Emergencies Around Childbirth

Emergencies Around Childbirth

A Handbook for Midwives

Third Edition

Edited by

Maureen Boyle

University of West London
Ealing, UK

CRC Press

Taylor & Francis Group

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Boca Raton, FL 33487-2742

© 2017 by Taylor & Francis Group, LLC

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Version Date: 20160128

International Standard Book Number-13: 978-1-78523-135-3 (Paperback)

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Library of Congress Cataloging-in-Publication Data

Names: Boyle, Maureen, editor.

Title: Emergencies around childbirth : a handbook for midwives / [edited by] Maureen Boyle.

Description: Third edition. | Boca Raton : CRC Press/Taylor & Francis, 2016. | Includes bibliographical references and index.

Identifiers: LCCN 2016003697 (print) | LCCN 2016003986 (ebook) | ISBN 9781785231353 (paperback : alk. paper) | ISBN 9781498776356 (e-book)

Subjects: | MESH: Midwifery | Obstetric Labor Complications--therapy | Pregnancy Complications--therapy

Classification: LCC RG701 (print) | LCC RG701 (ebook) | NLM WQ 165 | DDC 618.5--dc23

LC record available at http://lccn.loc.gov/2016003697

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Contents

Contributors

Abbreviations

1    An overview of the professional issues that support safe practice

Kate Nash

2    Maternal and newborn resuscitation

Jenny Brewster

3    Antepartum haemorrhage

Luisa Acosta

4    Thromboembolism in pregnancy

Judy Bothamley

5    Pre-eclampsia and associated conditions

Maureen Boyle

6    Malpresentations and malpositions

Ona Stewart

7    Cord prolapse

Alison Meinel

8    Shoulder dystocia

Judith Robbins

9    Uterine complications

Marie Hall

10    Intrapartum and primary postpartum haemorrhage

Helen Crafter

11    Amniotic fluid embolism: Anaphylactoid syndrome of pregnancy

Maureen Boyle

12    Serious infection

Judy Bothamley and Maureen Boyle

13    Other causes of potential maternal collapse

Andrea Aras-Payne

14    Psychological considerations for emergencies around childbirth

Elisabeth Hallewell

Glossary

Index

Contributors

Luisa Acosta

University of West London

United Kingdom

Andrea Aras-Payne

University of West London

United Kingdom

Judy Bothamley

University of West London

United Kingdom

Maureen Boyle

University of West London

United Kingdom

Jenny Brewster

University of West London

and

Advanced Life Support in Obstetrics and Newborn Life Support (Resuscitation Council)

and

Royal Berkshire NHS Foundation Trust

United Kingdom

Helen Crafter

University of West London

United Kingdom

Marie Hall

Imperial College Healthcare NHS Trust

London, United Kingdom

Elisabeth Hallewell

University of West London

and

London North West Healthcare Trust

United Kingdom

Alison Meinel

Imperial College Healthcare NHS Trust

London, United Kingdom

Kate Nash

University of West London

and

Royal Berkshire NHS Foundation Trust

United Kingdom

Judith Robbins

Imperial College Healthcare NHS Trust

London, United Kingdom

Ona Stewart

Imperial College Healthcare NHS Trust

and

City University

London, United Kingdom

Abbreviations

ABG

Arterial blood gas

ABUO

Antepartum bleeding of unknown origin

AED

Automated external defibrillator

AES

Anti-embolic stockings

ALSO

Advanced Life Support in Obstetrics

ALT

Alanine transaminase (a liver enzyme)

AN

Antenatal

APH

Antepartum haemorrhage

ARDS

Acute (formerly adult) respiratory distress syndrome

ARM

Artificial rupture of membranes

AST

Aspartate transaminase (a liver enzyme)

BMI

Body mass index

CCT

Controlled cord traction

CEMD

Confidential Enquiries into Maternal Deaths (report – now under MBRRACE)

CPR

Cardiopulmonary resuscitation

CS

Caesarean section

CT

Computerized tomography

CTG

Cardiotocograph (fetal monitoring)

CVP

Central venous pressure (line)

DIC

Disseminated intravascular coagulation

DKA

Diabetic ketoacidosis

DSM

Diagnostic and Statistical Manual of Mental Disorders (American Psychiatric Association)

ECG

Electrocardiogram

ECV

External cephalic version

EmCS

Emergency caesarean section delivery

ERCS

Elective repeat caesarean section

ERPC

Evacuation of retained products of conception

FBC

Full blood count

GAS

Group A streptococcal (infection)

GCS

Graduated compression stockings

GP

General practitioner (family doctor)

HELLP

Haemolysis, elevated liver enzymes and low platelets (syndrome)

HIE

Hypoxic ischaemic encephalopathy

IM

Intramuscular (injection)

IOL

Induction of labour

IPH

Intrapartum haemorrhage

ITU/ICU

Intensive therapy/care unit

IUD

Intrauterine death

IUGR

Intrauterine growth restriction (of the fetus)

IV(I)

Intravenous (infusion)

LCHAD

Long-chain acyl-CoA dehydrogenase

LFT

Liver function test

LMWH

Low molecular weight heparin

LSA

Local Supervising Authority

LSCS

Lower segment caesarean section

MAP

Mean arterial pressure (reading)

MBRRACE-UK

Mothers and Babies: Reducing Risk through Audits and Confidential Enquiries across the UK

MDT

Multi-disciplinary team

MEOWS

Modified early obstetric warning score

MOET

Managing Obstetric Emergencies and Trauma

MOH

Major (or massive) obstetric haemorrhage

MRI

Magnetic resonance imaging

MSV

Mauriceau-Smellie-Veit (delivery of head following breech)

NHS

National Health Service

NICE

National Institute for Health and Care Excellence UK

NICU

Neonatal intensive care unit

NMC

Nursing and Midwifery Council UK

NSAID

Nonsteroidal anti-inflammatory drug

O₂

Oxygen

OA

Occipito anterior (fetal position)

OHSS

Ovarian hyperstimulation syndrome

OP

Occipitoposterior (fetal position)

PCR

(urinary spot) Protein:creatinine ratio

PEFR

Peak expiratory flow rate

PND

Postnatal depression

POP

Persistent occipitoposterior position (delivery)

PPH

Postpartum haemorrhage

PPROM

Prolonged preterm rupture of membranes

PRECOG

Pre-eclampsia community guideline

PROMPT

PRactical Obstetric Multi-Professional Training

PTSD

Post-traumatic stress disorder

RCOG

Royal College of Obstetricians and Gynaecologists (UK)

RCT

Randomized controlled trial (seen as the ‘gold standard’ of research)

RFT

Renal function test

Rh

Rhesus (factor)

ROM

Rupture of membranes

RUQ

Right upper quadrant (of the abdomen)

SBAR

Situation, background, assessment, recommendation (a tool for handover)

SROM

Spontaneous rupture of membranes

TEDS

Thromboembolic deterrent stockings

TOP

Termination of pregnancy

U&E

Urea and electrolytes

UAD

Umbilical artery Doppler

UH

Unfractionated heparin

UK

United Kingdom

UKOSS

UK Obstetric Surveillance System

US(S)

Ultrasound (scan)

VBAC

Vaginal birth after caesarean

VE

Vaginal examination

VTE

Venous thromboembolism

1

An overview of the professional issues that support safe practice

KATE NASH

Introduction

Accountability and duty of care

Risk assessment and management

Working together: Teamwork, multiprofessional training and creating a positive culture

Communication and record-keeping

Conclusion

References

INTRODUCTION

You uphold the reputation of your profession at all times. You should display a personal commitment to the standards of practice and behaviour set out in the Code. You should be a model of integrity and leadership for others to aspire to. This should lead to trust and confidence in the profession from patients, people receiving care, other healthcare professionals and the public.¹

The terms professional and professionalism are used widely within the midwifery literature and help shape the roles and responsibilities of midwives within both their work and personal lives. The National Health Service (NHS) Constitution² was developed to specify the rights that the public have when using the NHS and sets out a list of principles that guide the NHS and govern the way that it operates. A central tenet of these principles is that patients should be treated with a professional standard of care by appropriately qualified and experienced professionals.

The concept of professionalism is multifaceted³ and encompasses a specific set of skills, knowledge, attitudes and behaviours which carry certain responsibilities and duties. The Nursing and Midwifery Council (NMC) is the professional regulator for nursing and midwifery in the United Kingdom and has created a structure and set of professional rules and standards for both professions. The criteria for the professional behaviours, attitudes, knowledge, skills and competencies of midwives are also set out by the NMC and are neither negotiable nor discretionary.1,4 These rules and standards reinforce the professionalism of midwifery and must inform and underpin midwifery practice at all times.¹ Midwives commit to upholding these standards when they join the NMC register and subsequently renew their registration. They are an essential part of protecting the public and the delivery of a high standard of safe midwifery care.¹ They also provide a benchmark upon which midwifery practice can be scrutinised and for which midwives may be called to account and ultimately removed from the register should they fail to uphold them (Table 1.1).

Table 1.1  A summary of the principles and values to be upheld within the code – professional standards of practice and behaviour for nurses and midwives

Prioritise people

•  Treat people as individuals and uphold their dignity.

•  Listen to people and respond to their preferences and concerns.

•  Make sure that people’s physical, social and psychological needs are assessed and responded to.

•  Act in the best interests of people at all times and respect people’s right to privacy and confidentiality.

Practice effectively

•  Always practise in line with the best available evidence.

•  Communicate clearly and work cooperatively.

•  Share your skills, knowledge and experience for the benefit of people receiving care and your colleagues.

•  Keep clear and accurate records relevant to your practice.

•  Be accountable for your decisions to delegate tasks and duties to other people.

•  Have in place an indemnity arrangement which provides appropriate cover for any practice you take on as a nurse or midwife in the United Kingdom.

Preserve safety

•  Recognise and work within the limits of your competence.

•  Be open and candid with all service users about all aspects of care and treatment, including when any mistakes or harm have taken place.

•  Always offer help if an emergency arises in your practice setting or anywhere else.

•  Act without delay if you believe that there is a risk to patient safety or public protection.

•  Raise concerns immediately if you believe a person is vulnerable or at risk and needs extra support and protection.

•  Advise on, prescribe, supply, dispense or administer medicines within the limits of your training and competence, the law, our guidance and other relevant policies, guidance and regulations.

•  Be aware of, and reduce as far as possible, any potential for harm associated with your practice.

Promote professionalism and trust

•  Uphold the reputation of your profession at all times.

•  Uphold your position as a registered nurse or midwife.

•  Fulfil all registration requirements.

•  Cooperate with all investigations and audits.

•  Respond to any complaints made against you professionally.

•  Provide leadership to make sure people’s well-being is protected and to improve their experiences of the healthcare system.

Source:  Nursing and Midwifery Council (NMC). 2015a. The Code. Professional Standards of Practice and Behaviour for Nurses and Midwives. London: NMC, p. 15. Available at http://www.nmc.org.uk/standards/code/ (accessed July 26, 2015).

This chapter aims to explore the various components that are essential for the professional practice of midwives. Whereas each component can be considered on an individual basis, it is important to be aware that they are mutually dependent and coexist together to support and inform the care that midwives must provide at all times. Issues such as communication, record-keeping and team working might seem an obvious consideration in the provision of safe and effective care; however, consecutive published reports into failing Trusts and maternal deaths have shown that these are areas which often fall short of the required standard. Because of this they urgently need to be improved to prevent unnecessary maternal and neonatal morbidity and mortality.

Responding to emergencies around childbirth can be both a stressful and potentially devastating time for all those involved. It is during such times that the provision of a high standard of professionalism by the practitioners involved is crucial in minimising the potential psychological and physiological sequelae for the mother and her family both during and following the event. It is hoped that through reading this chapter the midwife will gain an understanding of what it means to be a professional and how accountability, effective leadership, a positive safety culture and multiprofessional collaboration, communication and training are vital to achieving this.

ACCOUNTABILITY AND DUTY OF CARE

There are many definitions of accountability presented within the literature; however, it is best explained in terms of how it can be applied to midwifery. The roles and responsibilities of a midwife are set in statute, and midwives are personally answerable for the actions and omissions that they make during their working lives, and have a duty of care to the women, babies and families that they care for. Midwives are accountable to both the criminal and civil courts to ensure that their activities conform to legal requirements, to their employer to follow their contract of duty and to the NMC to ensure that the rules and standards that govern midwifery practice are adhered to.⁵ Midwives are also accountable to the women and babies to whom they have a duty of care and must be able to provide evidence that this duty has been met. Midwives can therefore be held to account to a range of higher authorities with whom they have a legal relationship in order to provide justification for their actions.⁶ Failure to do this can result in disciplinary or legal action, the application of sanctions and possible removal from the register or recognised training programme (for student midwives).

It is important that midwives have the necessary knowledge, skills and competencies to enable them to fulfil their professional responsibilities. The NMC Code and standards of competence and guidance for registered midwives sets out the professional standards that midwives must meet when they qualify and which they must maintain consistently throughout their careers in order to remain on their professional register.7,8 Midwives must keep their knowledge and skills up to date and ensure that they have undertaken sufficient practice hours in order to maintain their skills and competence. In April 2016, the NMC introduced the process of revalidation to provide a robust mechanism for ensuring that midwives and nurses meet the requirements to remain on the professional register. This has replaced the post-registration education and practice (Prep) standards previously set by the NMC.⁹

The International Confederation of Midwives (ICM) have considered the implications of midwives’ accountability and emphasised the importance of midwives not undertaking any actions that they have not received the appropriate training for.¹⁰ This is also supported by the Midwives Rules and Standards⁴ which stipulates that midwives must not provide any care, or undertake any treatment, that they have not been trained for except in an emergency. In an emergency, either inside or outside the work setting, nurses and midwives have a professional duty to provide care and may be called to account if they do not respond to the emergency.¹¹ It is important, however, that midwives act only within the limits of their knowledge and competence¹ and should call for help from other health or social care professionals with the necessary skills and experience to provide assistance in the provision of care.⁴

The accountability of midwives also extends to any delegation of tasks that they might make and midwives must ensure that they only delegate those tasks and duties that are within the other person’s scope of competence.¹ While health care support workers can document unsupervised tasks within the maternity records on their own responsibility, it is the midwife who has delegated the task who is accountable and should ensure the countersigning of these at the end of the shift.

RISK ASSESSMENT AND MANAGEMENT

Having the expert knowledge and skill to recognise, assess and manage risk, both at an individual level and within the wider realms of the maternity unit and healthcare organisation is an integral part of ensuring that midwives maintain their accountability and uphold their duty of care. Risk assessment forms part of the broader clinical governance strategy within healthcare organisations which is crucial to their ability to carry out their functions effectively and safeguard the provision of quality care. It is paramount that midwives are able to identify risk and initiate referral and the implementation of appropriate care and information. However, it is important that maternity units and Trusts have systems and processes in place to facilitate this and ensure that risk assessment and management is undertaken in a systematic and robust way.

The publication of An Organisation with a Memory¹² emphasised the need for healthcare organisations to learn from critical safety incidents to improve care and act to reduce risks and increase safety. A holistic systems approach to understanding failure in health care was advocated which emphasised the inherent presence of human factors within an organisation which may predispose individuals to make mistakes. The report stressed the importance of considering the broader environmental context to help minimise those circumstances and situations which may contribute to the occurrence of error. Far from being random, the report found that human errors tended to fall into recurrent patterns whereby the same set of circumstances may provoke individuals to make the same mistake. Risk management strategies should therefore focus on removing such situational ‘error traps’.¹² This has become a predominant theme in more recent publications that have sought to expose the human factors that may lead to mistakes being made and consider ways that these can be minimised.13,14 Table 1.2 provides an overview of human factors that are often identified as a contributing factor in patient safety incidents¹³ alongside some examples that are pertinent for the provision of optimum care during childbirth emergencies.

Following the publication of An Organisation with a Memory,¹² the National Patient Safety Association (NPSA) was developed in 2001 with the aim of identifying and reducing risks to patients receiving NHS care and assisting all those involved in health care to identify and learn when things go wrong. Historically patient safety incidents were not always reported locally, often because of fears of disciplinary action, and it was recognised that there was a need to move from blaming individuals to understanding the underlying factors within the system that are more often responsible for incidents.¹⁵ The key functions developed by the NPSA were transferred to the NHS Commissioning Board Special Health Authority in 2012.

The National Reporting and Learning System (NRLS) is a central database which was established in 2003 and receives confidential reports of patient safety incidents from healthcare staff across England and Wales. Clinicians and safety experts analyse these reports to identify common risks to patients and opportunities to improve patient safety. Resources of the NRLS include the publication and dissemination of Patient Safety Alerts through the Central Alerting System (CAS) and the provision of regular feedback from the data collected to identify themes and causes. All healthcare organisations within England and Wales should report any patient safety incidents to the NRLS whose data the NHS Commissioning Board Authority will use to analyse risk, promote learning and tackle important patient safety issues at their root cause.¹⁶

Table 1.2  An overview of possible human factors that contribute to risk

Human factors that may contribute to patient safety incidents¹³

Possible examples during childbirth emergencies

•  Cognition and mental workload

•  Distractions

•  The physical environment

•  Physical demands

•  Service/product design

•  Teamwork

•  Process design

•  Stress and fatigue

•  Several professionals in the room

•  Lack of communication or people talking at once if a clear leader is not identified

•  Peripheral noise

•  Poor lighting and clutter

•  Possible need to make complicated drug calculations/ lack of prefilled syringes for high-risk drugs

•  Lack of equipment, for example in Resuscitaire/PPH trolley

•  Seeing what you expect to see – remember to check labels/drugs

The National Health Service Litigation Authority (NHSLA) was established in 1995 as a Special Health Authority whose duties include the provision of legal and professional advice to the NHS and Department of Health (DH), assisting the NHS with risk management and managing claims made against the NHS.¹⁷ As part of its safety and learning service the NHSLA publishes reports based on analysis drawn from their national database of claims. The latest report analysed 10 years of maternity claims between April 1, 2000 and March 31, 2010.¹⁸ During this time there had been a total of 5087 maternity claims with a total value of 3.1 billion pounds. The management of labour was the number one claim category within maternity, with shoulder dystocia being the eighth most common claim.¹⁸

The NHSLA is a partner in the Safer Births Initiative with The Kings Fund, Royal College of Obstetricians and Gynaecologists (RCOG), Royal College of Midwives (RCM), Centre for Maternal and Child Enquiries, Mothers and Babies: Reducing Risk through Audits and Confidential Enquiries across the UK (MBRRACE – UK) and the NRLS. There are many initiatives and strategies in place at a strategic level to assess and manage risk and which may feed into and inform the day-to-day practice of midwives on the front line. Lessons can be learnt from the analysis of safety incidents at both national and local levels. Many of the initiatives implemented within the workplace today have been done so in response to previous lessons learnt and there are many tools available to promote effective risk management and safe working within maternity. While it is important that safety incidents do not elicit a ‘knee-jerk’ response, midwives have a responsibility to act immediately should they believe that there is a risk to the safety of women and babies.¹

More recently there have been a number of high-profile cases and reports published that have reviewed the safety of the NHS and maternity services.19,20 A key issue that lies at the heart of these is that of culture. The Health and Care Professions Council (HCPC) have emphasised the role that organisations themselves play in the development of professionalism³ and how culture can exert a significant influence on the professional behaviour of practitioners and either help or hinder the extent to which they are able to carry out their professional duties.

Recent published reports following investigations into failing Trusts have revealed that poor organisational culture is synonymous with poor patient care and its associated impact on morbidity and mortality rates.19,20 Various initiatives implemented over the past decade have also sought to address the culture within which midwives work. The challenge of historical interprofessional and departmental barriers, drive for increased transparency and a commitment to report, investigate and learn from incidents to improve patient safety all serve to improve the clinical environment and promote a culture of openness and safety. Despite this, the Confidential Enquiry into Maternal Deaths and Morbidity 2009–2012²¹ has revealed that only 29% of the women who died were considered to have received good care which could not have been improved. Improvements to care were required in the remaining 71% of maternal mortalities with such improvements judged as having the potential to change the outcome in 52% of these cases.²¹ A key concern for the enquiry assessors was the apparent lack of information about the lessons that were learned locally following the maternal deaths as evidence of local reflection was missing for a high proportion of cases.

The Nursing and Midwifery Order 2001 grants the NMC authority to regulate midwifery and nursing in the United Kingdom. The Order also contains an additional set of powers for the NMC to set rules related to midwifery. These rules have provided midwives with an extra layer of regulation known as ‘statutory supervision’.²² The Order requires that a Local Supervising Authority (LSA) is established within each of the four countries of the United Kingdom. Midwives are required to give notice of their intention to practice to their LSA via their Supervisor of Midwives and each LSA must ensure the effective supervision of midwives in their area and investigate any concerns about midwives’ practice.

The effective supervision of midwives has the potential to challenge organisational culture and poor standards of care while promoting high standards of practice and woman-centred care.²³ In this way it can form an essential part of the risk management process within maternity services. However, effective supervision is often dependent upon the organisational structure within which it operates and can potentially serve to perpetuate the very culture that it is required to investigate or challenge. The primary function of supervision has recently been called into question following the publication of the report of the Morecambe Bay investigation which exposed systemic flaws in the quality of midwifery supervision.²⁰ A potential conflict of interest between midwifery supervision and regulation revealed that the supervisory and regulatory roles of supervisors of midwives were often confused, which failed to protect the interests of mothers and their babies.²⁴ This has led to a call for changes in the legislation regarding the supervision of midwives.²⁴ Individual cases reviewed also revealed that current supervisory arrangements may lead to inadequate escalation of information about poor care into Trust clinical governance and regulatory systems, leading to a failure to learn from mistakes.²⁴ The Kings Fund was subsequently commissioned to undertake a review of midwifery regulation by the NMC²² and in January 2015 the NMC requested a change in its legislation in order to remove the additional layer of regulation applying to midwives. The Secretary of State for Health in England announced in July 2015 that the government will change the legislation governing the regulation of midwives and supervision will be removed from the regulatory legislation.²⁵ Work is currently being undertaken to plan for the future with regards to supervision and its role within midwifery, in the meantime, the current rules and standards set by the NMC continue to apply. It is envisaged that supervision will continue to exist within midwifery but the focus will be on leadership, support and advocacy.²⁶

WORKING TOGETHER: TEAMWORK, MULTIPROFESSIONAL TRAINING AND CREATING A POSITIVE CULTURE

Creating a positive culture

Whereas a positive working culture can increase patient safety, a negative working culture which encompasses the elements of poor engagement, a lack of teamwork and suboptimal communication can expose women and babies to unnecessary harm and the devastating impact that this can have on people’s lives.19,20,27,28 It has been suggested that leadership is the most influential factor in shaping organisational culture²⁹ and the need for Trusts to develop appropriate leadership strategies and behaviours to improve the delivery of care is well recognised.29,30 Such strategies have the potential to make a significant difference to the outcomes and experiences for both mothers and their partners²⁷ and midwives have a significant role to play in the delivery of such strategies.31,32

A substantial review of the published literature surrounding leadership and leadership development in health care was undertaken³⁰ and identified five key elements necessary for sustaining positive work cultures that ensure high-quality, compassionate care for patients. A summary of these five elements is shown in Box 1.1.

BOX 1.1: The five elements required to sustain a positive working culture³⁰

•  Shared vision to improve care and optimise outcomes

•  Clear, aligned objectives for all teams, departments and individual staff

•  Supportive and enabling people management and high levels of staff engagement

•  Learning, innovation and quality improvement embedded in the practice of all staff

•  Effective teamwork

The importance of all staff having shared values and mutually agreed objectives³³ has been emphasised as this enables practitioners to work together effectively to coordinate their efforts, knowledge and resources to successfully deliver highly complex clinical care.²⁹ This is particularly important when responding to emergencies within childbearing where everyone is working together towards the common goal of optimising outcomes for the mother and her baby using the best available methods. Effective leadership is important when coordinating the activities of team members in response to an emergency situation and leadership duties should include ensuring that the evolving plan of care is clear to all, information is shared, resources are procured and the environment managed so that team members are able to complete their roles and responsibilities effectively where possible.³⁴

There may be occasions where situational leadership is required whereby the initial clinician responding to the emergency assumes leadership until more senior help is available.³⁴ A lack of leadership was a feature in three deaths from postpartum haemorrhage in the latest Confidential Enquiries and the need for clinicians to step up to assume responsibility for the coordination of care was emphasised.³⁵ Perceived hierarchies within the team may deter junior clinicians from speaking up³⁴ and a key recommendation from the Kings Fund Inquiry was the need to build upon multiprofessional relationships to support and enable team working27,36 so that clinicians are empowered to speak up, raise concerns and assume leadership responsibilities when needed.³⁷

Investing in staff team building on the labour ward is a key element of improving the function and capability of the multiprofessional team and both management and lead clinicians should strive to develop creative ways to engage staff and provide opportunities for team building.²⁷ While resource issues often mean that staff are unable to leave the workplace to attend team-building days, other ways of developing staff engagement and team working include regularly scheduled in-house forums and training opportunities. Labour ward forums, case reviews, CTG review meetings and perinatal mortality meetings provide an opportunity to enhance team working and communication and break down interprofessional barriers. Such meetings may also offer the potential for the debriefing of staff following an emergency and provide an opportunity for individual and team learning while events remain fresh.³⁸ However, it is important that these forums are managed in such a way that the focus remains on the problem or incident itself rather than the allocation of individual blame. In this way individuals are able to give and receive both constructive and positive feedback in order to learn from incidents and help foster a culture of safety.

Teamwork and multiprofessional training

Midwives have a duty to maintain their knowledge and skills to ensure that they practice safely and effectively.¹ The deployment of a well-trained and skilled workforce is at the heart of safe maternity care³⁷ and important to ensure the prompt recognition of, and response to, emergency situations during childbirth. The failure of staff to recognise or respond appropriately to an acute situation is an ongoing theme within the Confidential Enquiries21,39 and there may be occasions when junior members of staff feel overwhelmed or lack the required skill and confidence to respond appropriately when faced with an emergency situation in the hospital or the community.²⁰

The effectiveness of local interprofessional training is recognised within the obstetric literature and ‘it has long been recognised that professional groups who work together should also train together to promote understanding of each other’s practice and foster good team working’.²⁷ Maternity units within the United Kingdom are required to implement local interprofessional training around childbirth emergencies in order to improve clinical skills while developing communication and team working.40–42 This is particularly significant when responding to emergencies during childbirth as optimal teamwork is essential in order to prevent avoidable morbidity and mortality for mothers and babies.21,27,28

Local interprofessional training is associated with significant improvements in clinical outcomes.²⁰ It helps reduce interprofessional stereotyping, and flattens hierarchies while facilitating collaboration and a positive working environment.28,43 It also provides clinicians with the opportunity to refine and develop existing leadership and clinical skills within a safe environment and develop the confidence to take charge of and refer appropriately within an escalating clinical situation.

The Simulation and Fire drill Evaluation (SaFE) study group received a research grant from the Department of Health to conduct a regional randomised controlled trial with the aim of reviewing obstetric emergencies training and to determine if including teamwork training in the obstetric emergencies courses improved the team’s management even further. Eight hospitals across the South West of England took part in the SaFE study and the trial demonstrated the importance of teamwork and clear communication and revealed improvements in knowledge, clinical skills and team working during simulated emergencies following training.44–46

More recently studies have continued to demonstrate the value of interprofessional training using simulation. A large retrospective cohort study was undertaken in eight public hospitals in Southern Australia to assess the introduction of PRactical Obstetric Multi-Professional Training (PROMPT) into maternity units and evaluate the effects on organisational culture and perinatal outcomes in maternity units.⁴⁷ The results showed significant improvements in staff attitudes towards safety and teamwork in addition to improvements in neonatal outcomes. Other studies have also reported significant improvements in communication⁴⁸ and safety culture⁴⁹ as well as clinical outcomes.45,50 The RCOG cautions, however, that not all studies have shown an improvement in outcomes following the introduction of training and recommend that hospitals monitor the neonatal injury rate after the introduction of training to ensure it is effective.⁵¹

It is imperative that emergency training prepares clinicians for all possible outcomes and prompts them to consider the wider clinical picture at all times during an emergency. This has been referred to as situational awareness³⁸ whereby clinicians survey their environment and think ahead to ensure they remain aware of the various factors that may impact upon care and include the possibility of all eventualities within their planning.³⁴ The importance of keeping a ‘critical mind, anticipating risk factors and explaining observations rather than accepting them’³⁵ forms a part of developing situational awareness and may help prevent delays in recognising and responding to emergencies within childbirth. The Latest Confidential Enquiry has emphasised the importance of the ‘ongoing clinical scrutiny of the woman’³⁵ which may prevent practitioners from making inaccurate assumptions or failing to detect significant changes in the rapidly deteriorating woman.

COMMUNICATION AND RECORD-KEEPING

Communication

While the most recent Confidential Enquiries into maternal deaths shows a decrease in the overall rate of maternal death across the United Kingdom, a lack of optimal communication and teamwork remains a continuing theme from previous enquiries.21,39 Many factors contribute to suboptimal communication and having an explicit strategy to facilitate communication within acute situations is important to ensure that individuals, teams and departments communicate effectively.21,52 The use of the SBAR (situation, background, assessment, recommendation) tool can lead to improved communication between team members and its use is recommended to improve communication during emergencies in childbirth.³⁷

The multiprofessional development and use of evidence-based clinical guidelines and care pathways have been shown to facilitate the organisation of multiprofessional care, communication and teamwork.⁵³ There is some evidence that care pathways are effective interventions for improving teamwork, increasing the organisational level of care processes and decreasing risk of burnout for healthcare teams in an acute hospital setting.⁵⁴ The European Pathway Association (E-P-A) has defined a care pathway as ‘a complex intervention for the mutual decision making and organisation of care processes for a well-defined group of patients during a well-defined period’.55,56 Defining characteristics of care pathways include having clearly stated goals and objectives of care that are evidence based and the coordination and sequencing of the care process and activities of the multiprofessional team.⁵⁶ In this way they are a useful tool to use to facilitate the coordination, communication and documentation of care by the multiprofessional team during an emergency. However, they should be communicated, reviewed and adapted to the requirements of the individual woman or baby.

The use of proformas and early warning systems are other tools that can be used to facilitate communication and have been shown to reduce mortality and improve care.57,58 Care bundles such as the UK Sepsis Trust ‘Sepsis Six Care Bundle’⁵⁹ should be used as a matter of urgency when dealing with a confirmed diagnosis of sepsis60–62 and the use of MEOWs charts can provide a framework to encourage the undertaking of observations and recognition and escalation of abnormalities.³⁵

It is vital that documented findings are escalated and acted upon appropriately although published reports suggest that this is not always the case.20,21,39 The findings of the report into the Morecambe Bay investigation have shown that there was evidence of ‘a lack of situation awareness, with a deficiency in understanding of basic observations, their clinical significance and how they should be managed. There were many instances where symptoms and signs, observations, progress in labour, and the concerns of patients, parents and families were recorded, but were not underpinned by a clinical plan or escalation of clinical decision-making’.²⁰ Clear communication and record-keeping enable observations to be shared with others to help maintain an ongoing awareness of the clinical situation³⁴ and staff should have a low threshold for seeking assistance should they have any concerns or are unsure.⁶³ Within the latest enquiry into maternal deaths and morbidities there was a common tendency for junior doctors and midwives to not inform their senior colleagues in a timely way.²¹ This was particularly pertinent in the cases of those women who died from sepsis and cases were cited where earlier referral may have changed the outcomes for the women and their families.⁶² Interprofessional communication could also have been improved to ensure that all those involved with the care were aware of significant risk factors or concerns.

Multiprofessional communication is a vital component of the overall safety culture of a maternity unit and the importance of learning lessons from safety incidents has been discussed previously within this chapter. Members of the multidisciplinary team need to engage to provide mutual support and review the evidence when things go wrong. Through systematic multiprofessional scrutiny of cases, feedback can be provided and acted upon to ensure that any necessary improvements to the systems and processes in place are made. It also enables any local training or individual practitioner behavioural, knowledge and competency issues that may become apparent to be dealt with constructively. The use of cross-monitoring has been advocated as a means of monitoring the actions of other team members to facilitate situation awareness and the self-correction of tasks in order to reduce error in the provision of health care.34,64 This enables the actions of the members of the team during an emergency to be monitored in a supportive way by colleagues with the purpose of sharing the workload, facilitating communication between teams and ensuring that a safe standard of care is provided.

When faced with immediate concerns regarding maternal and fetal well-being, most women would value safety and good communication with staff to autonomous choice.⁶⁵ The Being Open Framework⁶⁶ emphasises the importance of effective communication with patients when things go wrong and midwives have a duty of candour to the women that they provide care for.¹ Communication between staff and women has a significant influence on the maternal experience and women’s perception of the care they have received.⁴¹ Effective communication is of paramount importance when responding to childbirth emergencies. A phenomenological study undertaken to explore women’s experiences of their birth emergencies⁶⁷ found that the quality of women’s interactions with midwives and doctors was integral to how they felt about their experience. Non-verbal cues such as facial leakage, whereby the facial expressions of clinicians revealed their own anxiety, perpetuated the fear and distress that women felt both during and after the event. Women valued supportive interactions from clinicians and issues with communication included poor communication, a lack of interaction and inadequate or inappropriate explanations.

Compassion in Practice, the national strategy for nurses, midwives and care staff, was launched in December 2012 and emphasises the government’s commitment to the delivery of high-quality, compassionate care by nurses, midwives and care staff.⁶⁸ Part of this was ensuring that the six ‘Cs’ (care, compassion, competence, communication, courage and commitment) are embedded within clinical practice. The NMC Code is also clear about the need for nurses and midwives to communicate clearly and treat people as individuals with kindness, respect and compassion.¹ While this may seem to be stating the obvious, recent surveys into women’s experiences suggest that this is not always being achieved.19,20 Whereas the findings from the most recent survey of women’s experiences of maternity care⁶⁹ showed that improvements were made in some areas, a significant proportion of women expressed concerns about communication between maternity staff and themselves. Creating an open safety culture and having access to goodquality multiprofessional simulation training ensures that midwives have the necessary skills, knowledge and confidence to respond appropriately to emergencies during childbearing. It stands to reason that when clinicians feel supported and prepared, they will feel less anxious and be empowered to offer effective support and care to women.

Record-keeping

Record-keeping is an integral part of the professional practice of midwives and midwifery records can serve to reflect the standard of midwifery practice provided.¹ Ultimately midwives can be called to account through their records as to whether they have met their duty of care. This is because records provide the evidence that care has been provided as well as the justification for such care. Records completed to a high standard adhere to the principles of good record-keeping and provide evidence that midwives are practicing in a safe and competent way.⁷⁰ Such principles have been set out within the NMC guidance for recordkeeping document, Midwives Rules and Standards and the Code.1,4,70

The Data Protection Act section 68 (2) has defined health records as ‘consisting of information relating to the physical or mental health or condition of an individual made by, or on behalf of, a health professional in connection with the care of that individual’.⁷¹ This includes all records that are relevant to midwives’ scope of practice and the principles of good record-keeping apply to all types of records and communication methods and are not just confined to the maternity notes.⁷⁰ Such records are legal documents that can be called as evidence within a court of law, coroner’s inquests and fitness to practice panels. Within a court of law it is generally viewed that if something is not recorded, then it has not been done5,72 and failure to maintain a good standard of record-keeping is one of the main reasons that midwives and nurses appear at a NMC Fitness to Practice panel.⁵

Record-keeping serves many vital functions and an overview of these are included within Table 1.3 alongside a list of the various different formats that records might take.

The principles of good record-keeping specify that records should be clearly written in indelible ink and be factual, accurate, follow a logical sequence and use accepted professional terminology so that they can be understood by both colleagues and women.70,73 Notes should be contemporaneous or when this is not possible be written as soon as is possible following the event, identifying the time when written.¹ Records should also identify any risks or problems that have arisen and show the action taken to deal with them including assessment details, reviews, actions and plans for future care.

Record-keeping can be especially difficult during an emergency situation when a high level of stress may be present. The allocation of a scribe to contemporaneously record events as they unfold should be used where possible.⁷⁴ The RCOG has recommended the use of proformas which can be adapted for local use and provides guidance for critical points to include in record-keeping during specific childbirth emergencies.51,63 An adaption of these is presented as an example within Table 1.4.

Local training in record-keeping has been recommended to be included as part of multiprofessional childbirth emergency training (‘skills drills’) provided by maternity units, to ensure that records include the required critical elements.51,75 It should be assumed that all records will be scrutinised following a childbirth emergency in order to ensure that a safe standard of care was provided, learn lessons and provide answers for women and their families. It is important that documentation is accurate and reflects the reality of what occurred during the emergency. This was investigated as part of the previously mentioned SaFE trial by comparing a written record with a videotape of the simulation and an electronic record of the force applied to the baby during the simulation of shoulder dystocia.⁷⁴ The authors also sought to compare the quality of record-keeping with and without the use of a proforma. Both video and force recording for each simulation were obtained which enabled the comparison of the written records with the actual events. The study findings suggested that record-keeping during childbirth emergencies is a complex process fraught with many influencing factors. Although the use of a proforma demonstrated improved completeness of documentation, it may have reduced the accuracy of recording in some areas and the immediate written recollection of events by clinicians may often be both inaccurate and incomplete.⁷⁴

Table 1.3  Functions of record-keeping

The types of records used within midwifery practice

Various purposes of record-keeping

•  Handwritten/computer clinical notes

•  E-mails and letters to and from other health professionals

•  Laboratory reports

•  X-rays

•  Printouts from monitoring equipment

•  Incident reports and statements

•  Photographs

•  Videos

•  Tape recordings of telephone conversations

•  Text messages

•  Provides an accurate account of care planning, decision making, treatment and care given as well as responses to care and further action taken

•  Promotes the ability to detect problems at an early stage detailing the reasoning behind any action taken

•  Demonstrates continuity of care

•  Facilitates and supports interprofessional and client communication

•  Supports clinical audit/research, allocation of resources and service planning

•  Helps to address complaints and/or legal processes

•  Improves accountability

Source:  Adapted from the Nursing and Midwifery Council (NMC). 2009b. Record Keeping – Guidance for Nurses and Midwives. London: NMC Available at http://www.nipec.hscni.net/Image/SitePDFS/nmcGuidanceRecordKeepingGuidanceforNursesandMidwives.pdf (accessed March 14, 2016).

Table 1.4  Critical points to include in record-keeping

Childbirth emergency

Critical points

Shoulder dystocia

Time of delivery of the head and time of delivery of the body

Position of fetal head at delivery

Position of anterior shoulder at the time of the dystocia

Manoeuvres performed, their timing and sequence

Degree of axial traction applied

Maternal perineal and vaginal examination

Estimated blood loss

Assessment of the mother

Staff in attendance and the time they arrived

General condition of the baby (Apgar score)

Umbilical cord blood acid–base measurements

Neonatal assessment of the baby

Postpartum haemorrhage

The staff in attendance and the time they arrived

The sequence of events

The time of administration of different pharmacological agents given, their timing and sequence

The time of surgical intervention, where relevant

The condition and overall assessment of the mother throughout the different steps

Identification and timing of the fluid and blood products given

Source:  Adapted from the Royal College of Obstetricians and Gynaecologists (RCOG). 2012a. Green-Top Guideline No. 42 Shoulder Dystocia. 2nd ed. London: RCOG Available at https://www.rcog.org.uk/globalassets/documents/guidelines/gtg42_25112013.pdf (accessed April 8, 2015); Royal College of Obstetricians and Gynaecologists (RCOG). 2009. Green-Top Guideline No. 52 Prevention and Management of Postpartum Haemorrhage. London: RCOG. Available at https://www.rcog.org.uk/globalassets/documents/guidelines/gt52postpartumhaemorrhage0411.pdf (accessed April 8, 2015).

The authors concluded that there were different virtues associated with the use of a proforma and writing longhand, and postulated that writing longhand may encourage more careful thought than simply ticking preformatted boxes. The use of a proforma however appeared to act as an aide-memoire for more comprehensive documentation although may encourage the practitioners to record things of which they have no true recollection and miss items that are not included within the proforma.⁷⁴ The use of a scribe within an emergency situation to record events contemporaneously may circumvent this by increasing the accuracy of recordings while having the benefit of helping to ensure all critical components of care are documented.⁷⁴

As well as the potential for maternal psychological sequelae to occur as a result of childbirth emergencies there is evidence that those midwives directly involved with the emergency may also suffer a degree of traumatisation during and following the event.⁷⁶ It is important to bear in mind how individual perceptions of events may become distorted and in turn impact upon the quality and completeness of subsequent recordkeeping. A recent prospective observational study that assessed the quality of midwifery documentation from reviewing the intrapartum notes and partograms of 61 consecutive women found that fatigue may also play a role in suboptimal documentation towards the middle and end of the shift.⁷⁷ The provision of support from senior staff or a Supervisor of Midwives may help improve the standard of record-keeping following such events.

Social media

Within today’s society the use of social media is commonplace and firmly embedded within the working and personal lives of most practitioners via Facebook, Twitter and various other electronic vehicles. Midwives have a professional duty to maintain the confidentiality of those in their care and this duty extends to both their online professional and personal lives.⁷⁸ The NMC has recently published guidance for social networking⁷⁹ and midwives may put their registration at risk as well as jeopardise their professional integrity by behaving online in a way that may be deemed as inappropriate or unprofessional.

