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Obstetric Emergencies.pdf

Obstetric Emergencies

Diogo Ayres-de-Campos

Obstetric Emergencies

A Practical Guide

Diogo Ayres-de-Campos

Medical School

University of Porto

Porto

Portugal

ISBN 978-3-319-41654-0 ISBN 978-3-319-41656-4 (eBook)

DOI 10.1007/978-3-319-41656-4

Library of Congress Control Number: 2016951938

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Pref ace

When I started practicing Obstetrics and Gynecology in Porto, some 25 years ago,

obstetric emergencies were looked upon by healthcare professionals as events of an

almost “supernatural” nature. After such emergencies occurred, people almost

invariably put on an expression of fear and fatality. “I pray that this never happens to

me when I’m on call” was commonly heard. The occurrence was usually recounted

in detail from individual to individual, with some consequent distortion of the facts,

and normally very little was learnt from it. Some doctors appeared to be very sure of

what should have been done, but opinions frequently differed among them. As a

junior doctor at the time, I felt very unsure of what to do should an obstetric emergency happen to me. Memories remain of very stressful cases of acute fetal hypoxia,

shoulder dystocia, and postpartum hemorrhage, with many people talking at the

same time, contradictory orders and some adverse neonatal and maternal outcomes.

The wide dissemination of evidence-based practice did not do a lot to improve

this situation. Acute events are poor candidates for studies providing the highest

levels of evidence. Obstetric emergencies were consequently given limited relevance at scientifi c meetings and medical journals, as there was not a lot of good

evidence to discuss, and also because doctors who become well-know in these environments were frequently not involved in the clinical activities where the majority

of these situations occur.

The largest contribution to the management of obstetric emergencies over the

last decades probably came from the development of clinical guidelines, many of

which were based mainly on expert opinion and small case series. Another strong

contribution came from the development of more realistic obstetric simulators and

the dissemination of simulation-based training courses.

After being involved in the co-ordination of local, national and international

guidelines on these subjects, having run simulation-based courses in obstetric emergencies for more than 10 years, and being a medical advisor for the development of

a high-fi delity obstetric simulator, I felt the time had come to share some of these

experiences in a book. A lot can be learned from observing multiprofessional teams

manage obstetric emergencies in the protected environment of simulation, and then

formulating an objective and structured way of teaching them to junior doctors.

Similar experiences can be gained from developing the requirements of a highfi delity simulator. Priorities can be reconsidered and the relevance of existing recommendations can be re-evaluated.

With the natural limitation of the quality of existing scientifi c evidence to support many of the recommendations, I trust that the present book will constitute a

useful contribution to healthcare professionals involved in the clinical management

of obstetric emergencies, and an opportunity to revise and re-think some of the

necessary attitudes.

Preface

vii

Contents

1 Introduction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1

Part I Predominantly Fetal Emergencies

2 Acute Fetal Hypoxia/Acidosis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 7

2.1 Defi nition, Incidence and Main Risk Factors . . . . . . . . . . . . . . . . . . . . 7

2.2 Consequences . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 10

2.3 Diagnosis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 10

2.3.1 Reversible Causes . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 11

2.3.1.1 Uterine Hypercontractility . . . . . . . . . . . . . . . . . . . . 11

2.3.1.2 Sudden Maternal Hypotension . . . . . . . . . . . . . . . . . 12

2.3.1.3 Maternal Supine Position with Aorto-Caval

Compression . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 13

2.3.2 Irreversible Utero-Placental-Umbilical Disorders . . . . . . . . . . 13

2.3.2.1 Major Placental Abruption . . . . . . . . . . . . . . . . . . . . 13

2.3.2.2 Uterine Rupture . . . . . . . . . . . . . . . . . . . . . . . . . . . . 14

2.3.2.3 Umbilical Cord Prolapse . . . . . . . . . . . . . . . . . . . . . 15

2.3.3 Maternal Cardiorespiratory Disorders . . . . . . . . . . . . . . . . . . . 16

2.3.4 Usually Occult Causes. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 16

2.3.4.1 Occult Cord Compression . . . . . . . . . . . . . . . . . . . . 16

2.3.4.2 Major Fetal Haemorrhage . . . . . . . . . . . . . . . . . . . . 17

2.3.5 Specifi c Mechanical Complications of Labour . . . . . . . . . . . . 18

2.4 Clinical Management . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 18

2.4.1 Immediate Actions in Face of a Prolonged Deceleration . . . . 18

2.4.2 Uterine Hypercontractility . . . . . . . . . . . . . . . . . . . . . . . . . . . . 20

2.4.3 Sudden Maternal Hypotension . . . . . . . . . . . . . . . . . . . . . . . . 20

2.4.4 Major Placental Abruption . . . . . . . . . . . . . . . . . . . . . . . . . . . 21

2.4.5 Uterine Rupture . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 21

2.4.6 Umbilical Cord Prolapse . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 22

2.4.7 Maximum Time Limits for Reversal

of a Prolonged Deceleration . . . . . . . . . . . . . . . . . . . . . . . . . . 22

2.5 Clinical Records and Litigation Issues . . . . . . . . . . . . . . . . . . . . . . . . 23

viii

3 Shoulder Dystocia . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 27

3.1 Defi nition, Incidence and Main Risk Factors . . . . . . . . . . . . . . . . . . . 27

3.2 Complications . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 29

3.3 Diagnosis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 31

3.4 Clinical Management . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 31

3.4.1 Anticipating the Situation . . . . . . . . . . . . . . . . . . . . . . . . . . . . 31

3.4.2 Clearly Verbalising the Diagnosis . . . . . . . . . . . . . . . . . . . . . . 32

3.4.3 Avoiding Manoeuvres That Increase the Risk

of Fetal Injury . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 32

3.4.4 Asking for Help . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 32

3.4.5 External Manoeuvres . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 32

3.4.6 Internal Manoeuvres . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 33

3.4.7 All-Fours Manoeuvre (Gaskin’s Manoeuvre) . . . . . . . . . . . . . 35

3.4.8 Exceptional Manoeuvres . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 36

3.5 Clinical Records and Litigation Issues . . . . . . . . . . . . . . . . . . . . . . . . 37

4 Retention of the After-Coming Head . . . . . . . . . . . . . . . . . . . . . . . . . . . . 41

4.1 Defi nition, Incidence and Main Risk Factors . . . . . . . . . . . . . . . . . . . 41

4.2 Consequences . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 42

4.3 Diagnosis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 43

4.4 Clinical Management . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 43

4.4.1 Guaranteeing the Conditions for a Safe Vaginal

Breech Delivery . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 43

4.4.2 Anticipate the Situation . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 44

4.4.3 Attempts to Deliver the Fetal Head . . . . . . . . . . . . . . . . . . . . . 44

4.4.4 Clearly Verbalising the Diagnosis . . . . . . . . . . . . . . . . . . . . . . 45

4.4.5 Asking for Help . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 45

4.4.6 McRobert’s Position . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 46

4.4.7 Episiotomy . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 46

4.4.8 Fetal Monitoring . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 46

4.4.9 Insertion of a Vaginal Retractor. . . . . . . . . . . . . . . . . . . . . . . . 46

4.4.10 Forceps to the After-Coming Head . . . . . . . . . . . . . . . . . . . . . 46

4.4.11 Exceptional Manoeuvres . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 48

4.5 Clinical Records and Litigation Issues . . . . . . . . . . . . . . . . . . . . . . . . 48

Part II Predominantly Maternal Emergencies

5 Eclampsia . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 53

5.1 Defi nition, Incidence and Main Risk Factors . . . . . . . . . . . . . . . . . . . 53

5.2 Complications . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 54

5.3 Diagnosis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 54

5.4 Clinical Management . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 54

5.4.1 Anticipate and Prevent the Situation . . . . . . . . . . . . . . . . . . . . 54

5.4.2 Ask for Help . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 55

5.4.3 Avoid Lesions During the Eclamptic Seizure . . . . . . . . . . . . . 55

Contents

5.4.4 Left Lateral Safety Position, Inspect Airway

and Monitor . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 55

5.4.5 Prevention of New Seizures . . . . . . . . . . . . . . . . . . . . . . . . . . 56

5.4.6 Other Non-emergent Measures . . . . . . . . . . . . . . . . . . . . . . . . 56

5.4.7 Decreasing Blood Pressure . . . . . . . . . . . . . . . . . . . . . . . . . . . 56

5.4.8 Recurrent Seizures . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 57

5.4.9 Maintenance Dose of Magnesium Sulphate . . . . . . . . . . . . . . 58

5.4.10 Fluid Balance . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 59

5.4.11 Thromboprophylaxis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 59

5.4.12 Evaluation of Laboratory Results and Fetal Evaluation . . . . . 59

5.4.13 Programming Birth . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 59

5.5 Clinical Records and Litigation Issues . . . . . . . . . . . . . . . . . . . . . . . . 60

6 Postpartum Haemorrhage . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 63

6.1 Defi nition, Incidence and Main Risk Factors . . . . . . . . . . . . . . . . . . . 63

6.2 Consequences . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 65

6.3 Diagnosis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 66

6.4 Clinical Management . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 66

6.4.1 Anticipating the Situation . . . . . . . . . . . . . . . . . . . . . . . . . . . . 66

6.4.2 Clearly Verbalising the Diagnosis . . . . . . . . . . . . . . . . . . . . . . 66

6.4.3 Asking for Help . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 66

6.4.4 Initial Evaluation of the Cause of Haemorrhage . . . . . . . . . . . 67

6.4.5 Support of Maternal Circulation

and Oxygenation . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 67

6.4.5.1 Venous Catheterisation and Blood

Volume Replacement . . . . . . . . . . . . . . . . . . . . . . . . 67

6.4.5.2 Maternal Monitoring . . . . . . . . . . . . . . . . . . . . . . . . 67

6.4.5.3 Bladder Catheterisation and Measurement

of Urinary Output . . . . . . . . . . . . . . . . . . . . . . . . . . . 67

6.4.5.4 Maintain Maternal Oxygen Supply

to the Brain . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 67

6.4.5.5 Decision to Start Colloids . . . . . . . . . . . . . . . . . . . . 68

6.4.5.6 Decision to Administer Blood Products . . . . . . . . . . 68

6.4.5.7 Maintain Body Temperature . . . . . . . . . . . . . . . . . . 68

6.4.6 Treatment of Uterine Atony . . . . . . . . . . . . . . . . . . . . . . . . . . 68

6.4.6.1 Initial Measures . . . . . . . . . . . . . . . . . . . . . . . . . . . . 68

6.4.6.2 Medical Treatment . . . . . . . . . . . . . . . . . . . . . . . . . . 69

6.4.6.3 Mechanical Treatments . . . . . . . . . . . . . . . . . . . . . . 69

6.4.6.4 Surgical Treatments . . . . . . . . . . . . . . . . . . . . . . . . . 71

6.4.6.5 Pelvic Tamponade . . . . . . . . . . . . . . . . . . . . . . . . . . 73

6.4.7 Treatment of Birth Canal Injuries . . . . . . . . . . . . . . . . . . . . . . 73

6.4.8 Treatment of Placental Retention . . . . . . . . . . . . . . . . . . . . . . 75

6.4.8.1 Complete Placental Retention . . . . . . . . . . . . . . . . . 75

6.4.8.2 Partial Placental Retention . . . . . . . . . . . . . . . . . . . . 75

6.4.9 Treatment of Rare Causes of Postpartum Haemorrhage . . . . . 75

6.4.9.1 Uterine Inversion . . . . . . . . . . . . . . . . . . . . . . . . . . . 75

Contents

6.4.9.2 Uterine Rupture . . . . . . . . . . . . . . . . . . . . . . . . . . . . 76

6.4.9.3 Abnormally Adherent Placenta . . . . . . . . . . . . . . . . 76

6.4.9.4 Maternal Bleeding Disorders . . . . . . . . . . . . . . . . . . 77

6.4.10 Postpartum Haemorrhage at Caesarean Section . . . . . . . . . . . 77

6.5 Clinical Records and Litigation Issues . . . . . . . . . . . . . . . . . . . . . . . . 77

7 Maternal Cardiorespiratory Arrest. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 81

7.1 Defi nition, Incidence and Main Risk Factors . . . . . . . . . . . . . . . . . . . 81

7.2 Consequences . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 82

7.3 Diagnosis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 82

7.4 Clinical Management . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 82

7.4.1 Anticipating the Situation . . . . . . . . . . . . . . . . . . . . . . . . . . . . 82

7.4.2 Clearly Verbalising the Diagnosis . . . . . . . . . . . . . . . . . . . . . . 82

7.4.3 Asking for Help . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 83

7.4.4 Maternal Monitoring . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 83

7.4.5 Support of Maternal Oxygenation and Circulation . . . . . . . . . 83

7.4.5.1 A (Airway): Guarantee the Patency

of the Airway . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 83

7.4.5.2 B (Breathing): Maintain Oxygen Supply

to the Lungs . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 83

7.4.5.3 C (Circulation): Cardiac Massage

and Vein Catheterisation . . . . . . . . . . . . . . . . . . . . . 84

7.4.6 Bladder Catheterisation and Measurement

of Urinary Output . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 85

7.4.7 Fetal Monitoring . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 85

7.4.8 In Situ Caesarean Section . . . . . . . . . . . . . . . . . . . . . . . . . . . . 85

7.4.9 Defribrillatory Rhythms . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 85

7.4.10 After Cardiorespiratory Arrest Reverses . . . . . . . . . . . . . . . . . 86

7.4.10.1 Hypotension . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 86

7.4.10.2 Termination of Pregnancy . . . . . . . . . . . . . . . . . . . . 86

7.4.10.3 Monitoring in an Intensive Care Unit . . . . . . . . . . . 86

7.4.10.4 Maintain Body Temperature . . . . . . . . . . . . . . . . . . 87

7.4.10.5 Looking for an Underlying Cause . . . . . . . . . . . . . . 87

7.4.11 Pulmonary Thromboembolism . . . . . . . . . . . . . . . . . . . . . . . . 87

7.4.12 Amniotic Fluid Embolism Syndrome . . . . . . . . . . . . . . . . . . . 88

7.5 Clinical Records and Litigation Issues . . . . . . . . . . . . . . . . . . . . . . . . 89

Contents

D. Ayres-de-Campos, Obstetric Emergencies,

DOI 10.1007/978-3-319-41656-4_1

1 Introduction

Obstetrics is a unique area of healthcare, in that the vast majority of situations in

pregnancy and childbirth have normal outcome, even when there is no intervention

from healthcare professionals. However, serious complications do occur in a smaller

number of cases, and increased knowledge on their diagnosis and treatment has

made a tremendous difference to maternal and fetal outcomes over the last 200

years. One could even say that obstetrics is somewhat a victim of its own success,

as improvements have been so striking that much of society has erroneously perceived adverse outcomes to have disappeared and, when they occur, frequently

judges them to be due to malpractice.

Progress achieved over the last decades in high-resource countries has resulted in

marked decreases in maternal and perinatal mortality. In the last 80 years, maternal

mortality decreased almost a 100-fold in many European countries, to values that

are currently between 5 and 10 per 100,000 births. Perinatal mortality also decreased

more than tenfold, to values between 3 and 10 per 1000 births. Equally important,

but less well documented, is the decrease in long-term maternal and child morbidity

consequent to the complications of pregnancy and childbirth.

In spite of the unquestionable success of modern obstetrical care in reducing the

burden of disease associated with the reproductive process, there is still margin for

improvement. According to confi dential enquiries into maternal and perinatal

deaths carried out over the last two decades in the United Kingdom, substandard

care continues to be identifi ed in around 50 % of cases.

Healthcare professionals working in moderate-sized European centres usually

maintain experience in management of most obstetric situations by literature review

and day-to-day clinical practice, but rare situations exist where lack of familiarity

with the clinical entity causes apprehension and uncertainty. Some of these situations are not acute in nature, so they allow time for consultation of the literature, but

others require immediate action in order to guarantee a positive outcome. These are

the most feared, and sometimes even healthcare professionals with decades of experience in obstetrical care have limited practice in their management.

Acute complications of pregnancy and childbirth, posing risk to the mother and/

or the fetus, and whose resolution requires an almost immediate response from the

healthcare team (usually in a few minutes) in order to guarantee a favourable outcome – this is the concept that best describes obstetric emergencies .

Resolution of these situations not only requires a thorough knowledge of their

diagnosis and management but also specifi c technical skills (in this case manual

skills) that because of reduced exposure are diffi cult to learn and to maintain

competence. Unless healthcare professionals regularly attend simulation-based

courses, most fi nd it diffi cult to retain profi ciency, for instance, in executing internal

manoeuvres for the resolution of shoulder dystocia, applying forceps to the aftercoming head, executing the Zavanelli manoeuvre or symphysiotomy or inserting a

Bakri balloon.

Management of these situations usually requires the collaboration between multiple professionals within a healthcare team, so teamwork skills are also important.

The latter includes the capacity of a team member to assume leadership and to hand

it over when a more experienced person arrives, as well as the capacity of the

remaining team to cooperate with the leader. Inherent to these concepts are the skills

for adequate task distribution , feedback and support between team members.

Communication skills assume a central role in all of these aspects, not only for the

interactions between healthcare professionals but also with patients and their

families.

Finally, it should not be forgotten that organisational aspects of healthcare

facilities may also play a part in the resolution of these situations. Ease of contact

and timely availability of healthcare professionals are crucial for successful management, as is the accessibility to clinical materials and the guarantee of their

usability.

Given the rarity of these situations, the social burden of adverse outcomes and

the diffi culty in maintaining adequate clinical competence, simulation - based

training courses in obstetric emergencies , initially developed in the United States

and United Kingdom in the 1990s, have been introduced in many European countries. These courses use patient actors and a new generation of obstetric simulators

developed over the last two decades, to allow realistic and interactive multiprofessional team training.

Regular attendance of such courses has become a routine part of training and

accreditation in many centres, and there is data to suggest that it is associated with

reduced incidence of adverse perinatal outcomes, including brachial plexus injury

and hypoxic-ischaemic encephalopathy.

This book provides a practical guide to the diagnosis and management of obstetric emergencies. It can be used for review and consultation of specifi c clinical procedures, and it is also a useful reference manual for simulation-based courses. The

topics covered include “predominately fetal” emergencies – acute fetal hypoxia/

acidosis, shoulder dystocia, and retention of the after-coming head; as well as “predominately maternal” emergencies – eclampsia, cardiorespiratory arrest, and postpartum haemorrhage.

1 Introduction

Suggested Reading

Black RS, Brocklehurst P (2003) A systematic review of training in acute obstetric emergencies.

BJOG 110:837–841

CEMACH (2006) Confi dential enquiry into maternal and child health. Perinatal mortality surveillance 2004: England, Wales and Northern Ireland. CEMACH, London

CEMACH (2007) Saving mothers’ lives 2003–2005. CEMACH, London

CESDI (1997) Confi dential enquiry into stillbirths and deaths in infancy. 4th annual report.

Maternal and Child Health Research Consortium, London

Draycott TJ, Sibanda T, Owen L, Akande V, Winter C, Reading S, Whitelaw A (2006) Does training in obstetric emergencies improve neonatal outcome? BJOG 113:177–182

Draycott TJ, Crofts JF, Ash JP, Wilson LV, Yard E, Sibanda T, Whitelaw A (2008) Improving neonatal outcome through practical shoulder dystocia training. Obstet Gynecol 112:14–20

World Health Organization (2006) Neonatal and perinatal mortality: country, regional and global

estimates. WHO Press, Geneva

Suggested Reading

Part I

Predominantly Fetal Emergencies

D. Ayres-de-Campos, Obstetric Emergencies,

DOI 10.1007/978-3-319-41656-4_2

2 Acute Fetal Hypoxia/Acidosis

2.1 Definition, Incidence and Main Risk Factors

Fetal hypoxia refers to the condition in which there is decreased oxygen concentration in fetal tissues, and this is insuffi cient to maintain normal cell energy production by way of aerobic metabolism. Oxygen is supplied to fetal tissues via a long

pathway that involves the maternal respiratory system, maternal circulation, gas

exchange at the placenta and fi nally the umbilical and fetal circulations (Fig. 2.1 ).

Problems occurring at any of these levels may result in decreased oxygen concentration in the fetal circulation (hypoxaemia) and ultimately in fetal tissues (hypoxia).

Acute fetal hypoxia refers to the condition in which there is a rapid reduction in

oxygen levels, i.e. occurring over the course of a few minutes. Its main causes are

considered in Table 2.1 .

In the absence of oxygen, fetal cells may continue to produce the energy required

for maintenance of basic homeostatic functions during a few more minutes, by

resorting to anaerobic metabolism . However, the latter yields much less energy

than aerobic metabolism and results in the production of lactic acid. The intra- and

extracellular accumulation of hydrogen ions, due to increased lactic acid production, results in the development of metabolic acidosis (decreased pH caused by

acids of intracellular origin) and, because these ions are taken away by the fetal

circulation, metabolic acidaemia. The whole process of decreased oxygen concentration in tissues is therefore known as hypoxia / acidosis .

