7 Labour analgesia, 563 inhalational agents, 564–65 non–pharmacological methods, 564 opioids, 565–66 regional, 566–71 Lactation suppression, 703 Lactic dehydrogenase (LDH), 142, 181, 182 Lambda sign, 401–2 Laparoscopy in pregnancy, 20, 24, 27, 114, 354 Large for date gestational age, 158, 479 Large loop excision of transformation zone (LLETZ), 351 Liley zones, 442 Liver failure, acute, 106, 254–55 Lochia, 626, 696 Lovset manoeuvre, 547 Low–molecular–weight heparin, 32, 97, 118, 191, 214, 238, 275, 276, 285, 392, 628, 687 Lumbar epidural analgesia, see Epidural analgesia

Index  763

Lupus flare, 237, 238 Lupus nephritis, 237, 270, 271

M Macrosomia, 97, 158, 162, 164, 478, 598 Magnesium sulphate, 170, 194, 201–4, 465, 467, 469, 471, 750 Malaria, 318–19 Malpresentation, 91, 97, 340, 342, 427, 536–55 Management of third stage, 221, 226, 363, 417, 525–26, 624, 662–63 active management, 526, 662–63 controlled cord traction, 526, 624, 663 early versus late cord clamping, 526, 663 Manual removal of placenta, 363, 436, 575, 629, 643, 665 Maternal mortality, 2–4, 89, 92, 110, 116, 119, 128, 153, 202, 215, 225, 611, 617, 641 causes, 2–3 definition, 2 maternal mortality rate (MMR), 3 Mauriceau–Smellie–Veit manoeuvre, 545 Measurement of postpartum blood loss, 660–62 Meconium–stained liquor, 431, 478, 480, 507, 556, 583, 587, 733 Mendelson syndrome, 619, 689–90 Mentzer index, 134 Metroplasty, 35, 337–38 Middle cerebral artery, 82, 304, 385, 390, 440, 499 Miscarriage, 18–38 complete, 21, 26 incomplete, 21, 26 inevitable, 21, 26 missed, 22, 27 mortality, 37 recurrent, 32, 36 septic, 28–32 sequelae, 37 threatened, 21, 25–26 Misgav Ladach method, 627 Mitral stenosis, 212, 222–23 Morbid adherence of placenta, 364–70, 665 Moulding of fetal head, 515, 524, 533 Mullerian agenesis, 334 Multifetal pregnancy reduction, 418 Multiple gestation, 404 acardiac twin, 408 antepartum management, 413–15

chromosomal anomalies, 405 conjoined twins, 399, 407 fetal complications, 405–6 intrapartum management, 415–17 maternal complications, 404–5 preterm labour, 411–12 preterm premature rupture of membranes, 412 single fetal demise, 406–7 Myomectomy in pregnancy antepartum, 344 intrapartum, 636

N National Diabetes Data Group (NDDG), 163 National Health Policy 2017 recommendations, 12 National Institute for Health and Care Excellence, 9, 163, 166 National Rural Health Mission (NHRM), 3 Nausea and vomiting, 102–7, 198, 242, 250 Near miss, 4 Neonatal complications, 4–5, 158, 161–62, 200, 263, 276, 470, 620–21 hyperbilirubinaemia, 161, 590 hypocalcaemia, 161 hypoglycaemia, 161, 170 hypomagnesaemia, 162 polycythaemia, 162 respiratory distress syndrome, 161 Neonatal examination, 717–29 assessment of gestational age, 720–21 Neonatal exchange transfusion, 445, 450–51, 591 Neonatal jaundice, 590 Neonatal lupus, 237, 270 Neonatal resuscitation, 732–34 chest compressions, 739 endotracheal intubation, 738–39 Neonatal thrombocytopenia, 252 Neural tube defects, 36, 49–50, 413, 426 Neurological injury, 654–55 Newborn, 699–701 Nitric oxide donors, 468, 583 Non–haemorrhagic shock, 683–84 Non–stress test, 169, 276, 492–95 Normal labour, 515 first stage, 521–22 first stage abnormalities, 522–24 management, 522–27