CONCLUSION

The NHS Constitution has set out the standards that those accessing their services should expect.² Midwives are knowledgeable and skilled practitioners who must behave in a way that reflects high standards of personal integrity and justify the trust that is placed in them by the women and families who access their care. This chapter has introduced the reader to an overview of the components that are essential to professional practice and which must entwine together to underpin midwifery care.

The adverse aspects of risk and patient safety have been emphasised within maternity services in recent years and this has been as a result of both individual tragedies and a wider concern that has been expressed about the infrastructure in place to support maternity services.²⁷ While much of the language that centres on risk and patient safety is negative²⁷ it is important to remember that midwives hold a privileged position in society today and have the potential to shape the experiences and outcomes for mothers and their families during a momentous period in their lives. The provision of good-quality safe midwifery care is accomplished through the tireless commitment of individual clinicians and the robust processes and systems of care that are in place within maternity units and hospitals. It is vital that all midwives have an understanding of what professionalism means and how it must be promoted and enhanced to safeguard the future of midwifery and maternity care.

REFERENCES

1.  Nursing and Midwifery Council (NMC). 2015a. The Code. Professional Standards of Practice and Behaviour for Nurses and Midwives. London: NMC, p. 15. Available at http://www.nmc.org.uk/standards/code (accessed July 26, 2015).

2.  Department of Health (DH). 2015. The NHS Constitution. London: Crown Copyright. Available at https://www.gov.uk/government/uploads/system/uploads/attachment_data/file/480482/NHS_Constitution_WEB.pdf (accessed March 14, 2016).

3.  Health and Care Professions Council (HCPC). 2011. Professionalism in Healthcare Professionals. London: Health and Care Professions Council. Available at http://www.hpc-uk.org/assets/documents/10003771Professionalisminhealthcareprofessionals.pdf (accessed November 1, 2014).

4.  Nursing and Midwifery Council (NMC). 2012. Midwives Rules and Standards. London: NMC. Available at http://www.nmc.org.uk/standards/additional-standards/midwives-rules-and-standards (accessed July 26, 2015).

5.  Dimond B. 2005. Legal Aspects of Midwifery. 4th ed. London: Quay Books, MA Healthcare.

6.  Griffith R, Tengnah C, Patel C. 2010. Law and Professional Issues in Midwifery. Exeter: Learning Matters.

7.  Nursing and Midwifery Council (NMC). 2009a. Standards for Pre-Registration Midwifery Education. London: NMC Available at http://www.nmc.org.uk/standards/additional-standards/standards-for-pre-registration-midwifery-education (accessed March 1, 2015).

8.  Nursing and Midwifery Council (NMC). n.d. Standards of Competence for Registered Midwives. Available at http://www.nmc.org.uk/standards/additional-standards/standards-of-competence-for-registered-midwives (accessed February 28, 2015).

9.  Nursing and Midwifery Council (NMC). 2011. Prep Handbook. London: NMC. Available at http://www.nmc.org.uk/standards/additional-standards/prep-handbook (accessed March 1, 2015).

10.  International Confederation of Midwives (ICM). 2014. Position Statement: Professional Accountability of the Midwife. Available at http://www.internationalmidwives.org/assets/uploads/documents/Position%20Statements%20-%20English/Reviewed%20PS%20in%202014/PS2008_014%20V2014%20Professional%20Accountability%20of%20the%20Midwife%20ENG.pdf (accessed November 1, 2014).

11.  Nursing and Midwifery Council (NMC). 2008. Providing Care in an Emergency Situation Outside the Work Environment. London: NMC. Available at http://www.em-online.com/download/medical_article/37178_Providing%20Care%20In%20An%20Emergency%20Situation%20Outside%20The%20Work%20Environment.pdf (accessed March 14, 2016).

12.  Department of Health. 2000. An Organisation with a Memory. London: Crown Copyright. Available at http://webarchive.nationalarchives.gov.uk/20130107105354/http://www.dh.gov.uk/prod_consum_dh/groups/dh_digitalas-sets/@dh/@en/documents/digitalasset/dh_4065086.pdf (accessed July 26, 2015).

13.  Carthey J, Clarke J. 2010. The ‘How to Guide’ for Implementing Human Factors in Healthcare. London: Patient Safety First.

14.  National Health Service (NHS) England. 2013. Human factors in healthcare. A Concordat from the National Quality Board. Available at http://www.england.nhs.uk/wp-content/uploads/2013/11/nqbhum-fact-concord.pdf (accessed March 1, 2015).

15.  Stephenson T. 2005. The National Safety Patient Agency. Archives of Disease in Childhood, 90:226–228.

16.  National Patient Safety Agency. 2010. Transfer of Patient Safety Function to the NHS Commissioning Board Special Health Authority. Available at http://www.npsa.nhs.uk/corporate/news/transfer-of-patient-safety-function (accessed March 1, 2015).

17.  NHS Litigation Authority. n.d. About Us. Available at http://www.nhsla.com/AboutUs/Pages/Home.aspx (accessed July 20, 2015).

18.  NHS Litigation Authority. 2012. Ten Years of Maternity Claims: An Analysis of NHS Litigation Authority Data. London: NHS Litigation Authority. Available at http://www.nhsla.com/safety/Documents/Ten%20Years%20of%20Maternity%20Claims%20%20An%20Analysis%20of%20the%20NHS%20LA%20Data%20-%20October%202012.pdf (accessed July 26, 2015).

19.  Francis R. 2013. Report of the Mid Staffordshire NHS Foundation Trust Public Inquiry. London: HMSO.

20.  Kirkup B. 2014. The Report of the Morecambe Bay Investigation. London: The Stationary Office. Available at https://www.gov.uk/government/uploads/system/uploads/attachment_data/file/408480/47487_MBI_Accessible_v0.1.pdf (accessed July 26, 2015).

21.  Knight M, Kenyon S, Brocklehurst P, Neilson J, Shakespeare J, Kurinczuk JJ (Eds.), on behalf of MBRRACE-UK. 2014. Saving Lives, Improving Mothers’ Care – Lessons Learned to Inform Future Maternity Care from the UK and Ireland Confidential Enquiries into Maternal Deaths and Morbidity 2009–12. Oxford: National Perinatal Epidemiology Unit, University of Oxford. Available at https://www.npeu.ox.ac.uk/downloads/files/mbrrace-uk/reports/Saving%20Lives%20Improving%20Mothers%20Care%20report%202014%20Full.pdf (accessed March 1, 2015).

22.  Baird B, Murray R, Seale B, Foot C, Perry C. 2015. Midwifery Regulation in the United Kingdom. London: The Kings Fund. Available at http://www.nmc.org.uk/global-assets/sitedocuments/councilpapersand-documents/council-2015/kings-fund-review.pdf (accessed July 26, 2015).

23.  LSAMO National Forum (UK). 2009. Modern Supervision in Action. London: NMC. Available at http://www.lsamoforumuk.scot.nhs.uk/media/3091/modern_supervision_in_action_august_09_1_.pdf (accessed July 27, 2015).

24.  Parliamentary and Health Service Ombudsman. 2013. Midwifery Supervision and Regulation: Recommendations for Change. London: The Stationery Office.

25.  Nursing and Midwifery Council. 2015b. Review of Midwifery Regulation: An Update on Midwifery Regulation – 16 July 2015. Available at https://www.nmc.org.uk/news/news-and-updates/nmc-response-to-secretary-of-states-statement-on-midwifery-supervision/ (accessed March 14, 2016).

26.  Gillman LJ. 2015. Re-Framing Midwifery Supervision: A Discussion Paper. Available at https://www.rcm.org.uk/news-views-and-analysis/views/first-iteration-of-a-paper-on-supervision (accessed July 26, 2015).

27.  Kings Fund. 2008. Safe Births: Everybody’s Business: An Independent Inquiry into the Safety of Maternity Services in England. London: The Kings Fund. Available at http://www.kingsfund.org.uk/sites/files/kf/field/field_publication_file/safe-births-everybodys-business-onora-oneill-february-2008.pdf (accessed April 8, 2015).

28.  Cornthwaite K, Edwards S, Siassakos D. 2013. Reducing risk in maternity by optimising teamwork and leadership: An evidence-based approach to save mothers and babies. Best Practice and Research Clinical Obstetrics and Gynaecology, 4:571–581.

29.  West MA, Lyubovnikova J. 2013. Illusions of team working in health care. Journal of Health Organization and Management, 27(1):134–142.

30.  West M, Armit K, Loewenthal L, Eckert R, West T, Lee A. 2015. Leadership and Leadership Development in Healthcare: The Evidence Base. London: Faculty of Medical Leadership and Management.

31.  Department of Health. 2009. Delivering High Quality Midwifery Care: The Priorities, Opportunities and Challenges for Midwives. London: Crown Copyright.

32.  Midwifery 2020. 2010. Delivering Expectations. Available at https://www.gov.uk/government/uploads/system/uploads/attachment_data/file/216029/dh_119470.pdf (accessed December 1, 2014).

33.  West M, Dawson J, Admasachew L, Topakas A. 2011. NHS Staff Management and Health Service Quality. London: Department of Health.

34.  Deering S, Johnstone LC, Colacchio K. 2011. Multidisciplinary teamwork and communication training. Seminars in Perinatology, 35(2):89–96.

35.  Paterson-Brown S, Bamber J, on behalf of the MBRRACE-UK haemorrhage chapter writing group. 2014. Prevention and treatment of haemorrhage. In: Knight M, Kenyon S, Brocklehurst P, Neilson J, Shakespeare J, Kurinczuk JJ. (Eds.), on behalf of MBRRACE-UK. Saving Lives, Improving Mothers’ Care – Lessons Learned to Inform Future Maternity Care from the UK and Ireland Confidential Enquiries into Maternal Deaths and Morbidity 2009–12. Oxford: National Perinatal Epidemiology Unit, University of Oxford, pp. 45–55.

36.  Smith A, Dixon A. 2007. Health Care Professionals’ Views about Safety in Maternity Services. London: The Kings Fund. Available at http://www.kingsfund.org.uk/sites/files/kf/field/field_document/health-care-profs-view-maternity-safety-maternity-services-inquiry.pdf (accessed July 26, 2015).

37.  Thomas V, Dixon A. 2012. Improving Safety in Maternity Services. A Toolkit for Teams. London: The Kings Fund. Available at http://www.kingsfund.org.uk/publications/improving-safety-maternity-services (accessed July 26, 2015).

38.  Leonard M, Graham S, Bonacum D. 2004. The human factor: The critical importance of effective teamwork and communication in providing safe care. Quality and Safety in Health Care, 13(Suppl. 1):i85–i90.

39.  Centre for Maternal and Child Enquiries (CMACE). 2011. Saving Mothers’ Lives: Reviewing maternal deaths to make motherhood safer: 2006–08. The Eighth Report on Confidential Enquiries into Maternal Deaths in the United Kingdom. BJOG: An International Journal of Obstetrics and Gynaecology, 118(Suppl. 1):1–203.

40.  Royal College of Obstetricians and Gynaecologists RCOG. 2014. Green-Top Guideline No. 50 Umbilical Cord Prolapse. London: RCOG. Available at https://www.rcog.org.uk/globalassets/documents/guidelines/gtg-50-umbilicalcordprolapse-2014.pdf (accessed April 8, 2015).

41.  Royal College of Obstetricians and Gynaecologists (RCOG). 2015. Joint RCOG and RCM Statement: Kirkup Report into Maternity Services at Morecambe Bay NHS Trust. Available at https://www.rcog.org.uk/en/news/joint-rcog-and-rcm-statement-kirkup-report (accessed April 8, 2015).

42.  Royal College of Midwives RCM. 2015. Joint Statement from the Royal College of Midwives and the Royal College of Obstetricians and Gynaecologists on the Kirkup Report into Maternity Services at Morecambe Bay. Available at https://www.rcm.org.uk/news-views-and-analysis/news/joint-statement-from-the-royal-college-of-midwives-and-the-royal (accessed April 8, 2015).

43.  Siassakos D, Fox R, Hunt L, et al. 2011. Attitudes towards safety and teamwork in a maternity unit with embedded team training. American Journal of Medical Quality, 26:132–137.

44.  Draycott TJ, Sibanda T, Owen L, Akande V, Winter C, Reading S, Whitelaw A. 2006. Does training in obstetric emergencies improve neonatal outcome? BJOG: An International Journal of Obstetrics and Gynaecology, 113(2):177–182.

45.  Siassakos D, Crofts JF, Winter C, Weiner CP, Draycott TJ. 2009a. The active components of effective training in obstetric emergencies. BJOG: An International Journal of Obstetrics and Gynaecology, 116(8):1028–1032.

46.  Siassakos D, Hasafa Z, Sibanda T, et al. 2009b. Retrospective cohort study of diagnosis-delivery interval with umbilical cord prolapse: The effect of team training. BJOG: An International Journal of Obstetrics and Gynaecology, 116:1089–1096.

47.  Shoushtarian M, Barnett M, McMahon M, Ferris J. 2014. Impact of introducing practical obstetric multi-professional training (PROMPT) into maternity units in Victoria, Australia. BJOG: An International Journal of Obstetrics and Gynaecology, 121(13):1710–1718.

48.  Noblot E, Raia-Barjat T, Lajeunesse C, et al. 2015. Training program for the management of two obstetric emergencies within a French perinatal care network. European Journal of Obstetrics and Gynecology and Reproductive Biology, 189:101–105.

49.  van der Nelson HA, Siassakos D, Bennett J, Godfrey M, Spray L, Draycott T, Donald F. 2014. Multiprofessional team simulation training, based on an obstetric model, can improve teamwork in other areas of health care. American Journal of Medical Quality, 29(1):78–82.

50.  Draycott TJ, Crofts JF, Ash JP, et al. 2008. Improving neonatal outcome through practical shoulder dystocia training. Obstetrics and Gynecology, 112(1):14–20.

51.  Royal College of Obstetricians and Gynaecologists (RCOG). 2012a. Green-Top Guideline No. 42 Shoulder Dystocia. 2nd ed. London: RCOG. Available at https://www.rcog.org.uk/globalassets/documents/guidelines/gtg42_25112013.pdf (accessed April 8, 2015).

52.  National Institute for Health and Care Excellence. 2007. CG50. Acutely Ill Patients in Hospital, Recognition of and Response to Acute Illness in Adults in Hospital. Available at http://www.nice.org.uk/guidance/cg50 (accessed April 8, 2015).

53.  Deneckere S, Euwema M, Van Herck P, Lodewijckx C, Panella M, Sermeus W, Vanhaecht K. 2012. Care pathways lead to better teamwork: Results of a systematic review. Social Science and Medicine, 75(2):264–268.

54.  Deneckere S, Euwema M, Lodewijckx C, Panella M, Mutsvari T, Sermeus W, Vanhaecht K. 2013. Better interprofessional teamwork, higher level of organized care, and lower risk of burnout in acute healthcare teams using care pathways: A cluster randomized controlled trial. Medical Care, 51(1):99–107.

55.  European Pathway Association. n.d. Clinical Care Pathways. Available at http://e-p-a.org/care-pathways/ (accessed March 14, 2016).

56.  Vanhaecht K, De Witte K, Sermeus W. 2007. The impact of clinical pathways on the organisation of care processes. PhD dissertation. KU Leuven: Katholieke Universiteit Leuven.

57.  Daniels R, Nutbeam T, McNamara G, Galvin C. 2011. The sepsis six and the severe sepsis resuscitation bundle: A prospective observational cohort study. Emergency Medicine Journal, 28(6):459–460.

58.  Miller RR, Dong L, Nelson NC, Brown SM, Kuttler KG, et al. 2013. Multicenter implementation of a severe sepsis and septic shock treatment bundle. American Journal of Respiratory and Critical Care Medicine, 188(1):77–82.

59.  UK Sepsis Trust. 2013. Clinical Tools. Available at http://sepsistrust.org/professional/educational-tools/ (accessed March 14, 2016).

60.  Royal College of Obstetricians and Gynaecologists. 2012b. Green-Top Guideline No. 64a. Bacterial Sepsis in Pregnancy. Available at https://www.rcog.org.uk/en/guidelines-research-services/guidelines/gtg64a (accessed July 28, 2015).

61.  Royal College of Obstetricians and Gynaecologists. 2012c. Green-Top Guideline No. 64b. Bacterial Sepsis following Pregnancy. Available at https://www.rcog.org.uk/globalassets/documents/guidelines/gtg_64b.pdf (accessed July 28, 2015).

62.  Churchill D, Rodger A, Clift J, Tuffnell on behalf of the MBRRACE-UK sepsis chapter writing group. 2014. Think Sepsis. In: Knight M, Kenyon S, Brocklehurst P, Neilson J, Shakespeare J, Kurinczuk JJ. (Eds.), on behalf of MBRRACE-UK. Saving Lives, Improving Mothers’ Care – Lessons Learned to Inform Future Maternity Care from the UK and Ireland Confidential Enquiries into Maternal Deaths and Morbidity 2009–12. Oxford: National Perinatal Epidemiology Unit, University of Oxford, pp. 27–43.

63.  Royal College of Obstetricians and Gynaecologists RCOG. 2009. Green-Top Guideline No. 52 Prevention and Management of Postpartum Haemorrhage. London: RCOG. Available at https://www.rcog.org.uk/globalassets/documents/guidelines/gt52postpartumhaemorrhage0411.pdf (accessed April 8, 2015).

64.  Agency for Healthcare Research and Quality. 2014. Labor and Delivery: Cross Monitoring: Team STEPPS Training Video. October 2014. Rockville, MD. Available at http://www.ahrq.gov/professionals/education/curriculum-tools/teamstepps/instructor/videos/ts_ldcrossmon/crossMonitorIntern.html (accessed May 1, 2015).

65.  Kingdon C, Neilson J, Singleton V, Gyte G, Hart A, Gabbay M, Lavender T. 2009. Choice and birth method: Mixed-method study of caesarean delivery for maternal request. BJOG: An International Journal of Obstetrics and Gynaecology, 116(7):886–895.

66.  National Patient Safety Agency and National Reporting and Learning Service. 2009. Being Open – Communicating Patient Safety Incidents with Patients, Their Families and Carers. London: NPSA/NRLS. Available at http://www.nrls.npsa.nhs.uk/ (accessed July 28, 2015).

67.  Mapp T, Hudson, K. 2005. Feelings and fears during obstetric emergencies – 1. British Journal of Midwifery, 13(1):30–35.

68.  Department of Health/NHS Commissioning Board. 2012. Compassion in Practice. Nursing, Midwifery and Care Staff. Our Vision and Strategy. London: Crown Copyright. Available at http://www.england.nhs.uk/wp-content/uploads/2012/12/compassion-in-practice.pdf (accessed July 27, 2015).

69.  Care Quality Commission (CQC). 2013. National Findings from the 2013 Survey of Women’s Experiences of Maternity Care. Available at http://www.cqc.org.uk/sites/default/files/documents/maternity_report_for_publication.pdf (accessed November 4, 2014).

70.  Nursing and Midwifery Council (NMC). 2009b. Record Keeping – Guidance for Nurses and Midwives. London: NMC. Available at http://www.nipec.hscni.net/Image/SitePDFS/nmcGuidanceRecordKeepingGuidanceforNursesandMidwives.pdf (accessed March 14, 2016).

71.  Data Protection Act. 1998. Meaning of ‘Accessible Record’. Available at http://www.legislation.gov.uk/ukpga/1998/29/section/68 (accessed July 20, 2015).

72.  Andrews A, O’Malley M. 2009. The ball’s in your court. Midwives, 12(5):24–25.

73.  Northern Ireland Practice and Education Council (NIPEC). 2010. Evidencing Care – Improving Record Keeping Practice. A Guide on Mandatory Requirements. Belfast: NIPEC. Available at http://www.nipec.hscni.net/recordkeeping/docs/RecordKeepingGuidanceMandatoryRequirementsFinal.pdf (accessed March 1, 2015).

74.  Crofts JF, Bartlett C, Ellis D, et al. 2008. Documentation of simulated shoulder dystocia: Accurate and complete? BJOG: An International Journal of Obstetrics and Gynaecology, 115(10):1303–1308.

75.  Deering S, Poggi S, Hodor J, Macedonia C, Satin AJ. 2004. Evaluation of residents’ delivery notes after a simulated shoulder dystocia. Obstetrics and Gynecology, 104:667–670.

76.  Sheen K, Slade P, Spiby H. 2014. An integrative review of the impact of indirect trauma exposure in health professionals and potential issues of salience for midwives. Journal of Advanced Nursing, 70(4):729–743.

77.  Bailey S, Wilson G, Yoong W. 2015. What factors affect documentation by midwives? A prospective study assessing relationship between length of shift, workload and quality of note keeping. Midwifery, 31(8):787–792.

78.  National Health Service (NHS) England. 2014. Confidentiality Policy. Available at http://www.england.nhs.uk/wp-content/uploads/2013/06/conf-policy-1.pdf (accessed July 25, 2015).

79.  Nursing and Midwifery Council. 2015b. Guidance on Using Social Media Responsibly. London: NMC. Available at http://www.nmc.org.uk/globalassets/sitedocuments/nmc-publications/social-media-guidance-30-march-2015-final.pdf (accessed September 1, 2015).

2

Maternal and newborn resuscitation

JENNY BREWSTER

Maternal resuscitation

Newborn resuscitation

Summary of midwifery responsibilities

References

MATERNAL RESUSCITATION

Resuscitation of a pregnant woman or a new mother is a rare event. However, midwives should always be prepared for both this eventuality, and the possibility that they may, either in the working or social environment, witness and assist at the resuscitation of a member of the public. A statement within the Nursing and Midwifery Council (NMC) Code¹ requires all registered personnel to assist at an emergency, be it while on or off duty. The principles of basic life support remain the same, although modifications are required when resuscitating a pregnant woman due to the physiological changes that occur during pregnancy.

The incidence of cardiac arrest related to childbirth is unknown as data on morbidity are not collected. The Royal College of Obstetricians and Gynaecologists² estimate the rate of maternal collapse to be in the region of 14 to 600 per 100,000 births. However, due to changes to the demographics of pregnancy in recent years with older women and those with pre-existing conditions, especially cardiac, becoming pregnant and maintaining a pregnancy, the numbers may well be expected to rise.

Maternal cardiac arrest is not only rare, but can frequently be unexpected. Therefore all midwives, obstetricians and support workers should ensure that they remain proficient and up to date in their basic life support skills by attending regular training and updating in resuscitation, including ‘skills drills’ in the clinical area, and that they are familiar with the resuscitation equipment. All resuscitation equipment and the expiry date of drugs should be checked on a daily basis.³ Equipment on resuscitation trolleys varies slightly from hospital to hospital. A suggested list may be found on the Resuscitation Council website.⁴ In areas with pregnant women, Harper and Wilson⁵ recommend that this should also include the basic equipment of a pre-mounted scalpel blade, gloves and cord clamps in case a perimortem caesarean section is required. It is frequently acknowledged that skills drills should also include recognition of the need for a perimortem caesarean section.⁶

In the recognition and initial treatment of maternal collapse, it is important that the cause is identified and appropriate management commenced.² The causes of cardiac arrest have been identified by the Resuscitation Council (UK)2,7 as belonging to one of eight categories, which are known by the 4Hs and 4Ts. These are identified in Box 2.1 together with the more common obstetric causes of cardiac arrest. Knight et al.⁸ recognised the most common causes of maternal death directly related to pregnancy as being thrombosis and thromboembolism (see Chapter 4), genital tract sepsis (see Chapter 12), pre-eclampsia and eclampsia (see Chapter 5) and haemorrhage (see Chapters 3 and 10). Cardiac disease is the most common cause of maternal death.⁸ All these conditions can lead to a need for resuscitation.⁹

BOX 2.1: 4Hs and 4Ts2,7

Hypoxia – eclampsia, cardiac conditions, severe asthma, high spinal block, Mendelsohn syndrome

Hypovolaemia – haemorrhage (antenatal, intrapartum, postnatal), disseminated intravascular coagulation (DIC)

Hyperkalaemia, hypokalaemia, hypocalcaemia, acidaemia, and other metabolic disorders

Hypothermia

Tension pneumothorax – severe asthma, trauma, complication from inserting a central venous pressure (CVP) line

Tamponade – trauma

Toxic substances – magnesium sulphate toxicity, septic shock, anaphylaxis

Thromboembolism – amniotic fluid embolism, pulmonary embolism

The main focus of care of all women should be to be aware of any known risk factors, to work continually to recognise these and any deterioration in condition to prevent maternal collapse where possible. However, when collapse does occur, the aim is to identify the cause as soon as possible and work to correct this while continually assessing bodily functions and commencing general resuscitation.¹⁰

Physiological changes in pregnancy

During pregnancy, there are many changes in the maternal body systems, some of which will lead in cases of maternal collapse to a rapid onset of hypoxia and acidosis due to reduced oxygencarrying capabilities, difficulties in ventilation and difficulties with performing effective chest compressions.

From around 20 weeks’ gestation, the weight of the gravid uterus may compress the inferior vena cava, and, to some extent, the aorta, when the woman is lying supine, reducing venous return and thus cardiac output, by up to 40%.2,11 This leads to supine hypotension, which may lead to maternal collapse, and certainly hinders effective resuscitation. Supine hypotension may be relieved by turning the woman onto the left lateral position, or by manually displacing the uterus to the left (see section entitled ‘Modifications to resuscitation for pregnant women’).

During pregnancy, there is an increase in the circulating blood volume of 30%–50%, which leads to physiological anaemia caused by haemodilution and a reduction in the oxygen-carrying capacity of the blood.2,11 The increased blood volume also leads to an increase in the cardiac output as well as the maternal pulse rate. The amount of blood circulating to the uterus increases dramatically throughout the pregnancy in order to supply the fetus through the placenta with the oxygen and nutrients required for its growth and development, from 100 mL/min in the first trimester to 500 mL/min by term.¹¹ The sizable volume of blood circulating to the uterus means that large amounts of blood may be rapidly lost. This, however, may not be immediately apparent as the extra circulating volume masks the symptoms of haemorrhage, and up to 35% of the circulating blood volume may be lost before the woman becomes symptomatic.²

The major changes in the respiratory system affecting resuscitation in pregnancy are due to the growth of the uterus which affects the functional capacity of the lungs, as well as increase in ventilation by up to 40% caused by the increased progesterone levels in the body,2,11 in order to supply the feto-placental unit. These factors lead to the rapid onset of hypoxia when there is a lack of ventilation to the lungs.² Intubation is also more difficult during pregnancy due to weight gain and the possibility of laryngeal oedema.

Physiological changes when body systems are not maintained

For the body to survive cardiopulmonary collapse, blood circulation and respiration must be maintained with an adequate circulating volume. Once the heart stops beating, blood stops circulating around the body, the cells become hypoxic and the metabolism within the cells alters leading to an acidotic state. The normal level of blood pH is between 7.35 and 7.45 (see Box 2.2).

Cells require oxygen to produce adenosine triphosphate (ATP), the energy source that is needed to power the cells’ functions. As a by-product of this, carbon dioxide and water are produced. Carbon dioxide under normal circumstances is a stimulator of respirations. However, where the levels build up in conditions of collapse, this is detrimental to the balance of body fluids. When oxygen is not supplied to the cells in sufficient amounts, the metabolism within the cells changes to be anaerobic, and this leads to an acidosis. The respiratory system also fails, meaning that not only is the blood not supplied with oxygen but carbon dioxide is no longer being excreted, leading to an increase of the levels in the capillaries. The kidneys are also no longer able to excrete harmful substances as they are not supplied with filtrate or oxygen to assist with the breakdown of elements within the blood. Without oxygen, the brain cannot function, and this leads to a rapid death of the cells.

The arterial base deficit of blood measures the amount of buffering solutions that are available to physiologically correct the acid–base balance, the normal range being between −2 and +2 mmol/L. Serum lactate levels also look at the levels of acidosis and should be <2.5 mmol/L, although they can be altered by liver damage or sepsis, so may not always be an accurate indicator of acidosis.¹² (Normal blood levels are given in Box 2.2.)

BOX 2.2: Normal blood pH levels

Lactate <2.5 mmol/L

Base Deficit −2 to +2 mmol/L

pH 7.35–7.45

pCO₂ 35–45 mm Hg

pO₂ 80–100 mm Hg

Recognition of maternal collapse

Many cases of maternal collapse are instantaneous, with no prior warning. In other cases, there may be signs of a deterioration in the woman’s condition, or signs of shock, such as a weak, thready pulse and low blood pressure, and an increase in the respiration rate due to the increase in oxygen requirements. Other signs of hypoxia that may be seen are disorientation, a fall in the level of consciousness, cold extremities, feeling clammy to the touch and/or showing signs of pallor or cyanosis.

Ineffectual gasping respirations may also be noted and are an indication of imminent cardiac arrest;¹³ when the heart stops beating, respirations cease. This will lead to irreversible brain and organ damage unless resuscitation is commenced immediately with the aim of maintaining a blood circulation around the body to supply oxygen to the tissues by artificially pumping the heart, and ensuring oxygen enters the lungs.

Basic life support

The initial approaches to a maternal collapse are the same as those for any person found collapsed. In order for all those working in a healthcare setting to be able to give initial care, a call for help must be made and basic resuscitation commenced.

Annual updates in resuscitation training should be attended. For those working in maternity, these sessions should include the modifications that are required for pregnant women.

Clear guidance on the sequence of events in the case of any collapse is provided by the UK Resuscitation Council for both in-hospital resuscitation¹⁰ (Figure 2.1) and resuscitation commenced by a bystander.¹⁴ Further guidance is also published for adult advanced life support.⁷ Guidance is also provided on the modifications that are recommended for pregnant women suffering a cardiac arrest after 20 weeks’ gestation.² These are discussed in the next section. The guidance published in October 2015 stresses the importance of early recognition of a cardiac arrest, providing chest compressions that are of a high quality with minimal interruptions as well as early and appropriate use of an automated external defibrillator where one is available. This applies in both hospital and community settings.7,10,14

Figure 2.1  In-hospital resuscitation. (Reproduced with the kind permission of the Resuscitation Council [UK].)

The first priority in approaching a collapsed person either in hospital, in the home or in the street, is to ensure the personal safety of the rescuer. Therefore it is essential to check floor areas for wires, spillages, and other potential dangers before approaching the person. Consideration should also be given to the potential for the spread of infection, so gloves should be applied at the earliest opportunity.⁷

An initial assessment should be made to see if the person is able to respond or if they are conscious by gently shaking the shoulders and asking loudly and in each ear ‘Can you hear me?’ Where there is a response, help may be summoned in the form of the emergency medical team in hospital, or by calling an ambulance if outside the hospital. An assessment of the condition should be made by using the ABCDE¹⁰ approach, looking at

•  Airway

•  Breathing

•  Circulation

•  Disability

•  Exposure

In cases where there is no response, it is essential that the appropriate help is summoned at the earliest opportunity. In hospital, the initial call for help will be by using a call or emergency bell if by a bed space, but in other areas the initial call may just be by shouting for help to attract attention while further assessment is carried out.

The patient should be moved onto his or her back and the airway opened by placing two fingers of one hand under the chin, the palm of the other hand onto the forehead and tilting the head back in a head tilt/chin lift in order to open the airway. At this point, an assessment is made for signs of life by looking for chest movement, feeling for breath on the rescuer’s cheek, and listening for breath sounds, for which the rescuer’s ear needs to be close to the patient’s nose, all of this should take no more than 10 seconds. If the breaths are infrequent, noisy, or there is any uncertainty as to whether the breathing is normal, then be prepared to start cardiopulmonary resuscitation (CPR).¹⁴

If signs of life are present, appropriate help should be called and assessment for the cause of collapse made, as well as evaluation of the person’s condition.

Where there is no sign of life, if not done already, it is now imperative that emergency help is called. In hospital, this would be the cardiac arrest team, (using the emergency 2222 number in the UK), and in cases of pregnancy, the obstetric team and obstetric anaesthetist are also called. Outside the hospital setting, a paramedic ambulance should be called (in the UK by dialing 999), and if available, a portable defibrillator brought to the scene. If there is no assistance available, then the recovery position should be used while help is called, and resuscitation attempts only commenced once further assistance is on the way.

Chest compressions should be commenced as soon as possible at a ratio of 30 chest compressions to 2 ventilation breaths. For effective chest compressions, the heel of the hand should be placed in the centre of the chest with the other hand on top¹⁴ (Figure 2.2). With each compression, the chest should be compressed to a depth of 5–6 cm at a rate of 100–120 compressions per minute, while allowing the chest to recoil completely between each compression to allow the heart to refill with blood. The chest compressions should continue with minimal interruption.

Ventilation breaths should be delivered after 30 compressions using an appropriate airway device, such as a pocket mask or bag valve mask to minimise the risks of cross-infection (Figure 2.3). Where qualified help is available, a laryngeal mask airway may also be inserted by those trained to do so, or tracheal intubation may be attempted. If no airway device is available, direct mouth-to-mouth breaths may be given, or if there are concerns regarding hygiene or infection risks, compressions should be continued at a rate of 100 per minute until further help arrives.

Figure 2.2  Hand position for maternal chest compression.

Figure 2.3  Head position for performing mouth-to-mask ventilation.

Chest compressions are tiring, so it is ideal to have at least two people and rotate between compressions and breaths every two or three cycles. When the cardiac arrest team arrives, one person will coordinate a regular change around to ensure that no one becomes exhausted.

Advanced life support

As soon as is possible, a defibrillator should be brought to the scene and the self-adhesive electrodes applied so that the cardiac rhythm can be analysed. Automated external defibrillators (AEDs) are now available both in hospital and in many community settings. Where defibrillation occurs within 5 minutes of a collapse, the survival rates are 50%–70%.¹⁴ AEDs give clear directions as to what to do, showing where the pads are to be placed (Figure 2.4), saying to ‘pause’ while the cardiac rhythm is analysed, and will then instruct as to whether CPR should continue, or a shock be delivered.

The cardiac rhythms that may be reversed through a shock are ventricular fibrillation (VF) and pulseless ventricular tachycardia (VT). The AED will instruct that the charge button should be pressed. Before delivering the shock, the lead person must ensure that everyone is standing clear of the patient.⁷ The shock works by depolarising the mass of the myocardium allowing the pacemaking tissue of the heart to resume control.¹⁵

However, these shockable rhythms are uncommon in cases of cardiac arrest in pregnancy, where it is more likely to see asystole, or pulseless electrical activity (PEA). These rhythms are seen where there is extreme blood loss, as although the heart continues to beat, there is no blood to pump around the body.¹⁵ In these cases, CPR should be continued while attempts to stabilise the woman are made.

FLUID REPLACEMENT

As soon as there are any concerns about the condition of the woman, IV access, if not already in place, should be obtained, using wide-bore, 16-gauge cannula and intravenous fluid replacement commenced in an effort to help stabilise the woman by maintaining her blood pressure and the chemical components of the body. IV access can be gained during an arrest situation on arrival of additional help and support.

Figure 2.4  Electrode pad placement for defibrillation.

The types of fluids and drugs that are needed will depend on the cause of the arrest. Caution is needed in the administration of fluids as, if they are cold, they could disturb the thermal balance of the body and lead to further difficulties with resuscitation. Care in maintaining accurate records of the fluids that are administered is also required, with consideration being given to the possibility of fluid overload, especially in situations complicated by pre-eclampsia (see Chapter 5) and sepsis (see Chapter 12).

DRUGS

The drugs used during resuscitation will be administered by the resuscitation team, although the midwife should have a working knowledge of those frequently used so that she can anticipate and prepare the drugs in advance. Following intravenous administration of each individual medication, a flush of 20 mL normal saline should be given.

The drugs most commonly used during a cardiac arrest are listed in Box 2.3.

Modifications to resuscitation for pregnant women

For pregnant women who suffer a cardiac arrest, the principles of resuscitation remain the same, however, some modifications are required due to the physiological changes that occur in pregnancy which were discussed earlier in this chapter.

As soon as it is recognised that the woman has collapsed, specialist help should be summoned, with the obstetrician, obstetric anaesthetist and neonatologist being required in addition to the cardiac arrest team. CPR should be commenced as for any person in cardiac arrest, ensuring that the chest compressions are of good quality and that these are disrupted as little as possible.

Due to the weight of the pregnant uterus compressing the inferior vena cava and aorta, venous return and cardiac output can be affected (Figure 2.5). Traditionally, this has been countered by ensuring a left lateral tilt using a variety of methods. However, this does not allow for effective compressions to be carried out unless the woman is on a firm surface such as a tilting table or spinal board so that good-quality chest compressions can be maintained. Research¹⁶ has shown that a stable tilt is unlikely to be achieved by using a soft wedge such as a pillow or the knees of an assistant on the floor.

BOX 2.3: Drugs used during a cardiac arrest⁷

ADRENALINE (EPINEPHRINE)

•  1 mg (10 mL 1:10,000 or 1 mL 1:1000) given IV.

•  In shockable rhythms, given after the third shock, then every alternate shock.

•  For pulseless electrical activity and asystole, given when IV access is available, and repeated every 3–5 minutes.⁷

•  A sympathomimetic drug which works by causing vasoconstriction, thus increasing coronary and cerebral perfusion.

AMIODARONE

•  300 mg, given as an IV bolus.

•  Only indicated for VF and pulseless VT.

•  An antiarrhythmic drug.

MAGNESIUM

•  2 g given IV, repeated after 10–15 minutes.

•  Used for VT.

•  Improves the ability of the myocardium to contract.

CALCIUM

•  10 mL, 10% calcium chloride given IV.

•  Used for PEA caused by hyperkalaemia or hypocalcarmia.⁷

•  Plays a vital role in the cell mechanisms supporting myocardial contraction.

•  Do not give at the same time as sodium bicarbonate by the same route.

Figure 2.5  Aortal and inferior vena caval compression in dorsal position. (a) Showing compression of vessels by gravid uterus with woman lying supine and (b) shows how compression is relieved by tilting the woman to the left.

Current guidelines¹⁷ recommend that from about 20 weeks’ gestation when the uterus is visible, the uterus should be manually displaced to the maternal left side to relieve this compression as it has been demonstrated that the risk of supine hypotension is significantly less using this method as opposed to tilting to the left side.¹⁸ This can be carried out from the left side using two hands (Figure 2.6a), or from the right side with one hand, depending on how the resuscitation team is positioned (Figure 2.6b).

In cases of maternal cardiac arrest, the best chance of survival for the mother, and possibly the fetus, is to deliver the infant as soon as possible. Hypoxia will develop in the pregnant woman far more rapidly than in the non-pregnant person, and they are at risk of brain damage within 4–6 minutes of cardiac arrest.⁵ Therefore, preparation for a perimortem caesarean section should be undertaken once the diagnosis of cardiac arrest has been made, with the aim of commencing the procedure within 5 minutes of the arrest if initial resuscitation attempts fail.2,5,17 By delivering the fetus, the maternal oxygen consumption will reduce, venous return and cardiac output will improve and the empty uterus will allow for easier and more effective chest compressions and ventilation.² All resuscitation trolleys within a maternity unit should be prepared for this eventuality, with a pre-mounted scalpel handle and blade, cord clamps and sterile gloves being an addition to the required equipment.2,5 Preparation should also be made for the potential resuscitation of a viable newborn, with appropriate equipment and the neonatologists present.

Figure 2.6 (a) Left uterine displacement from left side of patient. (b) Left uterine displacement from right side of patient.

A perimortem caesarean section should be carried out by an experienced obstetrician where the resuscitation is taking place, and should not be delayed by moving the woman to theatre. Resuscitation should be continued throughout the procedure, with the aim to deliver the fetus and placenta within 1 minute of commencing the caesarean section.⁵ As there is no established circulation, no anesthetic is required and there will be minimal blood loss. Where resuscitation is then successful, there should be prompt transfer to theatre to complete the operation.²

As a perimortem caesarean section is seen as being in the best interests of the patient, this is performed without consent.²

While dealing with the arrest situation and the potential for a perimortem caesarean section, midwives will not only have to consider the needs of family members who may witness the arrest and subsequent interventions, but also potentially will need to give support and consideration to other women and possibly their families if this occurs within a ward setting. In some cases, it may be appropriate for the family members to be brought in to observe the resuscitation so that they are aware that everything possible is being done.¹⁹ However, this will require careful preparation by the professionals involved, with clear information given to the relatives at all times. If possible it would be ideal for a midwife not directly involved in the hands-on resuscitation to stay with relatives to support them.

Following the resuscitation of a woman during pregnancy or the postpartum period, the family may have to face a number of outcomes and will need support and guidance during this difficult time. In the best situation, the resuscitation will have been successful, resulting in a healthy mother and baby. In situations where the outcome may not be so good, families may have to face loss of the mother, loss of the baby, and in some cases the loss of both. In any situation the family, and the mother if she survives, will need support and information to help them cope with what has happened.

Following any arrest situation, the personnel involved will also need support, guidance of where to gain further help if needed and a clear debriefing. In cases of maternal arrest, the Supervisor of Midwives will be involved in this process, offering individual support to the midwives involved.