Some constituents of fetal blood are capable of neutralising (buffering) hydrogen

ions. These are called bases , and they include bicarbonate, haemoglobin and plasma

proteins. However, their availability is limited, and their depletion ( base defi cit ) is

directly related to the severity of metabolic acidosis. As there is no direct method of

quantifying oxygen concentration within fetal tissues, the only objective way of

diagnosing intrapartum fetal hypoxia/acidosis is to measure pH and base defi cit in

the umbilical cord blood at delivery or in the newborn circulation during the fi rst

minutes of life. Metabolic acidosis is defi ned as a pH below 7.00 and a base defi cit

in excess of 12 mmol/l (or alternatively a lactate value in excess of 10 mmol/l) in

either of these circulations. The umbilical cord does not need to be clamped for

sampling, but it is important to obtain blood from both artery and vein as soon as

possible after birth, to guarantee the quality of results. Sampling of the wrong vessel

may occur when the needle crosses the artery to pierce the vein, and this may also

result in mixed sampling. After blood is drawn into two heparinised syringes, existing air bubbles are removed and the syringes capped and rolled between the fi ngers

to mix blood with heparin; blood gas analysis should be performed within the next

Fig. 2.1 Pathway of oxygen

supply to the fetus

2 Acute Fetal Hypoxia/Acidosis

30 min. When the difference in pH between the two samples is less than 0.02 and

the difference in pCO 2 is less than 5 mmHg (0.7 Kilopascal), samples are likely to

be mixed or to have been obtained from the same vessel. When hypoxia/acidosis is

of acute onset, there is usually also a large difference in pH between artery and vein.

Increasing concentrations of hydrogen ions that are no longer buffered because

of base depletion affect energy production and cell homeostasis, leading to disrupted cell function and ultimately to a cascade of biochemical events that results in

cell death. When hypoxia is suffi ciently intense and prolonged to disrupt neurological, respiratory and cardiovascular control, this is refl ected in reduced Apgar scores

at birth. Apgar scores however are much less specifi c indicators of fetal hypoxia

than umbilical blood gas values, as they can be affected by other factors such as

prematurity, central nervous system depressors administered to the mother, birth

trauma without hypoxia (i.e., subdural haematoma), infection, meconium aspiration, congenital anomalies, pre-existing lesions and early neonatal interventions

such as vigorous endotracheal aspiration.

The overall incidence of fetal hypoxia/acidosis, as defi ned by the incidence of

newborn metabolic acidosis, varies substantially between different European hospitals, depending on the risk characteristics of the population and on labour management strategies. Reported rates vary between 0.06 and 2.8 %.

The major risk factors for acute fetal hypoxia/acidosis are the ones responsible

for its underlying causes: i.e. labour induction and augmentation with prostaglandins or oxytocin are major risk factors for uterine hypercontractility, regional analgesia is a major risk factor for sudden maternal hypotension, and early amniotomy

is a risk factor for uterine hypercontractility and umbilical cord prolapse. A detailed

description of the risk factors for all causes of acute fetal hypoxia/acidosis is beyond

the aim of this book.

Table 2.1 Main causes of acute fetal hypoxia/acidosis

Reversible causes

Uterine hypercontractility

Sudden maternal hypotension

Maternal supine position with aorto-caval compression

Irreversible causes

Major placental abruption

Uterine rupture

Umbilical cord prolapse

Maternal cardiorespiratory disorders

Severe asthma, haemorrhagic shock, cardiorespiratory arrest, pulmonary thromboembolism,

amniotic fl uid embolism, generalised seizures, etc.

Usually occult causes

Occult cord compression (true cord knot, low-lying cord, nuchal cord with stretching)

Major fetal haemorrhage (fetal-maternal haemorrhage, ruptured vasa praevia)

Specifi c mechanical complications of labour

Shoulder dystocia

Retention of the after-coming head

2.1 Defi nition, Incidence and Main Risk Factors

2.2 Consequences

Most newborns with metabolic acidosis and low Apgars recover quickly and do not

develop short- or long-term functional impairments. However, when fetal hypoxia/

acidosis is suffi ciently intense and prolonged, changes in neurological function may

become apparent in the fi rst 48 h of life, manifested by hypotonia, seizures and/or

coma, a situation that is termed hypoxic - ischaemic encephalopathy . In its mild

forms (grade 1), a short period of hypotonia is documented, but very rarely it evolves

into permanent handicap. When the newborn develops seizures (grade 2), the risk of

mortality or long-term neurological sequelae is about 20–30 %. When a comatose

state occurs (grade 3), perinatal death or long-term handicap is frequent.

Not all cases of neurological dysfunction occurring in the fi rst 48 h of life (neonatal encephalopathy) are caused by fetal hypoxia/acidosis, so to establish the diagnosis of hypoxic-ischaemic encephalopathy, it is necessary to document metabolic

acidosis in the umbilical cord or in the newborn circulation in the fi rst minutes of

life.

Cerebral palsy of the dyskinetic or spastic quadriplegic types is the long-term

neurological sequela most strongly associated with fetal hypoxia/acidosis, although

only 10–20 % of cases are caused by this entity. Perinatal infection, congenital diseases, metabolic diseases, coagulation disorders and the complications associated

with birth trauma and prematurity constitute the majority of causal factors.

The speed of installation and intensity of acute fetal hypoxia/acidosis varies from

case to case, so fetal risk is not uniform. In some cases, there may be a sudden and

almost total reduction in oxygen supply, while in others, it may be less intense or of

slower onset. The insults can also be transitory and repetitive in nature (uterine

hypercontractility, occult cord compression). Finally, there is also some individual

variation in the capacity to react to hypoxia/acidosis.

For all these reasons, it is diffi cult to establish how long a hypoxic insult may last

before important injury occurs. However, some information can be extrapolated

from cases of sudden maternal cardiorespiratory arrest. No long-term neurological

sequelae were reported when the interval between arrest and birth was under 12

min, and perinatal death was common when more than 15 min had elapsed. This

evidence is frequently used as an indicator of a 12-min margin of safety for the

fetus, in situations where sudden and complete interruption of fetal oxygenation

occurs. It is likely that this rule of thumb is only valid for normally grown fetuses at

term, receiving adequate oxygenation before the insult occurred, and needs to be

adapted in other situations.

2.3 Diagnosis

Acute fetal hypoxia/acidosis almost always manifests as a prolonged deceleration – a sudden and sustained decrease in the fetal heart rate (FHR), with an amplitude exceeding 15 bpm and lasting more than 3 min (Fig. 2.2 ). When the duration

exceeds 10 min, it is called fetal bradycardia .

2 Acute Fetal Hypoxia/Acidosis

Decreased oxygen concentration in fetal arterial blood triggers chemoreceptors

located near the aortic arch to transmit neurological impulses to brain stem nuclei

controlling the vagus nerve and causes a parasympathetically mediated drop in

FHR. When fetal hypoxia/acidosis affects the central nervous system, the sympatheticparasympathetic modulation of FHR is decreased, and this results in diminished signal oscillations, a phenomenon known as reduced variability (Fig. 2.2 ).

Other clinical symptoms and signs may appear in association with a prolonged

deceleration, related to the underlying cause of fetal hypoxia/acidosis (see below).

2.3.1 Reversible Causes

The underlying cause of fetal hypoxia/acidosis is frequently reversible, as occurs

with uterine hypercontractility, sudden maternal hypotension or aorto-caval compression by the pregnant uterus when the mother is in the supine position.

2.3.1.1 Uterine Hypercontractility

Uterine contractions compress the blood vessels running inside the myometrium,

and this may cause a temporary reduction in placental perfusion. The umbilical cord

may also be compressed between fetal bony parts or between the fetal head and the

uterine wall, transitorily reducing umbilical blood fl ow. Usually these phenomena

occur during the peak of uterine contractions, and the intervals between these events

are suffi cient to re-establish normal oxygenation. The frequency, duration and

intensity of uterine contractions will determine the magnitude of the disturbances,

and how much they affect fetal oxygenation.

Fig. 2.2 Cardiotocographic (CTG) tracing with prolonged FHR deceleration and reduced

variability within the deceleration

2.3 Diagnosis

Hypercontractility may be spontaneous or induced in nature and refers to an

increased frequency, intensity and/or duration of contractions leading to reduced

fetal oxygenation. Rather than exhibiting a single prolonged deceleration

(Fig. 2.2 ), uterine hypercontractility usually manifests by repetitive decelerations

that may merge to become a prolonged deceleration and ultimately exhibit loss of

variability but with a tendency for FHR recovery between contractions (Fig. 2.3 ).

Most cases of uterine hypercontractility are iatrogenic in nature, caused by oxytocin or prostaglandin administration. Local practices for labour induction and

acceleration will therefore determine the incidence of this entity, and respecting

established doses and intervals for drug administration limits its occurrence. Little

is known about the incidence and risk factors of spontaneous uterine hypercontractility, but some cases have been described in association with myometrial infection

and partial placental abruption.

Increased abdominal pain is usually referred, but in the context of epidural analgesia, the diagnosis will rely mainly on the detection of increased contraction frequency

by cardiotocography (CTG) or on uterine fundus palpation. More than fi ve contractions in 10 min on two successive 10-min periods or averaged in the last 30 min is the

defi nition of tachysystole – increased frequency of uterine contractions. With external monitoring of uterine contractions, using a tocodynamometer or fundal palpation,

only frequency of uterine contractions can be reliability assessed. Evaluation of their

intensity and duration, as well as of basal uterine tone, requires the use of an intrauterine pressure sensor, a technique that is nowadays seldomly used. A sustained rise in

uterine contraction baseline or the detection of a permanently contracted uterine fundus is very suggestive of increased basal tone (hypertonus), but intrauterine pressure

measurement remains the gold standard for this diagnosis.

2.3.1.2 Sudden Maternal Hypotension

Sudden maternal hypotension is nearly always an iatrogenic complication associated with epidural or spinal analgesia, due to blocking of sympathetic nerves that

Fig. 2.3 CTG with uterine hypercontractility (tachysystole), prolonged decelerations with

attempts to recover between contractions and reduced variability at the end

2 Acute Fetal Hypoxia/Acidosis

regulate vessel tonus. It can manifest by nausea, dizziness, vomiting, blurred vision

and loss of consciousness and is usually accompanied by a prolonged deceleration.

The drop in blood pressure is usually moderate but suffi cient to cause a decrease in

placental perfusion and gas exchange.

When epidural analgesia began to be used in labour, maternal hypotension and

the resulting CTG changes occurred in almost a third of cases. Prophylactic fl uid

administration before catheter placement reduced this incidence to about 2 %, and

recent developments in the technique with lower doses of local anaesthetics have

almost eliminated the need for prophylactic fl uid administration.

2.3.1.3 Maternal Supine Position with Aorto-Caval Compression

Adoption of the maternal supine position can lead to important aorto-caval compression by the pregnant uterus, with a resulting reduction in placental perfusion and gas

exchange. This position has also been associated with uterine hypercontractility due

to sacral plexus stimulation. Asking the mother to adopt the upright, half- sitting or

lateral recumbent position is usually followed by normalisation of the CTG pattern.

2.3.2 Irreversible Utero-Placental-Umbilical Disorders

These are rare events of an irreversible nature that pose great risk to fetal oxygenation. They include major placental abruption, uterine rupture and umbilical cord

prolapse. All of them require rapid delivery to avoid adverse perinatal outcome, and

the fi rst two can also be associated with profuse maternal haemorrhage.

2.3.2.1 Major Placental Abruption

Major placental abruption can be defi ned as a separation between the chorion and

decidua of suffi cient area to condition fetal oxygenation and/or is associated with

maternal haemorrhage of suffi cient volume to produce the same effect (Fig. 2.4 ).

Placental abruption affects about 1 % of all labours, but the vast majority of cases

are insidious and of small dimension. Placental function needs to be reduced by about

50 % before fetal oxygenation is affected. Blood originating from vessels located

behind the placenta may detach the fetal membranes and drain to the vagina, or it may

accumulate to form a retroplacental haematoma. Occasionally, blood will infi ltrate the

myometrium and originate a Couvelaire uterus, a structure of petrous consistency that

can be palpated through the abdomen when located anteriorly and/or fundally.

The main risk factors for placental abruption are a previous history of similar

episodes, hypertensive diseases of pregnancy, abdominal trauma, maternal cocaine

consumption, maternal smoking and fetal growth restriction.

Sudden abdominal pain, abdominal tenderness, vaginal bleeding and maternal

haemodynamic changes may be present, but frequently the fi rst manifestation is a

prolonged deceleration. FHR sounds have been reported to be dulled when there is

a large anterior placental haematoma, and in these cases it may be necessary to

confi rm heart movements on ultrasound. When the presenting part is fully engaged,

blood may not exteriorise through the vagina and will accumulate inside the uterine

cavity, draining after birth.

2.3 Diagnosis

Uterine contractility may be increased in small placental detachments, but in

major abruption, it is generally irregular and ineffi cient, predisposing to postpartum uterine atony. Myometrial infi ltration causes the release of thromboplastins

into the maternal circulation and may result in disseminated intravascular

coagulation.

2.3.2.2 Uterine Rupture

Only about 30 % of cases of uterine rupture are associated with fetal hypoxia/acidosis, because lacerations are frequently limited to the caesarean section scar and do

not involve important myometrial vessels irrigating the placental bed nor is there an

accompanying major abruption. Acute hypoxia/acidosis is more frequent when the

fetus is exteriorised into the peritoneal cavity. Maternal mortality associated with

uterine rupture is currently low in high-resource countries. On the other hand, there

is a relatively high rate of peripartum hysterectomy.

Uterine rupture affects about 0.003 % of all births, and the incidence does not

appear to have increased over the last decades. In the majority of cases, there is a

Fig. 2.4 Major placental

abruption

2 Acute Fetal Hypoxia/Acidosis

previous history of caesarean section, and the incidence in this population is about

0.1 %. Other risk factors include high multiparity, uterine malformations, oxytocin

or prostaglandin use, forceps delivery, placenta percreta, external cephalic version,

fetal macrosomia, fetal-pelvic disproportion, abnormal fetal presentation and previous uterine surgery, including curettage and hysteroscopy.

Continuous lower abdominal quadrant pain (3–50 %) and vaginal bleeding (8–12 %)

are the most suggestive symptoms of uterine rupture, but a prolonged deceleration

(70 %) is frequently the only manifestation. Upward displacement of the presenting

part has been reported, but does not seem to be frequent nor is it easy to recognise.

Sometimes the diagnosis is only apparent at the time of surgery, where caesarean section scar dehiscence is the most frequent fi nding. Uterine rupture may extend anteriorly

to affect the posterior bladder wall or laterally towards the broad ligaments and the

uterine arteries, in the latter case causing severe haemorrhage. Extension to the posterior uterine wall is rare in the absence of previous uterine surgery.

Adherence to established guidelines for labour induction and acceleration and

continuous FHR monitoring in women with previous uterine scars are required for

avoiding and/or rapidly detecting these situations.

2.3.2.3 Umbilical Cord Prolapse

Umbilical cord prolapse is defi ned as the presence of a loop of umbilical cord below

the presenting part, after the membranes have ruptured. The loop usually passes

through the cervix into the vagina (Fig. 2.5 ), but it can also remain in the uterine

cavity or pass through the vaginal introitus to the exterior.

Fig. 2.5 Umbilical cord

prolapse

2.3 Diagnosis

With umbilical cord prolapse, the loop may be continuously compressed between

the presenting part and the maternal pelvis, but it can also only be subject to intermittent compressions during contractions. Rarely, no cord compression occurs, a

situation that is more frequent with earlier gestational ages, anomalous fetal presentations and in the absence of labour. Cord prolapse can also be complicated by

vascular spasm, which has been described when the cord is exposed to cold or is

manipulated. During labour, umbilical cord prolapse is almost always associated

with repetitive decelerations or with a prolonged deceleration.

Umbilical cord prolapse is reported to affect 0.1–0.6 % of all labours, but the

incidence may reach 1 % in breech presentations. Older studies report severe fetal

hypoxia/acidosis to occur in 25–50 % of cases, but this number has been decreasing

in the last decades, probably due to increased awareness, faster diagnosis and management. Recent studies report perinatal mortality rates between 3.6 and 16.2 %,

with causes of death more related to prematurity than to fetal hypoxia/acidosis.

The main risk factors for umbilical cord prolapse are anomalous fetal presentations (transverse lie, knee or footling breech), polyhydramnios, multiparity, long

umbilical cord, multiple gestation, preterm labour and low-lying placenta. In a

recent case series, 47 % of cases were preceded by an obstetrical intervention such

as amniotomy, fetal electrode placement, intrauterine pressure sensor placement

and external cephalic version or by expectant management of preterm premature

rupture of membranes.

2.3.3 Maternal Cardiorespiratory Disorders

Fetal hypoxia/acidosis may be caused by a number of acute maternal circulatory

and respiratory disorders, including severe asthma, haemorrhagic shock, and cardiorespiratory arrest. During labour, however, the most common causes are pulmonary thromboembolism and amniotic fl uid embolism. A more detailed description

of these complications is provided in Chap. 7.

2.3.4 Usually Occult Causes

It is not always possible to diagnose the causes of a prolonged deceleration before

birth, as there is no clear symptom or sign pointing to an aetiology. The occult

causes of acute fetal hypoxia/acidosis include occult cord compression and major

fetal haemorrhage.

2.3.4.1 Occult Cord Compression

Occult cord compression may occur because of a tight umbilical cord knot, a lowlying loop compressed by the fetal head or a tight nuchal cord that is stretched during descent of the fetal head. Different degrees of compression may occur, resulting

in varying levels of circulatory compromise. In the majority of situations, decreased

fetal oxygenation and the accompanying FHR changes only occur during

2 Acute Fetal Hypoxia/Acidosis

contractions, and the intervals between these events are suffi cient to recover fetal

oxygenation. The diagnosis is usually retrospective and established at the time of

vaginal delivery or caesarean section, but even there low-lying loops may be missed.

Depending on the degree of circulatory compromise during and in between contractions, the situation may be relieved by acute tocolysis and by positioning the mother

on the left or right lateral, half-sitting or upright positions.

2.3.4.2 Major Fetal Haemorrhage

Fetal haemorrhage of suffi cient volume to result in reduced oxygen transport capacity may be chronic, acute or recurring in nature and can be due to fetal-maternal

haemorrhage, ruptured vasa praevia or very rarely to lacerations of an umbilical or

placental vessel.

In almost all deliveries, there is some degree of fetal - maternal haemorrhage ,

but this is usually of small quantity. A fetal-maternal haemorrhage of more than

20 ml is reported to occur in 0.46 % of births, more than 30 ml in 0.38 % and more

than 80 ml in 0.07 %. An increased risk of adverse perinatal outcome is found when

blood loss exceeds 20 ml/kg of fetal weight, and about two-thirds of newborns die

when it exceeds 80 ml/kg. Other important factors to establish fetal prognosis are

the rate of haemorrhage and gestational age. Major fetal-maternal haemorrhage

can follow abdominal trauma, external cephalic version, amniocentesis and abruption, and it can also occur with placental chorioangiomas. The vast majority of

cases however arise spontaneously and have no identifi able cause. Fetal-maternal

haemorrhage is usually asymptomatic, although decreased fetal movements may

be reported. The volume of fetal blood present in the maternal circulation should

be estimated by the Kleihauer-Betke test or by fl ow cytometry, and newborn anaemia needs to be documented after birth. Rarely, in the presence of massive haemorrhage, the mother experiences a transfusion reaction with nausea, oedema, chills

and fever.

Ruptured vasa praevia refers to the laceration of fetal vessels coursing through

the membranes close to the internal cervical os , during spontaneous or artifi cial

rupture of membranes. It can occur because of velamentous insertion of the cord or

because of vessels running between lobes in a bilobed placenta. The reported incidence is 0.017–0.05 %. Perinatal mortality rate appears to be around 60 % when the

situation is diagnosed at membrane rupture, but it can be reduced to 3 % when antenatal diagnosis is followed by elective caesarean section. Ruptured vasa praevia

usually presents with vaginal haemorrhage at the time of membrane rupture. Very

occasionally the vessels may be palpated on vaginal examination before rupture

occurs, and their presence confi rmed with transvaginal Doppler ultrasound or with

an amnioscope. Risk factors for vasa praevia include bilobed placenta, low-lying

placenta diagnosed in the second trimester, multiple pregnancy and in vitro

fertilisation.

In major fetal haemorrhage of any cause, a sinusoidal FHR pattern is frequently

detected (Fig. 2.6 ), occasionally with fetal tachycardia during the acute phase,

recurrent late decelerations appearing when contractions start or a prolonged deceleration/bradycardia.