764  Ian Donald’s Practical Obstetric Problems mechanism, 520–21 second stage, 522 second stage abnormalities, 524–25 stages of labour, 521–22 third stage, 522, 525–26 Nuchal translucency, 9, 45, 46, 70–71, 168, 219, 271, 306, 403, 405, 418

O Obesity, 33, 96–98, 153, 482 Obstetric palsies, 654 Obstetric shock index, 662 Occiput–posterior, 534–36, 598, 603 Oligohydramnios, 81, 195, 238, 271, 370, 385, 388, 408, 429–32, 591 causes, 429–30 evaluation, 430–31 management, 431–32 Operative vaginal delivery, 596–612 contraindications, 598 failed, 610 indications, 597–98 Oral anticoagulants, 214, 286 Oral glucose tolerance test, see glucose tolerance test Oral hypoglycaemic agents, 153, 165 Outlet contraction, 600 Ovarian cancer, 354 Ovarian tumours in pregnancy, 353–54 Oxytocin, 195, 205, 221, 226, 374, 417, 468, 495, 526, 542, 556, 579, 583–88, 634, 663, 666, 667, 669, 692, 701

P Paracervical block, 566, 571 Parenteral iron, 136–39 Partial thromboplastin time, 182, 227, 275, 485 Partograph, 523 Parvovirus, 303–5, 482 Patient controlled analgesia (PCA), see PCIA Patient controlled epidural analgesia (PCEA), 567 Patient controlled intravenous analgesia (PCIA), 567 Pelvic diameters, 517–19 Pelvic floor trauma, 478, 616, 650–51 Pelvic infection, 630–31, 710 Pelvimetry, 531 clinical, 531–32 Pelvis, types, 517–19

android, 517 anthropoid, 517 gynaecoid, 517 platypelloid, 517–19 Pendulous abdomen, 91, 340 Penetrating abdominal injury, 123 Perimortem caesarean section, 123–24 Perinatal mortality, 4–5, 89, 92, 97, 123, 128, 152, 361, 375, 390, 414, 455, 497, 555, 645 Perinatal mortality rate (PNMR), 5 Perineal tear, 651–54 classification, 651 prevention, 652 repair of second degree, 652 risk factors, 651 Pfannenstiel incision, 620–21 Physiological changes in renal system, 233–34 Pinard manoeuvre, 546 Placental grading, 496 Placental localization, 359–60 Placenta praevia, 88, 91, 358–64 aetiology, 358–59 caesarean section, 362–63 clinical presentation, 359 examination under double set–up, 362 types, 358 vaginal delivery, 363 Placenta praevia accreta, 364 Plasmapheresis, 447, 687 Polyhydramnios, see Hydramnios Ponderal index, 719, 722 Positive pressure ventilation, 732, 737–38 Postdated pregnancy, see Prolonged pregnancy Postpartum blues, 711 Postpartum collapse, 683–92 Postpartum depression, 711–12 Postpartum haemorrhage, 92, 97, 417, 624, 659–79 atonic, 664 causes, 660 secondary, 678 Postpartum IUCD insertion, 205 Postpartum psychosis, 712 Postpartum stress urinary incontinence, 655 Postpartum thyroiditis, 265–66 Postpartum urinary retention, 655–56 Post–term pregnancy, see Prolonged pregnancy Power Doppler, 63, 65, 69, 365 Pre–eclampsia, 184 abnormal placentation, 185 aetiopathogenesis, 185–88 endothelial dysfunction, 186 fetal complications, 195