NEWBORN RESUSCITATION

At any birth, all those present wait for the expected cry of the newborn infant: the parents to know that all is well, and the midwives to observe that the first breath has been taken, replacing the fluid present in the lungs during the fetal period with air, making the transition from in utero to ex utero life. Gradually, as the oxygen starts to circulate through the body, the baby’s colour changes from blue to pink as normal respiration is established. In the majority of births, this happens immediately, or following stimulation and opening of the airway. However, there are times when there is silence in the room.

The Resuscitation Council²⁰ ‘Guidelines for Resuscitation and support of transition of babies at birth’ recognise that many newborn infants, rather than requiring resuscitation, require help and support with this transition from in utero to ex utero life. In many circumstances, the potential for newborn resuscitation can be predicted.²¹ A list of conditions that may predispose to this can be found in Table 2.1. Occasionally, the need for resuscitation is totally unexpected, and this is the situation that every midwife must be prepared for, be it in the hospital or home birth situation.

Prior to every birth, the room should routinely be prepared so that it is warm, draught free and all equipment is available and checked. If in hospital and the need for resuscitation at birth is suspected, the appropriate personnel, i.e. the neonatologist and further midwifery or neonatal unit nursing support, should also be present. At home, if a complication develops during labour, a paramedic ambulance should be called as support and be ready for transfer to hospital if this is required.

Some babies appear cyanosed when first born but have a good heartbeat and will generally respond to stimulation and an open airway. Babies who are pale, very floppy and with a slow or absent heartbeat will require more support and resuscitation in order to establish life.

Table 2.1  Predisposing/risk factors for neonatal resuscitation

Antenatal

Intrapartum

Maternal medical conditions such as diabetes, heart disease

Pre-eclampsia

Anaemia

Haemorrhage

Maternal infection

Multiple pregnancy

Maternal substance abuse

Intrauterine growth restriction (IUGR)

Placental abruption or placenta praevia

Prolapsed cord

Preterm labour

Precipitous labour

Prolonged rupture of membranes >18 hours

Abnormal presentation or malposition of the fetus

Meconium-stained liquor

Abnormal heart rate patterns on cardiotocograph (CTG)

Forceps or ventouse extraction

Emergency caesarean section and/or general anaesthesia

Note:  This list is not extensive, and there may be other risk factors which predispose to the need for neonatal resuscitation.

Similarly to maternal collapse, it is essential that the midwife maintains her or his skills and knowledge in newborn resuscitation as, being the lead carer in 70% of normal births, the midwife may be the first and potentially the only professional present at the time of birth. In these situations, the midwife will need to be able to recognise the need for resuscitation and initiate and carry out the procedures needed for the transition to life to be competed. The midwife should also ensure as she or he takes over the care of each woman that the newborn resuscitation equipment (including drugs) has been checked and is working.

Fetal physiology

As the fetus receives all its oxygen and nutritional requirements via the placenta in utero, adaptations are in place to ensure that the highest concentration of oxygen goes to the vital organs, such as the brain, and to essentially bypass the lungs, which are redundant in terms of oxygen transfer until birth (see Table 2.2). The excretion of waste products also occurs via the placenta to the maternal circulation. As the carbon dioxide enters the maternal system, the pH is altered for a very short period of time which again allows for greater levels of oxygen transfer from the maternal to the fetal system (the Bohr effect).²²

Table 2.2  Fetal adaptations in utero

Ductus venosus

Highly oxygenated blood from the umbilical vein bypasses the liver via the ductus venosus to join the inferior vena cava.

Foramen ovale

Highly oxygenated blood entering the right atrium is diverted through to the left atrium and thus to the general circulation to ensure that the heart and brain receive the oxygen required.

Ductus arteriosus

Diverts blood from the pulmonary trunk to the aorta, bypassing the lungs which are not used for oxygen transfer in utero.

Hypogastric arteries

These become the umbilical arteries, carrying deoxygenated blood away from the fetus to the placenta.

Higher haemoglobin levels

To support the high oxygen requirements of the fetus, the haemoglobin levels are higher, and also have different structure, allowing a higher binding capacity.

During labour, the oxygen supply to the fetus may be affected by compression of the cord and/or the action of the uterine contractions on the placenta, restricting oxygen transfer. The fetus that is in good condition will be able to cope well with these transient falls in the oxygen levels by altering the heart rate, and redistributing the blood flow so that the heart and brain, in preference to other internal organs and the peripheries, receive oxygenated blood. This is mediated by baroreceptors in the aortic arch and carotid sinuses which react to the changes in the partial pressure of oxygen within the fetal blood and chemoreceptors in the brain which are sensitive to the pH levels.

Where the oxygen levels fall so that aerobic metabolism is not able to be maintained, anaerobic metabolism takes over, which is less efficient and produces lactic acid as a by-product. This along with the accumulation of carbon dioxide in the fetus due to inefficient transfer of gases both to and from the fetus at the placenta lead to the development of an acidosis. The levels of the acidosis, measured by obtaining blood through fetal blood sampling, are important for helping with decision making underpinning optimum time for delivery where there are concerns over the fetal heart rate, as well as giving further guidance as to the condition of the baby at birth through analysis of cord blood gas. A pH level of over 7.25 is seen to be normal, 7.20–7.25 are pre-acidotic and anything below 7.20 indicates an acidosis. Attention is also paid to the base excess and lactate levels.

As the baby is born, adaptations to the circulatory and respiratory systems should be taking place so that the neonate’s oxygen supply comes from the lungs rather than the placenta. These changes are initiated by the first breaths that are taken, which pushes the fluid from the lungs into the interstitial spaces, filling the lungs with air, and changing the pressure ratio so that the blood supply to the lungs increases. The foramen ovale closes, helping to establish the pulmonary circulation, and the ductus venosus and arteriosus close anatomically over a period of time.

Equipment

The equipment for neonatal resuscitation varies according to the place of birth, so the midwife must ensure that she is familiar with what is available. The basic equipment needed for neonatal resuscitation includes towels, a stethoscope, means of delivering breaths, heat and light. In maternity units, Resuscitaires are generally available, giving a flat working surface with heat, light, a pressurised gas device with a ‘T’ piece for delivering breaths to the newborn, suction and storage for any other equipment, such as laryngoscopes, airways, saturation monitor and endotracheal tubes.

The pressurised gas device should initially be powered by air, with oxygen being introduced later in the resuscitation if this is indicated by the O₂ saturation readings on the baby (see later in this chapter). The pressures for a term baby should be set at 30 cm H₂O and 20–25 cm H₂O for a premature baby. The latest guidelines²⁰ recommend the use of a ‘T’ piece with a positive end-expiratory pressure (peep) device, which is set at 5 cm H₂O to help maintain the inflation in the lungs, for babies of all gestation.

While the pressurised devices deliver a constant pressure, midwives should also be familiar with and be able to use a bag/valve mask (Figure 2.7). At a home birth, this may be the only piece of equipment available, or will be needed if the main system fails.

With both pieces of airway equipment, an appropriate-sized mask is required, which should fit over the nose and mouth, without occluding the orbital ridges. For a good seal to be obtained, the mask should be rolled on from the cleft of the chin to the bridge of the nose. When holding the mask in place, the thumb and forefinger should hold the centre stem of the mask in a ‘C’ hold, applying gentle downward pressure to obtain the seal. The remaining three fingers should form an ‘E’ on the jaw line (Figure 2.8), with the ring finger on the angle of the jaw. This should be used to lift the jaw into the mask, applying a single-handed jaw thrust.

For more advanced resuscitation, a laryngoscope with appropriate-sized blade, appropriate-sized oral airways and a selection of endotracheal tubes with intubation stylets are required.

Figure 2.7  Bag and valve.

Figure 2.8  The ‘C’ grip for holding the mask.

Air or oxygen?

The aim of newborn resuscitation is to achieve ventilation of the lungs, removing the fluid present in utero, replacing it with air and thus changing the resistance within the lungs so that blood diverted in utero flows into the pulmonary circulation allowing gaseous exchange to take place. A systematic review by Davis et al.²³ found that although little research exists into the subject due to the ethics of studying newborns, available findings suggest that using 100% oxygen in a newborn resuscitation as has traditionally been done, in fact reduces the supply of cerebral oxygen and can delay the onset of spontaneous respirations. Babies resuscitated in air alone have been resuscitated at least as effectively as those receiving 100% oxygen, and the guidelines²⁰ recommend that the resuscitation commences in air. An oxygen saturation monitor should be applied, usually to the right hand, in the early stages of a resuscitation, and oxygen introduced if the saturation levels are below those shown in Table 2.3.

Preparation for birth

It is of vital importance that the newborn is kept warm in the immediate period following birth, whether support with transition or resuscitation is required or not.²⁰ The room should be warm and free of draughts, with a temperature of 23°C–25°C recommended.²¹ Babies who get cold will be more difficult to resuscitate as they will be using their glucose stores to produce heat, thus increasing their oxygen requirements for normal cell metabolism.²² The production of surfactant is also reduced in babies who are cold.

Table 2.3  Oxygen saturation levels in the newborn infant²⁴

Time from birth

Acceptable (25th percentile) right-hand saturation (%)

2 min

60

3 min

70

4 min

80

5 min

85

10 min

90

When to clamp and cut the cord

Recent national guidelines20,25 recommend that the cord is not cut before 1 minute of age to allow for fetal blood in the placenta to transfer to the newborn, thus allowing for improved iron status in the early months of life.²¹ However, where the infant requires resuscitation, the cord should be clamped and cut earlier to allow the baby to be moved to a suitable area, unless a resuscitation platform which slides over the bed is available. This then allows for the cord to remain unclamped and the fetal/placental unit to provide oxygen to the newborn while resuscitation commences.

Support during transition from in utero to ex utero life

The Resuscitation Council have clear guidelines of the systematic approach to aid the transition of babies at birth and for newborn resuscitation, outlined in Figure 2.9.

As the baby is born, the time of birth should be noted, and/or a stop clock started so that clear timings of events can be observed. The baby must be then dried thoroughly, and wrapped in a clean, warm, dry towel to minimise heat loss. Drying the baby will also act as stimulation, which along with the stress of the birth and change in temperature may be all that is needed to establish respirations.

While drying the baby, an assessment of the condition can be made. The colour is observed. The majority of babies appear blue initially, especially at the extremities, so this is not a good indication of oxygenation at birth, but babies who are acidotic will look pale, almost white at birth, thus indicating that intervention may be required.²⁰ Tone is an aid to assessing rapidly those babies where intervention may be needed. At birth, babies generally have a good tone, and appear well flexed. Those who are hypoxic will appear floppy. In assessing the heart rate, a stethoscope should be used to ascertain if the rate is normal (rate over 100 beats per minute), slow (between 60 and 100 beats per minute), or very slow (less than 60 beats per minute). Assessing the heart rate initially gives a baseline and can also be used to demonstrate inflation of the lungs with an increase of heart rate being one of the first signs of successful inflation.²⁴ Breathing activity should be observed. Normally, babies will breathe spontaneously soon after birth. Those in difficulty may demonstrate deep, intermittent gasping, or not be breathing at all. Where the baby is not breathing effectively, action needs to be taken to inflate the lungs, remove the lung fluid and establish respirations.

As soon as it is recognised that there is a potential resuscitation to carry out, help should be called for. At home, a paramedic ambulance should be alerted (by dialing 999 in the UK) and called to the house. In hospital in the UK, this will be via the 2222 phone number, calling for the neonatal resuscitation team. Additional help in the form of midwives or neonatal unit nurses may also be needed, plus a person allocated to keep note of the timing of the events to aid documentation at the end of the emergency.

Initially, the baby’s head should be moved into the ‘neutral’ position²⁰ to open the airway (Figure 2.10). This is where the face is parallel with the surface the baby is lying on. Airway obstruction in the newborn is usually due to lack of tone, causing the tongue to fall backwards obstructing the airway, rather than a mechanical obstruction. Many babies will respond and start spontaneous breathing purely with stimulation and an open airway.²²

If spontaneous breathing does not commence, then assistance must be given to help move the fluid from the lungs and replace it with air for effective lung ventilation to begin. Using either the ‘T’ piece and pressurised ventilation device or a bag/valve mask, five breaths should be delivered over a period of 2–3 seconds each, giving a sustained pressure of 30 cm H₂O in an effort to achieve the inflation of the lungs.²⁰ Following these inflation breaths, an increase in the heart rate will indicate that the lungs have been inflated. If the heart rate remains slow, this may be due to the fact that the lungs have not yet been inflated, or that the heart is not able to respond. This is determined by observing chest movement during the inflation breaths. Where the chest is seen to rise, this indicates that the lungs have been inflated.

Figure 2.9  Newborn life support. (Reproduced with the kind permission of the Resuscitation Council [UK].)

Figure 2.10  Head position for optimum airway opening.

Where the heart rate fails to increase, chest movement must be observed before moving on to further intervention. It should be ensured that the head is in the neutral position, that the mask fits without leaks, and the inflation breaths repeated with either a single-handed or a two-person jaw thrust (Figure 2.11) again observing for chest movement. On reassessment, if the heart rate remains low and no chest movement is seen, then the vocal cords should be visualised to observe for any mechanical obstruction such as meconium, vernix or a blood clot, which can be removed with a suction catheter. An oropharyngeal airway may also be inserted.²⁰ Both of these techniques are carried out with the aid of a laryngoscope. A skilled neonatologist may choose to intubate the baby with an endotracheal tube.

Cardiac compressions should only be considered once the fluid from the lungs has been replaced with air20,24 thus allowing for oxygen transfer to occur. If the heart rate remains below 60 beats per minute, and chest movement has been observed, compressions should be commenced at a ratio of three compressions to one ventilation breath. The rate should be at a speed so that 90 compressions and 30 breaths are achieved in 1 minute, and the chest being compressed by a third. When performing cardiac compressions on a newborn, the hands should be placed around the chest to form a firm platform, and the thumbs placed together on the sternum, just below the nipple line (Figure 2.12). It is also possible to perform compressions with two fingers placed centrally just below the nipple line, but this method is less effective and more tiring. However, where medical teams are working on the baby, this may be the only way in which the person performing compressions can reach the chest (Figure 2.12). Reassessment of the heart rate should be carried out every 30 seconds, with compressions being continued if the heart rate remains below 60 beats per minute. In the majority of cases, the heart rate will respond quickly once oxygenated blood starts circulating through the heart to the aorta and then to the coronary arteries.²⁰ The main reason for the heart not responding to chest compressions is that the lungs are not being ventilated, and the positioning of the airway should be checked once again.

Figure 2.11  Two-person jaw thrust.

Figure 2.12  Finger positions for neonate chest compressions.

Once the heart rate increases, ventilation of the lungs should be maintained until spontaneous breathing commences by giving breaths at a rate of 30 per minute, reassessing the heart rate every 30 seconds and ensuring that the lungs are being ventilated by observing for chest movement.

Drugs

Drugs are seldom required in a neonatal resuscitation, and their use usually indicates a baby that is in very poor condition.²⁰ Where drugs are required, the quickest access route is via the umbilical vein, and an umbilical venous catheter (UVC) should be inserted under aseptic conditions. The drugs commonly used are

•  Sodium bicarbonate to correct acidosis

•  Adrenaline, which may be given via the endotracheal tube

•  Dextrose to provide energy

A saline flush should be given between each drug. If there has been a blood loss from the baby, then volume in the form of 0.9% normal saline may also be given. Consideration may also be given to administering a blood transfusion.

Outcome

If there is no heart rate following 10 minutes of good quality resuscitation, then the prognosis for the baby if further resuscitation is successful is very poor. At this point in time, it may be appropriate to discontinue the resuscitation attempt.²⁰ This decision is generally made by the neonatologists following discussion with all involved in the resuscitation.

Meconium

Any baby born in the presence of meconium, be it thin or significant, who cries at birth, should be dried and handed to the mother for skin-to-skin contact. Where there is significant meconium, and the baby is floppy and unresponsive at birth, then a laryngoscope should be used to quickly inspect the airway and any visible meconium suctioned, using a wide-bore suction catheter, before resuscitation attempts are commenced.²⁰ Where meconium is inhaled, it indicates that the fetus in utero has been hypoxic to the extent that the primitive breathing centres have been triggered, causing the fetus to take deep gasping breaths. It should be kept in mind that where there has been sufficient hypoxia to cause gasping in utero or during birth, other particulate matter such as blood or vernix may also be inhaled and lead to obstruction.

Care following resuscitation

Throughout any resuscitation attempt, the parents should be kept fully informed of the condition of their baby and what is happening. They will continue to need support and explanations following the resuscitation, but more especially so where the baby is not able to be resuscitated. Many maternity units have specialist bereavement midwives who may become involved in their care at this point to give the appropriate information, support and guidance, although continued contact with the midwife present for the birth is often appreciated by the woman and the family.

Following successful resuscitation, the baby will need to be closely observed to ensure that there is no deterioration in condition. The condition of the baby will determine if transfer to the neonatal unit is required, again with the parents in this situation needing guidance and support as well as the opportunity to visit the baby as soon as is possible. All babies who have been resuscitated should have skin-to-skin contact at the earliest opportunity, and an early breastfeed, as their energy stores will have been depleted through the resuscitation. A blood glucose level test may be indicated to ensure the baby is not hypoglycaemic. As babies can lose heat rapidly, temperatures should be monitored and the baby kept covered while with the mother. Heart rate and respirations should also be monitored and documented according to the neonate’s condition.

As with all care, detailed records of the resuscitation should be made including times given for the varying interventions, time of birth and the time that respirations were established. Where possible, one person scribing the events as they occur aids with the accurate documentation of the resuscitation.

SUMMARY OF MIDWIFERY RESPONSIBILITIES

•  Keep up to date with maternal and newborn resuscitation techniques, in particular by attending regular ‘skills drills’ whenever possible.

•  Ensure both maternal and neonatal resuscitation equipment is checked regularly: Neonatal equipment should be checked before every birth by the midwife caring for the woman.

•  Recognise antenatally or in labour an ‘at risk’ situation that may lead to the need for neonate resuscitation and make all necessary preparations for it.

•  Call for appropriate help as needed.

•  Ensure appropriate monitoring of either mother (if she remains in midwifery care) or baby following any resuscitation.

•  Undertake and/or arrange follow-up care for parents as required.

REFERENCES

1.  Nursing and Midwifery Council (NMC). 2015. The Code: Professional Standards of Practice and Behavior for Nurses and Midwives. Available at http://www.nmc-uk.org (accessed April 24, 2015).

2.  Royal College of Obstetricians and Gynaecologists. 2011. Green-Top Guideline 56. Maternal Collapse in Pregnancy and the Puerperium. Available at https://www.rcog.org.uk/globalassets/documents/guidelines/gtg_56.pdf (accessed March 8, 2016).

3.  Knight M, Nair M, Shah A, Noor N, Acosta C. 2014. On behalf of the MBRRACE-IK AFE chapter writing group, Maternal Mortality and Morbidity in the UK 2009–2012: Surveillance and Epidemiology. In: Knight M, Kenyon S, Brocklehurst P, Neilson J, Shakespeare J, Kurinczuk JJ (Eds.), on behalf of MBRRACE-UK. Saving Lives, Improving Mothers’ Care – Lessons Learned to Inform Future Maternity Care from the UK and Ireland Confidential Enquiries into Maternal Deaths and Morbidity 2009–2012. Oxford: National Perinatal Epidemiology Unit, University of Oxford, pp. 9–26.

4.  Resuscitation Council (UK). 2015. Acute Care – Equipment and Drug List. Available at https://www.resus.org.uk/quality-standards/acute-care-equipment-and-drug-lists/ (accessed August 22, 2015).

5.  Harper A, Wilson W. 2014. On behalf of the MBRRACE-UK AFE chapter writing group, caring for women with amniotic fluid embolism. In: Knight M, Kenyon S, Brocklehurst P, Neilson J, Shakespeare J, Kurinczuk JJ (Eds.), on behalf of MBRRACE-UK. Saving Lives, Improving Mothers’ Care – Lessons Learned to Inform Future Maternity Care from the UK and Ireland Confidential Enquiries into Maternal Deaths and Morbidity 2009–2012. Oxford: National Perinatal Epidemiology Unit, University of Oxford, pp. 57–63.

6.  Jeejeebhoy F, Windrim R. 2014. Management of cardiac arrest in pregnancy, Best Practice and Research. Clinical Obstetrics and Gynaecology, 28(2014):607–618.

7.  Resuscitation Council (UK). 2015. Adult Advanced Life Support Guidelines. Available at https://www.resus.org.uk/resuscitation-guidelines/adult-advanced-life-support/ (accessed October 17, 2015).

8.  Knight M, Nair M, Shah A, Noor N, Acosta C. 2014. On behalf of the MBRRACE-UK Surveillance and Epidemiology chapter writing group, Maternal Mortality and Morbidity in the UK 2009–2012: Surveillance and Epidemiology. In: Knight M, Kenyon S, Brocklehurst P, Neilson J, Shakespeare J, Kurinczuk JJ (Eds.), on behalf of MBRRACE-UK. Saving Lives, Improving Mothers’ Care – Lessons Learned to Inform Future Maternity Care from the UK and Ireland Confidential Enquiries into Maternal Deaths and Morbidity 2009–2012. Oxford: National Perinatal Epidemiology Unit, University of Oxford, pp. 9–26.

9.  Soar J, Nolan J, Perkins G, Scott M, Mitchell S (Eds.). 2011. Immediate Life Support. 3rd ed. London: Resuscitation Council UK.

10.  Resuscitation Council (UK). 2015. In-Hospital Resuscitation Guidelines. Available at https://www.resus.org.uk/resuscitation-guidelines/in-hospital-resuscitation/ (accessed October 17, 2015).

11.  Rankin J. 2011. Respiration. In: Staples D, Rankin J. Physiology in childbearing. London: Elsevier, pp. 245–258.

12.  McCunn M, Dutin R. 2000. End points of resuscitation how much is enough? Current Opinion in Anaesthesiology, 13(2):147–153.

13.  Madams M. 2008. Maternal resuscitation: How to resuscitate mothers who die. British Journal of Midwifery, 16(6):372–378.

14.  Resuscitation Council (UK). 2015. Adult Basic Life Support and Automated External Defibrillation. Available at https://www.resus.org.uk/resuscitation-guidelines/adult-basic-life-support-and-automated-external-defibrillation (accessed October 22, 2015).

15.  Draycott T, Winter C, Crofts J, Barnfield S. 2010. PROMPT: Practical Obstetric Multiprofessional Training Course Manual. London: RCOG.

16.  Ip JK, Campbell JP, Bushby D, Yenis SM. 2013. Cardiopulmonary resuscitation in the pregnant patient: A manikin-based evaluation of methods for producing lateral tilt. Anaesthesia, 68:694–699.

17.  Resuscitation Council (UK). 2015. Prehospital Resuscitation. Available at https://www.resus.org.uk/resuscitation-guidelines/prehospital-resuscitation/ (accessed November 30, 2015).

18.  Kundra P, Khanna S, Habeebullah S, Ravishankar M. 2007. Manual displacement of the uterus during Caesarean section. Anaesthesia, 62:460–645.

19.  Royal College of Nursing. 2002. Witnessing Resuscitation: Guidance for Nursing Staff. London: RCN. Available at https://www.rcn.org.uk/__data/assets/pdf_file/0006/78531/001736.pdf (accessed June 25, 2015).

20.  Resuscitation Council (UK). 2015. Resuscitation and Support of Transition of Babies at Birth. Available at https://www.resus.org.uk/resuscitation-guidelines/resuscitation-and-support-of-transition-of-babies-at-birth/ (accessed October 17, 2015).

21.  Wyllie J, Bruinenberg J, Roehr CC, Rudiger M, Trevisanuto D, Urlesberger B. 2015. European Resuscitation Council Guidelines for Resuscitation 2015. Section 7. Resuscitation and support of transition of babies at birth. Resuscitation, 952015 249–263. Available at http://www.cprguidelines.eu (accessed October 17, 2015).

22.  Blackburn ST. 2013. Maternal, Fetal and Neonatal Physiology: A Clinical Perspective. 4th ed. Philadelphia: Elsevier.

23.  Davis PG, Tan A, O’Donnell CPF, Schulz A. 2004. Resuscitation of newborn infants with 100% oxygen or air: A systematic review and meta-analysis. Lancet, 364:1329–1333. Available at http://web.a.ebscohost.com.ezproxy.uwl.ac.uk/ehost/pdfviewer/pdfviewer?vid=5&sid=19cb1ba5-ac3e-4f57-a3ab-9ffaaa2cee5f%40sessionmgr4001&hid=4204 (accessed July 24, 2015).

24.  Resuscitation Council. 2011. Newborn Life Support. 3rd ed. London: Resuscitation Council.

25.  National Institute for Health and Care Excellence (NICE). 2014. Intrapartum Care: Care of Healthy Women and Their Babies During Childbirth. London: NICE.

3

Antepartum haemorrhage

LUISA ACOSTA

Introduction

Causes of APH

Risk and predisposing factors for APH

Placental abruption

Placenta praevia

Treatment of APH

Possible immediate outcomes of APH

Possible long-term outcomes of APH

Summary of midwifery responsibilities

References

INTRODUCTION

Antepartum haemorrhage (APH) is known to occur in approximately 2%–5% of all pregnancies and is defined as bleeding from the genital tract after 24 weeks’ gestation and before the birth of the baby.1,2 The basis of this definition is in keeping with the current national legal age of viability of the fetus in the United Kingdom.³ Similar bleeding while the woman is in labour is called intrapartum haemorrhage and is discussed in Chapter 10.

Any amount of bleeding in pregnancy is considered abnormal and has the potential to be serious for the fetus and the mother. APH is considered a major cause of perinatal morbidity and mortality worldwide. In the United Kingdom, the latest Confidential Enquiry Report⁴ identified three maternal deaths from APH between 2009 and 2012. Two maternal deaths were due to placental abruption and one was due to placenta praevia, which are the two most common identified causes for APH.

CAUSES OF APH

Approximately half of the women who present with an APH are found to have placental abruption or placenta praevia (see Table 3.1):

•  Placental abruption is the premature separation of a normally situated placenta.

•  Placenta praevia is when the placenta is wholly or partially attached to the lower uterine segment.

The causes of APH that are not associated with one of these two conditions are often not identified, or may be identified later (e.g. when inspecting the placenta after delivery). The bleeding that occurs may be described as ‘non-specific’, ‘unexplained’,¹ ‘unclassified’² or ‘antepartum bleeding of unknown origin (ABUO)’.5–7 This type of bleeding often includes small bleeds from marginal placental separation and therefore it is recognised that there is some overlap of unclassified bleeding and placental abruption2,8 (see Table 3.1).

Unclassified bleeding that is not from placental origin may be from varicosities, a ‘show’, genital tract trauma, polyps, tumours or infections such as cervicitis/vaginitis.

Vasa praevia, the only fetal cause of APH, occurs when there is a velamentous insertion of the umbilical cord. In this scenario the blood vessels run through the membranes and across the lower segment of the uterus in front of the presenting part. Bleeding will occur if the blood vessels are severed when the membranes rupture. See Chapter 10 for a description of vasa praevia.

Table 3.1  Causes of APH

Placental causes

Fetal causes

Antenatal bleeding of unknown origin (ABUO)

Placenta praevia (inevitable haemorrhage)

Placental abruption (accidental haemorrhage)

Vasa praevia

Unclassified placental causes Marginal bleeds ‘Show’

Genital tract causes
Cervicitis
Trauma
Vulvovaginal varicosities
Genital tumour
Genital infection

RISK AND PREDISPOSING FACTORS FOR APH

Risk factors are not always apparent and although there are overlapping risk factors for placental abruption and placenta praevia, the underlying aetiology is often different.

Yang et al.⁹ noted that placental abruption is more likely to be affected by conditions occurring during pregnancy, whereas placenta praevia is more likely to be affected by conditions existing prior to pregnancy. However, placental abruption, often triggered by events in pregnancy, is now frequently considered to be the result of chronic processes that may be present before and in early pregnancy.¹⁰

Some risk factors common to both placental abruption and placenta praevia follow.

Previous caesarean section

Suboptimal implantation of the placenta due to previous caesarean section is linked with both abruption and placenta praevia. A large, population-based cohort study of 400,000 women who gave birth in National Health Service (NHS) Trusts in England found that women who had a caesarean section in their first pregnancy were at a 60% higher risk of developing placenta praevia in their next pregnancy.¹¹ Yang et al.¹² studied a large group of women in the United States (n = 5,146,742), and found that women who had delivered by caesarean section in their first pregnancy had a 47% risk of placenta praevia and 40% risk of placental abruption in a second singleton pregnancy, and that the risk of abruption and placenta praevia increases with the number of previous caesarean sections.

High parity and older age

It has been suggested that women who have had three or more previous babies or who are more than 35 years old are at higher risk of developing an abruption or placenta praevia.¹³ However, a French study which examined the risk factors for placental abruption¹⁰ concluded that multiparity was a compounding risk factor for maternal age and therefore found no significant correlation between maternal age and placental abruption.

Early pregnancy bleeding

A systematic review by Saraswat et al.¹⁴ found that women who had threatened miscarriages were more likely to have placenta praevia and placental abruption; and twice as likely to have ABUO.

Vitamin/folic acid deficiency

Nilsen et al.¹⁵ investigated a possible association of supplemental folic acid and multivitamin use with placental abruption. They studied 280,127 singleton deliveries over a 6-year period in Norway and found that those women who had taken vitamin supplements during pregnancy showed a significantly lower risk of developing placental abruption. This could also imply that women from lower socioeconomic groups with poorer nutritional status may also be at higher risk of abruption. It is also thought that folate and vitamin deficiency is associated with placenta praevia, and Altvorst et al.¹⁶ found that folate supplements were associated with a decrease in ABUO.

Multiple pregnancy

Another risk factor for both placental abruption and placenta praevia is multiple pregnancy. There is usually a greater surface area of placental tissue with multiple pregnancies, and therefore more likelihood of it encroaching on the lower segment and becoming a placenta praevia.

PLACENTAL ABRUPTION

Placental abruption can be defined as the complete or partial separation of a normally implanted placenta occurring after 24 weeks’ gestation and prior to delivery, usually accompanied by abdominal pain and uterine bleeding. It is often confirmed after delivery by evidence of retroplacental bleeding or clot. Although the incidence is difficult to estimate it is generally reported to occur in approximately 0.4%–1.4% of pregnancies.¹⁷ The Health and Social Care Information Centre¹⁸ figures showed that in 2013–2014 it occurred in about 0.42% of pregnancies in NHS hospitals in England.

The associated perinatal mortality rate has been suggested to be as high as 32.5%¹⁹ of those diagnosed, with more than half the perinatal losses to fetal death occurring before the mother arrives in hospital.

Pathophysiology of placental abruption

The immediate cause of premature placental separation of a normally situated placenta is when maternal blood vessels in the decidua basalis are severed causing haematoma formation between the decidua and the placental wall. The pressure exerted by the haematoma forces the placenta to separate from the uterus causing the fetus to become deprived of oxygen and nutrients. The condition of the fetus will depend on the remaining placental area, the fetal reserves and the rapidity of recognition and treatment.

In a revealed haemorrhage, bleeding may track down between the membranes and the uterus and appear externally. This occurs in approximately 80% of cases. In 20% of cases the bleeding is more centrally located and may be retained behind the placenta. In this scenario the blood does not escape and it is said to be a concealed haemorrhage. In severe cases the bleeding infiltrates into the myometrium causing pain, uterine tenderness and irritability, as well as the diagnostic ‘board-like’ uterus. This is known as a Couvelaire uterus or uteroplacental apoplexy.

A mixed haemorrhage may have some revealed and some concealed bleeding.

The classification of haemorrhage from placental abruption can be seen in Figure 3.1.

Figure 3.1  Placental abruption.

Aetiology and risk factors

The aetiology of placental abruption is mainly unclear (see Table 3.2). Placental abruption is sometimes called ‘accidental’ haemorrhage. This suggests that the cause is traumatic and sudden. However, only a small proportion of cases occur spontaneously and involve trauma, implying that abruption is more commonly the end result of a chronic process,²⁰ with many cases of placental abruption involving a combination of both acute and chronic aetiology.21–23

ACUTE FACTORS

Direct trauma to the abdomen may result in placental abruption

It has been found that maternal trauma is associated with a sixfold increased risk of placental abruption.²⁴ Blunt abdominal trauma and/or sudden uterine decompression will cause the inelastic placenta to tear away from the uterine wall with uterine contraction or expansion.²³ Examples of direct trauma include a fall, a road traffic accident and domestic violence. Although domestic violence is difficult to quantify, current statistics show that approximately 30% of women ages 16–59 have reported that they have experienced domestic violence, and of these, about 28% experienced severe physical injury.²⁵ Pregnancy appears to be a trigger for further abuse and violent attacks during pregnancy seem to be focused on the abdomen, breasts and genitals. This is shown to be a cause of maternal and perinatal morbidity with an increased risk of placental abruption.²⁶ Furthermore, the psychological effects on the pregnant woman subjected to domestic violence may lead her to indulge in adverse lifestyle choices, which may include smoking²⁷ and/or substance or alcohol abuse. These in turn may further exacerbate the risk of abruption. Abruption may occur as a result of an external cephalic version (ECV). However, this is a rare complication only occurring in 0.12%–1.8% of women undergoing this procedure.28,29

Sudden decompression of the uterine cavity

Examples include spontaneous rupture of membranes where there is polyhydramnios or in a multiple pregnancy. Also after the delivery of the first twin the uterus is suddenly decompressed and may force the placenta to become separated.

Acute vascular changes in pregnancy

Vascular changes which are strongly associated with abruption are conditions involving vasoconstriction and sudden rise in blood pressure. Examples of this are fulminating pre-eclampsia or cocaine use (particularly in the third trimester).22,30

Chorioamnionitis

The bacterial colonisation and inflammation of the decidua may trigger the process of abruption.³¹ The opposite has also been hypothesised. Chorioamnionitis is a factor in preterm rupture of membranes, which too is a risk factor for placental abruption.

Although the factors above are considered acute or brought on by trauma, women who have underlying chronic aetiology (chronic and pregnancyinduced hypertension, maternal vascular disease, smoking, nutritional deficiencies, uterine abnormalities) will be at an increased risk of an abruption should they experience any of these events.

CHRONIC FACTORS

It is thought that many abruptions occur secondary to degenerative changes to the spiral arteries in early pregnancy leading to ischaemic placental disorders²³ as listed in Table 3.2.

Hypertensive disorders

Chronic and pregnancy-related hypertension including pre-eclampsia can predispose to placental abruption. Ananth et al.³² reviewed the literature to evaluate the joint influences of hypertensive disorders (chronic hypertension and pre-eclampsia) and smoking on the subsequent development of abruption and found an increased risk of placental abruption in relation to both smoking and hypertensive disorders during pregnancy. These combined factors exacerbate the risk of abruption due to placental hypoperfusion and related ischaemia.

Migraine

A small study by Sanchez et al.³³ has shown a correlation between women who experience migraines and placental abruption. This may be due to a shared underlying vascular pathophysiology.

Table 3.2  Risk and predisposing factors for placenta abruption and placenta praevia

Placental abruption

Placenta praevia

Socio-demographic and lifestyle risk factors

•  Maternal age

•  Multiparity

•  Smoking

•  Cocaine and other drug abuse

•  Alcohol

•  Socio-economic disadvantage

•  Dietary/Folic acid deficiency

•  Advanced maternal age

•  Multiparity

•  Smoking

•  Cocaine use

•  Lower educational level

Pre-pregnancy risk factors

•  Uterine abnormalities

•  Chronic hypertension

•  Thrombophilia

•  Pre-gestational diabetes

•  Previous caesarean section (CS)

•  Previous placental abruption

•  Miscarriage

•  Previous ischaemic placental disease

•  Stillbirth

•  Uterine scarring

•  Endometriosis

•  Assisted conception

•  Fibroids

•  Previous manual placenta removal

•  Previous termination of pregnancy (TOP)

•  Previous CS

•  Previous placenta praevia

•  Miscarriage

Current pregnancy risk factors

Acute factors

•  Sudden decompression: Rupture of membranes in polyhydramnios or multiple pregnancy

•  External cephalic version (ECV)

•  Abdominal trauma

•  Inflammatory conditions: Chorioamnionitis/premature rupture of membranes (PROM)

Chronic factors

•  Ischaemic placental disease

•  Pregnancy induced hypertension

•  Pre-eclampsia

•  Small for gestational age fetus

•  Oligohydramnios

•  Premature rupture of membranes

•  Placenta praevia

•  Placental abnormalities (e.g. circumvallate placenta)

•  Multiple pregnancy

•  Male infant

•  Early pregnancy bleeding

•  Multiple pregnancy

•  Male infant

•  Early pregnancy bleeding

Smoking

In women who smoke in pregnancy, there is evidence of reduced uteroplacental blood flow and decidual necrosis³¹ which may predispose to placental abruption. Since the mid-1950s smoking has been recognised as having an adverse effect on pregnancy outcome. Andres,³⁴ in his seminal work, reviewed the literature written about women who smoked in pregnancy and found that the risk of placental abruption and placenta praevia was increased in this group. The risk increased with the number of cigarettes smoked (10 a day or over), and the number of years over which they had smoked (6 years or more). Those women who gave up smoking during their pregnancy were shown to be at no greater risk of developing placental abruption than those who did not smoke. This indicates that smoking is a modifiable risk factor.³²

Placental implantation

When implantation occurs over uterine malformations (e.g. fibroids, bicornuate uterus) and in the case of a circumvallate placenta, it may pose a risk due to the instability of the site and decreased vascularisation of the placental area.23,30

Thrombophilias

There is a link between maternal thrombophilias and placental abruption.²²

Acute and chronic respiratory diseases in pregnancy

According to Ananth et al.,²⁰ women who require hospitalisation during their pregnancy because of acute and chronic respiratory disease are more likely to experience placental abruption.

Recurrence

Women who have previously had a placental abruption have 4%–8% chance of having another abruption in a subsequent pregnancy.³⁵ This is linked with possible underlying genetic aetiology.

Signs and symptoms

BLEEDING

As already described, the amount of blood seen when a woman presents with a placental abruption may not be associated with the severity of the abruption. Early warning scoring systems may help identify hidden bleeding by indicating that the woman is becoming compromised by her blood loss. The blood may be red if it is fresh loss, but there may be brown blood if it has been retained in utero for any length of time.

SHOCK

The woman’s skin may be pale and clammy and her vital signs may suggest hypovolaemic shock. She may also have altered levels of consciousness.

ABDOMINAL PAIN

This can be moderate or severe, intermittent or continuous and of either sudden or gradual onset. Backache may be present if the placenta is posterior and the uterus will be generally irritable.

ABDOMINAL EXAMINATION

In a concealed haemorrhage, there may be an increase in abdominal girth and the uterus may be firm or ‘board-like’ (Couvelaire) on palpation. The abdomen may be tender to touch.

EVIDENCE OF FETAL DISTRESS

The woman may report a history of reduced or excessive fetal movements. The fetal heart may show signs of distress on the cardiotocograph (CTG) or be absent.

ANXIETY

Any deviation from the norm in the progression of pregnancy can cause anxiety in women.

SIGNS AND SYMPTOMS OF CHRONIC PLACENTAL ABRUPTION

Bleeding may be intermittent and light and there will be signs of placental inflammation and dysfunction (oligohydramnios, pre-eclampsia, small for dates, PPROM).²¹

PLACENTA PRAEVIA

Placenta praevia is where the placenta is partially or wholly implanted in the lower uterine segment on either the anterior or posterior wall. It is associated with considerable maternal and neonatal mortality and morbidity and heightened demands on healthcare resources.³⁶ Placenta praevia poses significant challenges for the woman and the maternity staff due to the unpredictability and possible severity of bleeding and due to frequent hospital admissions.

Placenta praevia occurs in approximately 4 per 1000 pregnancies with a higher prevalence among Asian populations.³⁷ In NHS Trusts in England it was reported that placenta praevia had occurred in 0.7% of all births during 2013–2014.¹⁸ The perinatal mortality rate is about two to four times higher in pregnancies with placenta praevia than in those without.³⁸ The more preterm the gestation the greater is the increase in perinatal mortality and morbidity.³⁹

Classification is important in relation to how placenta praevia is managed for each individual woman. It pertains to the degree to which the leading edge of the placenta encroaches or covers the internal os of the cervix. Traditionally placenta praevia is divided into four types which can be simplified on clinical grounds to major or minor³⁶ (Figure 3.2):

•  Type I (lateral or low-lying): The placenta encroaches on the lower uterine segment but does not extend as far as the cervical os.

•  Type II (marginal): The edge of the placenta extends to the internal cervical os but does not cover it.

•  Type III (partial): The placenta partially covers the internal os.

•  Type IV (complete or central): The placenta completely covers the internal os.