2.3 Diagnosis

2.3.5 Specific Mechanical Complications of Labour

Acute fetal hypoxia/acidosis may be caused by specifi c mechanical complications

of labour, associated with umbilical cord compression and/or compression of

important fetal blood vessels. The most frequent situations are shoulder dystocia

and retention of the after-coming head in vaginal breech delivery. A more detailed

description of these situations is provided in Chaps. 3 and 4.

2.4 Clinical Management

The specifi c management of acute maternal cardiorespiratory arrest, shoulder dystocia and retention of the after-coming head is described in subsequent chapters.

The present section is dedicated to management of the remaining causes of acute

fetal hypoxia/acidosis.

2.4.1 Immediate Actions in Face of a Prolonged Deceleration

The immediate actions to take when a prolonged deceleration is detected are listed

in Table 2.2 . The order of these actions may be adapted, if there is a strong suspicion

of a specifi c cause.

Fig. 2.6 Sinusoidal FHR pattern in fetal-maternal haemorrhage

2 Acute Fetal Hypoxia/Acidosis

The fi rst consideration should be given to assuring the continuous acquisition of

a reliable FHR signal, so that the prolonged deceleration is confi rmed, the duration

is evaluated, and possible signs of recovery are documented. In addition, the occurrence of reduced variability within the deceleration is very suggestive of fetal

hypoxia/acidosis. For all these reasons, continuous CTG should be preferred, if

readily available. With external FHR monitoring, it is essential to assure that the

fetus rather than the mother is being monitored, so the maternal pulse needs to be

simultaneously evaluated to detect coincidences, and frequent repositioning of the

Doppler sensor may be required. It is therefore useful to assign one person to assure

a continuous good quality FHR signal and to evaluate the maternal pulse intermittently, for an adequate documentation of the situation.

The resolution of most situations of acute fetal hypoxia/acidosis requires a concerted action from a team of healthcare professionals, so therefore help should be

promptly summoned, and the presence of at least two midwives and a senior obstetrician assured.

Although many prolonged decelerations revert spontaneously without any intervention, it is sometimes diffi cult to predict the situations in which this occurs. With

the actions described in Table 2.2 , all reversible causes of fetal hypoxia/acidosis are

quickly identifi ed, and some are immediately corrected. A quick search of the

underlying cause is necessary to plan management, as some causes may be quickly

reversible (excessive uterine activity, acute maternal hypotension and maternal

supine position), while others are irreversible and pose extreme danger to the fetus

(major placental abruption, uterine rupture, umbilical cord prolapse). When it is not

possible to identify a cause, management should be based mainly on the duration of

the deceleration and the evaluation of variability (see below).

Even when there is no apparent tachysystole (see defi nition above), oxytocin perfusion should be stopped or prostaglandins removed (when possible) to reduce contraction frequency and help recover fetal oxygenation. A vaginal examination is essential

to diagnose umbilical cord prolapse and to evaluate the conditions for instrumental

vaginal delivery. Even if the patient is in the active second stage of labour, asking the

woman to stop pushing and temporary adopting the lateral decubitus position may

relieve aorto-caval compression and reduce uterine contraction frequency. In some

situations of occult cord compression, it may be the left or the right lateral decubitus

that causes the best effect, or alternatively the half-sitting or upright positions.

Table 2.2 Immediate actions in face of a prolonged deceleration

Assure a continuous and good quality FHR signal

Call for help (two midwives, senior obstetrician)

Stop oxytocin , remove prostaglandins. Evaluate contractility (CTG tocograph, palpate

uterine fundus to detect tachysystole and/or increased basal tone)

Vaginal examination (to detect umbilical cord prolapse and conditions for instrumental

vaginal delivery)

Patient in lateral decubitus (if there are no conditions for immediate delivery)

Evaluate state of consciousness and vital signs (talk to patient, evaluate breathing, radial

pulse and blood pressure)

2.4 Clinical Management

2.4.2 Uterine Hypercontractility

Uterine hypercontractility occurring when an oxytocin perfusion is in place usually

starts to revert 1–3 min after it is stopped, as the half-life of the drug is around

3–6 min. If a faster effect is required or when hypercontractility is spontaneous in

nature or prostaglandins cannot be removed, acute tocolysis should be considered

(Table 2.3 ).

Salbutamol and terbutaline should not be used in women with coronary artery

disease, history of cardiac arrhythmias, high blood pressure, hyperthyroidism or low

potassium levels. Their main side effects are tachycardia, tremor and nervousness.

Atosiban has no formal contraindications, but occasional side effects such as headaches, dizziness, vomiting, tachycardia, hypotension and fever have been reported.

Prolonged decelerations should start to revert 1–2 min after acute tocolysis

has begun, and waiting for this to occur is the fi rst option when hypercontractility

is strongly suspected. During the second stage of labour, instrumental vaginal

delivery may be an alternative if there are conditions for a quick and safe procedure. Otherwise, asking the parturient to stop pushing and waiting for reversal of

the deceleration is preferable to guarantee the return of adequate fetal oxygenation. It should not be forgotten that uterine hypercontractility may also occur in

the initial phases of placental abruption, so the maximum time limits for reversal

of a prolonged deceleration should be taken into account (see below).

2.4.3 Sudden Maternal Hypotension

Sudden maternal hypotension secondary to epidural or spinal analgesia is usually

quickly reversed by starting or increasing crystalloid perfusion and when this is

not enough administering ephedrine 3–6 mg in intravenous bolus over 5 min. The

bolus can be repeated after 5–10 min, until a maximum dose of 10 mg is reached.

The drug is contraindicated in patients with cardiac disease, hypertension, hyperthyroidism, phaeocromocytoma and closed angle glaucoma and those who have

taken monoamine oxidase inhibitors in the previous 14 days. The following side

effects have been reported: paleness, fever, dry mucosae, shortness of breath, chest

pain, tachycardia, anxiety, nausea and vomiting, headache, insomnia and mood

changes. It can also cause transitory fetal tachycardia.

Administration of colloids is not recommended in these situations, as they can

have a negative impact on coagulation, and rare cases of anaphylaxis and acute renal

insuffi ciency have been reported.

Table 2.3 Drugs used for acute tocolysis

Salbutamol 125 μg at 25 μ/min IV. One 1 ml vial (0.5 mg/ml) in 100 ml of crystalloid

solution, in intravenous perfusion at 300 ml/h for 5 min

Terbutaline 0.25 mg by subcutaneous injection

Atosiban 6.75 mg IV. One 0.9 ml vial (7.5 mg/ml) given by intravenous bolus during 1 min

2 Acute Fetal Hypoxia/Acidosis

Reversal of the FHR deceleration should start very soon after blood pressure

begins to normalise, and waiting for this to occur should be the fi rst option unless a

very fast and safe instrumental vaginal delivery can be guaranteed. It should not be

forgotten that hypotension may also be caused by maternal haemorrhage, as occurs

with major placental abruption or uterine rupture, so the maximum time limits for

reversal need to be taken into account (see below).

2.4.4 Major Placental Abruption

When major placental abruption is strongly suspected, rapid delivery is required to

guarantee the safety of both mother and fetus. Instrumental vaginal delivery may

occasionally be possible if there are very favourable conditions, but the majority of

cases will present before the active second stage of labour and require emergent

caesarean section. The anaesthesiologist and neonatologist should therefore be rapidly summoned and the operating theatre prepared.

Profuse retroplacental haemorrhage and disseminated intravascular coagulation

may occur in this situation, so continuous monitoring of maternal vital signs, oxygen saturation and ECG should be started, a vein catheterised with a large bore

needle, blood drawn for haemoglobin, coagulation studies and cross-matching and

a crystalloid infusion initiated. Blood results need to be monitored regularly in order

to identify the fi rst signs of disseminated intravascular coagulation and to anticipate

postpartum haemorrhage (see Chap. 7).

If fetal death has occurred and the mother is haemodynamically stable, it is preferable to induce or accelerate labour. In these situations, caesarean section is

reserved for absent labour progress, profuse bleeding and/or maternal haemodynamic instability.

As the diagnosis of major placental abruption is not always fi rmly established

before delivery, the maximum time limits for reversal of a prolonged deceleration

need to be taken into account (see below).

2.4.5 Uterine Rupture

Uterine rupture requires prompt delivery followed by surgical repair, in order to guarantee the safety of both mother and fetus. Similarly to major placental abruption,

when the diagnosis is strongly suspected, continuous monitoring of maternal vital

signs, oxygen saturation and ECG should be put in place, a peripheral vein catheterised with a large bore needle, blood drawn for haemoglobin, coagulation studies and

cross-matching and a crystalloid infusion initiated. The anaesthesiologist and neonatologist should to be rapidly summoned and the operating theatre prepared.

After confi rmation of uterine rupture at laparotomy and delivery of the fetus,

surgical correction with a double-layer suture may be technically possible. Several

case reports of successful subsequent pregnancies have been described after this

type of surgery, usually delivered by elective caesarean section at term. If suturing

2.4 Clinical Management

of the lesion is judged to be impossible, or when it is anticipated to be a lengthy

procedure in the context of an unstable patient, peripartum hysterectomy remains

the only alternative. Some centres report subtotal hysterectomy to be safer than total

hysterectomy in this context, with lower rates of ureteral complications and maternal mortality, but surgical experience should be the determining factor in this choice.

As the diagnosis of uterine rupture cannot always be safely established during

labour, particularly when the woman is under epidural or spinal analgesia, the maximum time limits for reversal of a prolonged deceleration need to be taken into

account (see below).

2.4.6 Umbilical Cord Prolapse

When umbilical cord prolapse occurs in the absence of continuous CTG monitoring, cord pulsatility should be evaluated, and if doubt remains as to the occurrence

of blood fl ow, heart movements should be quickly confi rmed on ultrasound. A few

cases of fetal survival have been reported when rapid action is taken in spite of an

apparently non-pulsatile cord. An exteriorised umbilical loop requires as little

manipulation as possible to avoid vascular spasm.

If the fetus is alive and the gestational age is viable, immediate measures should

be taken to reduce cord compression and quickly deliver the fetus, usually by caesarean section. Cord prolapse is very rare during the second stage of labour with the

head fully engaged, so instrumental vaginal delivery is usually not an option. The

patient should be rapidly placed in a head - down position and the presenting part

raised by a hand inside the vagina, measures that are maintained until delivery. An

anaesthesiologist and a neonatologist need to be rapidly summoned, the operating

theatre prepared and the patient transported there as quickly as possible.

When immediate caesarean delivery is not possible (i.e. when prolapse occurs in

a health facility that does not have an operating theatre), acute tocolysis should be

started (Table 2.3 ), the bladder catheterised and 500–750 ml of saline solution

instilled via the catheter in order to maintain the presenting part elevated. Continuous

monitoring by CTG or handheld Doppler is then maintained during patient transport, until a caesarean section is performed.

Currently, there is insuffi cient evidence on the safety of alternative treatments for

umbilical cord prolapse, such as digital reduction of the prolapsed cord followed by

expectant management, although there are a few reported cases of success in the

scientifi c literature.

2.4.7 Maximum Time Limits for Reversal

of a Prolonged Deceleration

Frequently, the underlying cause of a prolonged deceleration is not clear, and no

safe judgement can be made as to its reversible or irreversible nature, nor of the

probability of recurrence when contractility is resumed. Abundant vaginal bleeding

2 Acute Fetal Hypoxia/Acidosis

is highly suggestive of an irreversible cause (placental abruption, uterine rupture,

ruptured vasa praevia) and should prompt immediate delivery. The appearance of a

sinusoidal pattern is also very suggestive of fetal haemorrhage (fetal-maternal

haemorrhage or ruptured vasa praevia) and should also motivate rapid delivery.

Whatever the cause of fetal hypoxia/acidosis, maximum time limits for a prolonged deceleration need to be established in order to guarantee the absence of

permanent injury to the fetus.

Particular care is recommended when prolonged decelerations exceed 5 min and

there is no tendency to recover, especially when there is reduced variability within

the deceleration. The healthcare team should start preparing all the requirements

needed for a rapid caesarean section or instrumental vaginal delivery. The latter

should only be considered if a quick and safe procedure can be guaranteed; otherwise the operating theatre team should be prepared for an emergent caesarean section. The anaesthesiologist and neonatologist should be rapidly summoned. The

fi nal decision to intervene depends on local conditions, such as distance to the operating theatre and the team’s profi ciency with the surgery, as well as on additional

clinical information (normal or growth-retarded fetus, previous CTG changes,

appearance of vaginal bleeding or other symptoms suggesting an irreversible cause).

With an adequately grown and previously well-oxygenated fetus at term, this decision should rarely go beyond 7 – 8 min . The whole team must be aware of the

urgency of the situation, and the fetus needs to be delivered within 3 – 4 min , so that

the total duration of the hypoxic insult does not exceed 12 min.

2.5 Clinical Records and Litigation Issues

The complications of intrapartum fetal hypoxia/acidosis constitute major causes of

litigation in high- and medium-resource countries. Extreme care needs therefore to

be taken with clinical records, so that it is clear which healthcare professionals were

called, at what time they were called, when did they arrive, as well as who took

which decisions, and who performed which procedures.

It is also very important to document umbilical artery blood pH and base defi cit (or

alternatively lactate) in all situations where there has been an obstetric intervention for

suspected fetal hypoxia/acidosis and when Apgar scores are low. This information is

important to increase the team’s knowledge with management of these situations, and

it also allows a clarifi cation of many causes of neonatal encephalopathy, perinatal

mortality and cerebral palsy. A large number of these complications are not due to

intrapartum hypoxia/acidosis, and they can be ruled out with this information.

During caesarean section, it is important to look for causes of acute fetal hypoxia/

acidosis, as some may only be revealed at this time. Major placental abruption may

result in the formation of a retroplacental haematoma and/or a Couvelaire uterus,

and histological examination of the placenta will confi rm the diagnosis. Tight

nuchal chords, true cord knots, low-lying cord loops and ruptured umbilical/placental vessels can usually be detected during caesarean section or at subsequent inspection of the placenta and membranes. Fetal haemorrhage requires the documentation

2.5 Clinical Records and Litigation Issues

of newborn anaemia, and fetal-maternal haemorrhage can be detected by the

Kleihauer-Betke test or fl ow cytometry.

A clear explanation of the situation to the parents, during and shortly after it has

occurred, frequently removes main of the misunderstandings and uncertainties that

lead to litigation. The obstetric team also needs to remain informed of the health

status of the newborn, so that all information conveyed to the mother and family is

coherent and adapted to this evolution.

2 Acute Fetal Hypoxia/Acidosis

Suggested Reading

American College of Obstetricians and Gynecologists (1993) Fetal and neonatal neurologic injury

(technical bulletin number 163). Int J Gynecol Obstet 41:97–101

American College of Obstetricians and Gynecologists (1996) Umbilical artery blood acid-base

analysis (technical bulletin). Int J Gynecol Obstet 52:305–310

Ayres-de-Campos D, Arulkumaran S, for the FIGO Intrapartum Fetal Monitoring Expert

Consensus Panel (2015a) FIGO consensus guidelines on intrapartum fetal monitoring: physiology of fetal oxygenation and the main goals of intrapartum fetal monitoring. Int J Gynecol

Obstet 131:5–8

Ayres-de-Campos D, Spong CY, Chandraharan E, for the FIGO Intrapartum Fetal Monitoring

Expert Consensus Panel (2015b) FIGO consensus guidelines on intrapartum fetal monitoring:

cardiotocography. Int J Gynecol Obstet 131:13–24

Doria V, Papageorghiou A, Gustafsson A, Ugwumadu A, Farrer K, Arulkumaran S (2007) Review

of the fi rst 1502 cases of ECG-ST waveform analysis during labour in a teaching hospital.

BJOG 114:1202–1207

Giacoia GP (1997) Severe fetomaternal hemorrhage: a review. Obstet Gynecol Surv

52(6):372–380

Giwa-Osagie OF, Uguru V, Akinla O (1983) Mortality and morbidity of emergency obstetric hysterectomy. Obstet Gynecol 4:94–96

Goswami K (2007) Umbilical cord prolapse. In: Grady K, Howell C, Cox C (eds) Managing

obstetric emergencies and trauma. The MOET course manual, 2nd edn. RCOG Press, London

Hofmeyr G, Cyna A, Middleton P (2004) Prophylactic intravenous preloading for regional analgesia in labour. Cochrane Database Syst Rev (4):CD000175

Katz VL, Dotters DJ, Droegemueller W (1986) Perimortem cesarean delivery. Obstet Gynecol

68:571–576

Lin MG (2006) Umbilical cord prolapse. Obstet Gynecol Surv 61:269–277

Low JA, Lindsay BG, Derrick EJ (1997) Threshold of metabolic acidosis associated with newborn

complications. Am J Obstet Gynecol 177:1391–1394

MacLennan A for the International Cerebral Palsy Task Force (1999) A template for defi ning a

causal relation between acute intrapartum events and cerebral palsy: international consensus

statement. BMJ 319:1054–1059

Morgan JL, Casey BM, Bloom SL, McIntire DD, Leveno KJ (2015) Metabolic acidemia in live

births at 35 weeks of gestation or greater. Obstet Gynecol 126(2):279–283

National Collaborating Centre for Women’s and Children’s Health (2007) Intrapartum care: care

of healthy women and their babies during childbirth (clinical guideline). RCOG Press, London

Norén H, Carlsson A (2010) Reduced prevalence of metabolic acidosis at birth: an analysis of

established STAN usage in the total population of deliveries in a Swedish district hospital. Am

J Obstet Gynecol 202(6):546e.1–546e.7

Rasmussen S, Irgens LM, Bergsjo P, Dalaker K (1996) The occurrence of placental abruption in

Norway 1967-1991. Acta Obstet Gynecol Scand 75:222–228

Royal College of Obstetricians and Gynaecologists (2011) Placenta praevia, placenta praevia

accrete and vasa praevia: diagnosis and mangament (Green-top guideline no. 28). RCOG Press,

London

Rubod C, Deruelle P, Le Goueff F, Tunez V, Fournier M, Subtil D (2007) Long-term prognosis for

infants after massive fetomaternal hemorrhage. Obstet Gynecol 110(2 Pt 1):256–260

Ruth VJ, Raivio KO (1988) Perinatal brain damage: predictive value of metabolic acidosis and the

Apgar score. BMJ 297:24–27

van de Riet JE, Vandenbussche FPHA, Le Cessie S, Keirse MJNC (1999) Newborn assessment and

long-term adverse outcome: a systematic review. Am J Obstet Gynecol 180:1024–1029

World Health Organization, UNFPA, UNICEF, World Bank (2003) Managing complications in

pregnancy and childbirth. A guide for midwives and doctors. Prolapsed cord. WHO Press,

Geneva. S-97–98. [www.who.int/reproductive-health/impac/index.html]

Suggested Reading

D. Ayres-de-Campos, Obstetric Emergencies,

DOI 10.1007/978-3-319-41656-4_3

3 Shoulder Dystocia

3.1 Definition, Incidence and Main Risk Factors

The term shoulder dystocia describes a series of diffi culties encountered with

release of the fetal shoulders in cephalic deliveries and more objectively the need to

use additional manoeuvres when axial traction on the fetal head has failed. An overall incidence between 0.58 and 0.70 % of vaginal deliveries is reported in the largest

observational studies.

The main mechanism behind the occurrence of shoulder dystocia is the retention of the anterior shoulder behind the pubic symphysis, while the posterior shoulder is usually located in the maternal pelvis (Fig. 3.1 ). In rare situations, both

shoulders are retained above the pelvic brim.

The main risk factors for shoulder dystocia are listed in Table 3.1 . Previous shoulder dystocia stands out as a major risk factor for recurrence, and it is reported to be

Pubic

symphysis

Brachial

plexus

Fig. 3.1 The main

mechanism behind the

occurrence of shoulder

dystocia – retention of

the anterior fetal

shoulder above the pubic

symphysis

10-times higher than in the general population, for an overall incidence of 1–25 %. The

anatomical characteristics of the maternal pelvis that predispose to shoulder dystocia

and may cause it to be recurrent in nature are poorly understood. When additional risk

factors are present, such as maternal diabetes or suspected fetal macrosomia or when

previous fetal injury occurred in association with shoulder dystocia, serious consideration should be given to elective caesarean delivery, and this option should be discussed

with the mother. In the remaining situations, management remains controversial.

Another major risk factor is fetal macrosomia , and when coexistent with poorly

controlled maternal diabetes , an additional 2–4-fold risk is present, posed by the

increased diameter of the fetal shoulders.

With isolated macrosomia, there is recent evidence from a randomised controlled

trial that fetuses whose estimated weight is above the 95th percentile close to term

benefi t from induction of labour at 37–38 weeks, as it reduces the risk of shoulder

dystocia by about 70 % and also slightly increases the number of vaginal deliveries.

An estimated fetal weight above 5000 g is considered in many guidelines to be an

indication for elective caesarean section, and others include this recommendation

for estimated weights above 4500 g.