Index  765

immunological, 187 maternal complications, 195 oxidative stress, 187–88 pathophysiology, 188–89 prediction, 190–91 prevention, 191–93 renin–angiotensin–aldosterone system, 187 risk factors, 184 superimposed, 184 Pregnancy test, 21–22 Premalignant and malignant lesions of cervix, 349–52 Prematurity, 455, 538, 588 Prenatal diagnosis, 41, 146 indications, 44 Pre–pregnancy counselling, 6, 94, 147, 200, 215, 237, 270 Preterm labour, 48, 160, 411–12, 428, 455 antibiotics, 462–63 group B Streptococcus, 463 pathogenesis, 455–56 prediction, 458–60 prevention, 460–64 risk factors, 456 Preterm premature rupture of membrane (PPROM), 412, 470–72 Progestin only contraceptives (POC), 222 Progestin only pills, 171, 205, 222, 276 Prolapse with pregnancy, 340–41 Prolonged pregnancy, 477–80 Prostaglandins, 585, 634, 666 misoprostol, 586–87 PGE2, 586 PGF2–alpha, 585 Prostaglandin synthetase inhibitors, 428 Prosthetic valves, 224, 226–28 anticoagulation, 227 thrombosis, 229 Prothrombin time, 30, 182, 245, 248, 250, 253, 289, 485, 665 Pruritus, 251 Pudendal block, 571, 602 Puerperal fever, 705–12 breast infection, 709 pelvic infection, 708, 710–11 pelvic thrombophlebitis, 710 urinary tract infection, 710 wound infection, 711 Puerperium, 695–712 physiological changes, 695–97 Pulmonary embolism, 224, 283, 284, 631, 687 Pulmonary hypoplasia, 218, 430, 432, 470 Pulmonary thromboembolism, 687

R Recurrent pregnancy loss, 32–36, 94, 272, 338, 342 unexplained, 36–37 Renal disease, 94, 140, 156, 200, 233–43 Renal failure, acute, 131, 182, 189, 196, 240–42 Renal plasma flow, 233, 697 Renal transplant, 239 Renin–angiotensin–aldosterone system, 187 Repeat caesarean section, 632 Respiratory distress syndrome, adult, 30 Respiratory distress syndrome (RDS), fetal, 155, 161, 393, 412, 466, 590, 618 Respiratory infection, 631 Restitution, 521 Retained placenta, 369, 470, 646, 660, 674, 678 Reticulocytosis, 131, 145, 188, 277 Retroversion, 339–40 Rhesus alloimmunization, 435–51 amniocentesis, 441–42 antepartum prophylaxis, 449 antibody estimation, 450 cordocentesis, 442 estimation of fetomaternal haemorrhage, 437 flowcytometry, 438 genetics, 436 intraperitoneal transfusion, 445–46 intravascular transfusion, 444–45 Kleihauer test, 121, 375, 437, 483, 589 middle cerebral artery, 444 postpartum prophylaxis, 448–49 prevention, 448–50 Rh antibody titre, 438 ultrasound evaluation, 439–40 Ritodrine, 466 Robson’s classification, 617 Rubella, 2, 6, 294–96 Rudimentary horn, 114, 336, 643 Rudimentary uterus, 334 Rupture uterus, see Uterine rupture

S Sensorineural deafness, 295 Septate uterus, 35, 69, 335–38, 383, 552 Septic pelvic thrombophlebitis, 629, 630, 705, 710 Septic shock, 29–32, 684, 689

766  Ian Donald’s Practical Obstetric Problems Serum ferritin, 132, 133, 138, 140 Serum iron, 133, 146 Serum transferrin receptor, 134 Sheehan syndrome, 373, 679, 684 Short cervix, 338, 459–60 Shoulder dystocia, 97, 158, 164, 169, 170, 478, 515, 611, 651 Shoulder presentation, 551–53 Sickle cell disease, 43, 141, 144–48, Single gene disorders, 43 Small for gestational age, 48, 82, 98, 183, 197, 235, 309, 325, 348, 381, 431, 461, 479, 499, 538, 721 Stepwise uterine devascularisation, 670 Stillbirth, 2, 4–5, 34, 43, 54, 89, 93, 96, 148, 156, 159–60, 162, 223, 236, 240, 304, 309, 373, 389, 393, 457, 477, 480–85, 494, 591, 703 cytogenetic evaluation, 483 management, 485 Stress incontinence, 95, 650, 652 Subclinical hypothyroidism, 19, 260–61 Superfecundation, 398 Superfetation, 398 Sweeping of membranes, 479, 582 Symphysiotomy, 547, 551, 612, 656 Syphilis, 323–35 Systemic lupus erythematosus, 234, 268–72, 384, 481 Systemic Lupus International Collaborating Clinics (SLICC), 268