Pathophysiology of placenta praevia

Although it is not clear why some placentae implant nearer to the internal cervical os than the upper section of the uterus, it is thought that it may occur where the endometrium is less well vascularised due to scarring or abnormality. However, as the uterus grows and the lower segment develops and stretches, the placenta appears to migrate upwards and away from the os and the developing lower uterine segment (in other words the placenta stays in the same place on the growing uterus). A second hypothesis is that a process of ‘preferential migration’ occurs when the placenta itself grows towards an area of the uterus that is better vascularised and the part of the placenta lying over the less vascularised area atrophies.21,40–42 Oyelese and Smulian⁴¹ theorise that in some cases blood vessels may be left behind causing a vasa praevia. If the atrophy is incomplete a succenturiate lobe may be left behind.⁴¹

Bleeding from a placenta praevia usually occurs as a result of placental separation during the formation of the lower uterine segment and/or when cervical effacement occurs. Therefore, antenatal bleeding is more likely after 28 weeks’ gestation and torrential haemorrhage is more likely when labour begins.⁴³

Diagnosis and antenatal management of placenta praevia

Although a definitive diagnosis is almost always made with ultrasound scanning, there may still be situations where the midwife may become suspicious if a woman presents with any of the signs and symptoms discussed below, in which case immediate referral needs to be made.

It is commonplace in the United Kingdom for pregnant women to have a routine ultrasound anomaly scan at 20 weeks’ gestation. This should include screening for placental localisation.³⁶ This is done as the distance between the placental edge and the internal os is the best way to predict placenta praevia at term.⁴² At 20 weeks about 5%–6% of all placentae will appear low as the lower uterine segment is not yet formed. However, of these, more than 90% will be normally situated by full term.²¹ Therefore, only a minority of women who need to be re-scanned for this reason will be diagnosed with placenta praevia. Their subsequent management will be decided depending on their individual condition.

Figure 3.2  Placenta praevia.

The NICE⁴⁴ guidelines for antenatal care recommend that women who have a placenta that extends over the internal os at the 20-week scan should be offered further ultrasound scanning at 32 weeks. These women are at the highest risk of persistent placenta praevia and haemorrhage and therefore need to be advised as to what to do if bleeding occurs before the next scan. Where the placenta does not overlap the os and the woman is asymptomatic with no history of caesarean section, she will be managed expectantly and re-scanned at 36 weeks’ gestation.³⁶ As transvaginal scanning is safe and more accurate than transabdominal scanning, all women should be offered this should placenta praevia be suspected.³⁶

For women with an anterior placenta praevia and who have had a previous caesarean section, a morbidly adherent placenta (in particular placenta accreta) should be suspected. In this situation magnetic resonance imaging (MRI) may be used to diagnose the condition.³⁶ See Chapter 10 for further discussion.

As placenta praevia is usually diagnosed before bleeding occurs it follows that once it has been diagnosed staff must be aware that bleeding is inevitable in most cases. Hence, timely optimal management can be implemented. Management decisions will be based on both clinical and ultrasound findings.

Once a confirmed diagnosis is made, the woman needs to have an appointment with the obstetric consultant to discuss the increased risk of haemorrhage and preterm delivery, the need for hospitalisation and the possible need for a caesarean section, particularly if the placental edge is less than 2 cm from the internal os in the third trimester.³⁶ During this meeting the possibility of blood transfusion and hysterectomy should also be discussed.

Women who may refuse blood products should already have been identified routinely, however, this high-risk diagnosis will necessitate further discussion and additional planning. Staff need to be aware that there will be variations in products and techniques that are acceptable, and, of course the woman should always be given the opportunity to change her mind if the need arises (see Box 3.1).

As with the mode of birth, timing of the birth will depend on the degree of placenta praevia and whether any other symptoms are present. A woman who is asymptomatic with major placenta praevia will be delivered by caesarean section at 38 weeks’ gestation.³⁶

Signs and symptoms

BLEEDING

Bleeding is never concealed (as in placental abruption) and blood loss is fresh and red. Vaginal examination or coitus could possibly initiate bleeding. Pain is not usually a feature because the low-lying placenta allows the blood to escape, thus avoiding the formation of a retroplacental clot. A small amount of women may also present with uterine irritability alongside bleeding. This is similar to the presentation of placental abruption,⁴² and indeed coexisting abruption may be present.²

BOX 3.1: Managing women who refuse blood transfusion⁴⁵

Refusal of blood and blood components should be discussed and documented antenatally.

Other transfusion-sparing techniques should also be discussed and documented.

Anaemia should be corrected and Hb optimised prior to delivery.

Use of pharmacological, mechanical and surgical procedures to avert the use of blood and blood components should be considered early.

Intraoperative cell salvage should be considered with the above.

Additionally, every unit should have specific protocols for the management of women who refuse blood.

Conversations should be witnessed and documented.

SHOCK

This will correspond to the amount of blood loss. Due to increased blood volume, most healthy pregnant women can tolerate up to a 35% blood loss (or 1200–1500 mL) before showing any signs of shock, and assessment is further complicated by a delay in signs of shock in a pregnant woman who becomes hypovolaemic.⁴⁶

ABDOMINAL PALPATION

The uterus is usually soft and non-tender. There is often malpresentation and/or unstable lie because the placenta occupies the space in the pelvis where the baby’s head usually lies. Breech is particularly common. In any presentation, the presenting part will remain high.

FETAL CONDITION

The fetal heart rate is usually normal, although fetal tachycardia, reflecting maternal tachycardia, may be present. With severe haemorrhage, signs of fetal hypoxia will be present.

ANXIETY

Any deviation from the norm in the progression of pregnancy can cause anxiety in women.

TREATMENT OF APH

It is always important to remember that every woman who is experiencing an antepartum haemorrhage is different and should be treated sensitively and individually. A calm attitude and continual explanation of procedures is paramount in order to instil trust and confidence in the woman and her family.

Should a woman call the maternity unit from home with any signs and symptoms of bleeding or other related complications, she must be asked to come to triage or the labour ward immediately. If her signs and symptoms are severe, the assistance of the emergency services will be required to ensure a swift transfer to the nearest consultant-led maternity unit, ideally one with appropriate neonatal facilities.

If the midwife is attending the woman at home, her priority is to arrange to transfer her to the maternity unit as mentioned above. An intravenous infusion should be sited to initiate fluid replacement. The mother should be positioned flat and in a left lateral tilt so as to avoid supine hypotension, as this could exacerbate her state of shock and further compromise the fetus. Blood pressure, heart rate, respirations and temperature should be taken and recorded. The presence of pain and the nature of the blood loss must be noted. Any bloodstained sanitary pads, sheets or clothing should be kept to assist with an accurate estimation of blood loss.⁴⁷ A vaginal examination must not be undertaken, as this may cause heavy bleeding in the case of a placenta praevia.³⁶ Abdominal examination should also be avoided at this stage as this may cause uterine irritability which may exacerbate bleeding in the case of a placental abruption.⁴⁸

On arrival in hospital or at any time if already hospitalised, if signs and symptoms of an APH are recognised, assistance should be summoned immediately and a multidisciplinary approach must be taken. The immediate treatment will depend on the severity of the haemorrhage (see Box 3.2), the gestation and the condition of the mother and fetus.

BOX 3.2: The RCOG¹ definitions used for assessing the severity of an APH

•  Spotting: Staining, streaking or blood spotting noted on underwear or sanitary protection

•  Minor haemorrhage: Blood loss less than 50 mL that has settled

•  Major haemorrhage: Blood loss of 50–1000 mL, with no signs of clinical shock

•  Massive haemorrhage: Blood loss greater than 1000 mL and/or signs of clinical shock

The midwife must remember that any amount of bleeding could be serious and the condition of the mother and fetus can deteriorate rapidly. As blood loss may be concealed or underestimated, it is essential that frequent and thorough assessment for maternal and fetal compromise is undertaken and repeated as appropriate. Hence, despite the estimated amount of blood loss, any maternal compromise should prompt the initiation of a Major Obstetric Haemorrhage (MOH) protocol (see section entitled ‘Immediate management of a major/massive APH’).

Accurate and thorough history-taking will give the team information on the amount of blood loss, any associated pain, trauma, recent sexual intercourse or any previous episodes of bleeding. This will help in trying to determine the cause of the bleeding. The woman may have had a recent scan indicating placental location or she may have had previous hospital admissions with bleeding or other risk factors for APH.

Careful abdominal palpation can help to determine the cause of haemorrhage according to whether or not the abdomen is tender, soft or ‘board-like’. However, it should be performed gently so as to avoid pain and/or further separation. Abdominal palpation will also give an indication of the size of the baby. A history of repeated small bleeds during the pregnancy may be linked to placental insufficiency which can lead to associated intrauterine growth restriction.

Digital vaginal and/or rectal examinations must not be performed as this could aggravate the bleeding. A scan is necessary in most cases to determine the location of the placenta. Even if this has been done previously in pregnancy, it should be repeated as routine pregnancy ultrasound may not always accurately identify placental localisation. A placenta that is normally sited will indicate that the APH may be due to placental abruption. Separation may occasionally be seen on ultrasound if there is a particularly large retroplacental clot, although this is not usually the case.⁴⁹ A speculum examination may be carried out to exclude cervical or vaginal lesions as a cause for the bleeding.¹

The fetal condition is assessed by initial auscultation, a CTG and a description of the nature of recent fetal movements from the mother.

After 37 weeks and if the mother and fetus are stable (or if the baby has died), an induction of labour will be considered if the woman has experienced either a minor or major APH.¹

In the case of maternal or fetal compromise or in the case of major placenta praevia, delivery needs to be expedited via an emergency caesarean section.1,50 See Chapter 10, Box 10.4 for a description of the preparation necessary if an emergency caesarean section is planned. Delivery of the fetus and placenta will assist in controlling the bleeding by allowing the uterus to contract, thereby ensuring a more favourable outcome for the mother. Removal of the placenta may further assist as placental tissue factor may exacerbate any coagulation disorders.¹

Immediate management of a major/massive APH

Once the initial call for assistance has been made, a multidisciplinary approach is essential for optimum care.⁴⁹ Box 3.3 presents a list of personnel who may be involved.

All actions undertaken from the time the emergency has been recognised should be taken simultaneously, with priority given to resuscitating and stabilising the woman before delivering the baby. Initial management of the haemorrhage will be the same irrespective of the cause. Once the woman and fetus are stabilised specific treatment will be considered. Please see Chapters 2 and 10 for further discussion of maternal resuscitation and major obstetric haemorrhage, respectively.

BOX 3.3: Team members for managing a major/massive APH

•  Labour ward coordinator

•  Consultant obstetrician

•  On-call obstetric team

•  Midwives

•  Senior anaesthetist

•  Haematologist

•  Blood transfusion service

•  Porters to expedite blood product delivery

•  Operating theatre staff

•  Neonatologist

•  Neonatal unit nursing staff

•  An identified scribe to note events, fluids, drugs and vital signs

•  Any other staff to give assistance

The compromised woman needs to be positioned in a left lateral tilt with the bed flat. Should cardiopulmonary resuscitation be necessary, the woman should be moved back into a supine position and manual uterine displacement to the left should be used⁵¹ (see Chapter 2). Her airway needs to be kept patent and breathing assessed and assisted if necessary. High-flow oxygen must be administered via a mask at 15 L/min. Circulation must be evaluated and maintained.

Early intravenous access with wide-bore canulae is essential so that intravenous fluid replacement can be commenced to maintain blood pressure and circulating volume. Blood transfusion may be needed and any coagulopathy will need to be corrected promptly by the medical team.⁵⁰

Ongoing assessment for signs of shock must be carried out by looking for clammy skin, pallor and air hunger. The woman’s vital signs may include rising heart rate and respirations and lowering blood pressure, although low blood pressure is often a late sign of shock in the pregnant woman. The blood pressure may also not be particularly low in the early stages of shock for women with underlying hypertension alongside an APH, thus further masking the clinical signs of shock.

The blood tests which may be needed include

•  Full blood count

•  Group and save/crossmatch

•  Coagulation screen

•  Biochemistry screen in cases of hypertension (see Chapter 5 for details of the pre-eclampsia blood tests)

•  Urea and electrolytes

•  Kleihauer test (if the mother is rhesus negative)

•  Arterial blood gas

•  Bedside haematocrit

Further specific treatment of APH

PLACENTAL ABRUPTION

After a minor haemorrhage, the blood loss will probably all be revealed and the condition of the mother and fetus are not normally compromised. Treatment will therefore be conservative. If the woman has experienced a minor APH that is not associated with placenta praevia and has no further episodes of bleeding or other concerns, the pregnancy can continue normally and intermittent fetal auscultation during labour is deemed as appropriate.¹ However, if there are signs of placental insufficiency, continuous monitoring during labour is necessary.¹

If the gestation of the baby is between 24 and 34 weeks, corticosteroids can be administered to accelerate fetal lung maturity.1,52 If the woman is rhesus negative, an intramuscular injection of anti-D immunoglobulin is needed (a Kleihauer test will be done to gauge the dose required). The placental site will be determined by ultrasound scan to exclude placenta praevia. The woman may be allowed home after a period of observation if no further bleeding has occurred in the preceding 24 hours and frequent monitoring has indicated that the fetal heart rate is normal.

A major haemorrhage is where up to 1 L of blood has been lost and about one-quarter of the placenta separated. The blood loss may be partially concealed and partially revealed – a mixed haemorrhage. The condition of the mother is not compromised but she will be experiencing abdominal pain. Regular observation of these signs, as well as accurate measurements of maternal heart rate, respirations, oxygen saturations, blood pressure and fluid balance should be maintained, as she may become compromised suddenly and rapidly. Analgesia may be required. Fetal assessment needs to be maintained as appropriate.

With a massive haemorrhage, one or more litres of blood may have been lost and more than half of the placenta separated. It is possible that the fetus will have died. The mother will be shocked and in extreme pain with large quantities of the blood loss concealed behind the placenta. A central venous pressure line may be needed to monitor fluid levels. An in-dwelling urinary catheter should be inserted and analgesia administered as appropriate. Although the treatment is the same as for a major haemorrhage, the mother is more at risk of coagulation defects, renal failure and pituitary failure. Efficient teamwork and good communication between the labour ward and blood transfusion laboratories is essential.

PLACENTA PRAEVIA

Women with a major degree of placenta praevia tend to bleed earlier in pregnancy and more heavily than those with minor degrees. Only about 10% of women diagnosed with placenta praevia will reach term without bleeding.⁴²

The first bleeds suffered by women with placenta praevia do not normally compromise the mother or fetus and are sometimes referred to as ‘warning bleeds’. Severe bleeding usually occurs after the 34th week of pregnancy. About 50% of women with placenta praevia deliver at less than 35 weeks.⁵³

Expectant or conservative management is appropriate with slight to moderate bleeding, to minimise the problems of prematurity. This usually entails rest in hospital until the bleeding has stopped. Once in her third trimester it is important to remain in hospital until delivery if major placenta praevia has been diagnosed. Blood must always be available should the mother bleed again and need an urgent transfusion. Intraoperative cell salvage should also be discussed with the woman prior to a planned caesarean section if appropriate.³⁶

The treatment of women who remain in hospital includes correction of anaemia in the mother and serial ultrasound scans for fetal well-being. Anti-D and/or steroids should be administered as appropriate (as in placental abruption) and psychological care must be considered. The mother may become institutionalised and miserable with prolonged hospitalisation. She may be separated from other children and need help in organising their care. Parent education may be considered, including a visit to the neonatal unit. A date set for her delivery will give her something positive to focus on.

If the placenta praevia has been classified as marginal, induction of labour may be appropriate once the fetus has reached an adequate gestation. However, an artificial rupture of membranes should only be performed in controlled conditions, such as in the operating theatre, in the presence of appropriate staff and with blood available in case of haemorrhage. The fetal head should be below the placental edge and amniotomy attempted by a senior obstetrician. If any placental tissue can be felt, then the procedure should be abandoned and an emergency caesarean section performed.

POSSIBLE IMMEDIATE OUTCOMES OF APH

Woman

Postpartum haemorrhage: This is to be anticipated and an actively managed third stage is recommended.¹ However, following delivery of a woman with APH, uncontrollable bleeding may occur despite administration of oxytocics (see Chapter 10).

Hysterectomy: This may be necessary to control a massive haemorrhage, particularly as a result of Couvelaire uterus or coagulation defects.

Disseminated intravascular coagulation (DIC): DIC can arise from APH and haemorrhagic shock. The trigger for DIC seems to be the entry of tissue thromboplastin or endotoxin into the circulation, inducing thrombin activation. A consumption coagulopathy occurs where fibrinogen, coagulation factors and circulating platelets are depleted. The result is haemostatic failure with microvascular bleeding and an increased blood loss. See Chapter 10 for further discussion of the diagnosis and management of DIC.

Renal failure: Renal failure may occur as a result of severe blood loss.

Thromboembolism: Thromboprophylaxis should be commenced as soon as the immediate risk of haemorrhage is reduced. See Chapter 4 for further discussion.

Anaemia: A result of excessive blood loss or underlying disease, anaemia may require correction by blood transfusion, oral or intravenous iron therapy as appropriate.

Infection: Infection may be acquired through low resistance caused by shock, anaemia or through increased interventions.

Fetus/baby

Premature delivery and resulting sequelae: Any delivery occurring between 24 and 37 weeks’ gestation as a result of placental abruption or placenta praevia will require varying degrees of input from the neonatal team. Long-term follow-up may ensue under the responsibility of community and social services.

Fetal hypoxia: Fetal hypoxia may occur as a result of premature placental separation.

Fetal death: Death of the fetus is rare but more common in abruption.

POSSIBLE LONG-TERM OUTCOMES OF APH

Sheehan’s syndrome: Anterior pituitary necrosis or Sheehan’s syndrome is a rare complication of prolonged shock. It can result in failure of lactation, amenorrhoea, hypothyroidism and adrenocortical insufficiency following the pregnancy.

Coping with the preterm or sick infant: If separated from her baby, the mother may feel more vulnerable. The midwife needs to ensure that information about the baby’s condition is given and there is sufficient opportunity for her to bond with her baby. The woman may have breastfeeding difficulties and therefore the midwife will need to provide enhanced breastfeeding support.

Adverse psychological effects: Postnatal depression or post-traumatic stress syndrome (see Chapter 14 for additional discussion of these issues) may occur as a result of prolonged periods of hospitalisation, a traumatic delivery or negative fetal outcome. It may be also necessary to refer the mother for bereavement counselling. Information and advice about what has happened needs to be given and the woman should be encouraged to ask questions about her condition, the immediate and longterm effects of her condition and about her physical recovery and subsequent pregnancies and fertility.

Recurrence: Traumatic placental abruption is unlikely to recur. However, women who have chronic underlying causes can be advised on various lifestyle behaviours in order to lessen the risk. This may include encouraging the cessation of smoking, drug and alcohol abuse and measures to control hypertension.

SUMMARY OF MIDWIFERY RESPONSIBILITIES

•  Awareness of unit protocols and participation in skills drills training

•  Maintenance of good communication with the multidisciplinary team

•  Risk assessment

•  Antenatal correction of anaemia

•  Accurate recognition and diagnosis

•  Appropriate and timely referral/escalation

•  APH immediate management (some actions will take place simultaneously)

•  Call for appropriate help immediately/transfer to hospital if at home.

•  Continuously assess clinical situation.

•  Do not perform a vaginal examination.

•  Use left lateral tilt and oxygen therapy.

•  Perform resuscitation (with manual uterine displacement) if necessary.

•  Establish venous access and administer fluids.

•  Collect blood samples.

•  Replace blood loss as necessary (crystalloids, colloids, blood products as prescribed).

•  Continuously assess maternal and fetal condition.

•  Accurately monitor blood loss.

•  Maintain records (MEOWS) of observations (pulse, BP, respirations and O₂ saturations) and fluid balance.

•  Administer analgesia as necessary.

•  Assist with the delivery of the baby (if necessary) after mother stabilised.

•  Actively manage third stage.

•  Document time, action and reaction.

•  Present continual explanation and calm attitude.

•  Appropriate postnatal care to minimise complications

•  Consideration of long-term psychological complications (see Chapter 14)

•  Clinical incident reporting

REFERENCES

1.  Royal College of Obstetricians and Gynaecologists (RCOG). 2011. Antepartum Haemorrhage. Green-Top Guideline No. 63. November 2011. London: RCOG.

2.  Navti OB, Konje JC. 2011. Bleeding in late pregnancy. In: James D (Ed.). High Risk Pregnancy Management Options. Philadelphia: Saunders Elsevier, pp. 1037–1052.

3.  Great Britain, Human Fertilisation and Embryology Act. 1990. Chapter 37. London: HMSO Available at http://www.legislation.gov.uk/ukpga/1990/37/section/37 (accessed July 2, 2013).

4.  Patterson-Brown S, Bamber J, on behalf of the MBRRACE-UK haemorrhage writing group. 2014. Prevention and treatment of haemorrhage. In: Knight M, Kenyon S, Brocklehurst P, Neilson J, Shakespeare J, Kurinczuk JJ (Eds.), on behalf of MBRRACE-UK. Saving Lives, Improving Mothers’ Care – Lessons Learned to Inform Future Maternity Care from the UK and Ireland Confidential Enquiries into Maternal Deaths and Morbidity 2009-12. Oxford: National Perinatal Epidemiology Unit, University of Oxford, pp. 45–55.

5.  Magann EF, Cummings JE, Niederhauser A, Rodrigues-Thompson D, McCormack R, Chauhan SP. 2005. Antepartum bleeding of unknown origin in the second half of pregnancy: A review. Obstetrical and Gynecological Survey, 60:741–745.

6.  McCormack RA, Doherty DA, Magann EF, Hutchinson M, Newnham JP. 2008. Antepartum bleeding of unknown origin in the second half of pregnancy and pregnancy outcomes. BJOG: An International Journal of Obstetrics and Gynaecology, 115(11):1451–1457.

7.  Bhandari S, Raja EA, Shetty A, Bhattacharya S. 2012. Maternal and perinatal consequences of antepartum haemorrhage of unknown origin. BJOG: An International Journal of Obstetrics and Gynaecology, 121:44–52.

8.  Schoen C, Berghella V. 2013. Commentary on ‘Maternal and perinatal consequences of antepartum haemorrhage of unknown origin’. BJOG: An International Journal of Obstetrics and Gynaecology, 121:44–52.

9.  Yang Q, Wen SW, et al. 2009. Comparison of maternal risk factors between placental abruption and placental praevia. American Journal of Perinatology, 26(4):279–286.

10.  Boisramé T, Sananès N, Fritz G, Boudier E, Aissi G, Favre R, Langer B. 2014. Placental abruption: Risk factors, management and maternal-fetal prognosis. Cohort study over 10 years. European Journal of Obstetrics and Gynecology and Reproductive Biology, 179:100–104. doi: 10.1016/j. ejogrb.2014.05.026.

11.  Gurol-Urganci I, Cromwell DA, Leroy C, Edozien LC, Smith GCS, Onwere C, Mahmood TA, Templeton A, van der Meulen JH. 2011. Risk of placenta previa in second birth after first birth cesarean section: A population-based study and meta-analysis. BMC Pregnancy and Childbirth, 11:95. Available at http://www.biomedcentral.com/1471-2393/11/95 (accessed May 1, 2015).

12.  Yang Q, Wen SW, et al. 2007. Association of caesarean delivery for first birth with placenta previa and placental abruption in second pregnancy. BJOG: An International Journal of Obstetrics and Gynaecology, 114:609–613.

13.  Matsuda Y, Kawamichi Y, Hayashi K, Shiozaki A, Satoh S, Saito S. 2011. Impact of maternal age on the incidence of obstetrical complications in Japan. Journal of Obstetrics and Gynaecology Research, 37(10):1409–1412.

14.  Saraswat L, Bhattacharya S, Maheshwari A, Bhattacharya S. 2010. Maternal and perinatal outcome in women with threatened miscarriage in the first trimester: A systematic review. BJOG: An International Journal of Obstetrics and Gynaecology, 117(3):245–257. doi:10.1111/j.1471-0528.2009.02427.

15.  Nilsen RM, Vollset SE, et al. 2008. Folic acid and multivitamin supplement use and risk of placental abruption: A population-based registry study. American Journal of Epidemiology, 167(7):867–874.

16.  Altvorst MEWA, Chan EHY, Taylor RS, Kenny LC, Myers JE, Dekker GA, North RA, McCowan LME, and on behalf of the SCOPE Consortium. 2012. Antepartum haemorrhage of unknown origin and maternal cigarette smoking beyond the first trimester. Australian and New Zealand Journal of Obstetrics and Gynaecology, 52(2):161–166.

17.  Tikkanen M, Luukkaala T, Gissler M, Ritvanen A, Metsaranta M. 2013. Decreasing perinatal mortality in placental abruption. Acta Obstetricia et Gynologica Scandinavica, 92:298–305.

18.  Health and Social Care Information Centre (HSCIC). 2015. Compendium of Maternity Statistics – England 2013–2014. April 2015. Available at http://www.hscic.gov.uk/catalogue/PUB16725 (accessed June 2, 2015).

19.  Chhabra A, Pandit V, Gosavi M. 2014. Placental abruption: A persisting killer. International Journal of Reproduction, Contraception, Obstetrics and Gynecology, 3(3):604–609.

20.  Ananth CV, Oyelese Y, Prasad V, Getahun D, Smulian JC. 2006. Evidence of placental abruption as a chronic process: Associations with vaginal bleeding early in pregnancy and placental lesions. European Journal of Obstetrics and Gynecology and Reproductive Biology, 128(1–2):15–21.

21.  Francois KE, Foley MR. 2012. Antepartum and postpartum hemorrhage. In: Gabbe SG, Niebyl JR, Simpson JL, Landon MB, Galan HL, Jauniaux ERM, Driscoll DA (Eds.). Obstetrics: Normal and Problem Pregnancies. 6th ed. Philadelphia: Elsevier Saunders.

22.  Yeo L, Ananth CV, Vintzileoa AM. 2008. Placental Abruption. Global Library of Women’s Medicine. Available at http://www.glowm.com (accessed June 1, 2015).

23.  Ananth CV, Kinzler WL. 2015. Placental abruption: Clinical features and diagnosis. In: Lockwood CJ (Ed.). UpToDate. Waltham, MA. Available at http://www.UpToDate.com (accessed September 24, 2015).

24.  Cheng HT, Wanf YC, Lo HC, Sung FC, Hsieh CH. 2012. Trauma during pregnancy: A population based analysis of maternal outcome. World Journal of Surgery, 36(12):2767–2775. doi:10.10n07/s00268-012-1750-6.

25.  Office for National Statistics. 2014. Chapter 4–Intimate Personal Violence and Partner Abuse: Findings from the 2012/2013 Crime Survey for England and Wales (CSEW). February 13, 2014, p. 14. Available at http://webarchive.nationalarchives.gov.uk/20160105160709/http://www.ons.gov.uk/ons/dcp171776_352362.pdf (accessed March 2, 2016).

26.  Leone JM, Lane S, Koumans EH, DeMott K, Wojtowycs MA, Jensen J, Aubry RH. 2010. Effects of intimate partner violence on pregnancy trauma and placental abruption. Journal of Women’s Health, 19(8):1501–1509. Available at http://content.ebscohost.com.ezproxy.uwl.ac.uk/ContentServer.asp?T=P&P=AN&K=52680930&S=R&D=afh&EbscoContent=dGJyMMvl7ESep7M4yOvsOLCmr02eprRSsqa4SraWxWXS&ContentCustomer=dGJyMPGqtU6yrLNRuePfgeyx4Hnx3%2BEA (accessed June 1, 2015). doi:10.1089/jwh.2009.1716.

27.  Cheng D, Salimi S, Terplan M, Chisolm MS. 2015. Intimate partner violence and maternal cigarette smoking before and during pregnancy. Obstetrics and Gynaecology, 125(2):356–362.

28.  Collaris RJ, Oei SG. 2004. External cephalic version: A safe procedure? A systematic review of version-related risks. Acta Obstetricia et Gynecologica Scandinavica, 83:511–518.

29.  Grootscholten K, Kok M, Oei S, Mol B, van der Post, JA. 2008. External cephalic version-related risks: A metaanalysis. Obstetrics and Gynecology, 112(5):1143–1151. doi:10.1097/AOG.0b013e31818b4ade.

30.  Blackburn ST. 2013. Maternal, Fetal, and Neonatal Physiology: A Clinical Perspective. 4th ed. Maryland Heights, MO: Elsevier Saunders.

31.  Tikkanen M. 2011. Placental abruption: Epidemiology, risk factors and consequences. Acta Obstetrica et Gynaecology Scandenavica, 90:140–149. doi: 10.1111/j.1600-0412.2010.01030.

32.  Ananth CV, Smulian JC, Vintzileos AM. 1999. Incidence of placental abruption in relation to cigarette smoking and hypertensive disorders during pregnancy: A meta-analysis of observational studies. Obstetrics and Gynaecology, 4:622–628.

33.  Sanchez SE, Williams MA, Pacora PN, Ananth CV, Chungfang Q, Aurora SK, Sorenson TK. 2010. Risk of placental abruption in relation to migraines and headaches. BMC Women’s Health 10(30). Available at http://www.biomedcentral.com/1472-6874/10/30 (accessed August 27, 2015). doi:10.1186/1472-6874-10-30.

34.  Andres RL. 1996. The association of cigarette smoking with placenta praevia and abruptio placentae. Seminars in Perinatology, 20(2):154–159.

35.  Rasmussen S, Irgens LM. 2009. Occurrence of placental abruption in relatives. BJOG: An International Journal of Obstetrics and Gynaecology, 116(5):693–699. doi:10.111 1/j.1471-0528.2008.02064.

36.  Royal College of Obstetricians and Gynaecologists (RCOG). 2011. Placenta Praevia, Placenta Praevia Accreta and Vasa Praevia. Diagnosis and Management. Green-Top Guideline No. 27. January. London: RCOG.

37.  Cresswell JA, Ronsmans C, Calvert C, Filippi V. 2013. Prevalence of placenta praevia by world region: A systematic review and meta-analysis. Tropical Medicine and International Health, 18(60):712–724.

38.  Ananth CV, Smulian JC, Vintzileos AM. 2003. The effect of placenta previa on neonatal mortality: A population-based study in the United States, 1989 through 1997. American Journal of Obstetrics and Gynecology, 188(5):1299–1304.

39.  Berham Y. 2014. Predictors of perinatal mortality associated with placenta previa and placental abruption: An experience from a low income country. Journal of Pregnancy, 2014. Article ID 307043. Available at http://dx.doi.org/10.1155/2014/307043 (accessed September 18, 2015).

40.  Oyelese Y. 2012. Placenta previa and related placental disorders. In: Queenan JT, Spong CY, Lockwood CJ (Eds.). Queenan’s Management of High-Risk Pregnancy: An Evidence-Based Approach. 6th ed. Oxford: Wiley-Blackwell, p. 382.

41.  Oyelese Y, Smulian JC. 2006. Placenta previa, placenta accreta and vasa previa. Obstetrics and Gynaecology, 107(4):927–941.

42.  Lockwood CJ, Russo-Stieglitz K. 2015. Clinical features, diagnosis, and course of placenta previa. UpToDate. Wolters Kluwer. Available at http://www.uptodate.com (accessed May 2015).

43.  Symonds I, Arulkumaran S. (Eds). 2013. Antepartum haemorrhage. In: Essential Obstetrics and Gynaecology. 5th ed. London: Churchill, p. 121.

44.  National Institute for Health and Care Excellence (NICE). 2008. Clinical Guideline 62: Antenatal Care: Routine Care for Healthy Pregnant Women. Modified in 2014. London: NICE.

45.  Royal College of Obstetricians and Gynaecologists (RCOG). 2015. Blood Transfusions in Obstetrics. Green-Top Guideline No. 47. May 2015. London: RCOG.

46.  Yanamandra N, Chandraharan E. 2013. Anatomical and physiological changes in pregnancy and their implications in clinical practice. In: Chandraharan E, Arulkumaran S (Eds.). Obstetric and Intrapartum Emergencies. A Practical Guide to Management. Cambridge: Cambridge University Press, pp. 1–8.

47.  Needham J. 2015. Antepartum haemorrhage. In: Bates K, Crozier K (Eds.). Managing Childbirth Emergencies in the Community and Low Tech Settings. 2nd ed. London: Palgrave, p. 26.

48.  Hutcherson A. 2011. Bleeding in pregnancy. In: Magill-Cuerden J, MacDonald S (Eds.). Mayes Midwifery. London: Bailliere Tindall.

49.  Winter C, Crofts J, Laxton C, Barnfield S, Draycott T. 2012. Practical Obstetric Multi-Professional Training (PROMPT) Course Manual. 2nd ed. Cambridge: Cambridge University Press.

50.  Nama V, Chandraharan E. 2013. Massive obstetric haemorrhage. In: Chandraharan E, Arulkumaran S (Eds.). Obstetric and Intrapartum Emergencies. A Practical Guide to Management. Cambridge: Cambridge University Press.

51.  Paterson-Brown S, Howell C (Eds.). 2014. The MOET Course Manual. Managing Obstetric Emergencies and Trauma. 3rd ed. Cambridge: Cambridge University Press.

52.  Roberts D, Dalziel SR. 2013. Antenatal corticosteroids for accelerating fetal lung maturation for women at risk of preterm birth. Cochrane Database of Systematic Reviews, 3. Available at http://ovidsp.tx.ovid.com/sp-3.18.0b/ovidweb.cgi?&S=BIFIFPEDHFDDGCKPNCJKOAFBEGONAA00&Link+Set=S.sh.22%7c1%7csl_50 (accessed July 2, 2013).

53.  Baskett TF. 2004. Antepartum Haemorrhage in Essential Management of Obstetric Emergencies. Bristol: Clinical Press.

4

Thromboembolism in pregnancy

JUDY BOTHAMLEY

Introduction

Epidemiology

Pathophysiology

Risk assessment

Risk factors

Medical and midwifery measures to prevent VTE

Deep vein thrombosis

Pulmonary embolism

Anticoagulation treatment and prevention of DVT and PE

Conclusion

Summary of midwifery responsibilities

References

INTRODUCTION

Venous thromboembolism (VTE) is one of the leading causes of maternal mortality and during the period 2010–2012, 26 women died of this complication in the United Kingdom.¹ The focus provided by reports from the Confidential Enquiry into Maternal deaths,² now MBRRACE-UK,³ has led to a welcome reduction in deaths through detailed risk assessment and timely and effective prophylaxis both in the antenatal and postnatal period. However, challenges remain. The rise in rates of obesity and medical comorbidities among pregnant women are contributing to persistent rates of women dying from this complication¹ and midwives need to remain knowledgeable in identifying both those at risk and those showing symptoms of a VTE.

Pulmonary embolism (PE) is the most common cause of death associated with VTE. It occurs when a clot from a deep vein, commonly in the leg, detaches itself and travels to the lungs where it lodges in a pulmonary blood vessel. Collapse and death will occur if the clot is large enough to compromise the pulmonary circulation. Pregnancy is a hypercoagulable state making pregnant women more prone to developing the deep vein thrombosis (DVT) that underlies this disorder. Prevention, detection and treatment of a DVT are crucial in limiting deaths from PE in pregnancy and the postpartum period. The management of a DVT, therefore, although not itself constituting an emergency, is discussed fully in this chapter alongside the immediate diagnosis and treatment of a woman presenting with a PE.

EPIDEMIOLOGY

VTE (which includes DVT and PE) is up to four times more common in pregnancy and up to 20 times more common in the postnatal period compared to non-pregnant women of a similar age.4–6 However, the diagnosis of VTE is relatively low with an overall incidence of around 1 in 1000 pregnancies.7,8 The pro-coagulant changes that underlie the development of VTE in pregnancy start early in gestation and a number of VTEs occur in early pregnancy,⁹ perhaps when carers are less likely to consider the risk. Although there appears to be a significant rise in incidence in the third trimester, the peak occurrence is in the 6 weeks following delivery (highest within the first 3 weeks) and then a steep decline to pre-pregnancy incidence at around 12 weeks postpartum.8,10,11

Of VTE events that occur in association with childbearing, about 80% are DVT and 20% are PE.¹² If a DVT is not recognised and treated, up to a quarter of women will develop a PE. Almost 15% of pregnant women with a PE will die and two-thirds of those deaths may occur within 30 minutes of the embolic event.⁶

PATHOPHYSIOLOGY

Clot formation normally occurs in response to injury in a vessel wall and is an important mechanism to prevent blood loss. It is a complex process involving a cascade of reactions whereby fibrinogen, a soluble protein in the blood, is converted to produce fibrin threads by the action of thrombin. Blood cells attach to the fibrin threads and clump together to form a clot. A DVT will develop when small deposits of fibrin collect in a vein (often iliofemoral, thigh or calf veins) usually as a result of slow blood flow. They may occur around the cusp of a venous valve, which can cause irreversible valve damage resulting in chronic valve insufficiency and a condition known as post-thrombotic syndrome. PE occurs when the clot extends and breaks off, traveling through the venous system to the lungs where it lodges in a pulmonary blood vessel, obstructing blood flow to the lungs. Symptoms of PE will vary depending on how much the pulmonary circulation and consequently oxygen exchange is affected (see section entitled ‘Pulmonary embolism’).

Rudolf Virchow (1821–1902) first described the triad of factors that are associated with venous thrombosis, all of which are present during pregnancy and the puerperium (see Figure 4.1).

Normal pregnancy is associated with alterations in the proteins of the coagulation and fibrinolytic systems, resulting in a relative state of hypercoagulability.⁵ These changes are an adaptive and preparatory mechanism for the control of bleeding in the third stage of labour and help maintain the placenta–uterine interface.⁵ Pro-coagulant factors, such as von Willebrand factor, factor VII, factor VIII, factor X and fibrinogen enhance thrombin production in pregnancy.⁴ In addition, an acquired resistance to the anticoagulant protein C and a reduction in protein S further contribute to the increased coagulability. Impaired fibrinolysis, resulting in slower breakdown of clots, also occurs.⁵

Figure 4.1  Triad of factors associated with venous thrombosis.

Venous stasis

Venous return from the lower limbs is reduced when the pregnant uterus compresses the inferior vena cava. In addition, reduction in the muscle tone of veins during pregnancy, caused by progesterone, leads to vasodilation and reduced velocity of blood flow. There can be up to a 50% reduction in blood flow (venous return) with peak effect occurring around 36 weeks’ gestation and taking about 6 weeks postnatally to return to pre-pregnancy levels. ⁴ Blood remains in contact with the vessel wall for a longer time and this may be an important factor in the development of a DVT. Incompetent venous valves are a common source of morbidity in women of reproductive age and may also contribute to venous stasis. Blood flow within the veins depends on the action of voluntary muscles and periods of inactivity further slow blood flow. The anatomy of the venous drainage from the lower limbs, where the right iliac artery crosses the left iliac vein, means that DVTs are more common (more than 80%) in the left leg. ¹³

Vascular damage

The epithelial lining of veins is normally an intact, smooth, single layer of cells containing various substances to prevent platelet adhesion and clot formation.

Surgery or perineal trauma encourages the platelets to clump together and sets off a series of chemical reactions that activates the coagulation system forming a micro-environment that promotes fibrin formation and the formation of clots.¹⁴

RISK ASSESSMENT

Computer-generated and paper-based risk assessment tools, that aim to identify women at higher risk of VTE, have been in common use for the last decade. These have enabled timely thromboprophylaxis, which aims to prevent VTE, and includes anticoagulant medication (usually low molecular weight heparin [LMWH]) and mechanical means (thromboembolic deterrent stockings [TEDS] and Flowtron boots) (see section entitled ‘Medical and midwifery measures to prevent VTE’).

An assessment for risk factors for VTE should be made at booking, repeated if admitted to hospital or if factors change and again immediately postpartum.15,16

The midwife at the booking interview already gathers the required information (such as smoking, body mass index [BMI], previous medical or family history of VTE), required for risk assessment of VTE so completion of a risk assessment tool should not be onerous. Risk will be stratified into low, intermediate and high. Box 4.1 lists the risk factors commonly identified as associated with VTE. Some of these risk factors are explored in more detail in the section entitled ‘Risk factors’. The risk assessment tool devised by the Royal College of Obstetricians and Gynaecologists (RCOG) and an alternative numerical risk scoring tool have been reproduced with permission.¹⁶ (See Figures 4.2 through 4.4.)

Ideally, those women with a high risk of VTE should be offered pre-pregnancy counselling with a clinician who has expertise in thrombosis in pregnancy. ‘Booking’ often does not occur until the end of the first trimester after the stage when thromboprophylaxis should have begun. General practitioners, physicians, other health professionals and the general public need to recognise the need for pre-conception planning for the woman at high risk of VTE.