With maternal diabetes, labour induction at 38–39 weeks has been shown to

decrease the incidence of shoulder dystocia and is recommended in several guidelines. Some institutions recommend elective caesarean section when estimated fetal

weight is above 4250 g or above 4500 g.

The above recommendations have been criticised for the limited strength of the

evidence on which they are based. Weight estimation by ultrasound has a welldemonstrated inherent error, particularly in macrosomic fetuses. One should also

not forget that caesarean section for fetal weights above 4500 g is associated with a

2.5 % risk of trauma. Nevertheless, these recommendations remain important

sources of guidance, while stronger evidence is awaited.

Risk factors that only become apparent during labour are more diffi cult to integrate into the clinical decision process. In spite of signifi cant associations existing

between all of these risk factors and shoulder dystocia, none of them are suffi ciently

discriminative to allow an accurate prediction. The majority of cases of shoulder

dystocia occur in pregnancies that have no risk factors, and when one is present, the

majority of cases do not develop this complication. There is therefore wide agreement within the medical community that shoulder dystocia is generally an

Table 3.1 Main risk factors

for shoulder dystocia Previous shoulder dystocia

Fetal macrosomia and its associated risk factors

Pre-existing or gestational diabetes

Maternal obesity

Excessive weight gain during pregnancy

Post-term pregnancy

Slow progress of labour

Prolonged fi rst and/or second stage

Need for labour acceleration

Instrumental vaginal delivery

3 Shoulder Dystocia

unpredictable situation . Nevertheless, identifi cation of risk factors is useful for

anticipating of the situation, so that an experienced team can be on hand at the time

of delivery.

3.2 Complications

The most frequent complication of shoulder dystocia is brachial plexus injury , of

which Erb’s palsy is the usual presentation. The latter manifests by a characteristic

position of the affected arm that hangs by the side of the body and is rotated medially. The forearm is usually extended and pronate (Fig. 3.2 ). It affects about 0.15 %

of all births, and in some countries, the incidence appears to be decreasing. Older

studies report brachial plexus injury to occur in 2–16 % of shoulder dystocias, but

recent data from centres performing regular staff training refer that this can be

reduced to about 1.3 %. Brachial plexus injury appears to be related mainly to the

traction force applied on the fetal head. Improved awareness of the fact and

simulation- based training of the force that can be safely applied to the fetal head

may be responsible for the decreasing incidence of this complication.

The underlying cause for injury is believed to be exaggerated mechanical distention of the brachial nerve, but the mechanism is incompletely understood, as it may

also affect the posterior arm, and cases have been reported to occur in elective

Fig. 3.2 Newborn with a

right arm position typical

of Erb’s paralysis

3.2 Complications

caesarean section and vaginal delivery without shoulder dystocia. In 24–53 % of

brachial plexus injuries, no documentation of shoulder dystocia was found, and

4–12 % occurred after caesarean section, so it is possible that they are also caused

by abnormal intrauterine fetal positions.

Of all brachial plexus injuries diagnosed at birth, the majority disappear after

treatment, and only 10–23 % remain after 12 months. In the majority of cases of

residual paralysis, some degree of recovery is achievable after surgery.

Shoulder dystocia is also a cause of perinatal mortality , although the incidence

appears to have decreased in the last decades. Confi dential enquiries carried out in the

United Kingdom indicate that it may be responsible for about 8 % of intrapartum fetal

deaths. The main cause of perinatal death is acute fetal hypoxia/acidosis (see Chap. 2).

There is uncertainty about how many minutes may elapse before the fetus is at

risk of injury from acute hypoxia/acidosis. The phenomenon is probably faster

when there are nuchal cords and when cord clamping takes place before the shoulders are released. Five such cases with resolution taking 3–7 min were reported in

association with cerebral palsy, but it is uncertain whether intrapartum hypoxia/

acidosis was already present before delivery of the head. Sustained cord occlusion

is likely to occur in these situations, and therefore umbilical blood gas values may

not translate the severity of hypoxia/acidosis. Hypoxic-ischaemic encephalopathy

has been documented in cases with only moderate acidaemia on cord gas analysis.

Compression of fetal neck vessels may also play an important part in the pathophysiological mechanism, and it may be the main cause of cerebral injury when no

nuchal cords are present. Again, umbilical blood gas values may not translate the

severity of hypoxia/acidosis occurring in the brain, and hypoxic-ischaemic encephalopathy has been documented in cases with only moderate acidemia on cord gas

analysis. In a small but well-documented observational study, no cases of hypoxicischaemic encephalopathy were found when resolution took less than 5 min, and

only mild cases of hypoxic-ischaemic encephalopathy were reported when it lasted

5–9 min. Serious complications of hypoxia/acidosis were only described in one case

where more than 12 min elapsed.

Although there are no certainties as to the time that may elapse before the fetus

is at risk of injury from hypoxia/acidosis, it seems wise not to clamp nuchal cords

after the head is delivered unless there is no other alternative and to attempt resolution preferably within 5 min. When 12 min have elapsed, fetal prognosis is likely to

be poor. Different timings must be considered when fetal oxygenation is already

compromised before the occurrence of shoulder dystocia or when there is fetal

growth restriction.

Rarer complications of shoulder dystocia are fractures of clavicle and humerus ,

the majority of which are iatrogenic in nature, consequent to the manoeuvres used for

resolution of the situation, and they usually heal without sequelae after immobilisation.

The most frequent maternal complications are vaginal and perineal lacerations , and some studies report anal sphincter lacerations to occur in about 4 % of

shoulder dystocia cases.

Postpartum haemorrhage affects about 11 % of cases and can be caused by

birth canal lacerations and more frequently by uterine atony. Rare cases of uterine

3 Shoulder Dystocia

rupture, bladder rupture, dehiscence of the pubic symphysis and sacroiliac joint

dislocation have also been described.

3.3 Diagnosis

The most common defi nition of shoulder dystocia is the need to use additional

manoeuvres to release the fetal shoulders, after the usual axial traction on the

head has failed. However, it is important to add that traction should be continuous

and that it should not exceed a maximum force of 100 Newtons. No more than two

or three tractions should be applied before the diagnosis is established.

Other criteria have been proposed for the defi nition of shoulder dystocia, based

on the time interval between delivery of the fetal head and release of the shoulders,

and they consider cut-offs of 1 or 2 min. However, accurate measurement of these

intervals may not be practicable in many hospitals.

3.4 Clinical Management

3.4.1 Anticipating the Situation

When risk factors are identifi ed (Table 3.2 ) or when premonitory signs are detected,

steps should be taken to summon an experienced healthcare team, in case shoulder

dystocia occurs. Moving the mother closer to the end of the bed or removing the

lower part of the bed may also be useful, to improve access to the fetal head.

The most important premonitory signs are a marked descent of the fetal head

during pushing followed by an abnormal rise in between contractions and the turtle

sign, a situation where there is incomplete expulsion of the fetal head, so that the

fetal mandible and occiput remain depressing the maternal perineum (Fig. 3.3 ).

Fig. 3.3 Turtle sign, with

the lower structures of the

fetal head depressing the

maternal perineum

3.4 Clinical Management

3.4.2 Clearly Verbalising the Diagnosis

In these situations, it is important to convey the diagnosis to all healthcare professionals present in the room, so that the team may act accordingly, and therefore it

needs to be clearly verbalised, without unnecessarily alarming the labouring woman

and her companion.

3.4.3 Avoiding Manoeuvres That Increase the Risk of Fetal Injury

The manoeuvres most frequently associated with brachial plexus injury are excessive

traction on the fetal head, non-axial traction and forced rotation. Fundal pressure should

also be avoided, as it only serves to push the anterior shoulder against the pubic symphysis. Maternal pushing has a similar effect, so the mother should be asked to stop this.

3.4.4 Asking for Help

Management of shoulder dystocia requires a concerted effort from the healthcare team,

so one of the fi rst measures should be to summon at least two midwives and a senior

obstetrician. In addition, a neonatologist and an anaesthetist should be called, the fi rst

one because neonatal resuscitation is likely to be required and the second because uterine relaxation is sometimes needed for the internal manoeuvres (see below).

3.4.5 External Manoeuvres

External manoeuvres resolve the vast majority of shoulder dystocia cases and

should be attempted fi rst:

McRobert’s Manoeuvre Hyperfl exion of the mother’s thighs against her abdomen – this manoeuvre is performed by two assistants, one on each side of the

mother, each holding one leg and forcibly fl exing and abducing the thighs against

the lateral part of the abdomen (Fig. 3.4 ). After this is accomplished, gentle and

continuous axial traction on the fetal head is reattempted. With this manoeuvre, the

lumbosacral angle is straightened, and the pubic symphysis is moved anterosuperiorly, thus helping the anterior shoulder to slip under the pubic bone.

Suprapubic Pressure This is usually performed by one of the assistants executing

the McRobert’s manoeuvre (Fig. 3.4 ), with a closed hand applying fi rm and sustained pressure above the pubic symphysis. After this is in place, gentle and continuous axial traction on the fetal head is reattempted. The applied pressure helps the

anterior shoulder to slip under the pubic bone. As an alternative, some authors advocate the use of strong and intermittent suprapubic pressure (Rubin I manoeuvre), but

there is no evidence on comparative effi cacies.

3 Shoulder Dystocia

3.4.6 Internal Manoeuvres

Internal manoeuvres should be performed by the most experienced healthcare professional available, while two assistants maintain the McRobert’s manoeuvre. There

is no clear evidence on which order the internal manoeuvres should be performed,

so this depends more on the experience of the executor and the accessibility of the

different fetal structures. Nevertheless, the order presented here refl ects the logical

sequence of increasing diffi culty.

Rotation of the Anterior Shoulder (Rubin II manoeuvre) – One or two fi ngers are

introduced behind the anterior shoulder, and apply continuous and fi rm pressure to

slowly rotate it in the direction of the fetal thorax (Fig. 3.5 ). At the same time, one

of the assistants performing the McRobert’s manoeuvre applies suprapubic pressure

laterally, to help rotate the anterior shoulder in the same direction. Sometimes it is

possible to use one fi nger of the contralateral hand to simultaneously rotate the

Fig. 3.4 McRobert’s

manoeuvre performed

together with suprapubic

pressure

Fig. 3.5 Rotation of the

anterior shoulder

3.4 Clinical Management

posterior shoulder towards the fetal back. The shoulders should be rotated between

45° and 90°, after which axial traction is reapplied on the fetal head.

The need for an episiotomy or for extension of an existing one is controversial

in the management of shoulder dystocia. In the past, it was part of many management guidelines, but its role has since been questioned and it has ceased to be used

routinely in many centres. Nevertheless, it may be useful in situations where access

to the posterior shoulder for rotation or extraction of the posterior arm is made diffi cult by the maternal perineum.

Rotation of the Posterior Shoulder (Woods corkscrew manoeuvre) – Two fi ngers

are introduced behind the posterior shoulder or alternatively the whole hand is introduced around it, to rotate the shoulder slowly but fi rmly towards the fetal thorax

(Fig. 3.6 ). At the same time, lateral suprapubic pressure is applied by an assistant to

rotate the anterior shoulder in the direction of the fetal back. Sometimes, one fi nger

of the executer’s contralateral hand can be used simultaneously, to rotate the anterior

shoulder towards the fetal back. Again the rotation should be of 45–90° after which

axial traction is reapplied on the fetal head.

Extraction of the Posterior Arm The whole hand is introduced in the vagina

around the posterior shoulder, following the fetal arm until the elbow. Using the

tips of the fi ngers, the forearm is fl exed and the pulse grabbed to extract the

hand, followed by the arm, along the fetal body and head (Fig. 3.7 ). Once

extracted, the posterior arm is used as a lever to rotate the posterior shoulder

45–90° in the direction of the thorax, thus releasing the anterior shoulder. In

small observational studies, a 2–13 % rate of humeral fractures was reported

with this manoeuvre, but this could have been due to the relative inexperience

of the executors.

Fig. 3.6 Rotation of the

posterior shoulder

3 Shoulder Dystocia

Uterine relaxation is usually not required for executing the internal manoeuvres, but sometimes pressure inside the uterine cavity prevents mobilisation of the

shoulders or extraction of the posterior arm. Uterine relaxants may be useful in

these situations (Table 3.2 ).

3.4.7 All-Fours Manoeuvre (Gaskin’s Manoeuvre)

This manoeuvre consists of placing the labouring woman on her hands and knees

and applying continuous and gentle axial traction on the fetal head, to release what

was previously the posterior shoulder (Fig. 3.8 ). Its place in the shoulder dystocia

management protocol is currently unclear, particularly in hospital environments.

It is mostly used in community settings when only one birth attendant is present

and where an 83 % success rate has been reported. In hospital settings, it may be

attempted before the exceptional manoeuvres described below are considered.

Fig. 3.7 Extraction of the posterior arm

Table 3.2 Medications used for uterine relaxation

Nitroglicerin in slow intravenous bolus (50–100 μg IV slowly). One 5 ml vial (5 mg/ml) in

500 ml of saline. Slow intravenous injection of 1–2 ml (50–100 μg) with continuous blood

pressure monitoring

Salbutamol in intravenous perfusion (125 μg at 25 μ/min). One vial of 1 ml (0.5 mg/ml) in

100 ml of saline in intravenous perfusion at 300 ml/h during 5 min

3.4 Clinical Management

Fig. 3.8 All-fours

manoeuvre with axial

traction being applied on

the fetal head

3.4.8 Exceptional Manoeuvres

Situations of shoulder dystocia that are not resolved with the manoeuvres described

above are very rare, and by the time exceptional manoeuvres are considered, fetal

prognosis may already be poor. Nevertheless, the problem still requires resolution.

The patient needs to be transferred to the operating theatre , because general

anaesthesia with halogenated agents is required for the Zavanelli manoeuvre. Some

consider a fi nal repetition of the internal manoeuvres in the operating theatre under

general anaesthesia, because of the more effective uterine relaxation.

Zavanelli’s Manoeuvre (Cephalic replacement followed by caesarean section) – this

manoeuvre was described for the fi rst time in 1978, and it is performed in the operating

theatre under general anaesthesia with halogenated agents. The manoeuvre starts with

slow rotation of the fetal head to an occiput-anterior position, followed by fl exion of the

fetal neck and application of fi rm and continuous pressure for the reintroduction of the

fetal head in the maternal pelvis (Fig. 3.9 ). An immediate caesarean section follows. A

small number of case series are reported in the literature with varying success rates and

usually low maternal morbidity, but uterine rupture and subsequent need for hysterectomy have also been described. When fetal prognosis is reserved, maternal morbidity

becomes the main priority, and this is probably the less traumatic alternative for her.

Symphysiotomy This technique has been described for the resolution of obstructed

labour since the nineteenth century, but its current use in high-resource countries is

limited to cases of shoulder dystocia and retention of the after-coming head (see

Chap. 4). Symphysiotomy is associated with important maternal morbidity, so it

should probably be the last option when fetal prognosis is poor. The procedure can

be performed under regional, general and local anaesthesia with opiate sedation.

It should be preceded by antibiotic prophylaxis, bladder catheterisation, shaving and

disinfection of the pubic area. Before incision, two assistants hold the mother’s legs

60–80° apart, after removing them from the bed stirrups. This avoids sudden leg

abduction when the symphysis is opened, which can cause urethral injury. With a

hand introduced in the vagina to push the urethra aside, a transabdominal vertical

incision is performed with a long scalpel between the lower two-thirds and the upper

3 Shoulder Dystocia

Fig. 3.9 Zavanelli’s

manoeuvre

third of the pubic symphysis (Fig. 3.10 ). Pushing the handle upwards will open the

lower two-thirds. The scalpel is then reintroduced into the incision with the blade

facing upwards and the handle pushed downwards to open the remaining upper third.

It is usually possible to separate the pubic bones by about 2–3 cm, and this allows the

shoulders to be released. After closing the abdominal skin, the maternal pelvis is

bound with an orthopaedic strap, and bladder catheterisation is maintained for 48 h.

In the absence of complications, the patient is maintained in lateral decubitus for

two days, and assisted walking starts on the third. Among the reported complications

are para-urethral lacerations, vulval oedema and skin incision haematomas.

Diffi culties in mobilisation may persist for several months in 1–2 % of cases.

3.5 Clinical Records and Litigation Issues

A comprehensive understanding of the mechanism and consequences of shoulder

dystocia is not frequent in expecting mothers nor is the notion that the situation is usually unpredictable. Litigation continues to be common in cases of adverse outcome, so

strict adherence to management algorithms, together with carefully written clinical

records is required. It is important to document the time at which the head and the

3.5 Clinical Records and Litigation Issues

shoulders were released, which fetal shoulder was in the anterior position, who were

the healthcare professionals summoned, when they were called and when they arrived,

which manoeuvres were performed, when and by whom. It is usually convenient to

have a structured pro forma for registering the management of shoulder dystocia,

either in paper or in an electronic format, so that all these details are not forgotten.

Fig. 3.10 The main steps of symphysiotomy

3 Shoulder Dystocia

Complications secondary to fetal hypoxia/acidosis are the most serious, so it is important to document umbilical blood gas values and Apgar scores at birth.

Finally, a clear and frank explanation of the occurrence to the parents frequently

removes much of the suspicion, disinformation and misunderstanding that lead to

litigation. The healthcare team needs to remain informed of the health status of the

newborn, so that conveyed information is adapted to this evolution.

Suggested Reading

Allan RH, Bankoski BR, Butzin CA, Nagey DA (1994) Comparing clinician-applied loads for

routine, diffi cult and shoulder dystocia deliveries. Am J Obstet Gynecol 171:1621–1627

Boulvain M, Senat MV, Perrotin F, Winer N, Beucher G, Subtil D, Bretelle F, Azria E, Hejaiej D,

Vendittelli F, Capelle M, Langer B, Matis R, Connan L, Gillard P, Kirkpatrick C, Ceysens G,

Suggested Reading

Faron G, Irion O, Rozenberg P, Groupe de Recherche en Obstétrique et Gynécologie (GROG)

(2015) Induction of labour versus expectant management for large-for-date fetuses: a randomised controlled trial. Lancet 385(9987):2600–2605

Boulvain M, Stan C, Irion O (2001) Elective delivery in diabetic pregnant women. Cochrane

Database Syst Rev (2):CD001997

Bruner JP, Drummond SB, Meenan AL, Gaskin IM (1998) All-fours maneuver for reducing shoulder dystocia during labor. J Reprod Med 43:439–443

Buhimschi CS, Buhimschi IA, Malinow A, Weiner CP (2001) Use of McRoberts’ position during

delivery and increase in pushing effi ciency. Lancet 358:470–471

Chauhan SP, Blackwell SB, Ananth CV (2014) Neonatal brachial plexus palsy: incidence, prevalence, and temporal trends. Semin Perinatol 38(4):210–218

Crofts JF, Lenguerrand E, Bentham GL, Tawfi k S, Claireaux HA, Odd D, Fox R, Draycott TJ

(2016) Prevention of brachial plexus injury-12 years of shoulder dystocia training: an interrupted time-series study. BJOG 123(1):111–118

Evans-Jones G, Kay SP, Weindling AM, Cranny G, Ward A, Bradshaw A, Hernon C (2003)

Congenital brachial plexus injury: incidence, causes and outcome in the UK and Republic of

Ireland. Arch Dis Child Fetal Neonatal Ed 88:F185–F189

Gherman RB, Ouzounian JG, Satin AJ, Goodwin TM, Phelan JP (2003) A comparison of shoulder dystocia-associated transient and permanent brachial plexus palsies. Obstet Gynecol

102:544–548

Hinshaw K (2003) Shoulder dystocia. In: Johanson R, Cox C, Grady K, Howell C (eds) Managing

obstetric emergencies and trauma: the MOET course manual. RCOG Press, London,

pp 165–174

Hope P, Breslin S, Lamont L, Lucas A, Martin D, Moore I, Pearson J, Saunders D, Settatree R

(1998) Fatal shoulder dystocia: a review of 56 cases reported to the Confi dential Enquiry into

Stillbirths and Deaths in Infancy. Br J Obstet Gynaecol 105:1256–1261

Iffy L, Varadi V (1994) Cerebral palsy following cutting of the nuchal cord before delivery. Med

Law 13(3–4):323–330

Irion O, Boulvain M (2000) Induction of labour for suspected fetal macrosomia. Cochrane

Database Syst Rev (2):CD000938

Leung T, Stuart O, Sahota D, Suen S, Lau T, Lao T (2011) Head-to-body delivery interval and risk

of fetal acidosis and hypoxic ischaemic encephalopathy in shoulder dystocia: a retrospective

review. BJOG 118:474–479

Naef RW 3rd, Morrison JC (1994) Guidelines for management of shoulder dystocia. J Perinatol

14:435–441

O’Leary J (1993) Cephalic replacement for shoulder dystocia: present status and future role of the

Zavanelli manoeuvre. Obstet Gynecol 82:847–855

Poggi SH, Spong CY, Allen RH (2003) Prioritizing posterior arm delivery during severe shoulder

dystocia. Obstet Gynecol 101:1068–1072

Rouse DJ, Owen J (1999) Prophylactic caesarean delivery for fetal macrosomia diagnosed by

means of ultrasonography – a Faustian bargain? Am J Obstet Gynecol 181:332–338

Royal College of Obstetricians and Gynaecologists (2012) Shoulder dystocia (green-top guideline

no. 42). RCOG Press, London

Sandmire HF, DeMott RK (2003) Erb’s palsy causation: a historical perspective. Birth 29:52–54

Sokol RJ, Blackwell SC (2003) American College of Obstetricians and Gynecologists. Shoulder

dystocia (guideline no. 40). Int J Gynaecol Obstet 80:87–92

Verkuly DAA (2001) Symphysiotomies are an important option in the developed world. BMJ

323:809

World Health Organisation, Department of Reproductive Health and Research (2007) Shoulder

dystocia (stuck shoulders). In: Managing complications in pregnancy and childbirth: guidelines

for Midwives and for Doctors. WHO Press, Geneva, pp S83–S85

Wykes CB, Johnston TA, Paterson-Brown S, Johanson RB (2003) Symphysiotomy: a lifesaving

procedure. BJOG 110:219–221

3 Shoulder Dystocia

D. Ayres-de-Campos, Obstetric Emergencies,

DOI 10.1007/978-3-319-41656-4_4

4 Retention of the After-Coming Head

4.1 Definition, Incidence and Main Risk Factors

Retention of the after-coming head refers to the rare situation in which there is diffi culty in extracting the fetal head during vaginal breech delivery (Fig. 4.1 ). The

incidence of breech presentation in labour varies according to gestational age, from

about 23 % at 28 weeks to 3–4 % at term. The latter incidence depends also on local

practices for the promotion of external cephalic version. The number of vaginal

breech deliveries complicated by retention of the after-coming head is largely

dependent on local policies of case selection for elective caesarean section. Footling

or knee presentations, fetuses with estimated birth weights above 3800 g or below

1500 g and those with extended heads are common indications for caesarean section, but criteria may vary between centres. Some studies report retention of the

after-coming head to occur in as much as 10 % of vaginal breeches, but the criteria

used for the diagnosis are questionable.