T Tdap (tetanus, diphtheria and acellular pertussis) vaccine, 10 Teratogens, 42, 44 Terbutaline, 466 Thalassaemia, 6, 8, 42, 144–46, 427 Third degree perineal tear, 95–96, 651 Thrombin time, 30, 182, 245, 248, 250, 253, 289, 485, 665 Thrombocytopaenia, 177, 179, 188, 276–79, 294 Thrombophilia, acquired, see Antiphospholipid syndrome Thrombophilia, inherited, 33, 286, 287, 370 Thromboprophylaxis, 32, 148, 236, 286, 627–28, 677 Thyroid function in pregnancy, 259 TIBC, 133 Tocolytics, 124, 230, 362, 374, 465–68, 648 TORCH infections, 34, 94, 391, 483 Torsion of uterus, see Uterine torsion

Toxoplasmosis, 44, 315–17, 383, 426 Tranexamic acid, 124, 667 Transferrin saturation, 133 Transverse lie, see Shoulder presentation TRAP, twin reversed arterial perfusion, 408 Trauma in pregnancy, 119–24, 371 Trial of forceps, 610 Trial of labour, 90, 93, 170, 338, 344, 394, 417, 531, 591, 623, 634 Trichomonas vaginitis, 357 Triplets, 398, 403, 404, 405, 412, 414, 418, 455 Triploidy, 43, 54, 79 Trisomy 13, 43, 46, 54, 70, 71, 73, 76, 78, 382, 482, 740 Trisomy 18, 43, 46, 48, 54, 73, 76–77 Trisomy 21, see Down syndrome Tuberculin test, 326 Tuberculosis, 325–27 diagnosis, 325–26 treatment, 326–27 Turner syndrome, 46, 70, 78–79, 154 Twin pregnancy, see Multiple gestation Twin to twin transfusion syndrome, 408–11 Typhoid (enteric) fever, 110–11

U Ultrasound, 9, 45–47, 61–84 A–mode, 63 amniotic fluid assessment, 81 B–mode, 63 biparietal diameter, 79 colour Doppler, 81–83 crown–rump length, 67 femur length, 79 first trimester, 64 gestational age, 79 growth disorders, 80 head circumference, 79 mean sac diameter, 65 M–mode, 63 nasal bone, 71 safety of, 63 yolk sac, 65 2D ultrasound, 63 3D ultrasound, 63 4D ultrasound, 63 Umbilical artery Doppler, 82, 169, 389, 498–99 Umbilical cord blood gases, 510 Unfavourable cervix, 480, 580–81 Unfractionated heparin, 32, 285, 362 Unicornuate uterus, 69, 338

Index  767

Unstable lie, 553 Urinary tract infection, 111–12, 710 Ursodeoxycholic acid, see cholestyramine Uterine activity assessment, 519 Uterine artery Doppler, 190, 238, 276, 389, 498 Uterine infection, 37 Uterine inversion, 624, 646–49, 684 manual replacement (Johnson manoeuvre), 648 Haultain method, 648 Huntington method, 648 hydrostatic reduction (O’Sullivan technique), 648 Uterine malformations, 333–38 Uterine rupture, 26, 90, 92, 115, 541, 584, 588, 634, 642–46 causes, 642 classification, 642 consequences, 645 impending, 645 Uterine septum, see Septate uterus Uterine tamponade, 669 Uterine torsion, 341, 342, 345 Uterotonic agents, 666–67

Varicella–zoster, 301–3 Vasa praevia, 375–76, 589 Vault rupture, 645 VBAC, vaginal birth after caesarean section, 632–35 Venous thromboembolism, 283–89, 631 clinical features, 283 compression duplex ultrasound, 284 contrast venography, 284 pulmonary angiography, 284 risk factors, 286, 287 serial impedance plethysmography, 284 treatment, 288–289 Ventilation/perfusion (V/Q) scan, 284 Ventouse (vacuum extractor), 607–10 Vesicovaginal fistula, 95, 531, 606, 656 Vibroacoustic stimulation test, 493 Viral infections, 112, 294–310

W Walking epidural, see Epidural analgesia Wound infection, 631, 643, 652, 711

V

Z

Vaccinations, 744–46 Vanishing twins, 405

Zika virus, 112 Zygosity, 399–404