BOX 4.1: Risk factors for VTE in pregnancy and the postpartum period7,9,16,17

GENERAL FACTORS

•  Personal or family history of DVT, PE or thrombophilia

•  Acquired thrombophilia

•  Inherited thrombophilia

•  Age over 35

•  Obesity (BMI > 30)

•  Prolonged immobilisation

•  Major current illness, for example, malignancy, diabetes and/or heart, lung, kidney or bowel disease

•  Mechanical heart valves

•  Sickle cell disease

•  Long-distance air travel

•  Major varicose veins

•  Smoking

•  Combined oral contraceptive pill

PREGNANCY-RELATED FACTORS

•  Caesarean section

•  Parity ≥ three

•  Multiple pregnancies

•  Assisted reproduction

•  Ovarian hyperstimulation syndrome (OHSS)

•  Severe infection

•  Pre-eclampsia

•  Stillbirth

•  Preterm birth

•  Immobility (including bed rest, symphysis pubis dysfunction)

•  Surgical procedures in pregnancy

•  Prolonged labour, instrumental delivery

•  Dehydration, hyperemesis

•  Excessive blood loss

Figure 4.2  Obstetric thromboprophylaxis risk assessment and management: antenatal. (Reproduced from the Royal College of Obstetricians and Gynaecologists. 2015. Thrombosis and Embolism during Pregnancy and the Puerperium, Reducing the Risk. Green-Top Guideline No. 37a. London: RCOG, with the permission of the Royal College of Obstetricians and Gynaecologists.)

Figure 4.3  Obstetric thromboprophylaxis risk assessment and management: postnatal. (Reproduced from the Royal College of Obstetricians and Gynaecologists. 2015. Thrombosis and Embolism during Pregnancy and the Puerperium, Reducing the Risk. Green-Top Guideline No. 37a. London: RCOG, with the permission of the Royal College of Obstetricians and Gynaecologists.)

Figure 4.4  Risk assessment for VTE (numerical scoring). (Reproduced from the Royal College of Obstetricians and Gynaecologists. 2015. Thrombosis and Embolism during Pregnancy and the Puerperium, Reducing the Risk. Green-Top Guideline No. 37a. London: RCOG, with the permission of the Royal College of Obstetricians and Gynaecologists.)

BOX 4.2: Women who will be considered for antenatal prophylaxis with LMWH¹⁶

•  Those with previous VTE – This may have been while on oestrogen containing contraception, in a previous pregnancy or as an unprovoked event (A single previous VTE related to major surgery with no other risk factors is considered intermediate risk.)

•  Those with four or more risk factors (Figure 4.2)

•  Those admitted to hospital

•  Those with a diagnosis of a high-risk inherited or acquired thrombophilia

•  Those with a medical condition such as cancer, heart disease, SLE, complications of type 1 diabetes, IV drug user and those on anticoagulant medication (women with mechanical heart valves)

•  Hyperemesis, OHSS

•  Surgical procedures in pregnancy

A scoring system should not replace but rather complement a common-sense approach of individual assessment. Gathering information for risk assessment requires good communication and relevant questioning. An awareness of changing circumstances such as admission to hospital, the development of an infection or a period of immobility should prompt a reassessment of risk. Midwives need to involve women fully in both the risk assessment and discussion regarding the need for thromboprophylaxis. Verbal discussion should be followed up with written information. Communication between members of the multidisciplinary team should be clear. Accurate documentation and clear prescription of any medication required will be key to this.

Those women considered high risk should receive, or be considered for, antenatal thromboprophylaxis with low molecular weight heparin (LMWH) (see section on anticoagulation treatment and prevention of DVT and PE). Where identified this should commence as early in pregnancy as practically possible (in view of increased first trimester risk). The midwife needs to complete the risk assessment tool and identify those women and make timely and efficient referral to an obstetrician/physician/haematologist as appropriate so that a plan of management can be determined.

Box 4.2 lists some of the factors that would indicate the need for prompt referral in the early antenatal period. Depending on the scoring system being used, a score of four or more indicates the need for antenatal prophylaxis with LMWH from the first trimester. Intermediate risk (a score of three or more) indicates the use of LMWH prophylaxis from 28 weeks’ gestation. (See Figures 4.2 and 4.4 for details.)

The first 3 weeks’ postpartum is the period of greatest risk for VTE and triggers for risk will now be lower than they were in the antepartum period. The risk assessment at this time will indicate who requires thromboprophylaxis and for how long. Women at high risk of VTE will be recommended to have 6 weeks prophylaxis and those at intermediate risk will be advised to have at least 10 days of prophylactic LMWH.¹⁶ Some women may change to the oral anticoagulant warfarin about a week after delivery, especially those that were taking maintenance doses of warfarin before pregnancy.

Midwives should ensure all women, regardless of risk, mobilise and avoid dehydration during and following delivery. (See section on medical and midwifery measures to prevent VTE.)

RISK FACTORS

Previous history of VTE

Previous thrombosis is the most important risk factor for developing VTE in pregnancy. The risk for thromboembolism in pregnancy and the postnatal period is approximately 3%–12% although this reduces to 0%–2.4% in those on regular anticoagulation.⁸ The midwife should enquire carefully and document accurately the circumstances of the woman’s previous VTE. Women with recurrent VTE and those whose previous VTE was oestrogen related (while on combined oral contraceptive pill) or during a previous pregnancy are unsurprisingly more likely to have another pregnancy-related VTE. However, if the woman had a single-episode VTE associated with a fracture or surgery, but has no other risk factors she is likely to be deemed intermediate risk antenatally although third trimester and postnatal prophylaxis would still be advised.8,16 Timely referral for specialist advice early in pregnancy is essential. Women with a history of VTE may be recommended to have thrombophilia testing before pregnancy.

Inherited or acquired thrombophilia

The other significant risk factor for pregnancyrelated VTE is thrombophilia. Inherited thrombophilia is found in between 20% and 50% of cases of pregnancy-related VTE.⁸ An alteration in the balance between the coagulation and fibrinolytic systems caused by inherited or acquired disorders predisposes a woman to clot formation, although many women with thrombophilia do not develop thrombosis complications indicating that the development of VTE is multicausal. Women with antithrombin deficiency and antiphospholipid syndrome (APS) are thought to be at very high risk and require referral to a specialist physician expert in haemostasis in pregnancy. They may be prescribed a higher-dose LMWH in both the antenatal and postnatal period and require closer monitoring and adjustment to medication around the time of labour and/or caesarean section.¹⁶ Examples of thrombophilia disorders are listed in Box 4.3.

BOX 4.3: Thrombophilia conditions¹⁸

INHERITED

•  Factor V Leiden

•  Antithrombin deficiency

•  Protein C and protein S deficiency

•  Prothrombin gene mutation G 20210A

ACQUIRED

•  Antiphospholipid syndrome (APS)

Women with high-risk thrombophilia are likely to be on long-term oral anticoagulant medication such as warfarin. As this medication is associated with damage to the fetus during development the woman is advised to change over to LMWH when the pregnancy is confirmed, ideally within 2 weeks of her missed period and before the sixth week of pregnancy.¹⁸ When planning pregnancy she is advised to take regular pregnancy tests. The woman will require information, support and access to expert advice to facilitate this transition in her medication.

Raised BMI

In the 2006–2008 Confidential Enquiries report,² 16 out of the 20 women who died from VTE were overweight or obese. The significant and rising prevalence of obesity in the childbearing population is an important risk factor for VTE and this risk appears to increase with rising BMI.⁸

Inadequate anticoagulation caused by maternal weight not being taken into account when heparin was prescribed has been implicated in deaths. There should be clear local guidelines for weightrelated thromboprophylactic and treatment doses of LMWH adjusted against the woman’s booking weight.⁶ Immobility associated with obesity (with consequent venous stasis) increases complications of childbirth generally¹⁹ and use of the combined oral contraceptive pill²⁰ postnatally are all cofactors contributing to the risk of VTE in obese women.

Caesarean section

Elective caesarean section doubles the risk of developing a VTE in the postnatal period and an emergency caesarean section further doubles that risk.8,9 Clinical practice that promotes use of pneumatic compression devices, effective pain relief, early mobilization, hydration and risk assessment for use of LMWH prophylaxis have been successful in reducing mortality and morbidity although midwives should not be complacent.

Pre-eclampsia

Pre-eclampsia is associated with vascular injury, which in turn is related to a disturbance in coagulation, thereby suggesting a link with thromboembolism. Confounding factors, such as bed rest and caesarean section, may also contribute to the risk of thromboembolism in women with pre-eclampsia.

Immobility

Movement of calf muscles and deep respiratory effort promote venous return and prevent stasis. Most pregnant women are healthy and active, but there are occasions when they become less mobile and are susceptible to thromboembolism. Changes in patterns of antenatal and postnatal care have contributed to the avoidance of routine bed rest for pregnant women and probably account for the overall reduction in thromboembolism over the years. However, bed rest does occur after caesarean section and at a time of severe pre-eclampsia and preterm labour. Admission to hospital should warrant further assessment and consideration for LMWH prophylaxis.15,16 Admission to hospital with hyperemesis combines the risk effects of immobilisation and dehydration.

Long-distance air travel or indeed any travel for more than 4 hours may cause venous stasis and women should seek guidance prior to travel particularly if they have other risk factors.²¹ Moving around the cabin, doing leg exercises every 30 minutes and avoiding dehydration by drinking plenty of non-caffeine and non-alcoholic drinks will help prevent DVT. Women at high risk of DVT should discuss specific prophylaxis measures with an obstetrician/physician.²¹

The Confidential Enquiry report published in 1998²² included a paraplegic woman who died of PE in the postnatal period. Overcoming the problems of immobility for these women represents a particular challenge. More recently symphysis pubis dysfunction has been identified as another possible cause for sustained immobility in pregnancy.²³

Women with mechanical heart valves

Women with mechanical heart valves are likely to be taking long-term oral anticoagulation medication. They require a plan of care from the cardiologist to adjust their medication for pregnancy balancing the risks in changing medication with the risks to fetal development associated with use of warfarin. LMWH, which does not cross the placenta, is safer for the fetus but there may be more thromboembolic complications for the mother.⁹

MEDICAL AND MIDWIFERY MEASURES TO PREVENT VTE

The midwife plays an important role in the education and support of women with regard to the range of measures to prevent DVT (see Box 4.4). Options for prophylaxis include mechanical methods (mobilisation, compression stockings, intermittent pneumatic compression devices [Flowtron boots], foot impulse devices) or pharmacological agents, usually LMWH.⁹

It is recommended that women at increased risk of VTE should be given information about the signs and symptoms of DVT and PE along with details on how to self-refer so they can quickly contact medical advice if they are concerned.⁵

Compression stockings

There is some different terminology used for the stockings that are intended to prevent DVT and its complications. Most midwives will refer to them all as thromboembolic deterrent stockings (TEDS) but strictly there are two types and the difference between them is the amount of pressure they provide and the indications for their use. The external compression provided by stockings increases the velocity of blood flow within the veins, improves venous return and therefore reduces venous stasis.²⁴ Box 4.5 outlines guidance for correct use of compression stockings.

Anti-embolic stockings (AES) are synonymous with TEDS and provide 14–15 mm Hg pressure around the ankle. They aim to improve venous return, particularly in immobile women following surgery and/or those with significant risk factors. AES may be used in conjunction with LMWH, for women where LMWH is contraindicated (i.e. those with high risk of bleeding), and for women travelling by air.

There is lack of data with regard to pregnancy about which length AES (knee or thigh) offers greater benefit. Reviews on the non-pregnant population have been contradictory, although there appears to be benefits to knee-length stockings, in that they are cheaper, more likely to fit correctly and better tolerated by the people wearing them.25–27

BOX 4.4: Prophylactic measures that may be used to prevent thromboembolism

FOR THOSE AT HIGHER RISK

•  Thromboprophylaxis with prescribed LMWH

GENERALLY AS INDICATED, AND FOR THOSE WITH ADDITIONAL RISK FACTORS

•  Avoid long period of immobilisation

•  Wear correctly fitting anti-embolic stockings (AES)

•  Deep-breathing exercises to encourage venous return

•  Effective postpartum pain relief to enable mobility

•  Intermittent pneumatic compression devices used during operative procedures and while immobile

GENERAL MEASURES FOR ALL PREGNANT WOMEN

•  Leg exercises to encourage venous return

•  Drink plenty of water and avoid dehydration

•  Avoid sitting with legs crossed

•  Avoid prolonged immobilisation

•  Take regular breaks on long journeys

•  Seek specific advice about air travel in pregnancy²¹

BOX 4.5: Guidance for correct use of compression stockings32–34

•  Use manufacturer’s instructions for measuring, selecting correct size and fitting stockings.

•  Apply carefully, ensuring toe hole lies under toes, the heel patch is in the correct position and the thigh gusset is over the inner thigh.

•  Stockings should be smooth when fitted. Ensure they do not roll down which gives a tourniquet effect.

•  Remove daily for no more than 30 minutes.

•  Check fitting daily to detect changes in leg circumference.

•  Explain to women how the stockings work and why they can help reduce DVT and give advice about how to wear them.

Accurate fitting of stockings may be difficult in pregnancy due to changing levels of oedema. Correct fitting however is essential – too tight can result in tissue damage and will be uncomfortable; too large and there will be no therapeutic benefit. The RCOG¹⁶ recommend the use of properly applied thigh-length AES with knee length being considered if full-length stockings are ill fitting or when compliance is poor.

Graduated compression stockings (GCS) are different to AES in that they provide greater ankle compression (20–40 mm Hg) and are used in the treatment of DVT on the affected leg. They are helpful in reducing oedema and pain as well as aiming to prevent the long-term problems of postthrombotic syndrome (PTS).²⁸ PTS is caused by damage to venous valves and symptoms vary from mild oedema to incapacitating swelling with pain and ulceration. It occurs in around 42% of women following a DVT in pregnancy.²⁹ It has been recommended that GCS should be worn for up to 2 years to prevent PTS¹⁴ although the strength of evidence in supporting this recommendation is not clear.⁶ Moreover, prolonged use of LMWH (more than 12 weeks) appears more beneficial in preventing this debilitating condition.³⁰ National Institute for Health and Care Excellence (NICE) guidelines³¹ recommend that those with proximal DVT be offered below-knee GCS.

Intermittent pneumatic compression devices

These devices wrap around the leg and deliver pressurised air in a sequential manner up the leg. This produces a wave-like milking effect to promote venous return. They should not be used in women with a DVT or where a DVT is suspected as there is an increased risk of pushing emboli towards the lungs. They are often put in place prior to surgery and are useful in preventing VTE in women at risk of bleeding where anticoagulation treatment is temporarily stopped.15,16,35

DEEP VEIN THROMBOSIS

Clinical assessment for signs and symptoms of DVT

The diagnosis of DVT in pregnancy can be difficult. Signs and symptoms (see Box 4.6) will raise suspicion of a DVT but only a small percentage of women will have the diagnosis confirmed.8,36 During antenatal and postnatal assessments midwives will examine the woman’s legs noting the size, colour and any temperature difference between the limbs. Midwives are likely to be the first to whom women report their symptoms. It is important for the midwife to listen carefully to the woman when she is describing symptoms and put these in context. The general discomfort and swelling of a woman’s legs in pregnancy can confuse the diagnosis and assessment should be made in context of additional risk factors. Any signs and symptoms of DVT or possible minor or major PE should be referred immediately to medical staff and diagnosis actively pursued.

BOX 4.6: Symptoms and signs of DVT37,38

•  Pain in calf, thigh, groin, buttocks (especially unilateral pain)

•  Swelling (at least 2 cm difference between the two legs)

•  Redness or discoloration of the affected leg

•  Change in limb colour or temperature

•  Homan’s sign (pain on dorsiflexion of the foot) (unreliable)

•  Low-grade pyrexia (37.5°C)

•  Tachycardia

•  Lower abdominal pain

•  Limb symptoms on left side (>80%)⁹

•  Chest pain and shortness of breath (symptoms of PE)

DVTs in pregnancy may not be in the calf vein but higher up in the ileo-femoral region.⁹ The higher the location of the clot, the more likely it is to cause a PE and the more difficult it is to be seen on ultrasound. Lower abdominal pain, associated with clots in higher level veins, can be the presenting feature of DVT in pregnancy.³⁹ Ovarian vein thrombosis, which is more likely on the right side, presents with flank, back or groin pain. Cerebral venous thrombosis (rare) may present as severe headaches.³⁷ Referral to a senior obstetrician and careful evaluation of additional risk factors form an essential part of the clinical assessment of a woman presenting with symptoms of DVT.

Diagnostic tests for DVT

Accurate diagnosis is essential, not only to prevent PE, but also to protect women from unnecessary treatment with anticoagulants. Compression ultrasound is the primary diagnostic test for detecting DVT in pregnancy. Compression ultrasound of the whole leg is recommended looking for both proximal and distal DVT.¹⁴ When a thrombus is present, a relatively echogenic soft tissue mass, which prevents the vein collapsing after compression of the leg, is seen. The iliac veins are less easily seen and are particularly difficult to visualise in the presence of obesity.⁴⁰

Fibrin degradation products (D-dimers) are formed as a thrombus develops and can be measured in the blood to raise suspicion of a DVT. D-dimer assays are commonly used in conjunction with ultrasound in non-pregnant patients. A low D-dimer level in pregnancy is likely to suggest there is no DVT or PE and thus may provide additional reassurance when there is no evidence of DVT on the ultrasound⁸ but generally the use of D-dimers for evaluation of DVT or PE in pregnancy is not recommended.6,14,41

Management of DVT

Women with features of a DVT or PE should be treated with LMWH while objective tests are carried out.¹⁴ In addition to anticoagulation, other interventions that will aid recovery are aimed at promoting good venous return, thereby preventing further clot formation. Leg elevation is recommended when sitting, but in pregnancy inguinal congestion may occur, so the leg should not be raised at too acute an angle and pressure behind the knee should be avoided. Knee-length GCS stockings (ankle pressure greater than 23 mm Hg) need to be fitted and correctly applied to the affected leg to help reduce oedema. (See section entitled ‘Compression stockings’). Once LMWH treatment has begun, and stockings fitted, mobilisation should be encouraged.⁶

General measures to prevent DVT (see Box 4.4) should be emphasised. Midwives should provide women and their families with information about DVT and how to prevent further clot formation as well as inform them about signs and symptoms of PE and when to seek further medical aid.

PULMONARY EMBOLISM

The clinical signs of pulmonary embolism (PE) (see Box 4.7) are related to the size of the clot that is obstructing the pulmonary circulation. Large or multiple emboli will prevent adequate oxygenation of the blood. A woman with a major PE will collapse with severe breathlessness, cyanosis, hypotension and chest pain. Sudden respiratory or cardiac arrest may occur. Warning signs and symptoms indicative of smaller emboli include unexplained pyrexia, cough, chest pain and breathlessness, which may be incorrectly diagnosed as a chest infection or be explained away as normal breathlessness of pregnancy.

Midwives need to identify all possible pulmonary embolism symptoms so that prompt referral and pursuit of an accurate diagnosis and initiation of effective treatment can be made.¹⁴ Failure to identify the more subtle symptoms of a PE, especially in the presence of additional risk factors, has been identified as a contributing factor in some maternal deaths.²

Diagnostic tools for PE

The woman’s presenting symptoms and her clinical condition will determine the priority in which diagnostic testing will be done. Compression duplex ultrasound of both limbs will normally be the initial investigation in women suspected of having a PE who also have leg symptoms.8,41 The diagnosis of DVT will indirectly confirm the diagnosis of PE and treatment (which is the same for both conditions) can be maintained.6,8

BOX 4.7: Clinical manifestations of PE37,38

MOST FREQUENT SIGNS AND SYMPTOMS

•  Sudden or unexpected difficulty in breathing

•  Increased respiratory rate (tachypnoea)

•  Feeling faint

•  Tightness in chest or pleuritic chest pain

•  Increased pulse (tachycardia)

•  Cough

•  Crackles on lung auscultation

ASSOCIATED SIGNS AND SYMPTOMS

•  Coughing up blood (haemoptysis)

•  Distended neck veins

•  Cyanosis and collapse

•  Hypotension

•  Anxiety

•  Low-grade fever

These are assessed in combination with signs and symptoms of DVT.

The next investigation may be a chest x-ray. A chest x-ray will identify other causes for chest symptoms, such as pneumonia, as well as show changes that may be indicative of PE.8,41 The radiation dose from a chest x-ray is negligible particularly as compared to other more definitive tests for PE (see below). Depending on the findings of the ultrasound and the chest x-ray, further diagnostic testing may be required.

A ventilation/perfusion (V/Q) scan consists initially of assessment of the pulmonary blood flow (perfusion) following an intravenous injection of albumin labelled with a radioactive marker. Areas with reduced or absent perfusion are diagnostic of PE. The ventilation component of the V/Q scan collects information regarding the distribution of inhaled gas. This component may be omitted in pregnancy to reduce radiation exposure to the fetus.6,8 PE typically produces poor perfusion in an area of normal ventilation.³⁷

A computed tomography pulmonary angiogram (CTPA) can be used, in which the pulmonary arteries are assessed following the injection of a dye into the bloodstream. The scanner creates a computer-generated image from x-rays taken at angles through the chest. It is useful for diagnosis of pulmonary embolism but will also identify other pathologies that may be causing the woman’s symptoms such as pneumonia, pulmonary oedema and aortic dissection.⁶

V/Q and CTPA involve radiation exposure to mother and fetus. With both techniques the amount of exposure to the fetus is well below that which would cause any serious fetal abnormality or growth restriction but there is a very small increase in the risk of childhood cancer. CTPA delivers a lower radiation dose to the fetus than a V/Q scan.⁶ The concern with CTPA is the radiation exposure to the mother’s breast tissue, which again, although extremely small, is an increased lifetime risk of breast cancer. The pregnancy and postpartum changes to the breasts make the breasts more sensitive to radiation exposure,⁶ although using breast shields will reduce this exposure.⁴

Agreed protocols for testing will help keep tests to a minimum while still attaining an accurate diagnosis.4,6 McLintock et al.¹⁴ argue that the harm arising from a missed diagnosis of DVT or PE far outweighs the potential risk of the small amounts of radiation associated with the recommended radiological investigations, although this will be a difficult consideration for the woman and her family to process. The implications of both these tests should be discussed fully with the woman and informed consent obtained.⁴¹

Further assessments of the woman’s condition will be undertaken including a full set of basic observations including oxygen saturation monitoring. An electrocardiogram (ECG) and an echocardiogram (ECHO) may also be ordered to investigate PE and will also identify any cardiac causes for the woman’s symptoms.⁶

Treatment of pulmonary embolism

Early diagnosis and treatment are vital when PE is suspected, as deaths caused by PE can occur very quickly following an embolic event. The priorities for assessment, diagnosis and treatment will depend on the woman’s clinical condition. Where PE is suspected anticoagulation treatment should be started immediately and without waiting for a confirmed diagnosis.⁴⁰ The pharmacological treatment of choice for non-life-threatening PE is LMWH whereas in life-threatening PE, intravenous (IV) unfractionated heparin (UH) is often the treatment of choice due to its rapid effect and experience in its use.⁸

A woman presenting with massive pulmonary embolus may suffer cardiovascular collapse and therefore the cardiac arrest team should be called. Appropriate staff, including a senior anaesthetist, physician and ITU outreach team should also be urgently summoned to deal with this emergency or if the woman is at home, she should be immediately transferred to the closest accident and emergency department via ambulance. The surgical team and a radiologist may also be required.

Immediate treatment should include standard ABCDE assessment and resuscitation as necessary (see Chapter 2). The woman will require continuous vital-sign measurement as well as ECG, intravenous access and oxygen therapy. An urgent echocardiogram or CTPA needs to be arranged.⁶ Cardiac arrest procedures, including endotracheal intubation and mechanical ventilation, may be required. If the woman is making some respiratory effort it is advisable to put the head of the bed up by 30° and/or assist her to lean forward to help maximise lung expansion, along with delivery of oxygen via a face mask. If the cause of the collapse is thought likely to be PE, intravenous unfractionated heparin should be started immediately¹⁴ and given according to local guidelines (see section entitled ‘Anticoagulation treatment and prevention of DVT and PE’). The midwife should provide the necessary support to the anaesthetist, physician and/or obstetrician in instigating these therapies. Admission to the intensive care unit is likely.

Other specific midwifery management includes the assessment and documentation of respiratory and cardiovascular vital signs. Assessment of oxygen saturation levels should be made continuously with an oximeter, and then periodically via arterial blood gas monitoring. Intravenous access will have been established as soon as possible and bloods taken (full blood count, coagulation tests, urea and electrolytes, and liver function tests). Accurate recording of fluid balance, including hourly urine output after catheterisation, is important in preventing further insult to the cardiovascular system through fluid overload: a central venous pressure (CVP) line may be necessary. An arterial line may be inserted to facilitate arterial blood gas monitoring and BP assessment.

Women taking anticoagulation (particularly the therapeutic dosage prescribed as treatment of a PE) are at risk of significant bleeding and therefore should be frequently assessed for bleeding.⁴²

The woman, if conscious, will be extremely apprehensive and agitated. A calm, confident, sympathetic approach by the midwife can help to minimise this apprehension. Members of the woman’s family will also require support, guidance and information at the time and following this event. Midwifery staff may also need to take responsibility for the care of the newborn. Box 4.8 summarises the main responsibilities for the midwife, a number of which can be instigated in the home setting while emergency transfer to hospital is arranged.

Further medical or surgical interventions may be necessary in life-threatening pulmonary embolism. Thrombolytic therapy (‘clot busting’ drugs such as streptokinase) may be used, but this is not common in pregnancy except in a life-threatening situation, due to the risk of major haemorrhage and fetal loss.43,44 Inferior vena cava filters, which work by intercepting emboli travelling to the pulmonary vasculature, may be used in cases of confirmed recurrent VTE despite anticoagulation.⁸ Pulmonary embolectomy, which requires major cardiothoracic surgery, is rarely used and only as a life-saving measure.⁶

Treatment with therapeutic (as opposed to prophylactic) doses of LMWH should be continued for the remainder of the pregnancy and until at least 6 weeks postnatally.8,14 At least 3 months of treatment is required in total.⁶ Induction of labour or CS may be planned to enable a transition to UH so that the level of anticoagulation can be adjusted to safe levels for delivery.¹⁴

Anticoagulants commonly used are not contraindicated in breastfeeding but individual drugs should always be checked. Midwives will be involved in teaching women to give their daily injections, advise about side effects such as bleeding from gums and bruising and generally provide ongoing support following what may have been a very frightening experience.

ANTICOAGULATION TREATMENT AND PREVENTION OF DVT AND PE

Overview of heparin

Anticoagulation treatment aims to prevent extension of the clot, restore venous patency and limit the risk or recurrence of a PE. Low molecular weight heparin (LMWH) has largely replaced unfractionated (standard) heparin (UH) in the prevention and treatment of VTE in pregnancy. Unfractionated (standard) heparin can be administered via the IV or subcutaneous route. It is now mostly used only in acute treatment of major PE, for those at high risk of bleeding, those with cardiac and/or renal compromise and around the time of birth in those women at high risk of thrombosis.14,16 Midwives should familiarise themselves with local guidelines for intravenous heparin use in acute events.

Heparin (both LMWH and UH) does not break down a clot but prevents further clot formation by enhancing the action of antithrombin, allowing time for the normal process of fibrinolysis to break down the clot. This stabilises the clot, preventing fragmentation, and also prevents clot formation in other locations.⁴⁵ Heparin is a large molecule that does not cross the placenta, so the risk of teratogenesis or bleeding in the fetus is minimal. It is therefore considered safe for use during pregnancy and lactation.⁴⁶

BOX 4.8: Midwife’s responsibilities in pulmonary embolism emergency*

FOR WOMEN PRESENTING WITH CARDIOVASCULAR COLLAPSE

•  Assess airway, breathing, circulation (ABC assessment).

•  Summon the emergency response team or arrange emergency transfer by ambulance to hospital if at home.

•  Administer cardiopulmonary resuscitation (CPR) as required (see Chapter 2: Maternal and newborn resuscitation).

•  Assist with endotracheal intubation as necessary.

FOR ALL WOMEN SUSPECTED OF HAVING PE

•  Admit to hospital and refer to senior obstetrician, anaesthetist or physician.

•  Give heparin and other drugs according to medical orders.

•  Attach pulse oximeter.

•  Give oxygen via face mask if O₂ saturations are below 96% in air.

•  If appropriate, sit the woman up to maximise the respiratory effort.

•  Initiate IV access.

•  Record an ECG.

•  Take bloods (e.g. for full blood count [FBC], coagulation screen, urea, electrolytes and liver function tests).

•  Assess and record cardiovascular and respiratory vital signs.

•  Maintain accurate fluid balance.

•  Assess for bleeding.

•  Monitor fetal well-being/ensure safe care of the neonate as appropriate.

•  Support the woman and her family.

•  Maintain accurate and contemporaneous records.

*  Many actions may be performed simultaneously

Anticoagulation therapy can be influenced by renal and liver function. As conditions such as preeclampsia may affect renal and liver function, blood should be tested for full blood count, coagulation screen, urea, electrolytes and liver function tests. The risk of bleeding should be assessed before giving anticoagulants. The presence of active bleeding, liver disorders, low platelets and inherited bleeding disorders such as von Willebrand disease warrant individualised assessment by senior medical staff.³⁴

Low molecular weight heparin

There are several LMWHs and examples used in pregnancy include enoxaparin (Clexane) and dalteparin (Fragmin).⁴⁶ LMWH is administered by subcutaneous injection. LMWH is commonly used for prophylaxis or in the longer-term phase of treatment, but studies have now confirmed that LMWH is also safe and effective for treatment of acute thromboembolism in pregnancy.14,46,47 Both the prophylactic and therapeutic doses of LMWH are maternal weight dependent. The RCOG guidelines6,16 provide weight-related LMWH dose recommendations based on booking or early pregnancy weight. LMWH generally has minimal side effects although bleeding may be a problem in around 2% of pregnancies.⁹ LMWH is considered safe in breastfeeding.¹⁶

Anticoagulation therapy during labour and delivery

There is a high risk of major haemorrhage at delivery if women are fully anticoagulated at this time and therefore clear documentation of plans for labour is required, given the need to balance the risks of thrombosis against haemorrhage.⁹ The onset of labour is not predictable, delivery (both vaginal and CS) is associated with blood loss and the insertion of epidural or spinal catheters for pain relief or surgery are associated with bleeding risk.⁸

Women taking LMWH maintenance therapy for treatment of a DVT or PE need to be advised not to give their scheduled injection once they think labour has begun.⁸ They will need to be assessed (including a coagulation screen and platelet count) on admission to hospital. If delivery is planned, LMWH should be discontinued 24 hours before the planned delivery.⁶ Women who develop VTE close to delivery require specialist adjustment of their therapeutic dose of LMWH and may, if the birth is within 2 weeks of presentation, require changing to UH which is more easily adjusted.¹⁴ Regional analgesia such as an epidural block cannot be given until at least 24 hours after the last dose of therapeutic LMWH.⁶

Women taking prophylactic doses of LMWH may await spontaneous labour but need to be advised that they will require a 12-hour gap between the last dose of prophylactic LMWH and placement of an epidural catheter.9,16

The risk of developing an epidural/spinal haematoma for women taking LMWH is a possibility.9,37 Although the risk is extremely low, the presence of a coagulation disorder, such as haemolysis, elevated liver enzymes and low platelets (HELLP) syndrome, will increase the concern.⁹ Anaesthetists will need to be aware of women taking anticoagulants and will require recent results of clotting studies prior to epidural/spinal insertion (Table 4.1). Midwives need to be proactive in ensuring good verbal and written communication between the woman, midwife, obstetrician and anaesthetist in this situation to enable the best possible choices in pain relief to be available to this woman balanced against the need to prevent VTE.

Midwives need to follow the anaesthetist’s instructions and local policies regarding the timing of removal of an epidural catheter in relation to LMWH injections. The RCOG guideline⁶ recommends that LMWH should not be given for 4 hours after a spinal anaesthetic. An epidural catheter should not be removed within 12 hours of the most recent injection and the next dose of LMWH should not be given until 4 hours after the catheter has been removed. These timings may vary for individual risk, treatment doses and use of IV UH. Midwives should follow documented plans and prescription for anticoagulation treatment alongside assessment of bleeding risk, but should not hesitate to question if concerned or unsure. Pneumatic compression devices are recommended until the woman is mobilizing and anticoagulation can be resumed.⁴⁸ Box 4.9 provides a checklist for midwives regarding thromboprophylaxis and the use of LMWH around the time of delivery.

Warfarin is an oral anticoagulant and in contrast to heparin crosses the placenta, with particular risk of damage to the embryo if taken between 6 and 12 weeks’ gestation. It is also associated with an increased risk of fetal loss even when first trimester exposure is avoided.⁴ It may be used in the postpartum period as an alternative to LMWH although regular assessment of the international normalised ratio (INR) is necessary, particularly in the first 10 days of treatment, which can prove inconvenient for the newly delivered mother. Warfarin does cross into the breast milk but has been shown not to impact the newborn’s coagulation profile and is therefore considered safe during breastfeeding.4,6 Women with prosthetic heart valves may be taking warfarin prior to pregnancy and a plan in consultation with a cardiologist is needed before pregnancy on how best to maintain effective anticoagulation balanced against a risk to the fetus.

Table 4.1  Laboratory tests for monitoring heparin

Assay

Nature of the test

Comments

Activated partial thromboplastin time (APTT)

Measures time to clot formation after adding an activating agent

Can be difficult to measure and unpredictable in pregnancy

Used to monitor effect of heparin on coagulation

Protamine titration (PT)

Determines the plasma level of warfarin

International normalised ratio (INR)

Thrombin is added to the plasma and time to clot recorded

Used to monitor blood clotting in people who take warfarin

Anti-factor Xa assay

Measures the rate of factor-Xa inhibition by optical density determination

Expensive; LMWH-specific; not widely available

Source:  Adapted from Blann A. 2013. Routine Blood Tests Explained. 3rd ed. Oxford: M&K.

BOX 4.9: Checklist for midwives regarding thromboprophylaxis and the use of LMWH around the time of delivery

•  The woman should have a clear plan documented in her notes by the obstetric and medical team who have seen the woman in the antenatal period.

•  When giving telephone advice to pregnant women in early labour the midwife should enquire about any known complications including any regular medication. If they are taking LMWH the midwife should advise the woman to omit any scheduled dose but to come to hospital for assessment by the medical, obstetric and anaesthetic team.

•  As there will be a need to balance the risk of VTE against the risk of bleeding at the time of delivery, mechanical and non-pharmacological methods of preventing VTE will now be very important. Hydration, mobilisation, use of AES, use of intermittent pneumatic compression devices (known as Flowtron boots), leg exercises, deep breathing exercises and effective pain relief are all relevant interventions the midwife can promote to prevent VTE.

•  Flowtron boots should be applied prior to any surgery.

•  The midwife should liaise directly with the anaesthetist regarding the insertion and removal of the epidural catheter and the timing of the next LMWH dose. The plan should be documented in the notes and on the prescription chart and include specific instruction on the timing of removal of the epidural catheter.

•  The midwife, when removing the epidural catheter, should document the time of removal both in the clinical notes and on the epidural prescription chart.

•  Prior to giving the first dose of LMWH after delivery the midwife should check what time the epidural catheter was removed and follow any particular instructions given by the obstetric or anaesthetic team.

Education, advice and support for women taking anticoagulant treatment

For all women, three simple steps can be taken to reduce the risk of VTE:

1.  Encourage mobilization

2.  Avoid dehydration

3.  Reassess the risk of VTE if things change³⁴

Women generally show initial reluctance to give themselves heparin injections and the midwife should work through the requirements with the woman to develop her confidence. A clear incentive to achieving self-management will be the possibility of discharge from hospital. LMWH involves only small volumes, which are pre-loaded and given with a fine-gauge needle. The site of subcutaneous injection should rotate between thighs and abdominal wall. Grasping some flesh, the injection is made at right angles to the skin surface. Women should be advised not to rub the injection site. Bruising inevitably occurs at the site of injection although rubbing the site will make that worse.³⁴ The woman should take care to take precautions in situations that may cause bleeding or injury; for example, a soft bristle toothbrush will protect from bleeding gums. Arrangements for safe disposal of needles should be made.

A phone call or visit from the midwife within days of discharge from hospital may be timely to offer support to the woman as she comes to terms with what will be prolonged treatment. A discussion regarding the management of any future pregnancies should be made at an appropriate time, probably after delivery, and in conjunction with the physician. The woman’s risk of recurrent DVT and the use of the combined contraceptive pill should be discussed. Women should be given information about modification of any existing risk factors such as smoking cessation, weight management and avoiding immobilisation as relevant.

Women being discharged from the hospital postnatally taking prophylactic dose LMWH will need similar support and instruction. With implementation of recent guidelines published from the RCOG¹⁶ which advises LMWH prophylaxis for at least 10 days for those with two or more risk factors (see Box 4.1), there will be a significant number of women discharged home who will need instruction in self-administration of LMWH.

CONCLUSION

Prevention and detection of thromboembolism in pregnancy is essential in preventing deaths from PE. Risk assessment tools are used to aid midwives and doctors in identifying women at risk. Midwives need to be alert to the signs and symptoms of DVT, particularly in those with additional risk factors, and make appropriate referral. Prevention of thromboembolism in pregnancy includes the use of effective prophylactic measures and client education.

As in any emergency situation, if a woman collapses with a major PE, the midwife must summon senior medical staff and implement appropriate resuscitation procedures immediately.

SUMMARY OF MIDWIFERY RESPONSIBILITIES

•  Provide detailed booking assessment and complete risk assessment tool that uncovers the range of risk factors for VTE including a previous history of a VTE.

•  Repeat risk assessment tool on admission to hospital, when any change occurs and immediately postnatally.

•  Ensure appropriate and prompt referral in the early antenatal period of those women at high risk.

•  Support the implementation of the range of measures aimed at reducing the pregnancyrelated risk of VTE thromboprophylaxis.

•  Ensure women do not become dehydrated post-delivery, particularly after CS. The midwife can assess the concentration of the urine as an easy evaluation of hydration.

•  Provide effective pain relief, especially after CS to ensure women can take deep breaths (promote venous return) and can mobilise.

•  Provide instruction to the woman regarding self-administration of LMWH.

•  Ensure the correct fitting and use of compression stockings.

•  Educate all women regarding general measures such as mobilisation and hydration to prevent VTE and for women to recognise when and how to seek help.

•  Midwives need to be able to recognise features of DVT and/or a PE and seek prompt referral for diagnosis and treatment.

•  Administer appropriate life support in situations of life-threatening PE.

REFERENCES

1.  Knight M, Nair M, Shah A, Noor N, Acosta C (Eds.), on behalf of the MBRRACE-UK 2014. Maternal Mortality and Morbidity in the UK 2009–2012: Surveillance and Epidemiology. In: Knight M, Kenyon S, Brocklehurst P, Neilson J, Shakespeare J, Kurinczuk JJ (Eds.), on behalf of MBRRACE-UK. Saving Lives, Improving Mothers’ Care – Lessons Learned to Inform Future Maternity Care from the UK and Ireland Confidential Enquiries into Maternal Deaths and Morbidity 2009–12. Oxford: National Perinatal Epidemiology Unit, University of Oxford, pp. 9–26.

2.  Centre for Maternal and Child Enquiries (CMACE). 2011. Saving Mothers’ Lives: Reviewing maternal deaths to make motherhood safer: 2006–08. The Eighth Report on Confidential Enquiries into Maternal Deaths in the United Kingdom. BJOG: An International Journal of Obstetrics and Gynaecology, 118(Suppl. 1):1–203.

3.  Knight M, Kenyon S, Brocklehurst P, Neilson J, Shakespeare J, Kurinczuk JJ (Eds.), on behalf of MBRRACE-UK. 2014. Saving Lives, Improving Mothers’ Care – Lessons Learned to Inform Future Maternity Care from the UK and Ireland Confidential Enquiries into Maternal Deaths and Morbidity 2009–12. Oxford: National Perinatal Epidemiology Unit, University of Oxford, pp. 1–98.

4.  Bourjeily G, Paidas M, Khalil H. et al. 2010. Pulmonary embolism in pregnancy. Lancet, 375(Feb. 6):500–512.

5.  Lussana F, Coppens M, Cattaneo M, Middeldorp S. 2012. Pregnancy related venous thromboembolism: Risk and the effect of thromboprophylaxis. Thrombosis Research, 129:673–680.

6.  Royal College of Obstetricians and Gynaecologists (RCOG). 2015. Green-Top Guideline No. 37b: Thromboembolic Disease in Pregnancy and the Puerperium: Acute Management. London: RCOG.

7.  Jacobsen AF, Skjeldestad FE, Sandset PM. 2008. Incidence and risk patterns of venous thromboembolism in pregnancy and puerperium – A register-based case-control study. American Journal of Obstetrics and Gynecology, 198(2):234.e1–234.e7.

8.  Donnelly JC, D’Alton ME. 2013. Pulmonary embolus in pregnancy. Seminars in Perinatology, 37:225–233.

9.  McLintock C. 2014. Thromboembolism in pregnancy: Challenges and controversies in the prevention of pregnancy-associated venous thromboembolisation and management of anticoagulation in women with prosthetic heart valves. Best Practice and Research Clinical Obstetrics and Gynaecology, 28:519–536.

10.  Sultan AA, West J, Tata LJ, Fleming KM, Nelson-Piercy C. et al. 2012. Risk of first venous thromboembolism in and around pregnancy: A population-based cohort study. British Journal of Haematology, 156(3):366–373.

11.  Virkus RA, Lokkegaard EC, Bergolt T, Mogensen U. et al. 2011. Venous thromboembolism in pregnant and puerperal women in Denmark 1995–2005. A national cohort study. Thrombosis and Haemostasis, 106(2):304–309.