Fig. 4.1 Retention of the

after-coming head

Moulding of the fetal head to the birth canal is frequent during the course of

labour in cephalic presentations, but there is little time for this to occur in breeches.

In preterm fetuses head-to-pelvis ratios are higher, and this may allow the fetal pelvis to pass through an incompletely dilated cervix, while the head is later retained.

The risk factors for retention of the after-coming head are displayed in Table 4.1

and are mainly related to fetal head dimensions, fl exion of the fetal neck and dimensions of the maternal pelvis. An extended fetal neck predisposes to retention because

it increases the anteroposterior diameter of the head.

Currently, these risk factors are used mainly to select cases where elective caesarean section is proposed as the preferential mode of delivery, but in some centres

this is proposed to all women with breech presentations at term or in labour.

Independently of these practices, healthcare professionals need to maintain competence in management of retention of the after-coming head, because they may

always encounter it unexpectedly, particularly when women present in advanced

labour with the breech already delivering.

4.2 Consequences

The main complication of fetal head retention is acute hypoxia / acidosis , due to

umbilical cord compression between the fetal head and the surrounding maternal

tissues, while the airway is still not in contact with air. Additional complications

may arise from iatrogenic trauma caused by attempts to resolve the situation.

Perinatal mortality in some series reaches 4–8 % and is mainly due to hypoxia/

acidosis and intracranial haemorrhage, but it is also related to the increased risk of

malformations associated with breech presentation at term. Perinatal morbidity

includes hypoxic-ischaemic encephalopathy; dislocation or fracture of cervical vertebrae; stretching/lacerations of the brachial-cephalic plexus and cervical muscles;

dislocation of the lower jaw; fracture of the femur, humerus and clavicle; rupture of

abdominal organs (spleen, liver, kidney, suprarenal glands); external genital lesions;

meconium aspiration syndrome; infection; and neonatal sepsis.

Little is known about how long head retention may last before perinatal death

or long-term injury occur. The situation providing the closest parallel for comparison is shoulder dystocia with coexisting nuchal cords (Chap. 3). Although

there are no absolute certainties, less than 5 min of sustained cord compression

Table 4.1 Risk factors for

retention of the after-coming

head

Fetal macrosomia or macrocephaly

Extended fetal neck

Reduced maternal pelvic diameters

Prolonged second stage of labour

Incompletely dilated cervix at the time of delivery

Rapid descent of the fetus in preterm delivery

4 Retention of the After-Coming Head

is unlikely to put the fetus at risk, while a 5–9 min interval appears to be associated with mild short-term neurological dysfunction and full recovery, and more

than 12 min causes substantial risk of permanent damage. These timings require

adaptation when fetal oxygenation is previously compromised and when there is

fetal growth restriction. Because of sustained cord occlusion, umbilical blood

gas values may not refl ect the severity of hypoxia/acidosis, and the occurrence of

hypoxic-ischaemic encephalopathy will be the best predictor of long-term

outcome.

Maternal morbidity arises mainly from the manoeuvres used for fetal extraction and includes vaginal lacerations, urethral and bladder injuries, vesical-vaginal

and recto-vaginal fi stulae, endometritis, postpartum sepsis, uterine rupture and postpartum haemorrhage.

4.3 Diagnosis

Retention of the after-coming head is established after there have been two or three

unsuccessful attempts to extract the fetal head in a vaginal breech delivery. The

most commonly used methods for this extraction are the Mauriceau-Smellie-Veit

and the Bracht manoeuvres (see below).

4.4 Clinical Management

4.4.1 Guaranteeing the Conditions for a Safe Vaginal

Breech Delivery

When important risk factors for retention of the after-coming head exist (Table 4.1 ),

caesarean section should be proposed at all stages of labour before delivery of the

shoulders. In the remaining situations, it is important to guarantee the conditions for

a safe vaginal breech delivery. In high-resource countries, this usually means continuous cardiotocographic monitoring (internal or external), emptying the bladder before delivery and assembling the necessary material for resolving the

possible complications of vaginal breech delivery. It is useful to have a large swab

on hand, to hold the fetal body when it is too slippery and to also hold the extremities and umbilical cord when applying the Piper forceps (see below). A vaginal

retractor and an appropriate forceps (Piper forceps or similar) should also be kept

on hand, in case they are needed.

If time allows and the mother requests this, epidural analgesia should be put in

place. Venous catheterisation is routinely used in many centres, to anticipate the

situations in which uterine relaxation or emergency caesarean section is required.

For delivery, the largest reported experience is with the mother in lithotomy position

and the lower part of the bed removed. The hands and knees position is used as an

4.4 Clinical Management

alternative in some centres, but more data is required to establish its safety in generalised settings. Routine episiotomy was recommended in the past for all cases of

vaginal breech delivery, but an increasing number of centres have moved away from

this practice.

4.4.2 Anticipate the Situation

The prodromal signs suggestive of impending head retention are a prolonged second

stage of labour, descent of the breech during contractions followed by an immediate

return to the previous station and rapid descent of a preterm fetus with still incomplete cervical dilatation. When these are identifi ed, steps should be taken to summon

an experienced healthcare team, in case retention of the after-coming head occurs.

4.4.3 Attempts to Deliver the Fetal Head

Release of the fetal head in vaginal breech deliveries is classically accomplished by

the Mauriceau-Smellie-Veit or Bracht manoeuvres, with no robust evidence of the

advantages of either.

For the Mauriceau - Smellie - Veit manoeuvre, one hand and forearm support the

ventral part of the fetal body, while the second and third fi ngers are placed on the

upper lip to depress the malar eminences and thus fl ex the neck. The second and

fourth fi ngers of the contralateral hand are placed on the dorsal aspect of the shoulders, one on each side of the neck, and the 3rd fi nger pushes the occiput bone forward to fl ex the fetal neck. After the fetal neck is fl exed, moderate downward

traction is applied on the shoulders until the occipital region is observed. With an

assistant applying continuous suprapubic pressure, the fetal body is then slowly

raised to rotate the neck gently around the pubic symphysis in the direction of the

maternal abdomen (Fig. 4.2 ).

Fig. 4.2 The MauriceauSmellie- Veit manoeuvre

4 Retention of the After-Coming Head

In the Bracht manoeuvre , the fetal breech and thighs are grasped with two

hands, fl exing the lower limbs, and the hands are slowly lifted upwards and around

the pubic symphysis to deliver the fetal head (Fig. 4.3 ). No traction should be

applied during this movement, but continuous suprapubic pressure by an assistant is

required. Some authors propose the use of this manoeuvre after the umbilicus is

delivered, to extract the fetal shoulders and head, while others propose it only for

head extraction.

Both of these manoeuvres require particular care with mobilisation of fetal articulations and with pressure applied to the fetal thorax and abdomen, in order to avoid

iatrogenic injury.

4.4.4 Clearly Verbalising the Diagnosis

It is important that all healthcare professionals present in the room are aware of the head

retention, so that they can act accordingly. Therefore, the diagnosis needs to be clearly

verbalised, without unnecessarily alarming the labouring woman and her companion.

4.4.5 Asking for Help

One of the fi rst measures should be to summon at least two midwives and a senior

obstetrician . In addition, a neonatologist and an anaesthetist should be called, the

fi rst one because neonatal resuscitation is likely to be needed and the second one

because uterine relaxation may be required (see below).

Fig. 4.3 The Bracht

manoeuvre

4.4 Clinical Management

4.4.6 McRobert’s Position

Similarly to what occurs in shoulder dystocia (see Chap. 3), the McRobert’s position straightens the lumbosacral angle and widens the anteroposterior diameter of

the maternal pelvis, facilitating extraction of the fetal head. An additional attempt at

head extraction with the Mauriceau-Smellie-Veit manoeuvre should be considered

after adopting this position.

4.4.7 Episiotomy

If it is felt that the maternal perineum poses resistance to extraction of the fetal head,

an episiotomy should be performed. This will also be useful for the application of

forceps to the after-coming head.

4.4.8 Fetal Monitoring

When internal fetal heart rate monitoring is in place, the signal should continue to

be acquired after the fetal body is released. With external fetal heart rate, the Doppler

sensor located on the maternal abdomen will no longer pick up heart movements,

but fetal monitoring can be continued by placing the Doppler sensor directly on the

fetal thorax. Evaluating umbilical cord pulsatility may fail to provide a reliable measure of fetal heart rate, because of sustained cord compression.

4.4.9 Insertion of a Vaginal Retractor

Some guidelines recommend the temporary insertion of a vaginal retractor to push

back the posterior vaginal wall and thus to allow oxygen to reach the fetal airways

(Fig. 4.4 ). There is little evidence on the effi cacy of this procedure, but it takes little

time and is unlikely to cause harm.

4.4.10 Forceps to the After-Coming Head

The Piper forceps was specifi cally designed for managing retention of the aftercoming head. However, when these forceps are unavailable, it is possible to use

other types of forceps, such as Simpson’s or Tarnier’s.

To apply the Piper forceps, an assistant holds the fetal body, extremities and

umbilical cord with two hands (or with a large swab) and raises these structures

slightly to create space for inserting the forceps below (Fig. 4.5 ). The blades of the

forceps are inserted one at a time, on each side of the head, guided by the contralateral hand. Once the blades are articulated, the fetal body is rested on the forceps, one

of the executor’s hands grabs the handle, and the contralateral hand is applied around

the fetal shoulders, using a similar grip to that of the Mauriceau-Smellie- Veit

4 Retention of the After-Coming Head

Fig. 4.4 Insertion of a

vaginal retractor

Fig. 4.5 Piper forceps

applied and the trajectory

of fetal head rotation

4.4 Clinical Management

manoeuvre. Moderate traction is then applied to the forceps, initially slightly downwards until the fetal occiput is visible, and then to slowly rotate the fetal head around

the pubic symphysis while at the same time an assistant applies continuous suprapubic pressure to fl ex and descend it. If a vaginal retractor is in place, this needs to be

removed before applying traction on the forceps.

After extraction of the fetal head, the birth canal should be carefully inspected with a

speculum or with vaginal retractors for lacerations of the cervix, vagina, urethra, rectovaginal septum, perineum and anal sphincter, which may require surgical correction.

4.4.11 Exceptional Manoeuvres

When the manoeuvres described above fail to deliver the after-coming head, exceptional manoeuvres need to be considered:

Lateral cervical incisions (Duhrssen incisions) – When retention of the fetal head

is judged to be caused by incomplete cervical dilatation, as occurs in preterm

deliveries, the cervical diameter can be increased by making two or three small

incisions on the cervix. Sterilised rounded scissors are used to perform 1–2 cm

cervical incisions at 2 and 10 o’clock and if necessary a third incision at 6

o’clock. These require surgical correction after the placenta is extracted.

Zavanelli ’ s manoeuvre (replacement of the fetal shoulders in the maternal pelvis and

vacuum-assisted caesarean delivery) – This manoeuvre should be performed in the

operating theatre under general anaesthesia with halogenated agents. The shoulders are reintroduced one at a time into the vagina, and immediate caesarean section follows. A vacuum extractor is applied to the fetal head to release the remaining

body while an assistant pushes the fetal pelvis up to help reinsert it into the vagina.

Symphysiotomy – This technique is described in detail in Chap. 3, and its use has

been reported in a small number of cases of head retention. However, care must be

taken, as it associated with important maternal morbidity in inexperienced hands.

Occasionally, it remains impossible to extract the fetal head in a timely fashion,

despite all these efforts, and an adverse fetal outcome needs to be considered. Absence

of heart sounds when the Doppler sensor is placed directly on the fetal thorax will

confi rm the diagnosis. The situation still requires resolution, but in these cases, the

manoeuvres described above can be reattempted without the previous time pressure.

4.5 Clinical Records and Litigation Issues

The risk of adverse fetal outcome raises the possibility of litigation and the need for

careful clinical records. It is important to document the time at which the fetal

shoulders and fetal head were delivered, who were the healthcare professionals

summoned, when they were called and when they arrived, and which manoeuvres

were performed, when and by whom.

Umbilical blood gas values and Apgar scores should also be documented (see Chap.

2). Because of continued cord compression, pH values may not refl ect the severity of

4 Retention of the After-Coming Head

fetal hypoxia/acidosis, so hypoxic-ischaemic encephalopathy will establish the best

long-term prognosis in these cases. Strict adherence to guidelines, together with careful

recording of events is required to avoid an adverse legal resolution.

4.5 Clinical Records and Litigation Issues

Suggested Reading

Collea JV (1981) The intrapartum management of breech presentation. Clin Perinatol 8:173

Gimovsky ML, Petrie RJ (1989) The intrapartum management of breech presentation. Clin

Perinatol 16:975

Hannah ME, Hannah WJ, Hewson SA, Hodnett ED, Saigal S, Willan AR, for the Term Breech

Trial Collaborative Group (2000) Planned caesarean section versus planned vaginal birth for

breech presentation at term: a randomised multicentre trial. Lancet 356:1375–1383

Hickok DE, Gordon DC, Milberg JA et al (1992) The frequency of breech presentation by gestational age at birth: a large population-based study. Am J Obstet Gynecol 166:851

Mukhopadhyay S, Arulkumaran S (2002) Breech delivery. Best Pract Res Clin Obstet Gynaecol

16:31–42

Myers SA, Gleicher N (1987) Breech delivery: why the dilemma? Am J Obstet Gynaecol

156:6–10

Royal College of Obstetricians and Gynaecologists (2006) Practice guideline no. 20b. The management of breech presentation. RCOG Press, London

Society of Obstetricians and Gynecologists of Canada (2009) Practice guideline no 226. Vaginal

delivery of breech presentation. J Obstet Gynaecol Can 31(6):557–566

Westrgren M, Grundsell H, Ingemarson I et al (1981) Hyperextension of the fetal head in breech

presentation: a study with long-term follow-up. Br J Obstet Gynaecol 88:101

4 Retention of the After-Coming Head

Part II

Predominantly Maternal Emergencies

D. Ayres-de-Campos, Obstetric Emergencies,

DOI 10.1007/978-3-319-41656-4_5

5 Eclampsia

5.1 Definition, Incidence and Main Risk Factors

Hypertensive diseases of pregnancy remain a leading cause of maternal and perinatal mortality in both low- and high-resource countries, and eclampsia represents

their most serious manifestation. Eclampsia is characterised by the occurrence of

generalised tonic-clonic seizures (grand mal) in a woman who usually displays the

typical symptoms, signs and laboratory fi ndings of pre-eclampsia. The pathophysiologic mechanism behind eclamptic seizures remains incompletely understood, but

endothelial lesion, exaggerated microvascular permeability, cerebral oedema and

pericapillary haemorrhage are common fi ndings.

The episode usually starts with a slight tremor of the facial muscles, shortly followed by a generalised tonic seizure of 15–20 s and then develops into generalised

tonic-clonic seizures which may last over 1 min. The total duration of the episode

rarely exceeds 90 s. Occasionally, seizures may recur rapidly with uninterrupted

generalised contracture. No respiratory movements occur during tonic-clonic seizures, and this can have serious consequences on maternal and fetal oxygenation.

When the episode terminates, there is a deep and noisy inspiration followed by a

comatose state that is usually superfi cial and of variable duration, with slow recovery of consciousness. Subsequent agitation may develop, and the woman usually

refers amnesia to the event. Transient cortical blindness and focal motor defi cits

may follow. Cerebral haemorrhage complicates 1–2 % of cases.

Eclampsia may occur during pregnancy (40–50 %), in labour (13–20 %) or in the

postpartum period (28–40 %). With the implementation of policies for screening

and early diagnosis of pre-eclampsia, as well as the prevention of seizures and

prompt termination of pregnancy in cases of severe pre-eclampsia, the incidence of

eclampsia has decreased dramatically over the last decades. In high-resource countries, pre-eclampsia is currently reported to occur in 2–8 % of pregnancies and

eclampsia to complicate 0.2–0.3 % of these cases, for an overall incidence of 0.004–

0.02 % of births. In many low- and medium-resource countries, the reported incidences of pre-eclampsia and eclampsia are much higher.

The main risk factors for eclampsia are similar to those of pre-eclampsia and are

listed in Table 5.1 .

5.2 Complications

In high-resource countries, maternal mortality occurs in about 0.07 % of eclampsia cases, and the main causes are intracranial haemorrhage, acute pulmonary

oedema and multi-organ failure. Maternal morbidity includes acute pulmonary

oedema, disseminated intravascular coagulation, renal insuffi ciency and more rarely

intracranial haemorrhage and rupture of subcapsular hepatic haematoma. Prolonged

stay in intensive care units is frequently required in these cases.

Iatrogenic prematurity is frequent in severe pre-eclampsia and eclampsia and is

responsible for the majority of perinatal deaths , which complicate about 26 % of

eclampsia cases.

5.3 Diagnosis

Eclampsia is diagnosed when generalised tonic-clonic seizures are observed in a

pregnant woman or a recent mother who usually displays the typical symptoms,

signs and laboratory fi ndings associated with pre-eclampsia.

The other major cause of generalised tonic-clonic seizures is epilepsy, and this

can usually be identifi ed by a history of previous episodes provided by a family

member and/or a review of the patient’s medication. When no other obvious cause

exists, the episode should be treated as eclampsia, and other diagnoses can be later

investigated, if there is inadequate response to treatment.

5.4 Clinical Management

5.4.1 Anticipate and Prevent the Situation

In patients with pre-eclampsia, the prodromal symptoms of severe frontal headache, continuous epigastric pain and visual complaints (blind spots, fl ashes, double

vision and blurred vision) should alert to impending eclampsia. In patients with

Table 5.1 Risk factors for

pre-eclampsia and eclampsia Primigravid

Extremes of reproductive age

Family history of pre-eclampsia

Gestational or pre-existing diabetes

Chronic hypertension or renal disease

Multiple pregnancy

Gestational trophoblastic disease

Hereditary or acquired thrombophilia

5 Eclampsia

severe pre - eclampsia (papilloedema, hyperrefl exia, platelets under 100 × 10 9

/l,

liver enzymes above 75 IU/l, oliguria, pulmonary oedema, nausea and vomiting),

those with severe hypertension in the context of pre - eclampsia (blood pressure

exceeding 160/110 mmHg) and those with prodromal symptoms, intravenous

magnesium sulphate (see below) should be started to prevent seizures. Frequent

re-evaluation of prodromal symptoms, blood pressure, laboratory results, together

with seizure prevention with magnesium sulphate and termination of pregnancy if

the situation deteriorates; these are the key elements for preventing eclampsia.

5.4.2 Ask for Help

The person(s) witnessing an eclamptic seizure should trigger a communication

chain that results in the urgent summoning of at least two midwives , a senior

obstetrician , and an anaesthetist . The anaesthetist will usually focus on maternal

monitoring and maintenance of the airway, while the obstetrician will concentrate

on starting magnesium sulphate and fetal monitoring. When the two specialities are

not present, the person in charge needs to take all of these aspects into account.

5.4.3 Avoid Lesions During the Eclamptic Seizure

Restraining tonic-clonic movements is dangerous and confers no benefi t to patients,

so the recommended attitude during the seizure is to remove all objects that may

cause injury and wait until it ends, which usually takes less than 90 s.

5.4.4 Left Lateral Safety Position, Inspect Airway and Monitor

When the seizure ends, the patient should be placed in left lateral safety position

(Fig. 5.1 ) and the airway quickly inspected for patency . In a second step, oropharyngeal secretions may be aspirated if they are abundant, a Mayo tube inserted if the

patient remains unconscious and breathing is made diffi cult by the tongue and oxygen by mask should be started at 8 l/min.

Fig. 5.1 Left lateral safety position

5.4 Clinical Management

Maternal heart rate and oxygen saturation should be monitored continuously and blood pressure evaluated every 5 min. Maternal ventilation also

requires frequent re-evaluation. If the woman is still pregnant, continuous cardiotocography should be put in place to evaluate fetal oxygenation. Eclamptic

seizures usually condition a transitory fetal hypoxaemia and a short-lasting

deceleration. However, severe pre-eclampsia may also be associated with chronic

placental insuffi ciency and abruption, conditioning more serious fetal heart rate

changes.

5.4.5 Prevention of New Seizures

During or shortly after an eclamptic seizure, it is important for one of the team

members to gather all the necessary materials for vein catheterisation and magnesium sulphate infusion. In some centres, there are pre-prepared “ eclampsia boxes ”

containing these materials, and they can be rapidly fetched. However, regular maintenance of these boxes needs to be assured.

After the seizure has stopped, vein catheterisation should be rapidly performed

and the loading dose of magnesium sulphate started to avoid recurrences

(Table 5.2 ).

5.4.6 Other Non-emergent Measures

After the acute response to eclampsia described above, the situation still requires

continuous monitoring and further management. Blood should be drawn for haemoglobin , platelet count , liver and renal function and coagulation studies.

Bladder catheterisation should be performed to measure urine output , important

for fl uid balance and for optimising magnesium sulphate treatment.

5.4.7 Decreasing Blood Pressure

When maternal blood pressure rises above 160 / 105 mmHg, it becomes necessary to

reduce it, because of increased risks of cerebral haemorrhage, cardiac insuffi ciency,

myocardial infarction and placental abruption.

Table 5.2 Magnesium sulphate for the prevention of eclampsia and recurrent seizures

Loading dose Maintenance dose

4 g magnesium sulphate IV over 5–20 min

2 vials of 10 ml magnesium sulphate at 20 %

(2 g/10 ml) in 100 ml saline at 300–1200 ml/h

1–3 g magnesium sulphate IV per hour

8 vials of 10 ml magnesium sulphate at 50 %

(5 g/10 ml) in 1000 ml saline at 25–75 ml/h

5 Eclampsia

Labetalol is a quick-acting alpha- and beta-adrenergic antagonist, with little

effect on brain and uterine perfusion. It can be given orally in a 200 mg tablet,

which will usually result in a blood pressure fall within 30 min. The tablet can be

repeated after 60 min, if needed. Fixed doses are then started, varying from 200 mg

every 12 h to a maximum of 400 mg every 6 h. If there is no response to oral labetalol therapy or if the patient does not tolerate it, continuous intravenous infusion

can be started by diluting one 100 mg/20 ml vial in 100 ml of saline (1 ml = 0.83 mg)

and starting infusion at 50 ml/h, after which it is adjusted according to the blood

pressure, to values between 24 and 192 ml/h. For hypertensive crises, an intravenous labetalol bolus of 20 mg can be given over the course of 1 min, implying the

injection of 4 ml of a 100 mg/20 ml vial. The dose can be repeated every 10 min

until a maximum dose of 200 mg is reached (10 boluses). This medication should

be avoided in asthmatic women, and maternal heart rate should be maintained

above 60 bpm.

Nifedipine is a relatively rapidly acting calcium channel blocker that can be

administered orally in 10 or 20 mg tablets, given every 4–6 h. The sublingual route

should be avoided, as it is associated with marked maternal hypotension and

decreased placental perfusion. The classical contraindication to associate nifedipine

with magnesium sulphate, because of the risk of hypotension and pulmonary

oedema, has not been confi rmed in several recent case series.

Hydralazine is a peripheral vasodilator that can be given intravenously in a

5 mg bolus over the course of 5 min. This implies injecting 0.25 ml of a 1 ml vial

(20 mg/1 ml). The dose can be repeated every 20 min, for a maximum daily dose

of 20 mg. Alternatively, a continuous intravenous infusion can be started at 0.5–

10 mg/h. This is accomplished by diluting one 1 ml vial (20 mg/1 ml) in 100 ml of

saline (1 ml = 0.2 mg) and infusing it at 2.5–50 ml/h, to a maximum daily dose of

20 mg. Tachycardia, headache, nausea and sweating are common side effects.

Preloading or co-administration of 500 ml of intravenous crystalloid fl uid reduces

the risk of severe hypotension seen with intravenous hydralazine and should be

considered if delivery has not yet occurred.

During antihypertensive treatment, blood pressure should initially be monitored

every 5 min, and the interval is then spaced according to treatment results. The goal

is to maintain systolic blood pressure between 140 and 150 mmHg and diastolic

blood pressure between 80 and 100 mmHg. Lower diastolic blood pressures may

put cerebral and uterine perfusion at risk.

5.4.8 Recurrent Seizures

When recurrent seizures occur after magnesium sulphate infusion is initiated, an

intravenous bolus of 2–4 g of magnesium sulphate can be given over the course of

5 min. If seizures persist, the diagnosis of eclampsia should be reconsidered and a

re-evaluation carried out with the help of a neurologist. Intravenous diazepam is less

5.4 Clinical Management

effi cient than magnesium sulphate for preventing recurrent seizures and reducing

maternal mortality, but is a possible alternative, given in a 5 mg bolus over the

course of 5 min and repeated if necessary to a maximum of 20 mg. Prolonged use

of diazepam should be avoided, as it is associated with an increased risk of maternal

death and neonatal respiratory depression. If seizures persist, intubation and ventilation remain as a last resource, in an intensive care unit setting.

5.4.9 Maintenance Dose of Magnesium Sulphate

The maintenance dose of magnesium sulphate should be started as soon as the loading dose has fi nished, and the infusion is maintained at least until 24 h after birth or

after the last seizure, whichever occurs latest (Table 5.2 ).

Magnesium sulphate is a drug with a low safety margin and is capable of conditioning serious side effects, such as muscular paralysis, central nervous system

depression and cardiac arrest. It is predominantly excreted by the kidneys, so oliguria has a major impact on plasma concentrations. Treatment with magnesium sulphate requires frequent monitoring of urine output, respiratory frequency and the

patellar refl ex, evaluations that should be performed at least every 4 h. If urine output drops below 30 ml/h, patellar refl exes become week and/or respiratory frequency is under 16 cycles/min, serum magnesium levels should be evaluated, and

the measures described in Table 5.3 should be undertaken. In many centres, serum

magnesium levels are also routinely measured at 2, 6 and 12 h after the start of

treatment.

About 25 % of women report side effects with intravenous magnesium sulphate,

the most common of which is fl ushing.

Table 5.3 Serum magnesium, expected clinical fi ndings, interpretation and management

Magnesium (mg/l) Clinical fi ndings Interpretation and management

1.5–2.5 None Subtherapeutic levels

4–8 None Therapeutic levels

9–12 Loss of patellar refl ex,

sedation, nausea, diplopia,

respiration <12 cycles/min,

O 2 sat <95 %

Stop infusion, give oxygen and quantify

serum magnesium. Re-evaluate every

15 min. If no improvement – calcium

gluconate 1 g (1 g/10 ml) IV over

10 min. After recovery, restart infusion

at half dose

15–17 Muscle paralysis, respiratory

arrest, prolonged QRS

Calcium gluconate 1 g (1 g/10 ml) IV

over 10 min, intubation, intensive care

30–35 Cardiac arrest Cardiac massage, intubation and

ventilation, calcium gluconate 1 g

(1 g/10 ml) IV over 10 min, intensive

care

5 Eclampsia

5.4.10 Fluid Balance

The increased vascular permeability found in women with pre-eclampsia increases

the risk of acute pulmonary oedema, cardiac insuffi ciency and cerebral oedema. For

these reasons, total fl uid volume should not exceed 83 ml / h (2 l in 24 h) except if

there are other sources of fl uid loss, such as haemorrhage. Colloids should not be

administered except in life-saving situations. Oliguria does not usually require

additional measures beyond fl uid adjustments to the established limits, as it will

revert spontaneously 36–48 h after delivery.

5.4.11 Thromboprophylaxis

Women with severe pre-eclampsia and eclampsia are at increased risk of venous

thrombosis, so compression stockings and prophylactic doses of low molecular

weight heparin need to be considered according to local protocols, until the patient

is fully mobile.

5.4.12 Evaluation of Laboratory Results and Fetal Evaluation

The urgency of pregnancy termination and the method of delivery depend on the

clinical stability of the situation; on laboratory results depicting the severity of preeclampsia, particularly the degree of thrombocytopenia and liver enzymes; and on

the fetal condition. Pre-eclampsia may be associated with chronic placental insuffi ciency, so fetal ultrasound is required to evaluate fetal growth, amniotic fl uid volume and umbilical and cerebral blood fl ow.

5.4.13 Programming Birth

Pregnancy termination and placental extraction constitute the only known cure for

pre-eclampsia. Recurrence of seizures after the initial eclampsia event poses unacceptable health risks to the mother, so delivery needs to be programmed as soon as

blood pressure is stabilised and laboratory results are evaluated, independently of

gestational age or of fetal prognosis. If prodromal signs have disappeared, blood

pressure has been controlled, only mild changes are present in laboratory results and

conditions to induce labour are favourable, this should be attempted with the aim

of achieving delivery within 8 – 12 h . Both oxytocin and prostaglandins may be

used in conjunction with magnesium sulphate, but care must be taken not to exceed

the recommended hourly fl uid replacement volume. Continuous maternal monitoring and cardiotocography should be maintained throughout the full course of labour.

5.4 Clinical Management

Epidural analgesia may be used for pain relief if the platelet count is above 80 ×

10 9

/l. A slight decrease in blood pressure should be expected in these situations, but

fl uid preload is not recommended. Before 32 weeks, the Bishop score is seldom

favourable, and the success rate of induction is low. When cervical characteristics

are adverse and delivery is not expected to occur within 8–12 h or if there are other

obstetric contraindications to vaginal delivery, the benefi ts of elective caesarean

section should be explained to the patient and family. Both regional and general

anaesthesia may be used for surgery, and the patient’s platelet count needs to be

taken into consideration.

When eclampsia occurs between 24 and 34 weeks of gestation, a course of corticosteroids should be administered as soon as possible. The neonatologist should

be contacted in anticipation of an iatrogenic preterm delivery. Waiting for the full

course of corticosteroids is usually not recommended, but there are reported benefi ts from partial courses. Magnesium sulphate may cause hypotension, hypotonia,

respiratory depression and reduced suction refl ex in newborns, so the neonatologist

needs to be informed of this medication.

After delivery, it is prudent to transfer the woman to an intensive care unit until

the haemodynamic, neurological and laboratory situation are stabilised.

5.5 Clinical Records and Litigation Issues

Eclampsia may be associated with adverse maternal and perinatal outcomes,

so it is important to document the names of the healthcare professionals who

were called, when this occurred and when they arrived, as well as who was

involved in the decisions, when they were taken and who performed which

procedures.

A frank explanation of the situation to the patient and to her family is important to avoid much of the suspicion, disinformation and misunderstanding that

lead to litigation. When the latter occurs, strict adherence to existing guidelines

and careful recording of events are important to guarantee a favourable legal

outcome.

5 Eclampsia

Suggested Reading

Duley L, Gülmezoglu AM, Henderson-Smart DJ, Chou D (2010) Magnesium sulphate and other

anticonvulsants for women with pre-eclampsia. Cochrane Database Syst Rev (11):CD000025

Duley L, Meher S, Jones L (2013) Drugs for treatment of very high blood pressure during pregnancy. Cochrane Database Syst Rev (3):CD001449

National Institute for Health and Clinical Excellence (2011) Hypertension in pregnancy – the management of hypertensive disorders during pregnancy. RCOG Press, London

Tuffnell D (2003) Pre-eclampsia and eclampsia. In: Johanson R, Cox C, Grady K, Howell C (eds)

Managing obstetric emergencies and trauma: the MOET course manual. RCOG Press, London,

pp 151–70

Suggested Reading

D. Ayres-de-Campos, Obstetric Emergencies,

DOI 10.1007/978-3-319-41656-4_6

6 Postpartum Haemorrhage

6.1 Definition, Incidence and Main Risk Factors

Postpartum haemorrhage occurs more frequently in the fi rst 2 h after delivery and is

classifi ed as early or primary postpartum haemorrhage (i.e. occurring in the fi rst

24 h after birth). Late or secondary postpartum haemorrhage (appearing after the

fi rst 24 h) is outside the aim of this chapter.

There is no worldwide agreement on the defi nitions of postpartum haemorrhage and major postpartum haemorrhage. Some defi ne postpartum haemorrhage as blood loss exceeding 500 ml and major postpartum haemorrhage as

blood loss exceeding 1000 ml. Others defi ne postpartum haemorrhage as blood

loss exceeding 500 ml in vaginal deliveries and exceeding 1000 ml at caesarean

section. The limitation of all these defi nitions is the diffi culty in quantifying blood

loss accurately, particularly in vaginal deliveries. Collector bags can be used for

this purpose, but blood frequently falls outside; amniotic fl uid and urine may be

collected and both will affect quantifi cation. Weighing of swabs is routinely performed in some centres, but the practice is time-consuming and not widely disseminated, and similar inaccuracies to those referred for collector bags may occur.

The most widely used alternative is visual estimation of blood loss, but this has

well-known limitations, although improved accuracy may be achieved with visual

aids, where the appearance of different blood quantity losses is depicted on photographs/drawings (Fig. 6.1 ). An additional problem arises from the fact that

small women and those with pre-existing anaemia may decompensate with lesser

quantities of blood loss.

Another defi nition of postpartum haemorrhage is a reduction in the haematocrit

exceeding 10 %, but routine blood analysis before and after birth is rarely practised

in low-risk labours, where the majority of complications occur. The need for blood

transfusion is an alternative criterion, but it is used mainly in research settings, it

leaves out less severe cases of haemorrhage, and transfusion criteria may vary

between centres.

From a clinical point of view, the most important factor to defi ne postpartum

haemorrhage is the one that should trigger a response from the healthcare team.

In the majority of situations, this occurs because profuse and / or persistent genital bleeding is witnessed to occur spontaneously after birth or when uterine massage is performed. Bleeding may be mild and rapidly reversible, so it is important

to separate the concept of major postpartum haemorrhage , where more complex interventions need to be considered. Blood loss exceeding 1000 ml or a

heart rate approaching the systolic blood pressure is probably the most useful

criteria, from a clinical point of view. The “shock index”, defi ned as the heart rate

divided by systolic blood pressure, is used in other areas of Medicine and has

recently been applied to postpartum haemorrhage. It is considered abnormal when

exceeding 0.9.

The three major causes of early postpartum haemorrhage are uterine atony ,

which is responsible for about 70–80 % of cases, genital tract lesions accounting

for 10–15 % of cases and retained placental tissue . Partial placental retention is

usually associated with recurring uterine atony and haemorrhage. Abnormally

adherent placenta (accreta, increta and percreta) is normally associated with

haemorrhage when attempts are made to remove the placenta, and its incidence

has been increasing in some parts of the world because of escalating caesarean

section rates. Rarer causes of postpartum haemorrhage are uterine inversion ,

Fig. 6.1 Quantifi cation of blood loss based on drawings

6 Postpartum Haemorrhage

uterine rupture and maternal bleeding disorders . Uterine inversion is thought

to be caused mainly by mismanagement of the third stage of labour, namely by

excessive pressure on the uterine fundus, premature traction on the umbilical cord

or excess traction during manual removal of an abnormally adherent placenta.

Less frequently it occurs after an episode of coughing or vomiting during the third

stage of labour.

The incidence of early postpartum haemorrhage varies widely, depending on the

criteria used for the diagnosis, the population studied and the methods used for

prevention, but it is reported to occur in 2–10 % of all deliveries. The most important

risk factors are listed in Table 6.1 , but many cases occur in women where these are

not present.

6.2 Consequences

Postpartum haemorrhage remains an important cause of maternal mortality , in

both low- and high-resource countries. In European countries, maternal deaths due

to postpartum haemorrhage occur in about 0.003 % of all births, and this incidence

has not changed signifi cantly over the last 30 years.

Less is known about maternal morbidity associated with postpartum haemorrhage, but most of it is related to the side effects of treatment. Some surgical procedures are associated with loss of fertility (conservative treatments and hysterectomy),

infectious morbidity, urologic lesion and intensive care unit stay. Other complications are associated with allergic reactions to medication, colloids and blood

replacement products. Birth canal lacerations may also occur as a consequence of

mechanical treatments, but these seldom have long-term consequences. Decreased

perfusion of the pituitary gland for prolonged periods of time has been associated

with secondary panhypopituitarism (Sheehan’s syndrome), but this complication is

currently very rare in high-resource countries.

Table 6.1 Risk factors for

postpartum haemorrhage High parity

High uterine volume – multiple pregnancy, macrosomia,

polyhydramnios

Caesarean delivery and instrumental vaginal delivery

Prolonged or precipitate labour

Labour induction and acceleration

Placental abruption

Uterine leiomyomas and malformations

Maternal bleeding disorders

Corioamnionitis

Placenta praevia and abnormally adherent placenta

Pre-eclampsia

Amniotic fl uid embolism

Previous postpartum haemorrhage

6.2 Consequences

6.3 Diagnosis

Postpartum haemorrhage can be defi ned as profuse and / or persistent genital

bleeding occurring spontaneously after birth or when uterine massage is performed.

The diagnosis may be triggered by routine clinical re-evaluation, maternal complaints of dizziness and loss of vision, maternal paleness or by the detection of

tachycardia or hypotension. The main clinical usefulness of this defi nition is that it

constitutes a trigger for action from the healthcare team.

The diagnosis of major postpartum haemorrhage implies the same fi ndings,

but in addition blood loss exceeds 1000 ml (by quantifi cation or visual estimation)

or maternal heart rate approaches systolic blood pressure (the shock index

exceeds 0.9).

6.4 Clinical Management

Management of postpartum haemorrhage involves two major components – support

of maternal circulation/oxygenation and treatment of the underlying cause. When

an anaesthetist and an obstetrician are present in the room, the responsibility for

these two aspects is usually divided among them. In the remaining situations, the

person in charge needs to take care of both.

6.4.1 Anticipating the Situation

When the risk factors listed in Table 6.1 are identifi ed, increased surveillance usually allows earlier diagnosis and intervention. Continuous monitoring of maternal

pulse and blood pressure should be considered in the fi rst stages of any abnormal

genital bleeding, in addition to frequent re-evaluation of haemorrhage and uterine

contracture.

6.4.2 Clearly Verbalising the Diagnosis

It is important that the whole team of healthcare professionals is aware of the diagnosis of postpartum haemorrhage, so that they can act accordingly, and therefore

this needs to be clearly verbalised, without unnecessarily alarming the labouring

woman and her companion.

6.4.3 Asking for Help

One of the fi rst measures should be to summon urgently at least two midwives , a

senior obstetrician and an anaesthetist . As stated above, the presence of an anaesthetist guarantees a safer management of basic circulatory and respiratory

6 Postpartum Haemorrhage

functions, as well as fl uid balance. Care is however needed to maintain good communication between both sides at all times, so that there is coordinated management

of the situation.

6.4.4 Initial Evaluation of the Cause of Haemorrhage

A quick evaluation needs to be carried out to establish the most likely cause of

haemorrhage. This involves assessment of uterine contracture to diagnose uterine

atony, a speculum evaluation to detect lacerations of the birth canal and a reevaluation of the placenta to establish whether it is complete (no missing cotyledons

on the maternal side, no lacerated vessels on the placental margin on the fetal side).

Abnormally adherent placenta is usually diagnosed when placental extraction fails,

and uterine inversion is diagnosed by bimanual examination. The rarer causes of

uterine rupture and maternal bleeding disorders are usually considered only after

the initial measures for treatment of postpartum haemorrhage have failed.

6.4.5 Support of Maternal Circulation and Oxygenation

6.4.5.1 Venous Catheterisation and Blood Volume Replacement

One of the fi rst measures should be to guarantee adequate access for fl uid perfusion,

by catheterising a vein with a large bore catheter (14G or 16G). If major postpartum haemorrhage is identifi ed, a second vein should be catheterised and at the same

time blood collected for full blood count, coagulation studies and cross-matching.