12.  James AH. 2008. Thromboembolism in pregnancy: Recurrence risks, prevention and management. Current Opinion in Obstetrics and Gynaecology, 20:550–556.

13.  Chan W, Spencer FA, Ginsbergm JS. 2010. Anatomic distribution of deep vein thrombosis in pregnancy. CMAJ, 182(7):657–660.

14.  McLintock C, Brighton T, Chunilal S, Dekker G, McDonell N. et al. 2012. Recommendations for the diagnosis and treatment of deep venous thrombosis and pulmonary embolism in pregnancy and the postpartum period. Australian and New Zealand Journal of Obstetrics and Gynaecology, 52:14–22.

15.  National Institute for Health and Care Excellence (NICE). 2010. Venous Thromboembolism: Reducing the Risk, NICE Clinical Guideline 92. Available at http://www.nice.org.uk/guidance/cg92 (accessed March 3, 2016).

16.  Royal College of Obstetricians and Gynaecologists (RCOG). 2015b. Green-Top Guideline No. 37a: Reducing the Risk of Venous Thromboembolism during Pregnancy and the Puerperium. London: RCOG.

17.  Knight M, on behalf of UKOSS. 2008. Antenatal pulmonary embolism: Risk factors, management and outcomes. BJOG: An International Journal of Obstetrics and Gynaecology, 115:453–461.

18.  Galambosi PJ, Ulander V, Kaaja RJ. 2014. The incidence and risk factors of recurrent venous thromboembolism during pregnancy. Thrombosis Research, 134:240–245.

19.  Robinson S, Yu C. 2007. The epidemiology of obesity and pregnancy complications. In: Baker P, Balen A, Poston L. et al. (Eds.). Obesity and Reproductive Health. London: RCOG Press, pp. 113–126.

20.  Lidegaard O, Edstrom B, Kreiner S. 2002. Oral contraceptives and venous thromboembolism: A five year national case-control study. Contraception, 65:187–196.

21.  Royal College of Obstetricians and Gynaecologists (RCOG). 2013. Air Travel and Pregnancy: Scientific Impact Paper No 1. London: RCOG.

22.  Lewis G, Drife J. 1998. Why Mothers Die. Report on the Confidential Enquiry into Maternal Deaths in the UK 1994–1996. London: Department of Health.

23.  Jain S, Eedarapalli P, Jamjute P, Sawdy R. 2006. Symphysis pubis dysfunction: A practical approach to management. Obstetrician and Gynaecologist, 8:3153–3158.

24.  Walker L, Lamont S. 2008. Graduated compression stockings to prevent deep vein thrombosis. Nursing Standard, 22(40):35–39.

25.  Phillips S, Gallagher M, Buchan H. 2008. Use graduated compression stockings postoperatively to prevent deep vein thrombosis. BMJ, 336:943–944.

26.  Brady D, Raingruber B, Peterson J, Varnau W, Denman J. et al. 2007. The use of knee-length versus thigh-length compression stockings and sequential compression devices. Critical Care Nursing Quarterly, 30(3):255–262.

27.  Sajid MS, Desai M, Morris RW, Hamilton G. 2012. Knee length versus thigh length graduated compression stockings for prevention of deep vein thrombosis in postoperative surgical patients. Cochrane Database of Systematic Reviews 2012 May 16(5):CD007162. doi:10.1002/14651858.CD007162.pub2.

28.  Calderwood CJ, Thanoon OI. 2013. Venous thromboembolism in pregnancy. Obstetrics, Gynaecology and Reproductive Medicine, 22(8):227–230.

29.  Wik HS, Jacobsen AF, Sandvik L, Sandset PM. 2012. Prevalence and predictors for post-thrombotic syndrome 3 to 16 years after pregnancy-related venous thrombosis: A population-based, cross-sectional, casecontrol study. Journal of Thrombosis and Haemostasis, 10(5):840–847.

30.  Hull RD, Pineo GF, Brant R, Liang J, Cook R, Solymoss S. et al. 2009. LITE Trial Investigators. Home therapy of venous thrombosis with long-term LMWH versus usual care: Patient satisfaction and postthrombotic syndrome. American Journal of Medicine, 122:763–769e3.

31.  National Institute for Health and Care Excellence (NICE). 2012. Venous Thromboembolic Diseases: The Management of Venous Thromboembolic Diseases and the Role of Thrombophilia Testing. NICE Clinical Guideline 144. Available at http://www.nice.org.uk/guidance/cg144 (accessed March 18, 2016).

32.  Gray G, Ash A. 2006. A survey of pregnant women on the use of graduated elastic compression stockings on the antenatal ward. Journal of Obstetrics and Gynaecology, 26(5):424–428.

33.  Welch E. 2006. The assessment and management of venous thromboembolism. Nursing Standard, 20(28):58–64.

34.  Roberts L, Ayra R. 2013. Venous Thromboembolism (VTE) Prevention: A 15 Minute E-Learning Course Designed for Hospital Training Programmes. Available at http://kingsthrombosiscentre.org.uk/induction/index.html (accessed November 29, 2014).

35.  Kurtoglu M, Sivrikoz E. 2013. Venous thrombo-embolism prophylaxis: Intermittent pneumatic compression. Reviews in Vascular Medicine, 1:71–75.

36.  Clark P. 2008. Maternal venous thrombosis. European Journal of Obstetrics and Gynecology and Reproductive Biology, 139(1):3–10.

37.  Rodger M, Rosene-Montella K, Barbour L. 2008. Acute thromboembolic disease. In: Rosene-Montella K, Keely E, Barbour L. et al. (Eds.). Medical Care of the Pregnant Patient. 2nd ed. Philadelphia, PA: ACP Press, pp. 426–444.

38.  Farquharson RG, Greaves M. 2011. Thromboembolic disease Chapter 42. In: James DK (Ed.). High Risk Pregnancy: Management Options. 4th ed. Philadelphia, PA: Saunders Elsevier, pp. 753–762.

39.  Greer IA, Thomson AJ. 2001. Management of venous thromboembolism in pregnancy. Best Practice and Research Clinical Obstetrics and Gynaecology, 15(4):583–603.

40.  Scottish Intercollegiate Network (SIGN). 2010. Prevention and Management of Venous Thromboembolism (SIGN Publication 122). Edinburgh: SIGN.

41.  Leung AN, Bull TM, Jaeschke CJ. et al. 2012. American Thoracic Society documents: An official American Thoracic Society/Society of Thoracic Radiology Clinical Practice Guideline – Evaluation of suspected pulmonary embolism in pregnancy. Radiology, 262(2):635–646.

42.  Flanders SA, Zwernerman K. 2014. Pulmonary embolism: Prevention, recognition and treatment. Nursing Critical Care, 9(6):14–18.

43.  te Raa GD, Ribbert LS, Sniijder RJ, Biesma DH. 2009. Treatment options in massive pulmonary embolism during pregnancy: A case report and review of literature. Thrombosis Research, 124:1–5.

44.  Beebeejaun MY, Adenugba O. 2013. Use of thrombolytic agents to treat pulmonary embolism in pregnancy. Reviews in Obstetrics and Gynecology, 6(3/4):182–184.

45.  Marshal JE, Ramsay MM. 2012. Thromboembolism. In: Raynor M, Marshall J, Jackson K (Eds.). Midwifery Practice: Critical Illness, Complications and Emergency Case Book. Maidenhead: Open University Press, pp. 61–72.

46.  Greer IA, Nelson-Piercy C. 2005. Low molecular-weight heparins for thromboprophylaxis and treatment of venous thromboembolism in pregnancy: A systematic review of safety and efficacy. Blood, 106(2):401–407.

47.  Voke J, Keidan J, Pavord S. et al. 2007. The management of antenatal venous thromboembolism in the UK and Ireland: A prospective multicenter observational survey. British Journal of Haematology, 139:545–558.

48.  American College of Obstetrics and Gynecologists (ACOG). 2011. Practice bulletin: Thromboembolism in pregnancy: Number 124. Obstetrics and Gynecology, 118(3):718–728.

5

Pre-eclampsia and associated conditions

MAUREEN BOYLE

Pre-eclampsia

HELLP syndrome

Severe (fulminating) pre-eclampsia

Eclampsia

Acute fatty liver of pregnancy (AFLP)

Outcomes and postnatal issues for pre-eclampsia and associated conditions

Summary of midwifery responsibilities

References

PRE-ECLAMPSIA

Introduction

Pre-eclampsia may be described as an unpredictable and progressive condition with the potential to cause multi-organ dysfunction and failure that can be detrimental to the health of both the woman and her fetus. There is a suggestion that there may be two syndromes associated with pre-eclampsia, a maternal syndrome (hypertension and proteinuria with or without multi-organ involvement) and a fetal syndrome (intrauterine growth restriction [IUGR] and other fetal compromise).⁴ In fact, although the definition (see Box 5.1) appears clear, there are many presentations of pre-eclampsia, and presenting signs and symptoms may not always fit the classical definitions.

In resource-rich countries pre-eclampsia is considered a major cause of maternal mortality, but in other parts of the world with limited antenatal care, the numbers are much higher.⁴ Worldwide, pre-eclampsia is reported to account for more than 50,000 maternal deaths each year.⁵ Pre-eclampsia also contributes significantly to the number of premature births, stillbirths and neonatal deaths.⁶

According to the latest Confidential Enquiry report from MBRACCE-UK⁷ deaths from preeclampsia and associated conditions are at the lowest rate since these records began, and this is at a time when there are many more pregnancies at high risk for pre-eclampsia, and therefore more women with the condition. Of course the maternal mortality figures do not take into account the level of morbidity, both for mother and baby, making these figures only part of the picture.

APEC⁸ (Action on Pre-eclampsia) suggest about 10% of first pregnancies are complicated by mild pre-eclampsia, and 1%–2% by more serious disease. Other estimates vary, which underlines the challenge of defining pre-eclampsia, however, it is clear that large numbers of women will present with pre-eclampsia. Although the falling of mortality rates is encouraging, there is no place for complacency, as improvements in surveillance and care for these women will have likely caused the better outcomes, and this must be maintained and even improved upon. Also, although fatalities associated with pre-eclampsia in the United Kingdom are relatively low in comparison with much of the world, any fetal death causes anguish and a maternal death is an unimaginable tragedy for the family concerned, and is possibly an indicator of failure in the care system.

BOX 5.1: Definitions1–3

Chronic hypertension: Hypertension that is present at booking or before 20 weeks, or if the woman is already taking antihypertensive medication when referred to maternity services.

Essential hypertension (primary): No underlying cause.

Secondary hypertension: Associated with underlying disease, including obesity.

Gestational hypertension: New hypertension present after 20 weeks without significant proteinuria. Resolves within 3 months after birth. Sometimes called ‘pregnancy induced hypertension’ (PIH).

Pre-eclampsia: New hypertension presenting after 20 weeks with significant proteinuria.

Severe pre-eclampsia: Pre-eclampsia with severe hypertension and/or with symptoms and/or biochemical/haematological impairment.

Early onset pre-eclampsia: <34/40.

Midwives at the forefront of maternity care delivery are ideally placed for primary surveillance and early detection of pre-eclampsia. Although it is acknowledged that pre-eclampsia is a complex and frustrating condition especially with regard to the prediction of progression, the more efficient the woman’s care is in the early/mild stages the more likely it is that an ‘emergency’ response will be unnecessary, and is thus instrumental to the outcome of any individual pregnancy. However, pre-eclampsia is a particularly difficult disease, and all experienced midwives will recall women with severe symptoms who made an uncomplicated recovery, as well as women with relatively mild symptoms who suffered a tragic outcome; all emphasising pre-eclampsia is a particular challenge for health professionals.

Clinical features

PREDICTION

There is currently no way to reliably predict preeclampsia, however, there is much research and many theories around this subject, mainly based on ultrasound or blood component analyses. Second trimester umbilical artery Doppler (UAD) findings and analysis of PIGF, triglyceride and eptin levels are suggested as actions that could help to predict pre-eclampsia.⁹ It has also been found that a woman whose fetus is discovered to have unexplained IUGR with abnormal UADs appears to be at increased risk of pre-eclampsia compared to one whose fetus has normal Dopplers.¹⁰

Higher levels of liver enzymes AST and ALT during the first 20 weeks of pregnancy are associated with a higher risk for the development of severe pre-eclampsia in the second half of the pregnancy, however, no clinical cut-off value has yet been established.¹¹

PREDISPOSING/RISK FACTORS

Although it is acknowledged that pre-eclampsia is a very unpredictable disease and may occur in those with no predisposing factors, it may be useful to identify those who have been suggested as being at increased risk of developing this condition (see Box 5.2).

Multiple pregnancy has long been accepted as a risk factor for pre-eclampsia, but recent research has suggested that DC (dichorionic) twin pregnancies were at even more risk than MC (monochorionic) twin pregnancies.¹²

A study comparing risk factors for early onset (<34 weeks) pre-eclampsia with those for late onset (≥34 weeks) pre-eclampsia found younger maternal age, nulliparity and diabetes mellitus were more strongly associated with late-onset pre-eclampsia.¹³

Other conditions apart from those identified by National Institute for Health and Care Excellence (NICE)³ (see Box 5.2) have also been mentioned in the literature. Involvement of the father, such as second or subsequent pregnancy with a new partner¹⁴ and women with partners who previously fathered a baby resulting from a pregnancy with pre-eclampsia,15,16 as well as a pregnancy involving donor material¹⁴ have been cited. The presence of abnormal placental material such as hydatidiform mole, or other anomalies such as hydrops fetalis or polyhydramnios, are also considered risk factors for pre-eclampsia.¹⁷

BOX 5.2: Women at risk of developing pre-eclampsia³

HIGH RISK

•  Hypertensive disease during a previous pregnancy

•  Chronic kidney disease

•  Autoimmune disease such as systemic lupus erythematosus or antiphospholipid syndrome

•  Type 1 or type 2 diabetes

•  Chronic hypertension

MODERATE RISK

•  First pregnancy

•  Age 40 years or older

•  Pregnancy interval of more than 10 years

•  Body mass index (BMI) of 35 kg/m² or more at first visit

•  Family history of pre-eclampsia

•  Multiple pregnancy

There has also been an association suggested between some antidepressant medication use and a higher risk of pre-eclampsia,¹⁸ and even some evidence that air pollution may influence the development of pre-eclampsia.¹⁹

PATHOPHYSIOLOGY

The aetiology of pre-eclampsia remains unknown, but understanding of the pathogenesis has been advanced in recent years by laboratory work and evidence is becoming increasingly available that the various theories presented have some common features. In a healthy pregnancy uncomplicated by pre-eclampsia, trophoblastic cells invade the maternal uterine arteries at both the decidual and myometrial levels resulting in erosion of the muscle layer and enlargement of the lumen. Additionally, there is increased synthesis of prostacyclin, nitric oxide and thromboxane A2, which create a change in homeostatic balance and tendency to vasodilatation of the uterine arteries. This alteration in function results in lowered resistance in the arteries, absence of maternal vasomotor control and a massive increase in blood supply to the placenta to meet the demands of the developing fetus. The associated changes account for the transient lowering of maternal blood pressure seen in early pregnancy, which is then compensated for by the physiologic increase in circulating blood volume.

The changes seen in pre-eclampsia appear to be caused by a complex interplay of abnormal genetic, immunological and placental factors.²⁰ The early changes in the way the placenta embeds in the uterus are considered to be significant, in that trophoblastic invasion of the placental bed spiral arteries is confined to the decidual level. As a consequence of this arrested trophoblastic invasion, adrenergic nerve supplies to the uterine spiral arteries are not disrupted, systemic vascular resistance remains high and placental perfusion is poor. The resultant effect is tissue hypoxia, which is believed to cause liberation of substances that are toxic to endothelial cells.4,21 It has been suggested that this involves an inflammatory response.⁴

The total peripheral vascular resistance increases in pre-eclampsia (as contrasted with the reduction expected in a normal pregnancy), and this is one of the causes of raised blood pressure. In addition, enhanced contraction of damaged blood vessels facilitates aggregation of platelets at the site of injury and may predispose to problems with coagulation.

In the kidneys, glomerular capillary endothelial swelling occurs accompanied by deposits of fibrinogen within and under the endothelial cells, resulting in generalised renal function being impaired causing rising serum creatinine, uric acid and urea levels. In addition, increased glomerular permeability allows protein to escape into the urine.

The hypoalbuminaemia of pre-eclampsia causes a lower colloid osmotic pressure, affecting fluid transport across the capillaries, resulting in too much fluid in the interstitial spaces (oedema) and too little in the vascular compartment (hypovolaemia). In addition to the cardiovascular and renal affects described above, reduced organ perfusion in the liver, pulmonary system and the brain can contribute to the serious and potentially fatal outcomes seen in pre-eclampsia.

Antenatal screening and specific care

Women who have a pre-existing condition, especially those who are taking medication, should access pre-conception care to ensure they are in optimum health as well as to have their medication assessed. Those women with chronic hypertension taking ACE (angiotensin-converting enzyme) inhibitors and ARBs (angiotensin II receptor blockers) will be advised to change their drugs as there is an increased risk of congenital abnormalities if these are taken during pregnancy.³ If a woman is booking without accessing this care and is taking these drugs, the midwife must ensure the woman is referred urgently to medical colleagues for medication assessment.

Salt restriction is not generally recommended, but women with chronic hypertension should be encouraged to keep their dietary sodium intake low.³

Although there is some evidence to support thrombophilia treatment in those women at risk of IUGR, this remains in need of further research²² and is not recommended by NICE³ at present. However, aspirin treatment in those at risk of pre-eclampsia has become recommended care.3,14 Current advice is 75 mg aspirin daily from 12 weeks until birth of the baby³ for those at high risk or with more than one moderate risk factor (see Box 5.2).

All women, but in particular those with risk factors for pre-eclampsia, should be given information of symptoms of pre-eclampsia (see Box 5.3), and know how and when to self-refer if necessary.

Diagnosis

While the midwife may initiate many of the early biochemical and haematological investigations and is eminently able to interpret findings, she must remember the scope of her clinical practice and always act in accordance with the Midwives Rules and Standards,²³ referring the woman to a registered medical practitioner when there are signs of deviation from normal.

BOX 5.3: Symptoms of pre-eclampsia³

•  Severe headache

•  Problems with vision, such as blurring or flashing before the eyes

•  Severe pain just below the ribs

•  Vomiting

•  Sudden swelling of the face, hands or feet

BLOOD PRESSURE

PRECOG² (the pre-eclampsia community guideline) define hypertension as diastolic readings ≥90 mm Hg. Debates over incremental rise and recognition of systolic reading continue, although its importance is clear. It is recommended that a systolic reading over 150 mm Hg needs effective treatment and over 180 is considered a medical emergency.²⁴ NICE³ has divided blood pressure findings into categories (see Box 5.4).

The midwife can combine the information in Box 5.4 with her knowledge of physiology when screening women for pre-eclampsia. Equally, she needs to be aware of other factors such as any recent physical activity undertaken, the emotions of the woman and the time of day the blood pressure is recorded, as all of these may have an impact upon the accuracy of her observation. Blood pressure evaluation is such a routine part of midwifery practice it would be easy to become complacent. However when considered objectively, numerous factors such as the woman’s personal fluctuations, the possibilities of ‘white coat syndrome’, work stress, less than perfect auditory acuity, a noisy working environment and/or substandard equipment, all make blood pressure recording anything but straightforward or simple. Nevertheless, accuracy of assessment as part of professional midwifery practice is vital for women’s well-being.²⁵

Previous reports of Confidential Enquiries into Maternal Deaths in the UK over recent trienniums26,27 have warned against exclusive reliance on automated blood pressure recording systems. While useful for establishing a trend over several readings,²⁸ conventional mercury sphygmomanometers remain the instrument of choice in order to prevent underestimation of the blood pressure. However, since in many areas this equipment may not be easily available, care must be taken to check automated reading against another validated devise if concerned.

BOX 5.4: Definitions of hypertension³

•  Mild hypertension: 140–149/90–99

•  Moderate hypertension: 150–159/100–109

•  Severe hypertension: ≥160/ ≥110 (mean arterial pressure [MAP] >125 mm Hg)

The MAP is the average pressure responsible for driving blood forward into the capillary bed of tissues. This reading is often used to assess the progress of pre-eclampsia and to underpin medication, although there is conflicting evidence regarding the value of MAP in this regard.²⁵ The MAP will usually show up on automated blood pressure (BP) devices, or can be calculated as either

•  Systolic BP plus twice the diastolic, divided by three

•  Diastolic BP plus one-third (systolic BP minus diastolic BP)

Midwives are cautioned that any rise in blood pressure occurring after 20 weeks’ gestation in a previously normotensive woman should be cause for concern, as this may be the first indicator of a progressive disorder. However, blood pressure needs to be taken and interpreted in context with other signs and symptoms.

PROTEINURIA

Proteinuria should never be ignored – screening for pre-eclampsia and infection should be routine and these are the most common causes, but awareness of the possibility of less usual conditions (e.g. lupus nephritis) should ensure a woman has appropriate medical exploration if proteinuria is present.

Although proteinuria is often caused by a urinary tract infection, it is also possible that it may be the first sign of pre-eclampsia in a woman with normal blood pressure. In pre-eclampsia, increasing levels of proteinuria may be associated with adverse maternal and fetal outcomes,²⁹ although this may not always be true.¹⁴

However, the midwife needs to ensure accurate assessment of proteinuria.

The reagent strips (‘dipsticks’) commonly used in clinical practice should be considered a guide only to the presence of protein in the urine and not be accepted as an accurate quantification of protein excretion. It should also be ensured that manufacturer’s instructions concerning care of dipsticks (such as dating the opening of bottles and replacing lids after use) are followed to ensure accuracy is optimal.

When any amount of protein is detected, a ‘clean-catch’ mid-stream sample of urine should be tested to exclude the possibility of contamination. If protein is still detectable, the sample should be sent to the laboratory for exclusion of infection, together with a urine specimen for urinary spot protein:creatinine ratio (PCR). Dependent on local policy, action may be taken on the PCR result, or a 24-hour urinary collection may be necessary.³⁰ Results over 30 mg/mmol for the PCR and more than 300 mg in a 24-hour collection are considered significant and therefore abnormal.³

It should be remembered that the quantity of protein present in urine samples may not be indicative of renal damage, but instead may be a reflection of capillary leakage and more accurately a projection of the development of generalised oedema. Where protein loss is significant, the possibility of pulmonary and/or cerebral oedema as complications of pre-eclampsia is considerable.

SEROLOGY

While the worsening of the combination of two of the cardinal signs, proteinuria and hypertension, are acceptable as reasonable predictors of increasingly severe pre-eclampsia, it is as well to remember that women with blood pressures within the normal range, especially if taking antihypertensive drugs, or in whom proteinuria was absent have had eclamptic fits. The obvious presence of a single finding should prompt investigations for others by measuring known biochemical markers (see Box 5.5 for an example of blood routinely taken for pre-eclamptic toxaemia (PET) screening). Common findings to diagnose pre-eclampsia include a reduced platelet count, elevated urate, urea and creatinine, liver function test (LFT) abnormalities and coagulopathy.³¹

BOX 5.5: PET screening

While many tests can be undertaken, the following are of particular importance

•  Full blood count

•  Renal function tests

•  Liver function tests

•  Clotting studies

When blood tests are taken for a PET screening, if the results are within the normal range, they can act as a baseline for future tests. A changing level, even if still within the normal range, should act as a warning sign, and these blood results should be recorded in a way that any trend is easily identifiable.

Full blood count

A full blood count (FBC) is a valuable assessment in pre-eclampsia as much information can be gained. Normal pregnancy results in physiological haemodilution and lower levels of erythrocytes in a specified volume of blood, although their life span is not affected. In pre-eclampsia the reduction in intravascular volume causes a rise in haematocrit and polycythaemia, while erythrocytes are damaged by the friction of their forced passage within the damaged endothelial lining of blood vessels. Repeated damage significantly reduces the life expectancy of erythrocytes leading to increased haemolysis and anaemia.

Mild thrombocytopenia, the cause of which is unknown, has long been identified as an uncomplicated finding in normal pregnancy; but when present in pre-eclampsia the platelet levels should be closely and regularly monitored. Reduction in platelets is thought to be related to a shorter life span (can be reduced by almost 50% from 9 to 5 days) and additionally there is an increased level of activation and enhanced adhesion capacity at the site of endothelial cell damage. Acute presentation (indicated by a fall of platelets between 20%–30% from the baseline measurement in early pregnancy) is associated with severe pre-eclampsia and HELLP (haemolysis, elevated liver enzymes and low platelets) syndrome. NICE³ consider severe pre-eclampsia to be associated with a platelet count <100 × 10⁹/L.

Renal function tests

In pregnancy urea and creatinine clearance is high, but blood levels at the upper end of the range may be suggestive of impaired renal clearance. A rise in serum uric acid production is secondary to tissue ischaemia and increasing levels may be reflective of impaired renal clearance, renal medullary ischaemia and tubular damage.³² These findings may be the only clinical indicators of the seriousness of pre-eclampsia. The importance of this information is that a rise in serum uric acid can be detected before proteinuria becomes evident.

Leakage of albumin through the kidneys is a positive indication of glomerular endothelial damage, the consequences of which are lowering of serum albumin levels and leakage of fluid into the extracellular space, while a marked rise in creatinine is indicative of severe renal impairment. Severe pre-eclampsia is associated with serum creatinine >100 mmol/L.³

Liver function tests

Development of epigastric or right upper quadrant pain may be suggestive of liver involvement. Damage to the endothelial lining of blood vessels in the liver results in leakage of plasma and causes an increase in size and overstretching of the fibrous capsule. In addition, blood vessels may rupture and haematomas may form in the sub-capsular region, increasing the pressure on the liver peritoneum causing referred pain.

Raised levels of liver enzymes such as alanine aminotransferase, aspartate aminotransferase and bilirubin, in combination with placental alkaline phosphatase, are indicators of a significant level of liver cell damage and the development of HELLP syndrome.

Management

After the first diagnosis of pre-eclampsia, the consultant obstetrician should document a clear plan in the notes, with thresholds for elective birth before 34 weeks.³ This plan may of course be altered as pregnancy progresses and signs/symptoms change.

Women admitted to an antenatal ward with pre-eclampsia should receive specific midwifery care including

•  Monitoring of her vital signs, with frequency dependent on her condition, and attention paid to fluid balance.

•  Blood/urine testing dependent on her condition.

•  Medication as prescribed, with assessment of its effectiveness.

•  A course of corticosteroids/MgSO₄ are usually given if preterm birth is anticipated.

•  Appropriate fetal surveillance, usually involving regular cardiotocographs (CTGs), ultrasound growth scans, amniotic fluid volume assessment and umbilical artery Doppler velocimetry.

DRUGS

The choice of which drug is used in practice is dependent on individual unit policies, and this may be related to experience and familiarity, as this does instill confidence, a factor essential to the prompt and successful management of the woman’s condition. The midwife needs to ensure she knows the protocol and policies of her workplace, as these will be different from unit to unit.

Therapy for reducing hypertension

The aim of drug therapy is to prevent the development of severe hypertension and so avert the development of cerebrovascular accidents as well as reduce the risk of seizures and emergency preterm delivery of the baby. However, treatment is dependent on the individual woman’s condition and cannot be successfully predicted, so close observation is always necessary.

An array of antihypertensive treatments have been used to minimise the risk of cerebral damage associated with pre-eclampsia, but it must be borne in mind that these are not cures as they do not arrest the disease progression. Antihypertensives are considered vital when a blood pressure is >160/110³³ but medication is usually commenced before this level is reached. A brief description of the mode of action of some of the more common drugs used to manage pre-eclampsia follows

Labetalol

Labetalol belongs to the group of peripheral-acting sympatholytic drugs including alpha, beta and combined alpha + beta sympathetic blocking agents. Other examples the midwife may see, usually in the postnatal period, are Metoprolol and Atenolol. This group acts on blood vessels by altering the baroreceptor sympathetic reflex response of nerves to adrenergic vasoconstrictors such as prostaglandins. The resultant effects are vascular relaxation, lowered peripheral resistance and reduced cardiac output, thus lowering the blood pressure.

Oral Labetalol is the recommended first line of treatment for hypertension in pregnancy³ and can also be given in severe pre-eclampsia as an intravenous infusion.

Methyldopa

Methyldopa is a central alpha-II agonist, often used in pregnancy. It acts directly on the brainstem to create vasodilation and lowering of the blood pressure without adverse changes in heart rate, cardiac output, renal perfusion or uteroplacental blood flow. Lowering of the blood pressure is slow, thus where rapid onset of blood pressure reduction is desired an alternative drug is preferable. Methyldopa should be stopped within 2 days of birth to avoid possible side effects, and another antihypertensive used if necessary in the puerperium.¹⁴

Nifedipine (Adalat)

Nifedipine belongs to the group of calcium antagonists and has increasingly been used in pre-eclampsia as the second line in hypertensive management where early treatment with Labetalol or Methyldopa has failed to keep maternal blood pressure below the danger level, or when a rapid response is needed. It works by preventing transfer of calcium ions from extracellular space and inhibits uptake by smooth muscle cells. Vascular muscle response and reflex excitation contractility are reduced and relaxation is achieved, peripheral resistance is lowered and blood vessels dilate and blood pressure falls. The sublingual route is not normally used in pregnancy, because mucosal absorption is unpredictable.³⁴

Nifedipine may also be used as a tocolytic drug, with no apparent drop in the blood pressure for a woman who is normotensive.³⁴

Hydralazine

Hydralazine, an arteriolar dilator, is usually reserved for use in cases of very high blood pressure. Given intravenously, it acts directly on the smooth muscles of the arterial wall to bring about vasodilation in 10 to 20 minutes with the hypotensive effect lasting 6 to 8 hours. Side effects are headaches, nausea and vomiting (signs which mimic impending eclampsia) and a possible link to thrombocytopenia in the neonate has been reported. Doses are usually titrated to the woman’s blood pressure and care needs to be taken to avoid a very rapid drop in a pregnant woman’s blood presssure, which could lead to reduced placental perfusion and fetal distress.

Magnesium sulphate

Although magnesium sulphate is primarily an anti-convulsive, it also has a strong hypotensive effect, and if used further antihypertensive medication may not be necessary. It is recommended as a first-line treatment of eclampsia and to prevent eclampsia in those at high risk. (See later in this chapter for midwifery care when a woman is receiving a magnesium sulphate infusion.)

HELLP SYNDROME

HELLP (haemolysis, elevated liver enzymes and low platelets) syndrome is a serious complication usually associated with pre-eclampsia but in which many women do not develop significant hypertension or proteinuria.³⁵ Its development is a clear indication for close surveillance. Diagnosis is based on a combination of laboratory findings, clinical signs and symptoms (see Box 5.6), although these may vary significantly. It has been suggested that 20% of women had not been diagnosed with pre-eclampsia before delivery and one-third of women with HELLP syndrome will be diagnosed postnatally.³⁵

The full blood count is an invaluable screening tool for HELLP, as evidence of anaemia may indicate excessive breakdown of red cells, one of the early features. Irrespective of the cause of anaemia (haemolysis or iron deficiency) it must be borne in mind that its presence will increase the cardiac workload and thus exacerbate hypertension.

As in pre-eclampsia, thrombocytopenia develops from reduction of the life span of platelets and utilization at sites of endothelial damage. The multisystem failure in HELLP is also associated with changes in renal and hepatic function.

Reduced circulatory volume, ischaemia, renal tubular necrosis and reduced renal clearance lead to a rise in the levels of urea, creatinine and serum urate, which are indicators of marked maternal and fetal compromise. Infarctions and oedema occurring in the liver will impair its capacity to maintain adequate metabolic activities such as synthesis of clotting factors, while increase in liver size may lead to capsular rupture triggering a combined medical, surgical and obstetric emergency.

BOX 5.6: HELLP syndrome

POSSIBLE SIGNS AND SYMPTOMS

Right upper quadrant pain (and often with a positive liver recoil test)

Epigastric pain

Nausea and vomiting

Malaise

Fatigue

Generalised oedema

Headache

Gastro-intestinal bleed

Hypertension

Proteinuria

Reduced urine output

POSSIBLE LABORATORY FINDINGS

Haemolysis

Anaemia

Low platelet count (<100 × 10⁹/L)

Elevated liver enzymes:

•  Alanine aminotransferase (ALT)

•  Aspartate aminotransferase (AST)

•  Alkaline phosphate (ALP)

•  Gamma glutamyltransferase (GGT)

Elevated levels of bilirubin.

Management of HELLP syndrome

Hospitalisation is required to enable more intense monitoring of the maternal and fetal condition (see Box 5.7) with the aim of stabilisation and expediting the birth at the optimum time. The time available for measures to be initiated is dictated by the woman’s condition, fetal maturity and the clinical facilities available for safe delivery and management of a possible preterm infant. For some women the condition may develop rapidly and/or before a stage where fetal viability is a possibility, while for others the progression of the disease may be more gradual and/or occur later in the pregnancy.

BOX 5.7: Optimal management of HELLP syndrome

•  Timely diagnosis and ongoing accurate assessment of the severity

•  Control of blood pressure if necessary

•  Prevention of seizure

•  Management of fluid and strict fluid balance

•  Assessment and monitoring of fetal condition

•  Planning and management of delivery

•  Judicious care to manage the potential for haemorrhage

•  Maximum supportive care to enhance the baby’s survival

•  High dependency or intensive care for the woman postpartum, with awareness of the continued risk of multiple organ failure

Where timing permits, in that the woman’s condition does not present an immediate threat, strategies may be implemented to assess fetal wellbeing and improve survival rates. This may include biophysical assessment by ultrasound to determine the degree of hypoxaemia and fetal reserve, administration of corticosteroids to accelerate fetal lung maturity in prematurity and continual/frequent assessing of fetal well-being by CTG. The woman’s condition should be closely observed continuously for detection of the onset of labour or rapid disease progression, indicated by deterioration in her blood results or increasing severity of physical signs and symptoms.

SEVERE (FULMINATING) PRE-ECLAMPSIA

Severe pre-eclampsia is a potentially dangerous medical condition that should be thought of as an emergency. Fulminating pre-eclampsia is likewise severe, but is often used to describe very rapid progression of the disease. When a woman is diagnosed with severe (and/or fulminating) pre-eclampsia, it is essentially a fractional window of opportunity, the duration of which cannot be predicted with any certainty, when timely intervention and appropriate treatment may prevent a seizure or organ failure. Essentially there are two possible courses of action related to management, either immediate delivery undertaken when the risk to the woman would be greater if the pregnancy was continued, or prolongation of the pregnancy within a controlled environment once her condition has been stabilised. The latter course will permit administration of corticosteroids to assist fetal lung maturity and benefit the baby that will be born early. While an active search and treat programme is the goal of antenatal care, it offers no guarantee against development of severe pre-eclampsia or eclampsia and it is important that midwifery practitioners know that a convulsion may be the first and only indication of an underlying pathological process.

Changes associated with a worsening condition do not necessarily follow a logical, sequential or linear progression, nor are seizures predictable. Some women may have a very severe presentation of pre-eclampsia where the practitioner expects the condition to culminate in a convulsion, yet this does not happen. Conversely, some women first diagnosed with mild or moderate signs and symptoms, can become severely ill in a very short period of time. The introduction of modified early obstetric warning score (MEOWS) charts to record vital signs may be a useful aid to allow midwives, especially when changes of shift occur, to observe increasing trends. It is imperative that midwives remain watchful for new developments or subtle changes discernible through close physical observation and changes in levels of biochemical tests, and not let reassuring observations or test results diminish attentiveness or create a false sense of security. See Box 5.8 for signs and symptoms of fulminating or worsening pre-eclampsia.

Monitoring the woman with severe pre-eclampsia

BLOOD PRESSURE

The importance of blood pressure measurement has been introduced previously, but in severe preeclampsia observations are made and recorded at intervals of between 5 and 15 minutes. An arterial line may be inserted to enable continuous monitoring of blood pressure and allow easy access for arterial blood gas sampling. Blood pressure readings will underpin administration of medication in accordance with prescribed instructions. The purpose of this is to ensure an appropriate response that is finely balanced to avert seizure or cerebral vascular accident, yet protects against the occurrence of sudden devastating hypotension that can be detrimental to the woman’s cerebral function and fetal well-being.

BOX 5.8: Signs and symptoms of fulminating or worsening pre-eclampsia

•  Continuing rise in blood pressure

•  Increasing proteinuria

•  Oliguria

•  Development of epigastric or right upper quadrant pain

•  Nausea and vomiting

•  Cerebral disturbances (headache, altered consciousness)

•  Visual field disturbances (‘floaters’ or diplopia)

•  Papilloedema (congestion of optic disc)

•  Bleeding tendency (platelet count decreasing and/or clotting factors abnormality)

•  Clonus (large or repetitive muscular reaction from reflex or stretching)

•  Abnormalities in fetal assessment, including reduced liquor volume

RENAL FUNCTION

Low levels of serum albumin will result in excessive loss of intravascular volume, impact on the cardiovascular system and be evident as oedema. This is indicated as a rise in haematocrit, polycythaemia, reducing renal perfusion, impaired renal tubular function and poor reabsorption of protein, causing further leakage of fluid into the extracellular space and resulting in reduced urinary output – a vicious cycle is in motion. Rapidly progressive oedema³¹ is frequently easily observed on the woman’s face. The woman should be catheterised, the urine measured hourly (output should be 0.5 mL/kg/hr and should not fall below 30 mL/hr or 100 mL/4 hourly) and tested for the quantity of protein. Fluid restriction of input will be in place.

SEROLOGY

Blood for PET screening (see Box 5.5) will be done regularly, dependent on the woman’s condition and recorded carefully in order to see the trend. Walker³² suggests that a falling platelet count could be used as a guide to the timing of delivery, as it is associated with a worsening of the maternal and fetal condition. Adhesion of platelets to damaged endothelial blood vessel walls narrows the lumen, reduces end organ perfusion, exacerbates tissue damage through anoxia and predisposes the woman to development of eclampsia, placental abruption and possible fetal demise. Blood may also be sent for group and save as the likelihood of an imminent caesarean section is high.

Ongoing care of the woman with severe (fulminating) pre-eclampsia

Women admitted with fulminating or severe preeclampsia must be closely monitored (see Box 5.9) and medicated. NICE³ suggests discussion with neonatal paediatricians and obstetric anaethetists should take place and decisions made be clearly documented. The most effective approach is likely to be multidisciplinary, involving obstetrician and anaesthetist at consultant level, haematologist, paediatrician and appropriately experienced midwives who should all be involved in the planning and provision of care. The neonatal intensive care unit should be alerted.

One-to-one care supporting adequate ventilation and oxygen therapy and monitoring the fetal condition are all essential, as is easy availability of drugs and equipment for managing an eclamptic fit. Effective measures are needed to prevent convulsion, major organ failure, fetal demise and reduce the severity of postpartum exacerbation and long-term morbidity. The main aims are to control the blood pressure, restrict fluids, consider anticonvulsant therapy with magnesium sulphate and plan delivery.³¹

The first objective requires initiation of therapy to lower the blood pressure to a level where the potential for seizure is reduced, thereby protecting the woman’s cerebrovascular circulation and preventing a stroke.3,26 Along with this intense monitoring of the maternal condition for early detection of deterioration (impending seizure, organ failure, and/or pulmonary oedema), observation for the onset of labour and/or evidence of fetal compromise must be carried out.

BOX 5.9: Summary of midwifery care of the woman with severe pre-eclampsia

•  Monitor vital signs, particularly blood pressure, pulse, respirations and oxygen saturations.

•  Administer drugs and assess effect on blood pressure.

•  Monitor and record total fluid input (maintaining prescribed fluid restriction) and urinary output (and level of proteinuria).

•  Monitor fetal condition and assess for onset of labour.

•  Obtain blood samples as necessary and monitor results for changes reflecting deterioration.

•  Assess for symptoms of worsening condition.

•  Notify the obstetrician and/or anaesthetist of any significant changes in the woman’s condition.

•  Maintain a quiet, calm atmosphere.

•  Provide psychological support for the woman and her family.

The midwife should note vital signs (at a frequency determined by individual condition, but perhaps as often as every 5 minutes), with particular attention being paid to blood pressure, respirations, oxygen saturation readings, pulse and level of consciousness. Medication being used for control of blood pressure should be administered as prescribed, and the woman’s response to treatment carefully evaluated. The aim of anti-hypertensive treatment is usually to keep the systolic blood pressure below 150 mm Hg and the diastolic blood pressure between 80 and 100 mm Hg,3,25 which is thought to be a safe compromise as further reductions may well impair placental perfusion and affect fetal well-being. In some circumstances arterial line monitoring may be used for continuous BP monitoring, and this will also provide scope for frequent arterial blood gas (ABG) measurements. Continuous oxygen saturation monitoring may give an early warning of the onset of pulmonary oedema.