Fluid replacement with crystalloids (saline, Ringer’s lactate) at high perfusion

speeds should follow, avoiding dextrose solutions as they may worsen acidosis.

About three litres of crystalloids are required to replace one litre of blood loss,

because of loss to the extravascular space. In previously healthy women, a 1.5 l blood

loss can usually be compensated just with the use of crystalloids. With further loss,

replacement with colloids and blood products needs to be considered (see below).

6.4.5.2 Maternal Monitoring

Continuous monitoring of maternal heart rate and oxygen saturation should be

started promptly and blood pressure measured every 5–10 min. Consideration

should also be given to electrocardiographic monitoring , particularly with major

postpartum haemorrhage or when there is loss of consciousness.

6.4.5.3 Bladder Catheterisation and Measurement of Urinary Output

Bladder catheterisation is needed to measure urinary output, which should be kept

above 30 ml/h, and to allow more effective external uterine massage (see below).

6.4.5.4 Maintain Maternal Oxygen Supply to the Brain

It is important to guarantee adequate oxygen supply to the brain, and for this the

woman should be placed in a slight head - down position or alternatively her legs

6.4 Clinical Management

raised to increase venous return. Oxygen should be administered by face mask,

starting at 30 %, 10–15 l/min, and thereafter adapting according to oxygen saturation levels.

6.4.5.5 Decision to Start Colloids

When blood loss exceeds 1.5 l or there is diffi culty in maintaining normal maternal blood pressure with crystalloids, administration of colloids needs to be considered. The latter includes albumin, dextran, gelatin and hydroxyethylamide.

These substances assure a higher intravascular volume and some improve oxygen

transport in the microcirculation, but they all carry a small risk of anaphylaxis.

The frequency of severe reactions (shock, cardiorespiratory arrest) is 0.003 % for

albumin, 0.008 % for dextran, 0.038 % for gelatin and 0.006 % for hydroxyethylamide. Colloid volumes exceeding 1000–1500 ml per day may also affect coagulation tests.

6.4.5.6 Decision to Administer Blood Products

Administration of blood products should be considered when haemorrhage persists

and is approaching 2000 ml. It is usually also considered when there is prolonged

haemodynamic instability or a low haemoglobin count. The main objective is to

recover oxygen transport capacity, but there are also haemodynamic and clotting

benefi ts. In a shared decision with the hospital blood bank, 2–4 units of packed red

blood cells may be transfused initially. All obstetric units must have access to blood

from universal donors (O negative blood) in less than 30 min, but usually there is

time for cross-matching and individualised transfusion. There is currently no consensus on the ideal balance between transfusion of packed red cells and fresh frozen

plasma, but it is prudent to administer at least one unit of fresh frozen plasma for

each 4 units of packed red cells, in order to prevent consumption coagulopathy.

Additional blood transfusions, including cryoprecipitate, platelets and recombinant

factor VIIa, are usually decided in coordination with the hospital blood bank, and

serial evaluations of haemoglobin and coagulation tests are required to guide

decisions.

6.4.5.7 Maintain Body Temperature

In hypovolemic shock, low body temperature will contribute to peripheral hypoperfusion and tissue damage. This can be reduced by maintaining normal body temperature and by administering previously warmed fl uids.

6.4.6 Treatment of Uterine Atony

6.4.6.1 Initial Measures

The fi nding of a non-contracted uterus after placental delivery should lead to immediate external uterine massage in order to stimulate contraction. Previous catheterisation of the bladder facilitates this procedure and also allows measurement of

urine output (see above).

6 Postpartum Haemorrhage

6.4.6.2 Medical Treatment

The options available for medical treatment of uterine atony are displayed in

Table 6.2 . Regardless of whether or not it has been previously used for the prevention of postpartum haemorrhage, oxytocin should be the fi rst-line treatment for

uterine atony. It is preferably administered intravenously in rapid infusion, but can

also be given by slow 10 IU intravenous bolus, although the latter has been associated with rare cases of severe maternal hypotension. If the intravenous route is not

available, successful treatment of uterine atony with intramyometrial administration

of 10 IU oxytocin has been reported in a small number of cases, by transcervical

injection at 2 and 10 o’clock.

Uterine massage, bladder catheterisation and intravenous oxytocin resolve the

majority of cases of uterine atony. There is little scientifi c evidence on which to base

the order of subsequent treatments, so it depends mostly on local experience. Rectal

misoprostol appears to be effective and safe, having as contraindications infl ammatory bowel disease and a history of previous allergy to the drug. Transient hyperthermia may occur, but no measures are usually required to treat it. Other prostaglandins

are available in some countries and have asthma, cardiac disease, hypertension and

diabetes as contraindications.

6.4.6.3 Mechanical Treatments

Bimanual uterine compression is a simple procedure that generally controls

bleeding from uterine atony and other intrauterine causes (Fig. 6.2 ). A hand is

placed on the abdomen over the uterine fundus, and the contralateral one is inserted

in the vagina to compress the cervix and uterus against the abdominal hand. Pressure

should be sustained to collapse bleeding vessels and to promote coagulation in the

placental bed. The procedure may not be applicable in some women, if it causes

unreasonable pain or discomfort. The main diffi culty resides in the executor’s

capacity to maintain sustained pressure for long periods of time, so frequent substitution may be required. It may also be used as a temporary measure to control bleeding, while other treatments are being considered or prepared.

Uterine balloon tamponade has gained popularity in the last decades and can

be performed with devices especially developed for postpartum haemorrhage, the

Bakri (Fig. 6.3 ) and Ebb balloons, or those adapted from other settings, the gastric

part of the Sengstaken-Blakemore balloon (developed for oesophageal

Table 6.2 Uterotonic agents used for the medical treatment of uterine atony

Oxytocin 20 IU in 500 ml of saline, in IV perfusion at 250 ml/h

Prostaglandins :

Misoprostol 800–1000 μg rectal

Sulprostone 1 mg in 500 ml of saline, in IV perfusion at 125 ml/h, which can be increased

up to 500 ml/h. After contracture, it is reduced to the initial dose

Carboprost (15-methyl prostaglandin F2 alpha) 0.25 mg IM, repeated every 15 min for a

maximum of 8 doses

6.4 Clinical Management

haemorrhage), the Rusch balloon (developed for bladder haemorrhage) or a condom

adapted to a Foley catheter. The balloon is introduced through the cervix with a

guiding hand, or using a speculum and sponge forceps, and fi lled with saline (ideally warmed up to 37 °C) until it is felt or seen to slightly dilate the cervix. The

amount of fl uid varies according to uterine dimensions, but is usually around 300–

500 ml. Prophylactic antibiotics should be started and the balloon removed 12–24 h

later. The reported success rate with this technique is around 85–90 %.

Fig. 6.2 Bimanual uterine

compression

Fig. 6.3 Uterine

tamponade with the Bakri

balloon

6 Postpartum Haemorrhage

In centres where there is an experienced intervention radiologist, uterine artery

embolisation is another option. Angiography may be used to identify the bleeding

vessels and to defi ne the best strategy for embolisation. A catheter is then introduced

into the femoral artery under local anaesthesia and inserted under fl uoroscopic control until the tip lies at the root of the contralateral uterine artery. Embolisation may

be performed with gelatin sponge pledgets, microspheres of polyvinyl alcohol or

tri-acryl gelatin microspheres, all of which are absorbed in about 10 days. The complication rate depends on local experience, but is reported in about 5 % of cases. It

includes fever, deep vein thrombosis, pancreatitis, infection, uterine necrosis, vascular perforation and femoral artery occlusion. Several observational studies report

success rates of 90–95 % and cases of viable subsequent pregnancies.

In low-resource settings, antishock garments and aortic pressure may be used

as temporary measures to reduce bleeding and the resulting haemodynamic instability, allowing patient transfer or the consideration of other treatments. Aortic pressure is performed by placing a hand in the midline above the uterus and exerting

continuous downward pressure with the heel of the hand. These measures are seldom required in high-resource countries.

6.4.6.4 Surgical Treatments

When bleeding does not stop with the medical and/or mechanical methods described

above, consideration must be given to moving the patient to the operating theatre

and preparing for laparotomy.

Several compression sutures have been described, and they are most successful

when intraoperative manual uterine compression results in cessation of bleeding.

The B - Lynch suture (Fig. 6.4 , left) is perhaps the most widely used, with a reported

success rate of around 90 %. A pair of absorbable sutures is symmetrically placed on

either side of the midline, but a second pair may be needed in large uteri. The

B-Lynch suture was originally described for cases where there was a caesarean incision, and a modifi cation described by Hayman may be used when the uterus is

intact (Fig. 6.4 , centre). In addition to B-Lynch and Hayman sutures, transverse

uterine Pereira sutures may be employed for increased compression, if necessary

(Fig. 6.4 , right).

Fig. 6.4 The B-Lynch ( left ), the Hayman ( middle ) and the Pereira sutures ( right )

6.4 Clinical Management

For situations of continuous uterine bleeding from the lower uterine segment due

to placenta praevia, transfi xing vertical sutures are frequently successful in haemorrhage control (Fig. 6.5 ).

An alternative approach is progressive uterine devascularisation , involving a

stepwise ligation of the ascending branch of one of the uterine arteries, followed by

the contralateral one, the uterine branch of one of the ovarian arteries and the contralateral branch (Fig. 6.6 ). The sequence stops as soon as haemorrhage is controlled. For uterine artery ligation, the bladder is refl ected downwards, a small

opening is created in the broad ligament 2 cm below the level of a caesarean incision, and the needle is passed to transfi x the myometrium about 2 cm from the lateral margin. Success rates are reported to be around 85 %, and the technique is

easier to execute than internal iliac (hypogastric) artery ligation. Uterine blood fl ow

is maintained through anastomoses from the vesical and rectal arteries, and there is

subsequent recanalisation of the uterine arteries. Cases of subsequent pregnancy

have been reported.

Internal iliac ( hypogastric ) artery ligation has lost popularity over the last

decades, as it requires the presence of a surgeon with experience in retroperitoneal

dissection. Because of major collateral anastomoses present in the pelvis, the

reported success rate is only 40-70 %, and it is also associated with important maternal morbidity.

Fig. 6.5 Transfi xing

vertical sutures, used for

bleeding from the lower

uterine segment

6 Postpartum Haemorrhage

Peripartum hysterectomy is one of the last resorts in treatment of postpartum

haemorrhage, and it should be considered when the patient does not desire future

pregnancies and consents to the proposal or as a life-saving procedure when this

situation is protected by law. Surgical technique is similar to that of hysterectomy

performed for gynaecological reasons, but the pedicles are usually more thick,

oedematous and vascular, so double clamping and ligation are usually preferable.

Identifying the cervix may be diffi cult in these situations, and it is useful to insert a

fi nger through the cervix into the vagina and hook it up to isolate the cervical rim.

This will also guide the vaginal incision for total hysterectomy. Subtotal hysterectomy is usually easier to perform and is associated with less ureteral lesions. Recent

studies report low mortality with the procedure, but morbidity and prolonged intensive care unit stay are frequent.

6.4.6.5 Pelvic Tamponade

When pelvic vessels continue to bleed after hysterectomy, pelvic tamponade with

gauze inserted into a sterilised plastic bag and connected to a weight via the vaginal

opening has been reported in a small number of cases (Fig. 6.7 ). Prophylactic antibiotics are started, and the bag is opened 24 h later to extract the gauze pads one by

one, after which the bag is removed.

6.4.7 Treatment of Birth Canal Injuries

Birth canal injuries may be detected on the initial speculum examination or may

need to be carefully searched in a later re-evaluation, motivated by persistent

haemorrhage with the uterus fi rmly contracted. Adequate light, positioning and

Utero-ovarian

ligament

Hypogastric

artery

Uterine

artery

Ligature

Branch of ovarian

artery

Ligature Fig. 6.6 Progressive

uterine devascularisation

6.4 Clinical Management

analgesia are required for this, together with vaginal retractors and a systematic

approach to evaluate the cervix and vagina. Two ring forceps are usually used to

explore the cervix, moving them alternatively to visualise the whole circumference. Only cervical lacerations measuring more than 2–3 cm and those that are

actively bleeding need to be repaired, using continuous absorbable suture and

starting at the apex.

Vaginal wall lacerations should be visualised in their entire extension and corrected with a continuous absorbable suture. Any gushing arterial haemorrhage

should be clamped and ligated individually. Subsequent vaginal packing with large

swabs may be necessary to control minor bleeding, and when this occurs it is preferable to catheterise the bladder to avoid urinary retention. When located high in the

vagina, lacerations may extend to the uterus and be associated with haematomas of

the broad ligament and/or retroperitoneal space (see below).

Birth canal haematomas may be located in the vulva, vagina, broad ligament,

ischial-rectal or retroperitoneal spaces and may form over the course of minutes or

hours. They may occur in isolation or associated with vaginal lacerations and are

caused by a vessel bleeding into a newly formed space. Small and non-expanding

haematomas should be managed conservatively, with frequent re-evaluations of size

and accompanying symptoms. Large or expanding haematomas require surgical

drainage under anaesthesia. After removal of the blood and clots, bleeding vessels

should be searched and ligated individually. If there is continued oozing, the space

should be closed. Broad ligament and retroperitoneal haematomas can be diagnosed

by ultrasound, computer tomography or magnetic resonance imaging. They are

preferably treated conservatively, unless there is haemodynamic instability, infection or rapid expansion. Selective arterial embolisation by an intervention

Fig. 6.7 Pelvic tamponade

6 Postpartum Haemorrhage

radiologist is currently the preferential method of treatment. Surgical treatment of

retroperitoneal haematomas requires a surgeon with experience in the exploration

of this space.

6.4.8 Treatment of Placental Retention

6.4.8.1 Complete Placental Retention

Complete retention of the placenta associated with haemorrhage requires prompt

manual removal of the placenta under regional or general anaesthesia and subsequent uterine curettage if any fragments remain attached. This is followed by external uterine massage, prophylactic antibiotics and intravenous perfusion of uterotonic

agents (Table 6.2 ) for at least 2 h. If a cleavage plane between the uterine wall and

the placenta is not identifi ed, this establishes the diagnosis of abnormally adherent

placenta increta or percreta (see below), and when bleeding cannot be controlled

with the medical and mechanical methods described above, immediate laparotomy

should be undertaken.

6.4.8.2 Partial Placental Retention

A poorly contracted uterus or recurrent episodes of uterine atony should lead to the

suspicion of partial placental retention. Re-evaluation of the placenta will usually

help to establish the diagnosis, but transabdominal ultrasound is required to confi rm

it. Uterine curettage should be performed to remove the remaining placental fragments, under regional or general anaesthesia.

6.4.9 Treatment of Rare Causes of Postpartum Haemorrhage

6.4.9.1 Uterine Inversion

Uterine inversion is a very rare but potentially life-threatening situation. It can be

diagnosed by vaginal examination, with the inverted uterine fundus found in the

uterine cavity (partial inversion), in the vagina (complete inversion) or even in the

exterior. The placenta may still be attached to the uterus, and in these situations

bleeding may be less intense. Sudden hypotension, pallor and bradycardia occur

frequently with uterine inversion, caused by neurogenic shock due to traction on the

uterine ligaments. Profuse haemorrhage and hypovolemic shock usually follow.

Manual replacement should be immediately attempted, before the cervix causes

congestion of the inverted fundus, making the procedure increasingly diffi cult.

Continuous pressure is applied around the inverted fundus to push it up through the

cervical ring, and this may require 2–3 min. If unsuccessful, medications should be

administered for uterine relaxation (Table 6.3 ) and the manoeuvre reattempted. A

further reattempt can be made in the operating theatre under general anaesthesia

with halogenated agents. If the placenta remains attached to the uterine fundus, no

efforts should be made to remove it at this stage. Manual removal can be attempted

after the uterine fundus is replaced.

6.4 Clinical Management

Unless reversal is quickly obtained, a prompt decision to undergo laparotomy

under general anaesthesia with halogenated agents should be taken. Manual repositioning can then be reattempted, but if the cervical constriction ring is too rigid, a

posterior vertical incision on this ring usually allows passage of the uterine fundus,

after which the incision is closed. After repositioning the uterus, prolonged uterine

contracture should be stimulated with an uterotonic agent (Table 6.2 ).

6.4.9.2 Uterine Rupture

This diagnosis should be considered when bleeding persists in spite of medical and

mechanical treatments of uterine atony, particularly when there is a history of previous caesarean section or other surgery involving the myometrium. Digital exploration of the uterine cavity via the vaginal route may identify the wall defect, but the

diagnosis is usually only established at laparotomy. Surgical management of uterine

rupture is considered in Sect. 2.4.5.

6.4.9.3 Abnormally Adherent Placenta

Management of abnormally adherent placenta when it is diagnosed before labour

allows planning of delivery and is beyond the aim of this book. This section refers

to the acute management of undiagnosed abnormally adherent placenta at the time

of caesarean section or during the third stage of labour. Because these situations are

relatively rare, there is little scientifi c evidence on which to base decisions. Two different clinical situations may be encountered. The fi rst is the suspicion of deep

myometrial, peritoneal or adjacent organ invasion at the time of caesarean section,

before the uterus is incised. In these cases, confi rmation of placental location should

be made by intraoperative ultrasound, and the uterine incision needs to avoid the

placental bed. After the fetus is delivered, no attempt should be made to extract the

placenta. If haemorrhage is minimal and the haemodynamic condition is stable,

several approaches may be taken, depending on the patient’s desire for future fertility. For patients desiring more children or when these desires are unknown (i.e.

patients under general anaesthesia), partial resection of the uterine wall en bloc

with the placenta may be attempted if subsequent closure is judged to be anatomically possible. The alternative is to leave the placenta in situ , ligate the umbilical

cord with an absorbable suture close to the placenta and close the uterus in an

attempt of expectant management. This option is associated with important haemorrhagic and infectious morbidity, as well as prolonged surveillance, but with careful

follow-up has a very low mortality. For patients who do not desire to remain fertile,

peripartum hysterectomy may be an option when important adjacent organs are

Table 6.3 Uterine relaxants

Nitroglycerine in slow intravenous bolus (50–100 μg IV slowly)

1 vial of 5 ml (5 mg/ml) in 500 ml of saline. Slow intravenous injection of 1–2 ml (50–

100 μg) with continuous monitoring of blood pressure

Salbutamol in intravenous perfusion (125 μg at 25 μ/min)

1 vial of 1 ml (0.5 mg/ml) in 100 ml of saline in intravenous perfusion pump at 300 ml/h

during 5 min

6 Postpartum Haemorrhage

not involved in placental invasion. When there is important involvement of adjacent

organs or when the expertise for a peripartum hysterectomy is not available, it is

preferable to leave the placenta in situ and attempt expectant management, even if

this results in hysterectomy at a later date. With heavy bleeding and/or a haemodynamically unstable patient, the surgical alternatives described above need to be

decided quickly. It is well to remember that defi nite treatment can be deferred to a

later time, and haemorrhage control is the main priority in these situations. Uterine

and vaginal packing with gauze, balloon tamponade, B-Lynch sutures, Hayman

sutures, uterine and internal iliac artery ligation have all been reported to be successful in a small number of cases. Haemostatic sutures of the placental bed may

also be successful in limited areas.

6.4.9.4 Maternal Bleeding Disorders

Several maternal bleeding disorders may be responsible for or may aggravate other

causes of postpartum haemorrhage. The detailed description of these conditions is

beyond the aims of this chapter, but they are usually managed in collaboration with

a haematologist and the hospital blood bank.

6.4.10 Postpartum Haemorrhage at Caesarean Section

Postpartum haemorrhage is more frequent at caesarean section, and it is also easier

to quantify blood loss in these situations. Uterine atony remains the most frequent

cause, and treatment is not substantially different to that used in vaginal deliveries,

involving similar support of maternal circulation/oxygenation and uterotonic agents

as fi rst-line treatment (Table 6.2 ). However, because there is direct access to the

uterus, some procedures need to be adapted. Localised uterine atony may benefi t

from intramyometrial injection of oxytocin, sulprostone and/or carboprost.

Bimanual uterine compression is substituted by internal uterine compression, and

balloon tamponade can still be performed, but the balloon is usually introduced

transabdominally. Compression sutures (Fig. 6.4 ) are used more frequently, because

of ease of access, and they can be combined with balloon tamponade, a procedure

that some refer to as the “sandwich technique”. Uterine embolisation is seldom

employed, because the required equipment is usually unavailable in an operating

theatre. Birth canal injuries should still be considered as a possible cause of haemorrhage, particularly when caesarean section was performed during the second stage

of labour and/or when there was a diffi cult fetal extraction.

6.5 Clinical Records and Litigation Issues

It is important to document the names of the healthcare professionals who were

summoned, when they were called and when they arrived, which medication and

manoeuvres were performed and when and by whom. Inadequate documentation

may cause problems when there is medicolegal litigation, and it is therefore helpful

to use a structured pro forma for accurate record keeping.