Magnesium sulphate (see suggested regime under Eclampsia section) is usually prescribed to prevent eclampsia if a woman has severe hypertension and proteinuria or mild/moderate hypertension and proteinuria, with one or more of the following³:

•  Severe headache

•  Problems with vision

•  Severe pain below the ribs or vomiting

•  Papilloedema

•  Signs of clonus (≥3 beats)

•  Liver tenderness

•  HELLP syndrome

•  Platelet count falling to below 100 × 10⁹/L

•  Abnormal liver enzymes

Fluid management is vital to the successful management of pre-eclampsia. The importance of meticulous recording and evaluation of input and output cannot be over-emphasised. A former Confidential Enquiry into Maternal Deaths²⁶ credits better fluid management with the decreasing death rate from pulmonary causes in women with pre-eclampsia.

All unit policies for pre-eclampsia care will contain a section regarding fluid restriction, and midwives will need to remember that IV infusions, bolus drug infusions and oral intake should be included in the ‘allowed’ (usually about 80 mL/hr) amount of fluid. Hourly urine measurement, via an indwelling urinary catheter, is maintained until the woman’s medical state is deemed controlled. The urine should be tested frequently and the amount of protein quantified. If the woman has delivered and had a PPH (not an uncommon scenario), fluid management is a particular challenge. As a very fine balance between intake and output is required, this may be best achieved by monitoring via a central venous pressure (CVP) line to underpin fluid management.

Continuous monitoring of the fetal heart rate pattern via CTG is often undertaken depending on the situation, and deterioration of this may indicate a change in the woman’s condition, as well as a compromised fetus. Since IUGR is common, other forms of fetal surveillance such as growth scans, amniotic fluid measurement and umbilical artery Doppler assessment will be undertaken as necessary.

Clinical biochemical features of full blood count, urea and electrolyte (U&E), LFT, renal function test (RFT) and clotting studies should be assessed frequently and regularly as the woman’s condition dictates.

If the woman’s condition stabilises sufficiently to enable labour to be induced, an epidural anaesthesia is often selected if the clotting studies are satisfactory. This method of pain relief offers the additional benefits of lowering blood pressure, elimination of painful stimuli that may trigger convulsion and avoids the possibility of complications which may accompany general anaesthesia and exacerbate pulmonary oedema. Spinal/epidural anaesthesia is therefore the preference for caesarean section but requires particular caution with regards to the fluid load in order not to alter the stable balance previously attained.

During labour, whether induced or spontaneous, the woman with any level of pre-eclampsia will need a continuation of the monitoring that she was receiving antenatally. It is salutary to remember that one in five cases of eclampsia occur in labour, so vigilance should not be relaxed. Syntometrine should not be given for management of the third stage of labour as the ergometrine component is associated with increases of blood pressure.

Postnatal care needs to continue with the knowledge that, although delivery of the baby is deemed to be the ‘cure’ for pre-eclampsia, symptoms can continue or even escalate in the initial period after the birth, and therefore intensity of medications/monitoring may need to be maintained or even increased.

ECLAMPSIA

Eclampsia is the occurrence of convulsions that are associated with the signs and symptoms of preeclampsia. It is a Greek word meaning ‘lightning’ and often strikes with the same random ferocity and has similarly devastating effects. The randomness is illustrated by the fact that 38% of seizures occur before proteinuria and hypertension have been documented.³¹ The seizure that is the key feature of eclampsia is thought to be due to intense vasospasm of the cerebral arteries, oedema secondary to ischaemic damage of vascular endothelium and/or intravascular clot formation.

An eclamptic fit usually includes three defined phases:

•  Prodromal, in which the imminent fit is heralded by possible reports of visual disturbances, muscular twitching, facial congestion, foaming at the mouth and/or deepening loss of consciousness.

•  Tonic-clonic, where initially generalised muscular contractions are present and respiration is absent. This is followed by repeated strong jerky irregular muscular activity.

•  Abatement, which occurs within 60–90 seconds of onset during which time respiration is re-established and there is gradual return to consciousness, but perhaps with a confused and agitated state.

It is futile to attempt any action within the short interval of the tonoclonic phase apart from calling for urgent help and protecting the woman from injury. However, immediate subsequent care should be aimed at damage limitation by placing the woman in the recovery position once the seizure has passed. Suction should be used to clear secretions from the mouth and nasal passage to maintain a clear airway and oxygen should be administered. These measures help to boost the maternal oxygen saturation and improve delivery to the fetus which would have been deprived of oxygen during the tonoclonic phase of the seizure. Further urgent measures are now imperative to prevent the recurrence of further seizures and optimise maternal and fetal well-being (see Box 5.10).

Care of the woman will be by the multidisciplinary team, and include close monitoring (O₂ saturations, BP, pulse, respirations, ECG, blood glucose, urine output/fluid balance, CTG, serology as required, ABG if necessary, signs of magnesium toxicity if receiving a magnesium sulphate infusion [see Box 5.11] until delivery).³¹ In rare situations where seizures are recurrent or prolonged, the woman may need to be medically paralysed and ventilated.

BOX 5.10: Immediate care of the woman with eclampsia

•  Summon assistance (anaesthetist and obstetrician) urgently if in hospital/call for emergency paramedic help (dial 999 in the UK) if at home – immediate transfer to hospital is necessary.

•  Protect from injury during the tonoclonic phase.

•  Maintain airway (clear by suctioning if necessary).

•  Provide supplementary oxygenation.

•  Place woman in the left lateral (recovery) position.

•  Obtain intravenous access and monitor fluid balance.

•  Treat the convulsion.

•  Monitor vital signs and beware of abruption/PPH.

•  Achieve stability of maternal condition.

•  Assess fetal well-being (risk of fetal distress from hypoxia or abruption).

•  Plan mode of delivery if antenatal.

•  Execute plan without further delay.

Suggested treatment regime using magnesium sulphate

Various therapies combining hypotensive agents and anticonvulsants have been used in recent times to manage pre-eclampsia and eclampsia, but without any consensus on efficacy. However, recent research studies carried out in the United States and United Kingdom comparing treatments of eclampsia concluded that magnesium sulphate was effective both as an anticonvulsant and hypotensive agent, both for the treatment of eclampsia and as a preventative.1,36

BOX 5.11: Signs and symptoms of magnesium sulphate toxicity

•  Loss of tendon reflexes

•  Double vision

•  Depressed respiration

•  Slurred speech

•  Flushing

•  Weakness

•  Reduced urinary output <0.5 mL/kg/hr

•  Drowsiness

All maternity units will have a protocol outlining how magnesium sulphate is administered. NICE³ suggest it is given intravenously as a loading dose of 4 g over 5 minutes, followed by a maintenance infusion of 1 g/hr for 24 hours. A seizure or repeat seizure should be treated with a further dose of 2–4 g given over 5 minutes.

As magnesium sulphate is a powerful depressant of neuromuscular transmission, care must be taken to avoid sudden hypotension, in particular if the woman is concurrently receiving large doses (especially if administered intravenously) of antihypertensives. Additionally, as this drug is excreted via the kidneys, existing damage and impaired renal clearance could result in toxic levels being quickly reached.

A maximum blood magnesium level of 4 mmol/L is therapeutic, but around 7 mmol/L is associated with respiratory distress, while levels of around 12 mmol/L can trigger cardiac arrest. A serum magnesium level may be measured if urinary output is diminished, but it is more common to monitor renal function tests regularly while a magnesium sulphate infusion is in progress¹⁴ to identify failing renal function which could lead to magnesium toxicity. Positive screening characteristics (see Box 5.11) are indicative of approaching toxicity levels.

Apart from regular and frequent monitoring of vital signs while receiving magnesium sulphate, the woman’s deep tendon reflexes should also be monitored, usually hourly.

Magnesium sulphate toxicity can be treated with calcium gluconate IV, and the midwife should ensure this is easily available.

Once the woman’s condition has stabilised and the baby has been delivered, the aggressive approach to management needs to be maintained as the risk of eclamptic fits occurring during the first 24 hours of the postpartum period remains.

ACUTE FATTY LIVER OF PREGNANCY (AFLP)

AFLP is a rare, but potentially fatal condition. When first described in the 1930s, a maternal and fetal mortality rate of 85% was suggested; however, although there is still significant risk, earlier recognition and better treatment has allowed vast improvements to be made. Although maternal mortality of 10%–20% and perinatal mortality of 20%–30% has been suggested,³⁷ in the most recent extensive UK study,³⁸ the maternal mortality rate was 1.8% and perinatal mortality 10.4%.

There is controversy³⁹ about whether AFLP and pre-eclampsia are the same disease, and the degree of overlap with HELLP syndrome, however, most authorities accept that AFLP is part of the preeclampsia spectrum. Preliminary presentation can make it challenging to diagnose. AFLP can be confused initially with HELLP syndrome,⁴⁰ fulminant hepatitis of pregnancy,⁴¹ other liver diseases or pancreatitis⁴² but blood tests will usually identify the correct cause.

Although it is not known exactly what causes AFLP, it appears to be linked with a defect in fatty acid oxidation in the fetus, in particular an inherited enzyme deficiency (long-chain acyl-CoA dehydrogenase [LCHAD]). LCHAD is an autosomal recessive disorder which causes the fetus to be unable to metabolise some fatty acids, which can then build up, transfer across the placenta to the mother and affect her liver. However, not all babies who are later found to have LCHAD caused their mother to develop AFLP.⁴³

Predisposing/risk factors38,44,45

•  Multiple pregnancies

•  Male fetus

•  First pregnancies

•  Nonsteroidal anti-inflammatory drugs

•  BMI <20

Clinical features

AFLP usually appears after 30 weeks’ gestation, and frequently near term. Although it starts antenatally, it may not become apparent until after the birth.³⁷

Women usually report an illness of 1–2 weeks with right upper quadrant (RUQ) pain and generalised malaise, then the abdominal pain worsens, and anorexia, increased nausea and vomiting, abnormal thirst and jaundice may occur. About half of women will have signs of pre-eclampsia but proteinuria and hypertension are usually mild.³⁷ Abnormal LFTs, hypoglycaemia and impaired coagulation (disseminated intravascular coagulation [DIC] can occur) are common features. Later signs may be upper gastrointestinal haemorrhaging, acute renal failure, sepsis and pancreatitis.⁴³

Diagnosis is usually achieved by a combination of clinical signs and symptoms and blood tests called the Swansea criteria (see Box 5.12). Liver biopsy is the gold standard diagnostic test but is rarely done due to coagulopathy.

AFLP is considered a medical and obstetrical emergency,⁴³ and early diagnosis and treatment will help improve survival/recovery of both the woman and fetus. Following stabilisation of the woman’s condition, the baby will be delivered and, as the woman with AFLP is usually very ill she will be cared for in a High Dependency or Intensive Care unit. In acute cases a liver transplant may be considered.

BOX 5.12: Swansea criteria for diagnosis of acute fatty liver of pregnancy³⁸

Six or more criteria are required in the absence of another cause:

•  Vomiting

•  Abdominal pain

•  Polydipsia/polyuria

•  Encephalopathy

•  Elevated bilirubin >14 µmol/L

•  Hypoglycaemia <4 mmol/L

•  Elevated urea >340 µmol/L

•  Leukocytosis >11 × 10⁹/L

•  Ascites or bright liver on ultrasound scan

•  Elevated transaminases (AAT or ALT)

•  Elevated ammonia >47 µmol/L

•  Renal impairment; creatinine >150 µmol/L

•  Coagulopathy; prothrombin time >14 seconds or APPT >34 seconds

•  Microvesicular steatosis on liver biopsy

OUTCOMES AND POSTNATAL ISSUES FOR PRE-ECLAMPSIA AND ASSOCIATED CONDITIONS

Although delivery of the baby is necessary to ‘cure’ all the conditions discussed, care needs to continue into the puerperium, with the knowledge that many women become more ill before starting to improve, and the largest number of fits occur in the postnatal period.

Maintaining regular vital sign observations at a frequency depending on the woman’s condition is vital. NICE³ suggest that women with pre-eclampsia who have given birth need to be asked about severe headache and epigastric pain each time the blood pressure is measured. Attention needs to continue to be paid to fluid balance, at least until creatinine levels are within the normal range.³

Although there is controversy about the cause of AFLP, the association with LCHAD deficiency in the baby means there should be follow-up arranged for infants born to mothers with AFLP.

Pre-eclampsia, HELLP syndrome and AFLP are all conditions which can recur in a future pregnancy, and women should be aware of this risk, and may choose to access pre-conception counseling before becoming pregnant again. In particular, if a woman persists in requiring antihypertension medication, she should access pre-conception care when planning a further pregnancy, so her medications can be assessed and changed if necessary.

Women who have had gestational hypertension or pre-eclampsia should be informed that these conditions are associated with an increased risk of developing high blood pressure and its complications in later life3,46,47 and therefore she should ensure she receives long-term monitoring.

In addition to the physical care the woman requires, there is the need for psychological support as there may be many questions the woman wishes to have answered. The skills of the midwife as communicator will be essential in providing information that is timely, appropriate, accurate and as comprehensive as possible to assist with the process of adjustment to what may have been a life-threatening event. The midwife might also consider informing the woman and her partner about APEC (Action on Pre-eclampsia), an organisation where she may be able to obtain continued support and information at a time when she will find it beneficial (http://www.apec.org.uk).

SUMMARY OF MIDWIFERY RESPONSIBILITIES

•  Up-to-date knowledge of all aspects of PET and related conditions must be maintained, as this is an area where treatments, including drugs, change frequently.

•  All women should be screened at every encounter for PET, and should be informed of relevant signs and symptoms that they should report.

•  Midwives must ensure skills of assessment, including BP monitoring, are always optimum, and develop further areas of expertise, such as care of women with CVP and arterial lines, as these are frequently used for women with PET and associated conditions.

•  Many situations around PET can be true emergencies, requiring a prompt response. All midwives should have detailed knowledge of local policies, being able to access rarely used drugs and operate specialised monitoring equipment with speed and competence, while continuing to engender a feeling of safety in the woman.

•  When dealing with women with highly complex conditions, meticulous record-keeping is vital to ensure subtle changes in the woman’s signs and symptoms are observed, and communication between the multi-disciplinary team (MDT) and midwives changing shifts is optimum.

•  Pre-eclampsia and associated conditions are unpredictable and have the potential to be life-threatening – women will need high levels of psychosocial support to cope both during the time of diagnosis and treatment, and following. Referral for long-term support should be made if appropriate.

REFERENCES

1.  Duley L, Meher S, Abalos E. 2006. Management of pre-eclampsia. British Medical Journal, 332:463–468.

2.  Milne F, Redman C, Walker J, Baker P, Bradley J, Cooper C, de Swiet M et al. 2005. The pre-eclampsia community guideline (PRECOG): How to screen for and detect onset of pre-eclampsia in the community. British Medical Journal, 330:567–580.

3.  National Institute for Health and Clinical Excellence (NICE). 2010. Hypertension in Pregnancy. NICE clinical guideline 107 last modified: January 2011. Manchester: NICE.

4.  Sibai B, Dekker G, Kupferminc M. 2005. Pre eclampsia. Lancet, 365:785–799.

5.  Harutyunyan T, Armenian H, Petrosyan V. 2013. Interbirth interval and history of previous preeclampsia: A case-control study among multiparous women. BMC Pregnancy and Childbirth, 13: 244.

6.  Duley L. 2009. The global impact of preeclampsia and eclampsia. Seminars in Perinatalogy, 33:130–137.

7.  Knight M, Kenyon S, Brocklehurst P, Neilson J, Shakespeare J, Kurinczuk J (Eds.), on behalf of MBRRACE-UK Saving Lives. 2014. Improving Mothers’ Care – Lessons Learned to Inform Future Maternity Care from the UK and Ireland Confidential Enquiries into Maternal Deaths and Morbidity 2009–12. Oxford: National Perinatal Epidemiology Unit, University of Oxford, pp. 57–63.

8.  Action on Preeclampsia (APEC). Basic Information on Preeclampsia. Available at http://www.apec.org.uk/preeclampsiabasics.htm (accessed October 1, 2015).

9.  Diguisto C, Le Gouge A, Piver E et al. 2013. Second-trimester uterine artery Doppler, PlGF, sFlt-1, sEndoglin, and lipid-related markers for predicting preeclampsia in a high-risk population. Prenatal Diagnosis, 33(11):1070–1074.

10.  Mirza F, Strohsnitter W, Rivera J et al. 2012. Intrauterine growth restriction with abnormal umbilical artery Dopplers: A harbinger for preeclampsia? Journal of Maternal-Fetal and Neonatal Medicine, 25(12):2658–2661.

11.  Mei-Dan E, Wiznitzer A, Sergienko R et al. 2009. Prediction of preeclampsia: Liver function tests during the first 20 gestational weeks. Journal of Maternal-Fetal and Neonatal Medicine, 26(3):250–253.

12.  Sparks T, Cheng Y, Phan N et al. 2013. Does risk of preeclampsia differ by twin chorionicity? Journal of Maternal-Fetal and Neonatal Medicine, 26(13):1273–1277.

13.  Lisonkova S, Joseph K. 2013. Incidence of preeclampsia: Risk factors and outcomes associated with early versus late-onset disease. American Journal of Obstetrics and Gynecology, 209(6):544–546.

14.  Higgins L, Haezell A. 2012. Severe preeclampsia and eclampsia. In: Chandraharan E, Arulkumaran S (Eds.). Obstetric and Intrapartum Emergencies. Cambridge: Cambridge University Press.

15.  Lie R, Rasmussen S, Brunborg H, Gjessing HK, Lie-Nielsen E, Irgens L. 1998. Fetal and maternal contributions to risk of preeclampsia: Population based study. BMJ, 316:1343–1347.

16.  Skjaerven R, Vatten L, Wilcox A, Rønning T, Irgens L, Lie R. 2005. Recurrence of preeclampsia across generations: Exploring fetal and maternal genetic components in a population based cohort. BMJ, 331(7521):877–885.

17.  El-Moselhy E, Khalifa H, Amer S, Mohammad K, El-Aal H. 2011. Risk factors and impacts of pre-eclampsia: An epidemiological study among pregnant mothers in Cairo, Egypt. Journal of American Science, 7(5):311–323.

18.  Palmsten K, Huybrechts K, Michels K et al. 2013. Antidepressant use and risk for preeclampsia. Epidemiology, 24(5):682–691.

19.  Dadyand P, Figueras P, Basagaña X et al. 2009. Ambient air pollution and preeclampsia: A spatiotemporal analysis. Environmental Health Perspectives, 121(11–12):1365–1371.

20.  Bothamley J, Boyle M. 2009. Medical Conditions Affecting Pregnancy and Childbirth. Oxford: Radcliffe.

21.  Powrie R, Rosene-Montella K. 2008. Preeclampsia. In: Rosene-Montella K, Keely E, Barbour L et al. (Eds.). Medical Care of the Pregnant Patient. 2nd ed. Philadelphia, PA: ACP Press, pp. 163–181.

22.  Gibson P, Nerenberg K. 2014. TIPPing practice away from anticoagulation in pregnancy. Lancet, 384:1648–1649.

23.  Nursing and Midwifery Council (NMC). 2013. Midwifery Rules and Standards. London: NMC.

24.  CEMD. 2011. Saving Mothers’ Lives: Reviewing maternal deaths to make motherhood safer: 2006–2008. The Eighth Report of the Confidential Enquiries into Maternal Deaths in the United Kingdom. BJOG: An International Journal of Obstetrics and Gynaecology, 118(Suppl. 1):1–203.

25.  Nathan H, Duhig K, Hezelgrave N, Chappell L, Shennan A. 2015. Blood pressure measurement in pregnancy. Obstetrician and Gynaecologist, 17:91–98.

26.  Lewis G (Ed.). 2007. The Confidential Enquiry into Maternal and Child Health (CEMACH). Saving Mothers’ Lives: Reviewing Maternal Deaths to Make Motherhood Safer – 2003–2005. The 7th Report on Confidential Enquiries into Maternal Deaths in the United Kingdom. London: CEMACH, pp. 1–296.

27.  Lewis G. 2005. The Confidential Enquiry into Maternal and Child Health (CEMACH). Why Mothers Die: Reviewing Maternal Deaths to Make Motherhood Safer – 2000–2002. The 6th Report on Confidential Enquiries into Maternal Deaths in the United Kingdom. London: CEMACH, pp. 1–330.

28.  Bothamley J, Boyle M. 2008. How to use automated blood pressure monitoring. Midwives, April/May:19.

29.  Thangaratinam S, Coomarasamy A, O’Mahony F et al. 2009. Estimation of proteinuria as a predictor of complications of pre-eclampsia: A systematic review. BMC Medicine, 7(10):9.

30.  Cote A, Brown M, Lam E et al. 2008. Diagnostic accuracy of urinary spot protein:creatinine ratio for proteinuria in hypertensive pregnant women: Systematic review. British Medical Journal, 335(7651):103–106.

31.  Scottish Multiprofessional Maternity Development Programme. 2011. Scottish core obstetric teaching and training in emergencies. In: Magowan B and the SCOTTIE Working Group, on behalf of the Scottish Multiprofessional Maternity Development Group. ‘SCOTTIE’ Course Manual. Available at http://www.scottish-maternity.org (accessed February 13, 2015).

32.  Walker J. 2000. Severe pre-eclampsia and eclampsia. Baillières Clinical Obstetrics and Gynaecology, 14(1):57–71.

33.  Royal College of Obstetricians and Gynaecologists (RCOG). 2006. The Management of Severe Pre-Eclampsia/Eclampsia. Guideline 10(A) March. London: RCOG.

34.  Royal College of Obstetricians and Gynaecologists (RCOG). 2000. Nifedipine in pregnancy. British Journal of Obstetrics and Gynaecology, 107:299–307.

35.  Norwitz E, Hsu C, Repke J. 2002. Acute complications of preeclampsia. Clinical Obstetrics and Gynecology, 45(2): 308–329.

36.  Williams J, Mozurkewich E, Chilimigras J, Van de Ven C. 2008. Critical care in obstetrics: Pregnancy-specific conditions. Best Practice and Research Clinical Obstetrics and Gynaecology, 22(5):825–846.

37.  Cowie P, Johnston I. 2010. Acute fatty liver of pregnancy. Anaesthesia Tutorial of the Week 191, September: 1–5.

38.  Knight M, Nelson-Piercy C, Kurinczuk J, Spark P, Brocklehurst P. 2008. A prospective national study of acute fatty liver of pregnancy in the UK. Gut, 57:951–956.

39.  Vigil-De Gracia P. 2001. Acute fatty liver and HELLP syndrome: Two distinct pregnancy disorders. International Journal of Gynecology and Obstetrics, 73:215–220.

40.  Minakami H, Morikawa M, Yamada T et al. 2014. Differentiation of acute fatty liver of pregnancy from syndrome of hemolysis, elevated liver enzymes and low platelet counts. Journal of Medical Ethics, 40(3):641–649.

41.  Chen H, Yuan L, Tan J et al. 2008. Severe liver disease in pregnancy. International Journal of Gynecology and Obstetrics, 101(3):277–280.

42.  Fesenmeier M, Coppage K, Lambers D, Barton J, Sibai B. 2004. Acute fatty liver of pregnancy in 3 tertiary care centers. American Journal of Obstetrics and Gynecology, 192:1416–1419.

43.  Schutt V, Minuk G. 2007. Liver diseases unique to pregnancy. Best Practice and Research: Clinical Gastroenterology, 21(5):771–792.

44.  Ko H, Yoshida E. 2006. Acute fatty liver of pregnancy. Canadian Journal of Gastroenterology, 20(1):25–30.

45.  Saygan-Karamursel B, Kizilkilic-Parlakgumus A, Deren O, Onderoglue L, Durukan T. 2004. Acute fatty liver of pregnancy after aspirin intake. Journal of Maternal-Fetal and Neonatal Medicine, 16:65–66.

46.  Melchiorre K, Thilaganathan B. 2012. Maternal cardiac function in preeclampsia. Current Opinion in Obstetrics and Gynecology, 23(6):440–447.

47.  Sandvik M, Leirgul E, Nygard O et al. 2013. Preeclampsia in healthy women and endothelial dysfunction 10 years later. American Journal of Obstetrics and Gynecology, 209(6):569–572.

6

Malpresentations and malpositions

ONA STEWART

Introduction

Definitions

Breech

Transverse or oblique lie

Compound presentation

Occipitoposterior (OP) position

Brow presentation

Face presentation

Ongoing care

Conclusion

Summary of midwifery responsibilities

References

INTRODUCTION

The majority of singleton fetuses will adopt a vertex presentation, occiput anterior (OA) position towards term, however, it is vital that the midwife is able to both recognise and act appropriately when deviations from this norm occur. This chapter sets out to ensure a good understanding of both malpositions and malpresentations and identify the role of the midwife in supporting women and their families while dealing with challenging or emergency situations, referring appropriately and as needed, to ensure the safety of both mother and newborn.

DEFINITIONS

Abdominal palpation is used to determine the lie, presentation and position of the fetus during routine antenatal examinations and where there is uncertainty, needs to be confirmed by ultrasound. On admission in labour, when an internal assessment is performed, this can aid diagnosis.

Malpresentation

With malpresentation, the fetus has a body part other than the vertex presenting into the pelvic outlet. This could also involve an abnormal lie such as oblique or transverse. However, most commonly malpresentation refers to a breech presentation, where the fetal buttocks are presenting in the lower pole of the uterus and the head is in the upper pole. Other nonvertex presentations include face, brow or shoulder.

Malposition

Malposition refers to a fetus in a longitudinal lie, with a vertex presentation where the occiput (the denominator) is facing the posterior aspect of the pelvis; fetal malpositions may also include a deflexed or asynclitic head.

BREECH

Where the lie is longitudinal but with the breech presenting, experienced care is vital and current UK guidelines generally recommend pre-labour external cephalic version (ECV) or lower segment caesarean section (LSCS) as the preferred management.1,2 Worldwide in resource-rich areas, most breech presenting births are managed by LSCSs; however, there is a slow increase in the trend towards considering planned vaginal births in carefully selected cases with both Canada³ and New Zealand⁴ having published guidelines on when it is appropriate to offer vaginal birth with breech presentation. When a breech is first diagnosed in active labour, the evidence for the safest method of delivery is even less clear1,5–7 and it is important that all midwives are competent to support women with unanticipated breech presentations, regardless of location or ability to refer to other practitioners.

The incidence of breech presentation at 28 weeks has been found to be around 24% of fetuses, however by 37 weeks, the number of breech presentations will decrease to between 3% and 4% due to spontaneous version.¹ It has been suggested that as many as 1 in 100 births among low-risk women will be an undiagnosed breech in labour⁸ as it has repeatedly been found that clinical examination by abdominal palpation is only approximately 70% accurate and so will miss up to 1:3 breech pregnancies at term.9,10 However, improved diagnosis has not been found to improve outcomes⁷ and so there remains uncertainty regarding the clinical value of routine third trimester ultrasound examination for presentation and it is currently not recommended in pregnancies at low risk of complications.¹¹

Historical context

While there have been reports of the increased risks associated with breech births for centuries,¹² vaginal breech births remained the norm throughout most of the last century.¹³ However, as early as 1959 it was proposed that all breech presentations should be delivered abdominally to reduce perinatal morbidity and mortality.¹⁴ From around this time onwards, throughout most resource-rich areas of the world, the number of breech vaginal births has steadily declined,¹⁵ with the publication of the Term Breech Trial (also known as the Hannah Trial) in 2000¹⁶ leading to the almost universal recommendation for breech presenting births to be carried out as planned CSs. While the validity of their research findings have been much questioned and critiqued,15,17–19 the fact remains that in the United Kingdom very few current practitioners have clinical experience in delivering breech babies vaginally.

There is an increasing debate as to whether a straightforward breech presentation, where the labour is progressing well, should be considered an emergency20–22 or whether midwives should always refer such cases to their obstetric colleagues.23,24 However, in the United Kingdom planned vaginal breech births are currently very rare and most midwives, working within the National Health Service (NHS) will only experience them through skills drills and the occasional undiagnosed breech when women present in advanced labour. It is therefore valid to consider breech births within the context of emergencies, as combined with the higher rates of early neonatal morbidity16,25 and a clear lack of experience, both the risks and anxiety of those providing care are significantly increased. Additionally, almost all professional bodies continue to describe breech, particularly undiagnosed breech labours, when a clear plan has not been made antenatally, within the context of an emergency delivery.1,2,26 Although the finding of a breech presentation in labour would usually necessitate immediate referral to senior obstetricians, midwives at the point of qualification are expected to be able to carry out the safe delivery of an undiagnosed breech²⁶ with the EU directive stating that in ‘urgent cases’ a midwife should be able to conduct a spontaneous breech delivery (Directive 2005/36/EC of the European Parliament and of the Council [2005]). This underpins the importance of regular drills and practice to enable midwives to be as prepared as possible for the rare occasions when they may need to manage a breech birth with or without the backup of more experienced colleagues.

Classifications

There are three classifications of breech presentation (Figure 6.1):

Extended breech (Frank): The extended breech presents with flexion at the hips and extension at the knees so that the feet are lying near the fetal head (Figure 6.1a), which results in a well-fitting presenting part. This presentation is most common in primiparous women who have firm abdominal muscles.

Figure 6.1  Classifications of breech presentation. (a) Extended breech, (b) flexed breech, (c) footling breech.

Flexed breech (Complete): The flexed breech presents with flexion at the hips and the knees, with the feet beside the buttocks (Figure 6.1b), which results in a poor fitting presenting part and increases the risks of early rupture of membranes and cord prolapse.

Footling breech (Incomplete): The footling breech presents with extension at both the hips and the knees leading to one or both feet or knees presenting (Figure 6.1c). This is the rarest of the breech presentations and has a high risk of cord prolapse given the ill-fitting nature of the presenting part.

Risks/predisposing factors

Often there is no identifiable cause of breech presentation, however, there are features which make it more likely27–30:

•  Low gestational age/premature labour

•  Primiparity (tight abdominal muscles – harder to rotate to cephalic)

•  Grand multiparity (lax abdominal muscles)

•  Polyhydramnious

•  Major fetal abnormalities such as hydrocephaly (thought that the fetal head is better accommodated in the fundus of the uterus)

•  Older maternal age

•  Female infant

•  Smoking/intake of substances, which may cause reduced fetal movements such as anticonvulsive medications or alcohol

•  Septum or partial septum (bicornuate uterus)

•  Fibroids or uterine tumours

•  Placenta praevia

•  Previous uterine surgery

Consideration should also be given to the fact that for some women, all their babies adopt a breech presentation, suggesting that perhaps their pelvic shape is better suited to the breech position. Although pelvic classification is rarely practiced, obstetric texts frequently refer to an increased risk of breech with some pelvic shapes, making cephalic pelvic entry more challenging. Additionally, research has shown that if either parent was born breech their offspring is more than twice as likely to also be breech, suggesting a genetic predisposition to the position.³¹

Clinical features, diagnosis and reducing the incidence of breech presentation

Given that current practice and evidence highlight an increased risk of initial perinatal morbidity and mortality associated with vaginal breech births, diagnosis is ideally made in the antenatal period where appropriate referral and care planning can be made. This is particularly beneficial in ensuring that women and their families are able to make informed decisions about their care and options for birth, which is very challenging when a woman is already in established labour.8,32

Fetal presentation is not considered to be of clinical significance until 36 weeks’ gestation (unless in preterm labour), as the majority of fetuses will revert to a cephalic presentation by term. Often women with complex pregnancies will have multiple ultrasound examinations and so it is likely that these women will have breech presentations diagnosed early.

In the United Kingdom, women at low risk of complications are primarily seen by midwives where current practice does not recommend routine ultrasound scans after 20 weeks’ gestation11,33 and so the midwife’s skill in preforming an abdominal palpation is vital to diagnosis. While approximately 30% of breech presentations remain undiagnosed at term9,10 there is some evidence that those with less experience are more likely to mistake a breech for a cephalic presentation³⁴ and so vigilance and practice in abdominal palpation are vital. It is also suggested that a senior opinion is sought whenever there is any uncertainty.

Abdominal palpation

Prior to undertaking an abdominal palpation it is important for the midwife to undertake a thorough history as any of the above risk factors may alert the midwife to the possibility of a breech presentation. Additionally, mothers with a breech presentation often complain of increased discomfort under the ribs and heartburn which is caused by the proximity of the fetal head and so a discussion with the mother regarding her pregnancy symptoms and comfort can also provide the midwife with useful clues to the fetal position before she has even begun to palpate. That said, any woman may present breech and so a midwife should always be open to the possibility.

On inspection there is likely to be little difference; the lie is longitudinal although on palpation the size may palpate larger than expected particularly if the presenting part has not yet descended into the pelvis. Using a Pawlik’s grip the head is located in the fundus and palpated as a round hard mass, which may move independently of the back by gently balloting it between both hands. However, in a frank breech, if the feet are ‘splinting’ the head then the diagnosis may be more difficult.

Both poles may be grasped simultaneously to aid diagnosis and if the breech is movable above the symphysis pubis then it is likely that the fetal pelvis has not yet passed the maternal pelvic inlet (making the possibility of successful version to cephalic more likely). Typically the fetal back is felt on one side of the abdomen and the fetal small parts are felt on the other.

On auscultation the fetal heart sounds are often best heard at or above the level of the umbilicus and laterally on the side of the fetal back. Use of a Pinard stethoscope can be helpful, as they require more specific placement in terms of location.³⁵ It is generally recommended that if there is any suspicion of breech presentation by 36/40 then an ultrasound scan should be performed to confirm and assist in care planning.

Antenatal diagnosis

When midwives diagnose a breech presentation after 36 weeks (or according to local policy), referral to obstetric colleagues is usual. Prior to the onset of labour a woman with a breech presentation should ideally also be referred to a breech team or birth options clinic where she can be given full and in-depth information of the risks and benefits of ECV, elective CS or a planned vaginal breech birth.21,36,37 This discussion will need to include a clear explanation of the availability of personnel who are experienced in conducting vaginal breech births.

Turning breech to cephalic presentation

EXTERNAL CEPHALIC VERSION (ECV)

ECV is the manipulative transabdominal conversion of the breech to cephalic presentation and it has been a Royal College of Obstetricians and Gynaecologists (RCOG) recommended standard for many years.³⁸ This procedure has been carried out since the time of Hippocrates and was continued throughout the Middle Ages but during the 1970s and 1980s the practice fell out of favour and its availability diminished.³⁹ However, with further studies and as the option of vaginal breech birth decreased, it has since been widely reintroduced, with most consultant units now offering an ECV service.⁴⁰ The procedure has been the subject of significant scientific appraisal and a number of RCTs have been carried out which demonstrate that when offered at term there is a reduction in the rate of LSCS without increased risks to the baby.³⁹ Some skilled clinicians have a successful version rate of around 80%, although most areas achieve around a 50% success rate.41,42

Factors that increase the likelihood of success include43,44

•  Skilled ECV practitioner

•  Multiparity

•  Increased/normal amniotic fluid volumes

•  Posterior placenta

•  Non-frank breech

•  Body mass index (BMI) of less than 25

•  Black African ethnicity

While very safe,³⁴ it is recommended that the procedure should always be undertaken in a place where a baby can immediately be delivered by caesarean section should this become necessary.

Potential risks associated with ECV include39,45,46

•  Transient fetal heart rate anomalies

•  Persisting abnormal cardiotocography (CTG)

•  Inadvertent rupture of membranes (ROM)/cord prolapse

•  Placental abruption

•  Significant feto-maternal haemorrhage is possible but rare

•  Increase in instrumental vaginal births

•  Intrapartum LSCS rate doubles

Contraindications to ECV include46–48

•  Prior indication for CS

•  Placenta praevia

•  Rh sensitisation

•  Known fetal compromise

•  Intrauterine fetal death

•  Coagulation disorders

•  Ruptured membranes

•  Recent antepartum haemorrhage/placental abruption

•  Major uterine anomaly

•  Multiple pregnancy

Relative contraindications to ECV include

•  Pre-eclampsia

•  Intrauterine growth restriction (IUGR)

•  Oligohydramnios

•  Fetal anomaly

Current data suggest that ECV after one previous LSCS is safe.⁴⁷ While it may appear that there are many contraindications, it has been found that only 4% of breech presentations have a contraindication to ECV.⁴⁸

An obstetrician most commonly carries out the procedure but in some areas midwives are expanding their role to include ECV.42,49,50 What is most important is that the clinician is appropriately trained and skilled.⁴² Prior to the clinician performing the procedure, the woman must be fully informed of the potential risks and it is important to ensure she understands the procedure itself and that her informed consent is both given and documented. A CTG is performed to ensure a normal fetal heart pattern and a thorough ultrasound examination carried out to determine fetal position, where the legs are in relation to the body, head flexion and liquor volume. Once all is confirmed as suitable the woman should be given an appropriate tocolytic,³⁷ for example terbutaline, prior to the procedure.

The woman is required to either lie on her side with the fetal back uppermost, or on her back with an appropriate wedge tilt to the side. Using the palmer surfaces of both hands the practitioner will gently disengage the breech from the maternal pelvis (if needed). Once disengaged, the breech is encouraged laterally upward to encourage fetal flexion and for the fetus to ‘follow its nose’ around. The whole procedure should be gentle and unhurried.

The midwife should stay with the woman and be alert to any signs of discomfort as the procedure can be uncomfortable. If significant pain is experienced this would always be an indication to stop the procedure. Women should be reassured that most find the discomfort manageable⁵¹ and where needed Entonox may be used.⁵² The fetal heart should be auscultated after each attempt and a maximum of three attempts is considered appropriate.³⁹ A CTG should be repeated following the procedure and if the mother is Rhesus negative then blood for a Kleihauer test should be taken and Anti-D administered.

Following a successful ECV, it is important to discuss signs of spontaneous labour and when the woman should contact her midwife if there are any concerns, paying particular attention to fetal movements and any vaginal (per vagina [PV]) bleeding. If unsuccessful, plans should be made with the obstetrician for mode of delivery or, if appropriate, another ECV may be attempted at a later date.

ALTERNATIVE AND COMPLEMENTARY THERAPIES

Moxibustion

Moxibustion is a form of traditional Chinese medicine (TCM) in which moxa sticks (usually Artemesia vulgaria or a smokeless variety) are burned close to the skin of the outer aspect of the fifth toenails of both feet. This is a traditional acupuncture point called Bladder 67, which is the primary point selected for use because it is the most dynamic point to activate the uterus. The moxa burn with a slow but intense heat, which stimulates heat receptors on the skin of the toe and according to TCM theory, moxa has a tonifying and warming effect that promotes movement and activity. This warming and raising effect is utilised to encourage the fetus to become more active and thus increase the chance of spontaneous version to cephalic.⁵³

There is, however, conflicting evidence for the use of moxibustion,54–56 with a recent Cochrane review stating that there is some evidence that when used in conjunction with knee/chest positioning it may reduce the incidence of non-cephalic presentations at term and recommended further studies to evaluate its effectiveness.⁵⁷

While the evidence of its effectiveness is conflicting, it is non-invasive, appears to be safe and is an option some women are likely to consider in their desire to avoid an operative delivery. It is therefore important that midwives have a basic understanding of moxibustion as a treatment some women will seek out.

In some areas midwives have developed use of moxibustion as an extended skill which can be offered to women from 33 weeks’ gestation;⁵⁸ however, as with all things, midwives are reminded that they are accountable for their practice and so should only offer a service if properly trained and competent to do so.26,59

Other alternative therapies

It has been suggested that the following may also be beneficial in encouraging breech to cephalic version although research into their effectiveness has generally been small studies which lack scientific rigor. All would benefit from further evaluation⁶⁰ and should therefore not be routinely recommended:

•  Ginger paste

•  Homeopathy

•  Chiropractic

•  Fetal acoustic stimulation

•  Hypnotherapy

•  Yoga positions

Posture and positioning

Much has been written regarding the use of the knee-chest, all-fours position as a means of encouraging spontaneous version from breech to cephalic presentation.⁶¹ Evidence from a Cochrane review⁶² reviewed studies where women were encouraged to adopt this position for varying time periods in late pregnancy; however, the evidence was unable to demonstrate any significant benefit in breech version and so they concluded that there is no reason to recommend this intervention but suggested that further large-scale studies were warranted. However, as this is a non-invasive intervention, and so therefore may be considered a safe practice, it is likely that some women will continue to make use of it. Midwives should be cautious in recommending it; however, as there is some limited evidence from studies concerning maternal positioning to turn OP to OA, that if women are advised to carry out various postures/positions, and the fetus does not turn, they can suffer negative psychological effects.63,64 As mentioned above, if women are making use of moxibustion then it is possible that in conjunction with the knee-chest position the success rate may be improved.⁵⁷

Immediate care/treatment – undiagnosed breech in labour

It is not uncommon, even for women who have accessed regular antenatal care, to present in labour with an unknown breech presentation, which is ideally diagnosed on admission. Approximately 10% of all breech presentations at term will be undetected prior to labour²⁸ and as many as 1:3 when a third-trimester ultrasound has not been performed.¹ All midwives should be alert to the possibility of previous palpations and even vaginal examinations being incorrect (or even of a late position/presentation change by the fetus) and therefore each examination should be conducted without preconceived expectations (see Box 6.1).