6.5 Clinical Records and Litigation Issues

A frank explanation of the situation to the patient and her closest family by an

experienced member of the team is also required at the earliest available

opportunity.

6 Postpartum Haemorrhage

Suggested Reading

Abdel-Aleem H, Hofmeyr GJ, El-Sonoosy E (2006) Uterine massage and postpartum blood loss.

Int J Gynecol Obstet 93:238–239

B-Lynch C, Keith L, Lalonde A, Karoshi M (eds) (2006) A textbook of postpartum hemorrhage,

1st edn. Sapiens Publishing, Duncow

Chandraharan E, Arulkumaran S (2008) Surgical aspects of postpartum hemorrhage. Best Pract

Res Clin Obstet Gynaecol 22:1089–1102

Ramanathana G, Arulkumaran S (2006) Postpartum hemorrhage. Curr Obstet Gynaecol 16:6–13

Royal College of Obstetricians and Gynaecologists (2009) Prevention and management of postpartum hemorrhage (green-top guideline no. 52). RCOG Press, London

Royal College of Obstetricians and Gynaecologists (2011) Placenta praevia, placenta praevia

accrete and vasa praevia: diagnosis and management (green-top guideline no. 27). RCOG

Press, London

Suggested Reading

D. Ayres-de-Campos, Obstetric Emergencies,

DOI 10.1007/978-3-319-41656-4_7

7 Maternal Cardiorespiratory Arrest

7.1 Definition, Incidence and Main Risk Factors

Maternal cardiorespiratory arrest is estimated to occur in 0.003 % of pregnancies

and manifests by loss of consciousness and central cyanosis . There are a number

of possible aetiologies for this event (Table 7.1 ), but in high-resource countries,

pulmonary thromboembolism and amniotic fl uid embolism are among the leading

causes. A detailed description of the maternal conditions that may lead to cardiorespiratory arrest is beyond the aim of this book, so this chapter will focus on the acute

management of the situation and the initial treatment of the two most frequent

causes.

Table 7.1 Major causes of maternal cardiorespiratory arrest

Obstetric complications Major obstetric haemorrhage (abruption, uterine rupture,

postpartum haemorrhage)

Amniotic fl uid embolism

Anaesthetic complications High spinal anaesthesia

Pulmonary aspiration of gastric contents

Toxicity of local anaesthetic agents

Medical complications Pulmonary thromboembolism

Myocardial infarction

Aortic dissection

Peripartum cardiomyopathy

Anaphylaxis

Sepsis/septic shock

Air embolus

7.2 Consequences

Maternal cardiorespiratory arrest is associated with a high incidence of maternal

deaths and long - term neurological sequelae . It is also associated with important

perinatal mortality and long - term neurological sequelae for the child. Anticipation

of the problem and early recognition allow prompt resuscitation and other support

measures that have a profound impact on maternal and fetal prognosis.

7.3 Diagnosis

Maternal cardiorespiratory arrest manifests by loss of consciousness and central

cyanosis. Absence of respiratory movements and lack of a carotid pulse confi rm

the diagnosis. The maternal electrocardiogram may display a continuous line representing asystole , or there may be ventricular fi brillation , ventricular tachycardia or any other type of electric activity without a carotid pulse .

7.4 Clinical Management

Whatever the cause of maternal cardiorespiratory arrest, the initial response is similar and involves the support of maternal oxygenation and circulation and rapid

delivery of the fetus if the situation does not revert within 4 min . When both an

anaesthetist and an obstetrician are present, the responsibility for these two aspects

is usually divided among them. In the remaining cases, the most senior healthcare

professional needs to take charge of the whole situation. Management of cardiorespiratory arrest occurring after delivery does not differ signifi cantly from that occurring in the non-pregnant woman and is beyond the aim of this chapter.

7.4.1 Anticipating the Situation

The occurrence of sudden maternal shortness of breath (dyspnoea and tachypnoea)

associated with central cyanosis suggests a serious respiratory complication that

may be followed by cardiorespiratory arrest. When such symptoms occur, the

woman should be placed in left lateral safety position (Fig. 7.1 ), and several of the

aspects considered below can be anticipated, including maternal and fetal monitoring , vein catheterisation , summoning of appropriate staff and collection of

equipment that may later be required (emergency trolley).

7.4.2 Clearly Verbalising the Diagnosis

It is important that all members of the healthcare team are aware of the diagnosis of

maternal cardiorespiratory arrest, and therefore this needs to be clearly verbalised.

7 Maternal Cardiorespiratory Arrest

7.4.3 Asking for Help

One of the fi rst measures should be to summon urgently at least two midwives , a

senior obstetrician , an anaesthetist and the hospital resuscitation team . As stated

above, the presence of an anaesthetist guarantees a safer management of respiratory

and circulatory functions, as well as basic fl uid balance. Care is however needed to

maintain good communication between both sides at all times, so that there is coordinated management of the situation.

7.4.4 Maternal Monitoring

When cardiorespiratory arrest occurs in a hospital environment, maternal monitoring is a priority for objective assessment and response to treatment, so continuous

evaluation of heart rate , oxygen saturation and electrocardiography should be

started promptly and the blood pressure measured at least every 5–10 min.

7.4.5 Support of Maternal Oxygenation and Circulation

7.4.5.1 A (Airway): Guarantee the Patency of the Airway

To guarantee the patency of the airway, the patient should be turned onto her back,

the head tilted backwards, the chin lifted and the mouth opened and inspected for

objects that may cause obstruction. Secretions may be aspirated if abundant and a

Mayo tube temporarily introduced to prevent the tongue from occluding the airway,

if endotracheal intubation cannot be immediately performed.

7.4.5.2 B (Breathing): Maintain Oxygen Supply to the Lungs

To maintain oxygen supply to the lungs, ventilation with a bag - valve mask should

be immediately started at 15 cycles/min, using 100 % oxygen and 15 l / min , and

thereafter adapting according to oxygen saturation levels, which should be kept over

90 %. After obtaining the necessary material, early endotracheal intubation

should be performed to improve the effi cacy of ventilation and prevent aspiration of

Fig. 7.1 Left lateral safety position

7.4 Clinical Management

gastric contents. The ventilation cycles described above are maintained. If available,

capnography should be used to confi rm correct tube placement, as well as the adequacy of ventilation and cardiac massage. Pulmonary auscultation is necessary to

evaluate proper endotracheal tube placement and the presence of additional respiratory sounds. As soon as possible, arterial blood gas sampling should be performed

to evaluate whether the objective of maintaining partial pressure of oxygen above

60 mmHg is being achieved.

7.4.5.3 C (Circulation): Cardiac Massage and Vein Catheterisation

With maternal loss of consciousness and an absent carotid pulse, immediate

external cardiac massage should be started, independently of whether or not

cardiac activity is detected on the electrocardiogram. A hard board should be

placed underneath the woman, and if pregnancy is above 20 weeks, a hard object

is placed under this board to create a 30 ° left tilt (Fig. 7.2 – left). The objective is

to avoid aorto-caval compression by the pregnant uterus and the resulting decreased

venous return from the lower limbs. If this is not immediately available, an alternative is to shift the abdomen laterally and displace the uterus to the left

(Fig. 7.2 – centre).

Cardiac massage is performed by placing two interlocked hands on the inferior

portion of the patient’s sternum and with the arms fully stretched, applying rhythmic compressions at 100 cycles per minute, depressing the sternum by about 5 cm

(Fig. 7.2 – right). There is ample evidence that appropriately applied cardiac massage causes respiratory movements, so this should be the prioritised manoeuvre if

no one is available to guarantee ventilation. Cardiac massage is only stopped for

brief seconds every 2 min, to re-evaluate cardiac rhythm and the carotid pulse. The

procedure is only abandoned when an adequate cardiac rhythm and pulse are

detected, or when death is declared.

As soon as possible, vein catheterisation with a large bore catheter (14G

or 16G) should be carried out. In all situations of cardiorespiratory arrest,

adrenaline 1 mg in intravenous bolus should be given as soon as the venous

catheter is in place and repeated on alternate 2 min cycles of cardiac massage.

After the fi rst bolus is given, blood should be collected for complete blood

count, electrolytes, liver and renal function, coagulation studies and

Fig. 7.2 Hard board and 30° left tilt ( left ), left lateral abdominal displacement ( centre ), positioning of the body and hands for external cardiac massage ( right )

7 Maternal Cardiorespiratory Arrest

cross-matching. Fluid replacement with crystalloids (saline, Ringer’s lactate)

should follow.

7.4.6 Bladder Catheterisation and Measurement

of Urinary Output

Bladder catheterisation should be performed to measure urinary output and fl uid

balance adapted to maintain the latter above 30 ml/h.

7.4.7 Fetal Monitoring

At viable gestational ages, continuous cardiotocography should be performed

quickly started, although the measure should ideally anticipate cardiorespiratory

arrest (see Chap. 2).

7.4.8 In Situ Caesarean Section

When pregnancy is above 20 weeks and there is no reversal after 4 min of cardiorespiratory arrest, in situ caesarean section is indicated to improve the chances of maternal resuscitation and to avoid the consequences of prolonged acute fetal hypoxia in

viable pregnancies. Moving the patient to the operating theatre is not recommended in

these situations, as it delays the procedure, so caesarean section should be performed

at the site of arrest. Because of reduced circulation with external cardiac massage,

bleeding is usually minimal, and no anaesthesia is required as the patient is unconscious. The abdomen is previously disinfected, the abdominal skin is opened with a

scalpel, and fetal extraction is quickly carried out, as in normal caesarean delivery.

Cardiac massage and assisted ventilation are continued throughout the whole process.

After the fetus is delivered, the surgical procedure can be completed at a slower pace,

and more attention should again be given to maternal resuscitation.

7.4.9 Defribrillatory Rhythms

When ventricular fi brillation and ventricular tachycardia without pulse are

detected, electric defi brillation is frequently successful in reverting cardiorespiratory arrest. A 200 J biphasic or 360 J monophasic shock should be applied

(Fig. 7.3 ). Before this, the team must temporarily stop cardiac massage and ventilation, remove the oxygen source and step away from the patient and her bed. If there

is no reversal after the fi rst shock, a second shock is indicated. If the abnormal

rhythm persists after the second shock, adrenaline 1 mg in intravenous bolus

should be administered on alternate cardiac massage cycles and a third shock

applied. If the rhythm persists after the third shock, amiodarone 300 mg in intravenous bolus is administered.

7.4 Clinical Management

7.4.10 After Cardiorespiratory Arrest Reverses

If there is reversal of cardiorespiratory arrest, the situation requires re-evaluation in

a more serene context.

7.4.10.1 Hypotension

When there is sustained hypotension, ephedrine , dopamine , dobutamine and colloids need to be considered. The objective is to maintain mean arterial pressure

above 65 mmHg and urine output above 30 ml/h. In addition to these, blood products, including red blood cells, fresh frozen plasma, cryoprecipitate and platelets,

may be required, particularly when there is disseminated intravascular coagulation

and persistent haemorrhage (see Chap. 6).

7.4.10.2 Termination of Pregnancy

The decision to terminate pregnancy after reversal of cardiorespiratory arrest

has occurred depends on gestational age and on the clinical stability of the situation. A caesarean section is usually indicated if pregnancy is above 34 weeks

and the patient is haemodynamically stable. At earlier gestational ages, management depends mostly on the underlying cause, on haemodynamic stability and

on the results of cardiotocography and ultrasound. In some cases, it may be

justifi able to maintain vigilance or to wait 48 h for the effect of a corticosteroid

course.

7.4.10.3 Monitoring in an Intensive Care Unit

After the initial stabilisation, patients require transfer to an intensive care unit for

closer observation, where arterial catheterisation with invasive blood pressure

Fig. 7.3 Location of the

electric pads for

defi brillation

7 Maternal Cardiorespiratory Arrest

monitoring, serial blood gas analysis, central venous catheterisation and pressure

monitoring may be required.

7.4.10.4 Maintain Body Temperature

Low body temperature contributes to peripheral hypoperfusion and to tissue damage. This can be reduced by maintaining normal body temperature and by administering previously warmed fl uids.

7.4.10.5 Looking for an Underlying Cause

After the initial response to maternal cardiorespiratory arrest, further evaluation of

the underlying cause should be carried out as soon as the patient is stabilised

(Table 7.1 ). It is sometimes possible to suspect the diagnosis from analysis of clinical records and/or from a patient history obtained from a relative. Chest X - ray ,

d - dimers , electrocardiogram , echocardiogram and ventilation / perfusion scan

may be useful in establishing the defi nite diagnosis.

7.4.11 Pulmonary Thromboembolism

Pulmonary thromboembolism has a fatality rate of 1 % and is one of the leading

causes of maternal mortality in high-resource countries. The association of shortness of breath, tachypnoea, cough and pleuritic chest pain is very suggestive, but the

clinical presentation is variable. The presence of risk factors (Table 7.2 ) contributes

to the suspicion. Diminished respiratory sounds on auscultation are only found in

50 % of cases, and oxygen saturation is usually low.

Table 7.2 Risk factors for pulmonary thromboembolism

Pre-existing medical complications Cardiac disease

Hypertension, diabetes mellitus, obesity

Systemic lupus erythematosus

Smoking

Thrombophilia – protein S or C defi ciencies

Previous thromboembolic disease

Pregnancy complications Multiple pregnancy

Hyperemesis/dehydration

Antepartum or postpartum haemorrhage

Prolonged labour

Infection

Caesarean section and instrumental vaginal delivery

Artifi cial placental extraction or curettage

7.4 Clinical Management

Although the defi nite diagnosis requires a high degree of certainty, as it implies

prolonged therapy and increased vigilance, a reasonable suspicion should be enough

to initiate anticoagulant therapy (Table 7.3 ), except when there is an absolute contraindication, such as hepatic insuffi ciency or a high risk of bleeding, as delaying treatment will strongly condition outcome. Low molecular weight heparin does not

cross the placenta, is administered subcutaneously and does not require close monitoring of coagulation results, so it is usually the preferred method of treatment. The

alternative is heparin, administered intravenously at 80 units/kg for 12 h (maximum

of 10,000 units), followed by a perfusion of 18 units/kg/h (maximum of 2200 units/h).

Low molecular weight and unfractionated heparin have an equivalent effi cacy, but the

latter requires coagulation tests 6 h after the loading dose, or after any dose change,

and thereafter at least daily. In these situations, activated partial thromboplastin time

should be kept 1.5–2.5 times the basal value, and platelet count should be monitored

every other day. Treatment should be continued until the diagnosis is excluded.

Arterial blood gas analysis will frequently reveal hypoxaemia, and metabolic

acidosis may also be present. The chest X - ray is normal in about 50 % of the cases,

but several non-specifi c changes may appear, such as cardiac enlargement, small

opacities, atelectasis, pleural effusion or pulmonary oedema. This exam is also

important to exclude other diseases, such as pneumonia and pneumothorax.

D - dimers may be increased in the absence of thromboembolism, because of

increased fi brinolysis during pregnancy and after surgery, but the test has a high

negative predictive value, as normal values almost completely exclude the diagnosis. The electrocardiogram usually displays non-specifi c changes, such as sinus

tachycardia, but it is also important for other diagnoses. Doppler ultrasound of the

lower limbs is useful to establish the diagnosis of deep vein thrombosis, which

predisposes to pulmonary thromboembolism and has an identical treatment.

Ventilation / perfusion scan is commonly used in pregnant women to establish the

defi nite diagnosis of pulmonary thromboembolism, as it carries less risks of radiation than computerised tomography pulmonary angiography , but the latter has

the highest accuracy and may be necessary in some cases.

In severe cases of massive pulmonary thromboembolism associated with serious haemodynamic compromise, unfractionated heparin is the treatment of choice,

and thrombolytic therapy, thrombus fragmentation, thoracotomy and surgical embolectomy may all need to be considered.

7.4.12 Amniotic Fluid Embolism Syndrome

This syndrome appears to be caused by an anaphylactic reaction to amniotic fl uid or

to another unknown substance that gains access to the maternal circulation. It occurs

Table 7.3 Therapeutic doses of low molecular weight heparin (according to early pregnancy

weight)

<50 kg 50–69 kg 70–89 kg >90 kg

Enoxaparin 40 mg 12/12 h 60 mg 12/12 h 80 mg 12/12 h 100 mg 12/12 h

Dalteparin 5000 IU 12/12 h 6000 IU 12/12 h 8000 IU 12/12 h 10,000 IU 12/12 h

Tinzaparin 175 units/kg once daily

7 Maternal Cardiorespiratory Arrest

more frequently during labour or in the 30 min that follow, but may also arise during

pregnancy, particularly in association with second and third trimester abortion or in

the 4 h after delivery.

It is reported to occur in 0.002 % of all pregnancies, but sub-diagnosis is

likely. In high-resource countries, it accounts for approximately 10 % of all

direct maternal deaths. The common features are pulmonary arteriolar constriction followed by left ventricular failure . The resulting symptoms and

signs are profound hypotension , shortness of breath , central cyanosis , loss of

consciousness , seizures and cardiorespiratory arrest . In a second phase, there

is thromboplastin release into the maternal circulation, caused by activation of

the coagulation cascade, with resulting disseminated intravascular coagulation and postpartum haemorrhage . The main risk factors are displayed in

Table 7.4 .

Maternal mortality varies between 13 and 61 %, and about 10 % of survivors

develop neurological sequelae. Perinatal mortality affects 9–44 % of cases, and

almost 50 % of survivors will have long-term sequelae.

Currently, there is no gold standard test for this syndrome, so the diagnosis is

based on suggestive clinical features and the exclusion of other diagnoses such as

eclampsia, high anaesthetic blockade, systemic toxicity by local anaesthetics, gas

embolism, anaphylactic reaction to medications, peripartum cardiomyopathy and

myocardial infarction. Even when there is maternal death, fi ndings at autopsy are

unspecifi c. Chest X-ray, electrocardiogram and ventilation/perfusion scan should be

considered to exclude other possible causes.

Likewise, there is no specifi c treatment for amniotic fl uid embolism, beyond the

support measures described above, and correction of ensuing complications. Some

authors propose the use of 500 mg hydrocortisone IV every 6 h, to reduce the anaphylactic response, but there is insuffi cient proof of benefi t. Anticipation of postpartum haemorrhage is an essential part of treatment.

7.5 Clinical Records and Litigation Issues

It is important to document the names of the healthcare professionals who were

summoned, when they were called and when they arrived, which medication and

manoeuvres were performed, when and by whom. These aspects may be crucial if

there is medicolegal litigation.

Table 7.4 Risk factors for

amniotic fl uid embolism Advanced maternal age

High parity

Induction of labour

Multiple pregnancy

Caesarean section

Cervical laceration

Uterine rupture

7.5 Clinical Records and Litigation Issues

A frank explanation of the situation to the patient and her closest family needs

to be given by an experienced member of the team who was involved in management. The overall attitude and the words of healthcare professionals remain for a

long time in people’s memories, associated with such diffi cult moments.

Thoughtless words, a rushed or cold attitude will frequently be remembered as

negative experiences, while kindness and concern will usually be an important

source of comfort.

7 Maternal Cardiorespiratory Arrest

Suggested Reading

Benson MD, Kobayashi H, Silver RK, Oi H, Greenberger PA, Terao T (2001) Immunologic studies

in presumed amniotic fl uid embolism. Obstet Gynecol 97:510–514

Clark SL, Howkins GDV, Dudley DA, Dildy GA, Porter TF (1999) Amniotic fl uid embolism:

analysis of a national registry. Am J Obstet Gynecol 172:1158–1169

Conde-Agudelo A, Romero R (2009) Amniotic fl uid embolism: an evidence-based review. Am

J Obstet Gynecol 201(5):445.e1–445.e13

Greer I (2001) The acute management of venous thromboembolism in pregnancy. Curr Opin

Obstet Gynecol 13:569–575

James A (2008) Thromboembolism in pregnancy: recurrence risks, prevention and management.

Curr Opin Obstet Gynecol 20:550–556

Knight M, Tuffnell D, Brockelhurst P, Spark P, Kurinczuk JJ, on behalf of the UJ Obstetric

Surveillance System (2010) Incidence and risk factors for amniotic fl uid embolism. Obstet

Gynecol 115:910–917

Krivak T, Zorn KK (2007) Venous thromboembolism in obstetrics and gynecology. Obstet Gynecol

109:761–777

Royal College of Obstetricians and Gynaecologists (2007) Thromboembolic disease in pregnancy

and the puerperium: acute management (Green-top guideline no. 28). RCOG Press, London

Royal College of Obstetricians and Gynaecologists (2009) Reducing the risk of thrombosis and

embolism during pregnancy and the puerperium (Green-top guideline no. 37). RCOG Press,

London

Weiwen Y, Niugyu Z, Lauxiang Z, Yu L (2000) Study of the diagnosis and management of amni

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