When the diagnosis is made in labour, particularly advanced labour, it is much harder to ensure the woman is both given adequate information and is able to understand this in order to give informed consent to either a vaginal birth or, where available, an emergency CS. It is therefore vital that following the birth, regardless of outcome, the woman and her family are given adequate time to discuss and reflect on their birth experience with someone (ideally, the birth practitioner) who is able to answer any questions or unresolved issues they may have.⁶⁵

BOX 6.1: Vaginal examination

Prior to undertaking vaginal examination the midwife will gain consent and carry out an abdominal examination which, as described earlier, will hopefully alert the midwife to the possibility of a breech presentation. On vaginal examination, the smooth, hard round head with its familiar landmarks is absent. The presenting part is often high, soft and irregular, sometimes the anal orifice or male genitalia can be felt. If landmarks can be felt they will be in a line (e.g. the fetal ischial tuberosities and the anus), although in a very compressed breech, the cleft between the buttocks may be mistaken for the sagittal suture. After rupture of membranes, fresh meconium is often seen, especially on the examining finger after identification of the anus and this is diagnostic. Occasionally, the midwife may also feel a foot or rarely a knee. However, diagnosis of a breech from a vaginal examination, particularly in early labour, can be difficult and mistakes are sometimes made.

The first action when a breech is diagnosed in labour is to explain the finding to the mother calmly and to call for help. In a hospital setting this would initially be senior midwifery and obstetric assistance and prior to birth, anesthetic and neonatal colleagues should be on standby. If available, it would also be appropriate to call a specialist breech midwife or midwife with breech experience. In the community, emergency services should be called to enable swift transfer to an obstetric unit. It is important to liaise with the local obstetric unit to ensure that they are anticipating the transfer and so that appropriate personnel (including neonatal) are available on arrival.

MECHANSISM OF LABOUR: LEFT SACROANTERIOR (LSA)

An understanding of the mechanism of labour in a breech birth can assist the midwife in facilitating the process. The following describes the mechanism of labour in the LSA position:

•  Longitudinal lie.

•  Attitude of flexion.

•  Breech presentation.

•  Position LSA.

•  Denominator is the sacrum.

•  The presenting part is the anterior left buttock.

•  Engagement takes place when the bitrochanteric diameter has passed through the inlet of the pelvis.

•  Descent takes place with the increasing compaction. Since the breech is a less efficient dilator than the head, descent may be slow. (This should alert the midwife to the possibility of a breech if presentation was unsure.)

•  Flexion: Lateral flexion takes place at the waist. The anterior hip becomes the leading part.

•  Internal rotation of the buttocks: The anterior buttock reaches the resistance of the pelvic floor and rotates forward to lie beneath the symphysis pubis.

•  Increased lateral flexion occurs as the anterior buttock impinges under the symphysis pubis. With further flexion the buttocks are born and rise up the perineum.

•  Following expulsion of the legs the buttock then falls towards the maternal anus.

•  The anterior buttock restitutes to the right.

•  The shoulders enter the pelvis in the left oblique. The anterior shoulder rotates forward towards the symphysis pubis and is born. The posterior shoulder follows.

•  As the shoulders are at the outlet the head enters the pelvis with the sagittal suture in the transverse diameter of the brim. The occiput meets the pelvic floor and rotates forward so that the sagittal suture is in the anteroposterior diameter.

•  Externally, this action causes the sacrum to rotate back towards the pubis so the back is anterior.

•  As the nape of the neck pivots under the symphysis, the chin, mouth, nose, forehead and occiput are born by flexion.

Breech delivery

While it is anticipated that senior obstetric assistance will usually be available, every midwife must be familiar with, and able to support, a woman birthing in the breech position.

The temperature of the birthing room must be warm and without draughts, as the baby’s body will be exposed before drying/wrapping is possible and cold air can stimulate respiration before the head is born.

Prior to the birth it is important to ensure the woman’s bladder is empty.³⁵

Current management and most recommendations35,39 encourage birth in the semi-recumbent/lithotomy position with space at the end of the bed for the baby to hang. Kneeling/upright birth positions have long been advocated by some midwives experienced in supporting women with breech presentations who choose to birth at home;66–69 however, as there is currently no large case series data published on alternative birthing positions these are not generally recommended.³⁹ In the case of an unexpected breech birth it is suggested that, with the woman’s consent, whichever position the midwife feels most capable of supporting the mother in is likely to be the safest. However, if the woman prefers an upright position it is important that the midwife is able to support this also, and so ideally, both positions are prepared for.⁶⁵ In any position, the recommendations are that wherever possible, when there is good progress minimal handling or ‘hands off the breech’ is the best approach until the nape of the neck is visible, when assistance to ensure a slow delivery of the head is beneficial. It is vital that when there is a delay the midwife is able to understand what may cause this and assist as necessary to reduce the risk of cord compression, head entrapment or oxygen deprivation.

Full dilatation of the cervix must be confirmed before supporting/encouraging the woman to push. Active pushing should be avoided prior to the breech distending the introitus, anal dilation should be visualised. This will prevent head entrapment within a partially dilated cervix. If this occurs, a retractor or finger should be used to gently push aside the cervix in front of the baby’s face and delivery must then be expedited.

The principle of ‘hands off the breech’ is valid as long as there is good progress and clear signs of fetal well-being. Any handling of the baby is liable to stimulate premature respiration and therefore touching should only be done if necessary. Avoidance of traction is crucial to a safe birth. If the fetal back appears to be rotating away from the sacroanterior then this should be corrected.

The baby’s legs should deliver spontaneously, but if necessary they can be assisted by placing two fingers along the length of one thigh with the fingers in the popliteal fossa. Each leg is then flexed across the body and down, although traction or additional handling of the baby should be avoided.

Once the baby has birthed to the umbilicus and the legs have been delivered, the cord should be visualised. There is no evidence that pulling a loop of cord is beneficial and it could cause arterial spasm and should therefore be avoided.

With further expulsion the back arches and well-flexed arms may deliver spontaneously. If necessary the midwife can assess the position of the baby’s arms by placing her fingers on the baby’s chest, if she can feel elbows, the arms are flexed and are likely to deliver with the next contraction. If they do not deliver then it may be possible to simply hook them down from the elbow or with two fingers passed over the shoulder, gently push the humerus across the chest sweeping the arms across the body and downwards. However, if the arms are extended then Lovset’s manoeuver (see Box 6.2) will be necessary. Where traction has been used or the baby has been stimulated in any way, then it is more likely that the arms will be extended due to the ‘startle’ reflex.

DELIVERY OF THE HEAD

The head will move through the pelvis in a transverse position until it rotates spontaneously to bring the occiput under the symphysis pubis with the back anterior. It is important to wait for this to happen and for the nape of the neck to be visible before manoeuvres are used to deliver the head. If there appears to be a delay then an assistant should apply suprapubic pressure to assist flexion of the head.

While the fetal head may birth spontaneously and without problems,⁶⁵ it is important to ensure the birth of the head is not too rapid and so it may be prudent to carry out a modified Mauriceau-Smellie-Veit (MSV) manoeuvre (Figure 6.3). This is particularly important if the head is not well flexed as it aims to enhance flexion. The baby’s body is usually laid along the midwife’s dominant arm with the palm upwards supporting the chest. The index and second finger of that hand are placed on the malar (cheek) bones of the baby’s face. (Traditionally it was the index and ring fingers with the middle finger on the baby’s chin, however, this caused a risk that the practitioner might insert their middle finger in the baby’s mouth, which can fracture the jaw or cause trauma to the mouth and gums.) The midwife should then place her other hand across the baby’s shoulders with her middle fingers on the occiput to increase flexion. An assistant can continue to provide external support for flexion by providing suprapubic pressure throughout this manoeuvre.³⁵ As the head is flexed, gentle downward traction can be applied to the shoulders and the head is drawn out until the suboccipital region appears, the face is delivered, and the head is rotated around the symphysis pubis. It is important to ensure this is done gently and slowly as rapid delivery of the fetal head could lead to compression and decompression of the fetal skull bones, which may cause tentorial tears and intracranial haemorrhage to occur.

BOX 6.2: Lovset’s manoeuvre

Holding the baby carefully by the fetal pelvic girdle (avoiding any pressure on the soft tissues of the abdomen), gentle downwards traction is applied while rotation is carried out. Care must be taken to always keep the fetal back towards the mother’s front (i.e. the fetal back must be uppermost if the woman is in the semi-recumbent/lithotomy position). The baby is then rotated approximately 180 degrees so as to splint the posterior arm across the baby’s face and change it to an anterior position.

If the arm does not deliver spontaneously during the rotation, the midwife should draw it gently down over the chest by flexing the elbow with her finger. The baby is then rotated back in the opposite direction and the second arm is delivered (Figure 6.2), remembering to ensure that the back stays uppermost (baby’s back to mother’s front).

Figure 6.2  Lovset’s manoeuvre.

Figure 6.3  Delivery of the head.

It is also possible to perform MSV with the woman in an all fours position and practicing this in skills drills will enable midwives to be more competent in supporting women’s choices.⁶⁵

It is important to be aware of the time throughout the birth, as avoiding prolonged lack of oxygen to the fetus is crucial to good outcomes. It has been advocated that from the birth of the body to the birth of the head should be no more than 5 minutes.⁷⁰

Many babies will need resuscitation and so it is vital that this is prepared for prior to the birth regardless of location.

Emergency breech extraction

This is rarely undertaken and is inappropriate for a singleton term breech delivery.³ It would only be undertaken by an obstetrician as an emergency procedure to achieve immediate delivery if there is severe fetal distress and when an emergency LSCS is not an option. It would most commonly be used to deliver a second twin¹ in an oblique or transverse lie after internal podalic version.⁷¹ A hand must be placed into the uterus and if possible both feet are grasped. The legs are then pulled down and the head pressed upwards with the outside hand. Traction must be maintained on the delivered legs until the breech is fixed. Traction takes the place of contractions and the breech can then be delivered using the manoeuvers previously described. As the arms will be extended due to traction, Lovset’s (see Box 6.2) will be necessary.⁷²

Breech birth at home

There is very little literature outlining the risks and outcomes for planned breech births at home because they are not recommended and so few women choose this. It is therefore important that a woman considering a planned breech home birth be fully counselled and supported to consider the evidence available. It is vital that women understand the rationale for recommending birth within an obstetric-led labour ward;1,73 however, it is equally important that they do not feel coerced into a plan they are not happy with. Midwives work with women and are in a position to advocate for them, additionally, current UK practice would be to involve a Supervisor of Midwives (SOM)²⁰ in the planning discussions for women going against recommended practice.

While midwives have a duty to support women wherever they choose to birth, experience of breech births at home is extremely rare. With the continued dominance of CS not only is the hands-on experience of breech birth reduced but so too is the opportunity to observe vaginal breech births. Where a woman remains committed to her plan for a breech home birth it would be important to try and ensure experienced personnel are available to be on call for her and all those who are likely to attend would be recommended to refresh their skills in simulation training. As previously stated, it is crucial that all midwives continuously maintain and update their skills in managing vaginal breech births and it could be argued that this is even more important for midwives who work autonomously in home or birth centre settings where immediate backup is less readily available for unplanned breech births.

Besides having the necessary skills to enable a safe delivery, priorities for the midwife are to obtain help, maintain a calm environment and prepare for potential maternal postpartum haemorrhage (PPH) and/or neonatal resuscitation. The environment must be kept warm to prevent neonatal hypothermia and the ensuing hypoglycaemia, and early feeding is important.

Breech birth in hospital

The same priorities apply as above. However, preparing for a breech delivery in hospital is now usually associated with preparing for surgery.

Where a vaginal breech birth is planned it is vital that the most senior/experienced person is available to conduct the birth or support the midwife during the delivery. Continuous CTG monitoring is recommended¹ and labour progress should be good. Any thought of induction or augmentation should be considered with utmost caution and consultant obstetric input is essential.¹ In view of the increased likelihood of needing neonatal resuscitation it is recommended that a neonatal doctor/someone experienced in carrying out neonatal resuscitation is also present for the birth.

While many midwives have very limited experience of breech birth, it remains an essential skill that midwives must be competent to deliver a breech²⁶ and so it is imperative to maintain skills and update knowledge regularly to ensure women receive the best possible care whether undiagnosed or for women choosing a vaginal breech birth. See Box 6.3 for a summary of midwifery actions when undertaking a vaginal breech delivery.

Possible complications of a vaginal breech delivery which may need ongoing care

Baby:

•  Fractures of the humerus, clavicle or femur

•  Dislocation of the hip or shoulder

•  Erb’s palsy

•  Internal organ damage by rough or incorrect handling (e.g. kidneys, liver, spleen)

•  Dislocation of the neck

•  Spinal cord damage or fracture

•  Intracranial haemorrhage

•  Soft-tissue damage

•  Hypoxia/birth asphyxia; this may be due to cord compression, cord prolapse or premature placental separation

•  Cold injury and hypoglycaemia

•  Long-term neurological damage

•  Congenital dislocation of the hip, especially with frank breech; this is usually a complication of the presentation and not the birth process

Mother:

•  Urethral trauma

•  Vaginal or perineal trauma

•  Postpartum haemorrhage

The majority of these complications are rare and can be minimised by correct delivery techniques and immediate referral as appropriate.

BOX 6.3: Vaginal breech delivery checklist

•  Palpate abdomen.

•  Conduct vaginal examination to assess cervical full dilation.

•  Confirm bladder is empty.

•  Ensure woman is positioned appropriately.

•  Make sure room is warm and there are no draughts.

•  Perform continuous CTG/regular auscultation of the fetal heart.

•  Remember ‘hands off the breech’.

•  Note possible assistance may be necessary in delivery of extended legs.

•  Observe cord but avoid handling.

•  Check for position of the arms.

•  Keep baby’s back to mother’s front (i.e. back uppermost if mother is in semi-recumbent position).

•  Perform Lovset’s manoeuvre for arm/shoulder delivery if necessary.

•  Allow descent of the head through the pelvis (avoidance of traction improves the likelihood that the head remains flexed) and spontaneous rotation to OA.

•  Ensure slow delivery of the head (often using MSV).

•  Perform neonatal resuscitation if necessary.

•  Use third-stage management/observation for PPH.

•  Keep clear and contemporaneous records.

•  Maintain the baby’s temperature.

•  Give an early feeding.

•  Ensure there is a full neonatal assessment of the baby.

TRANSVERSE OR OBLIQUE LIE

Definition and incidence

A transverse lie denotes a fetus with its longitudinal axis perpendicular to the long axis of the uterus (Figure 6.4). The transverse lie can occur with either the curvature of the fetal spine orientated upwards (dorsosuperior) or downwards (dorsoinferior). In an oblique lie the head or the breech will be located within the iliac fossa (Figure 6.4). Most often these presentations form part of an unstable lie when the fetus moves between longitudinal, transverse and oblique lies after 37 weeks’ gestation. The incidence is difficult to estimate and varies significantly depending on population variables, however, where grand multiparity is uncommon the incidence is between 1:300 and 1:400.⁴⁶

Suggested causes and associations with transverse or oblique lie include

•  Grand multiparity

•  Contracted maternal pelvis

•  Placenta previa

•  Prematurity

•  Polyhydramnios

•  Uterine abnormalities such as transverse septum or leiomyomas (fibroids)

•  Fetal macrosomia

•  Fetal abnormalities

•  Multiple pregnancy (second twin)

Clinical features and diagnosis

Diagnosis is usually made antenatally. On inspection of the abdomen, the uterus appears broad and on palpation the fetal poles will not be felt in either the pelvis or the fundus. Additionally the woman may experience discomfort when the lower uterine segment is touched. Referral to the obstetrician should be made as appropriate, and ultrasound examination and review would be recommended to rule out any relevant causes/associations (see above) and to plan care and management.

On vaginal examination (VE) very little is likely to be felt as the presenting part remains high. It may be possible to feel the shoulder, ribs or on occasion the fetal arm may prolapse through the cervix. A cord prolapse is a very real risk in these situations and this too may be felt. It would be prudent to avoid VE until after ultrasound confirmation if oblique or transverse lie is suspected from palpation, due to the risk of cord prolapse following accidental ROM.

Figure 6.4  Transverse and oblique lie. (a) Transverse lie, (b) oblique lie.

Mechanism

There is no mechanism for labour and without version or emergency LSCS delivery, the labour becomes obstructed and contractions may become tonic with no relaxation of the uterus. Uterine rupture, death of the fetus and/or possible maternal death will ensue.

Immediate care/treatment

Antenatally, prior to term there is little clinical significance, however, the woman should be informed to attend immediately if she goes into premature labour or if there is pre-labour rupture of membranes as the risk of cord prolapse (see Chapter 7) is significant. The RCOG recommend considering inpatient care from 37+ weeks to reduce the risks associated with pre-labour rupture of membranes and cord prolapse.⁷⁴ Additionally, ECV may be attempted but in an unstable lie, the fetus may revert back. Where the fetus persists in a transverse/oblique lie at term or in early labour the obstetrician may attempt ECV possibly with a controlled ARM, however, in most cases CS is required.

If diagnosed in labour, it would be important to explain the situation to the mother and her birth partner clearly, while making an immediate referral to an obstetrican. If not in hospital, arrangements for urgent transfer to a labour ward must be made.

COMPOUND PRESENTATION

Definition and incidence

A compound presentation is when a fetal extremity presents alongside the presenting part. The majority of compound presentations involve the fetal hand or arm presenting with the vertex. The incidence of compound presentation is rare and usually described as less than 1:1000.⁴⁶

Suggested causes and associations with compound presentation include

•  Premature rupture of membranes

•  Premature labour, low gestational weight

•  Pelvic mass displacing the fetal pole

•  Induction of labour with a high presenting part

•  Multiple pregnancy

Clinical features and diagnosis

Compound presentation is a finding that may be diagnosed on vaginal examination when the extremity is felt alongside the presenting part. Most often a hand or fingers are felt alongside the vertex although rarely a foot may be felt beside the vertex or an arm may be present together with the breech.

Mechanism/Immediate care/treatment

In most cases, if the hand is presenting it will retract as labour progresses and care can continue as normal. Additionally, as the fetus already has the reflexes which are associated with newborns, it is possible to encourage retraction with a gentle pinch to the fingers. So long as labour is progressing normally a compound presentation can usually be safely ignored and the fetus is likely to self-correct the situation.

REFERRAL

If, however, the hand or arm has prolapsed below the presenting part it is likely the increased presenting diameter will necessitate a caesarean birth and therefore timely obstetric referral and transfer (if required) is necessary. Similarly, a foot presenting by the fetal head is more complicated as the size of the leg makes retraction less likely and significantly increases the diameter of the presenting part. Occasionally vaginal delivery may still occur but augmentation is to be avoided and instrumental delivery is contraindicated with a compound presentation.

OCCIPITOPOSTERIOR (OP) POSITION

Definition and incidence

When the fetal head descends into the pelvis it most often enters the pelvis in the lateral position and rotates to an occiput anterior (OA) position either prior to or during the early stages of labour. Occipitoposterior positioning occurs when the fetal occiput is malpositioned in the posterior of the pelvis. An OP position is present in approximately 20% of early labours and while spontaneous version to an OA position is likely, a persistent OP labour affects up to 10% of vertex births.⁷⁵

While some births will be straightforward even with an OP position, labours are frequently longer,⁷⁶ more painful, require greater use of analgesia, increased interventions⁷⁷ and result in higher rates of third-and fourth-degree tears.⁷⁸ It is important that the midwife is aware of these risks and is able to support mothers effectively to improve both outcomes and experiences.

Suggested causes and associations with OP positions include75,79

•  A previous OP labour

•  High inclination of the pelvis

•  Android- or anthropoid-type pelvis

•  Use of intrapartum epidural analgesia (which relaxes the pelvic floor muscles)

However, in most cases the aetiology of this malposition is unknown.

Additionally, it has been suggested that over 50% of persistent OP positions actually developed through malrotation during labour of an initially OA position.⁸⁰ While there is very little evidence to support the notion, there is a general perception that a sedentary lifestyle or adopting ‘slouched’ positions may lead to an increase in OP labours81,82 and discussion regarding the role of maternal posture and lifestyle continues to inform the debate regarding the position of the fetus.81,83

Clinical features and diagnosis

ABDOMINAL PALPATION

On inspection the abdomen may appear to flatten out, or a dip may be noted, around the umbilicus, marking the space between the fetal arms and legs. An OP position should be considered/suspected if engagement has not occurred by term in the primiparous woman, as the OP position makes it more difficult for the fetus to negotiate the pelvis.

The fetal back may be difficult to find or is found in a lateral position. The fetal head is often high. The fetal heartbeat is usually heard either laterally or at the umbilicus.

VAGINAL EXAMINATION

On vaginal examination the head may be high and an OP position is confirmed if the anterior fontanelle is located in the anterior and the posterior fontanelle is near the sacrum. However, vaginal examination can be complicated by the presence of caput and moulding.

Mechanism

LONG INTERNAL ROTATION

If engagement occurs in the right oblique diameter of the brim, descent follows in the right oblique diameter as a right OP (ROP) position. Descent continues to the pelvic floor and with a well-flexed head the progress can be good. As flexion increases, the occiput meets resistance of the pelvic floor and rotates anteriorly through approximately 135 degrees (three-eighths of a circle) to a direct OA position, labour and birth can then be expected to progress normally.

SHORT INTERNAL ROTATION

If engagement occurs in the right oblique diameter of the brim, descent follows in the right oblique diameter (ROP position). Descent continues to the pelvic floor and progress again depends on flexion of the head. If the fetal head remains deflexed, the sinciput reaches the resistance of the pelvic floor and rotates forward. The occiput settles into the hollow of the sacrum and the fetal chest restricts flexion of the head. Maternal soft tissues are stretched more and the midwife might suspect this position if there is gaping of the vagina and dilatation of the anus, when the fetal head is barely visible. Upward moulding and caput succedaneum are evident and the baby is born face to pubis (persistent occipitoposterior [POP]).

On delivery the sinciput will emerge under the symphysis and the midwife should aim to ensure a slow and controlled birth of the head. Whether hands on or hands poised it is vital to prevent a rapid expulsion of the occiput over the perineum although the increased risk of perineal trauma must be anticipated regardless.

DEEP TRANSVERSE ARREST

If engagement occurs in the right oblique diameter of the brim, descent follows in the right oblique diameter (ROP position). Descent continues to the pelvic floor and progress again depends on flexion of the head. As the head descends with a degree of flexion, the occiput meets the resistance of the pelvic floor and it begins a long rotation but – perhaps because of prominent ischial spines, or perhaps because it becomes less well flexed – the occipitofrontal diameter becomes trapped in the bispinous diameter of the outlet. On vaginal examination, the sagittal suture is felt in the transverse diameter and usually both fontanelles are palpable. The fetal head does not advance. Obstetric assistance should be sought and if the cervix is fully dilated and the head below the spines, a manual rotation may be attempted. A skilled practitioner may attempt an instrumental rotational delivery with either a vacuum or (now extremely rare) Kjelland’s forceps. However, more often these cases are now delivered by CS.

Instrumental deliveries with OP positions have been shown to increase maternal morbidity.84,85 Therefore if delivery is deemed to be difficult, the consensus is that CS is preferable.

EXTENSION TO BROW/FACE

On occasion an OP position may extend to either a brow or face presentation and it is important that the midwife is alert to these signs so that appropriate care and referral can be made as necessary.

Immediate care/treatment

Care and management of an OP labour in the home, birth centre or obstetric-led labour ward are similar. It has been demonstrated that there can be a variety of outcomes when a woman presents with an OP position in early labour and vigilance by the midwife is vital. Any sign of prolonged labour should alert the midwife to the possibility of an obstructed labour and obstetric assistance sought as necessary. Monitoring progress, documented on a partogram and detailed vaginal examinations will assist in labour care and planning. Encouraging maternal changes of position may enable greater coping strategies and improve comfort. Although adopting hands and knees positions at the end of pregnancy have not shown any reduction in the likelihood of OP labours,⁸⁶ during labour this position may reduce persistent back pain⁸⁷ making labour more bearable. Good psychological support for the mother is paramount, with continuity wherever possible.⁸⁸ Aware of the possible outcomes the midwife should act as an advocate for mothers, ensuring timely referral as needed while supporting full discussion to enable women to continue to make informed decisions about their care regardless of outcome.

REFERRAL

When labour progresses an OP labour is not out of the midwife’s scope of practice but an awareness of the risks will ensure appropriate referral as needed. There is some evidence that augmentation of a slow OP labour can help the fetus to rotate to an OA postion⁷⁵ and therefore if labour is not progressing it may be prudent to refer for oxytocin augmentation.

As with any labour if there is any concern about maternal and/or fetal well-being, referral to the obstetric team is advised and this is clearly necessary where the fetus arrests in the transverse diameter.

Summary of possible outcomes of OP malposition:

•  Long rotation to occipitoanterior and normal OA delivery

•  Short rotation to POP with face to pubis delivery

•  Deep transverse arrest

•  Conversion to brow presentation (may then convert to face or vertex; if not vaginal birth unlikely)

•  Conversion to face presentation (mentoanterior can deliver vaginally)

•  Medical assistance needed for delay or obstructed labour or non-vertex presentation

•  Medical intervention more likely with increased instrumental or operative delivery

BROW PRESENTATION

Definition and incidence

In a brow presentation, the fetal head is halfway between full flexion (vertex) and hyperextension (face: see next section). The presenting part of the fetal head is between the orbital ridge and the anterior fontanelle. The frontal bones are the point of designation and can present (as with the occiput in a vertex presentation) in any position relative to the maternal pelvis. Reported incidence varies significantly and has been stated to be between 1:177 and 1:1500.⁷⁵

Suggested causes and associations with brow presentation include

•  Post dates

•  Prematurity

•  Cephalopelvic disproportion

•  Associated with OP positions

Clinical features and diagnosis

Diagnosis prior to labour is difficult and a brow presentation may be suspected with a post-dates pregnancy where a large head is palpable abdominally.

On vaginal examination the pelvis may feel empty although it may be possible to reach the presenting part, which will usually remain high. The anterior fontanelle may be felt on one side of the pelvis and the orbital ridges on the other, however, if descent had taken place the landmarks may be obscured by oedema.

Mechanism

Where a brow presentation persists, the large mentovertical (13.5 cm) diameter is considered too large to fit through the pelvis, unless the fetus is small or preterm, and labour will become obstructed, necessitating a CS.

Immediate care/treatment

When a brow is suspected in early labour it may flex (to vertex position) or extend (to face presentation), possibly allowing labour to continue; therefore conservative management and a watch and wait approach⁷⁵ with appropriate multiprofessional collaboration is recommended.

REFERRAL

Where a brow presentation is suspected it is worth early discussion with the woman and obstetric team to reduce the risk of an emergency transfer of care or unanticipated surgical delivery.

FACE PRESENTATION

Definition and incidence

A face presentation is the result of a complete extension of the fetal head; where the area from the glabella (the flat area of bone between the eyebrows) to the underside of the mentum (chin) lies over the cervical os and the occiput is flexed against the upper back. The incidence of face presentation is reported to be between 1:500 and 1:1000.46,75 Occasionally the face may be the primary presenting part at the start of labour; however, more often a deflexed posterior presentation develops into a face presentation as labour progresses. This is called a secondary face presentation and is caused when the deflexed posterior position gets held up at the pelvic brim and contractions promote extension of the fetal head.

Suggested causes and associations with primary face presentation include

•  Tumours of the fetal neck, e.g. goitre or cystic hygroma (which are usually diagnosed during antenatal ultrasound)

•  Anencephaly (which is usually diagnosed during antenatal ultrasound)

•  Prematurity

•  Low birth weight

•  Uterine abnormalities

•  Loops of cord around the neck (preventing flexion)

•  Cephalopelvic disproportion

•  Fetal musculoskeletal abnormalities

•  Multiple pregnancy

•  Multiparity

Clinical features and diagnosis

Although almost impossible to diagnose from abdominal examination, palpation may suggest a high head with a sharp angulation noted between the fetal occiput and back. It is expected that most face presentations would not be diagnosed until labour.

On vaginal examination the presenting part is often high and will feel soft and irregular with the orbital ridges, nose, mouth and malar bones palpable. It is even possible that the fetal mouth may suck the examiner’s finger. Initially it can be hard to distinguish between a face presentation and a breech especially if oedema is present as this can distort the landmarks; however, the distinguishing features is that the mouth and two malar prominences will be felt as a triangle. Care must be taken during examination not to damage the eyes.

Mechanism

The mentum (chin) is the denominator, which is used to define the position with the submentobregmatic diameter (9.5 cm) being the largest diameter to pass through the pelvis. This is similar to the biparietal diameter and so a vaginal birth is often achievable; however, it must be remembered that face bones do not mould. Most often the face enters the brim of the pelvis in the transverse positon and with descent progresses into the mentoanterior (chin anterior) position in which case it is possible to expect a vaginal birth 60%–90% of the time⁷⁵ with the fetal head being born by hyperflexion of the neck (Figure 6.5). After anterior rotation and descent, the chin and mouth appear at the vulva. Then the nose, eyes, brow and occiput sweep the perineum and the head delivers by flexion. Restitution then takes place where the chin rotates back towards the side in which it entered the brim and the shoulders are delivered as normal. However, it is important to note that the occiput can cause significant perineal distension and so perineal trauma may be increased.

If the face presents and persists in the mentoposterior position vaginal birth is not possible as the fetal skull is unable to pass under the symphysis pubis and therefore a CS will be necessary.

Immediate care/treatment

It has been suggested that over 50% of face presentations are not diagnosed until the second stage of labour⁸⁹; however, a more recent study found around 70% diagnosis rates on admission in labour⁹⁰ and while in that study all proceeded to CS, it is generally agreed that intervention is only warranted when there is fetal distress or arrest of dilation/descent. It is vital that the midwife informs the woman and her birth partners immediately and sensitively of her findings so that they can be prepared, as most face presentation babies have significant bruising and facial swelling which, while it will generally resolve within a few days, can be distressing to parents. Additionally, this can delay the establishment of breastfeeding and so support to establish feeding may include teaching the mother to hand express. On rare occasions the neonate may need temporary admission to the neonatal unit for support if excessive oedema compromises respiration.

Figure 6.5  Face presentation (mentoanterior) and delivery.

REFERRAL

If a face presentation is suspected the midwife should discuss with obstetric colleagues and if at home or in a birth centre usually transfer into an obstetric labour ward. If birth is imminent in the community, paramedic help should be called for in case of resuscitation being necessary, and for subsequent transfer for a paediatrician examination.

While fetal heart rate abnormalities during labour may be more common it is important that fetal blood sampling, fetal scalp electrodes and ventouse delivery are avoided with a face presentation. Additionally, if required it is safer to perform a caesarean section in the first stage of labour with careful delivery of the fetal head as there is an increased risk of extension to the uterine incision and CS delivery becomes more challenging in the second stage.

ONGOING CARE

Possible complications associated with malpositions:

Mother:

•  Prolonged latent phase

•  Primary dysfunctional labour/slow progress

•  Prolonged second stage of labour

•  Exhaustion, dehydration and ketosis

•  Obstructed labour

•  Instrumental/operative interventions

•  Perineal lacerations and trauma

•  Trauma from operative or instrumental delivery

•  Risk of infection associated with prolonged rupture of membranes

•  Psychological trauma

Fetus/baby:

•  Hypoxia resulting from prolonged labour or cord prolapse (predisposed to by a high head with an ill-fitting presenting part)

•  Risk of infection if there is prolonged rupture of membranes

•  Cerebral haemorrhage from unfavourable upward moulding

•  Facial bruising with face presentation

•  Hypothermia or hypoglycaemia if hypoxic or if resuscitation has been required

CONCLUSION

Malpresentations and malpositions are often a part of the birth process; they may be a variation of the norm or an unexpected emergency situation. Midwives should therefore always expect and be prepared for the unexpected, even while promoting birth as a normal physiological and psychosocial event in the life of the woman and her family. Safe practice based on sound theory is vital and such knowledge must include all aspects of the birth process. Practice, judgment and clinical skills need to be constantly reviewed and updated.

SUMMARY OF MIDWIFERY RESPONSIBILITIES

•  Identify malpositions and malpresentations antenatally whenever possible, to enable forward planning and non-urgent informed decision making by the woman.

•  Monitor progress of labour and refer as appropriate.

•  Monitor well-being and position of the fetus.

•  Refer to obstetric colleagues and transfer to an obstetric labour ward when necessary.

•  Prepare for neonatal resuscitation, and potential PPH as appropriate.

•  Keep the baby warm.

•  Ensure early feeding.

•  Perform neonatal assessment.

•  Provide psychological and emotional support for the mother and her family.

•  Debrief as necessary (see Chapter 14).

REFERENCES

1.  Royal College of Obstetricians and Gynaecologists (RCOG). 2006. Management of Breech Presentation. December. London: RCOG.

2.  National Institute for Health and Care Excellence (NICE). 2011. Clinical Guideline 132: Caesarean Section. London: NICE. Available at https://www.nice.org.uk/guidance/cg132 (accessed March 4, 2016).

3.  Kotaska A, Menticoglou S, Gagnon R. 2009. Vaginal delivery of breech presentation: SOGC clinical practice guideline. Journal of Obstetrics and Gynaecology Canada, 31(6):557–566.

4.  The Royal Australian and New Zealand College of Obstetricians and Gynaecologists (RANZCOG). College Statement: Management of Term Breech Presentation (C-Obs 11). November 2009.

5.  Babay ZA, Al-Nuaim LA, Addar MH, Abdulkarim AA. 2000. Undiagnosed term breech: Management and outcome. Saudi Medical Journal, 21(5):478–481.

6.  Usta IM, Nassar AH, Khabbaz AY, Abu Musa AA. 2003. Undiagnosed term breech: Impact on mode of delivery and neonatal outcome. Acta Obstetricia et Gynecologica Scandinavia, 82:841–844.

7.  Nwosu EC, Walkinshaw S, Chia P, Manasse PR, Atlay RD. 1993. Undiagnosed breech. British Journal of Obstetrics and Gynaecology, 100:531–535.

8.  Walker S. Undiagnosed breech: Towards a woman-centred approach. 2013. British Journal of Midwifery, 21(5):316–322.

9.  Hemelaar J, Lim LN, Impey LW. 2015. The impact of an ECV service is limited by antenatal breech detection: A retrospective cohort study. Birth, 42(2):165–172.

10.  Nassar N, Roberts CL, Cameron CA, Olive EC. 2006. Diagnostic accuracy of clinical examination for detection of non-cephalic presentation in late pregnancy: Cross sectional analytic study. BMJ, 333:578–580.

11.  Bricker L, Medley N, Pratt JJ. 2015. Routine ultrasound in late pregnancy (after 24 weeks’ gestation). Cochrane Database of Systematic Reviews, (6). Art. No.: CD001451. doi:10.1002/14651858.CD001451.pub4.

12.  Sharp J. 1999. The Midwives Book: Or the Whole Art of Midwifry Discovered (ed. J Hobby). New York: Oxford University Press.

13.  Allison J. 1996. Delivered at Home. London: Chapman and Hall.

14.  Wright RC. 1959. Reduction of perinatal mortality and morbidity in breech delivery through routine use of cesarean section. Obstetrics and Gynecology, 14:758–763.

15.  Steen M. 2008. Vaginal or caesarean delivery? How research has turned breech birth around. Evidence Based Midwifery, 6(3):95–99.

16.  Hannah ME, Hannah WJ, Hewson SA, Hodnett ED, Saigal S, Willan AR. 2000. Planned caesarean section versus planned vaginal birth for breech presentation at term: A randomised multicentre trial: Term breech trial collaborative group. Lancet, 21:1375–1383.

17.  Glezerman M. 2006. Five years to the term breech trial: The rise and fall of a randomized controlled trial. American Journal of Obstetrics and Gynecology, 194(1):20–25.

18.  Deans CL, Penn Z. 2008. The case for and against vaginal breech delivery. Obstetrician and Gynaecologist, 10:139–144.

19.  Lawson GW. 2012. The term breech trial ten years on: Primum non nocere? Birth, 39:3–9.

20.  Marshall JE. 2010. Facilitating vaginal breech birth at term. In: Marshall JE, Raynor MD (Eds.). Advancing Skills in Midwifery Practice. Edinburgh: Elsevier, pp. 89–102.

21.  Dresner-Barnes H, Bodle J. 2014. Vaginal breech birth: The phoenix arising from the ashes. Practising Midwife, 17(8):30–33.

22.  Walker S. 2012. Breech birth: An unusual normal. Practising Midwife, 15(3):18–21.

23.  Evans J. 2012. Understanding physiological breech birth. Essentially MIDIRS, 3(2):17–21.

24.  Sanders R, Steele D. 2015. Re-engaging with vaginal breech birth: A philosophical discussion. British Journal of Midwifery, 22(5):326–331.

25.  Mattila M, Rautkorpi J, Heikkinen T. 2015. Pregnancy outcomes in breech presentation analyzed according to intended mode of delivery. Acta Obstetricia et Gynecologica Scandinavica, 94(10):1102–1104. doi:10.1111/aogs.12703.

26.  Nursing and Midwifery Council (NMC). 2009. Standards for Pre-Registration Midwifery Education. London: NMC.

27.  Cammu H, Dony N, Martens G. et al. 2014. Common determinants of breech presentation at birth in singletons: A population-based study. European Journal of Obstetrics and Gynecology and Reproductive Biology, 177:106–109.

28.  Penn Z. 2011. Breech presentation. In: James D, Weiner C, Steer P. et al. (Eds.). High Risk Pregnancy: Management Options. 4th ed. Philadelphia: Elsevier Saunders, pp. 1101–1122.

29.  Hofmeyr GJ. 2000. Breech presentation and abnormal fetal lie in late pregnancy. In: Enkin M, Keirse MJNC, Neilson J. et al. (Eds.). A Guide to Effective Care in Pregnancy and Childbirth. New York: Oxford University Press, pp. 185–195.

30.  Vendittelli F, Rivière O, Crenn-Hébert C. et al. 2008. Is a breech presentation at term more frequent in women with a history of cesarean delivery? American Journal of Obstetrics and Gynecology, 198:521.e1–521.e6.

31.  Nordveit TI, Melve KK, Albrechtsen S, Skjaerven R. 2008. Maternal and paternal contribution to intergenerational recurrence of breech delivery: A population based cohort study. British Medical Journal, 336(7649):872–876.

32.  Carlisle, N. 2012. An undiagnosed breech. RCM Student Life E-Newsletter. [online] Available at https://www.rcm.org.uk/content/an-undiagnosed-breech (accessed August 19, 2015).

33.  National Institute for Health and Care Excellence (NICE). 2008. National Collaborating Centre for Women’s and Children’s Health. Antenatal Care: Routine Care for the Healthy Pregnant Woman (Clinical guideline, no. 62). London: NICE.

34.  Leung VKT, Suen SSH, Sahota DS. et al. 2012. External cephalic version does not increase the risk of intra-uterine death: A 17-year experience and literature review. Journal of Maternal-Fetal and Neonatal Medicine, 25(9):1774–1778.

35.  Society of Obstetricians and Gynaecologists of Canada (SOGC). 2007. ALARM International Program Manual. 4th ed. Ottawa: Society of Obstetricians and Gynaecologists of Canada. Chapter 12: Vaginal Breech Delivery. Available at https://www.glowm.com/pdf/AIP%20Chap12%20Vaginal%20Breech.pdf (accessed July 21, 2015).

36.  CESDI. 2000. Confidential Enquiry into Stillbirths and Deaths in Infancy, 7th Annual Report. London: Maternal and Child Health Research Consortium.

37.  Royal College of Obstetricians and Gynaecologists (RCOG). 2006. External Cephalic Version and Reducing the Incidence of Breech Presentation. London: RCOG.

38.  Royal College of Obstetricians and Gynaecologists (RCOG). 2001. The Management of Breech Presentation. RCOG Green-Top Guidelines, No. 20b. London: RCOG.

39.  Patterson-Brown S, Howell C. 2014. Breech delivery and external cephalic version. In: Patterson-Brown S, Howell C. (Eds.). Managing Obstetric Emergencies and Trauma: The MOET Course Manual. Cambridge: Cambridge University Press, pp. 395–410.

40.  Koh LM, Mumdzjans A, Pradhan A. 2014. Survey of external cephalic version services in the East of England region: Comparison of services in 2007 and 2012. Journal of Obstetrics and Gynaecology, 9:1–3.

41.  Beuckens A, Rijnders M, Verburgt-Doeleman GHM. et al. 2016. An observational study of the success and complications of 2546 external cephalic versions in low-risk pregnant women performed by trained midwives [online version, February 2, 2015]. BJOG: An International Journal of Obstetrics and Gynaecology, 123(3):415–423.

42.  McCormick C, Cairns A. 2010. Reducing unnecessary caesarean section by external cephalic version. In: Marshall JE, Raynor MD (Eds.). Advancing Skills in Midwifery Practice. Edinburgh: Elsevier, pp. 47–55.

43.  Ben-Meir A, Erez Y, Sela HY. et al. 2008. Prognostic parameters for successful external cephalic version. Journal of Maternal-Fetal and Neonatal Medicine, 21(9):660–662.

44.  Burgos J, Melchor JC, Pijoan JI. et al. 2011. A prospective study of the factors associated with the success rate of external cephalic version for breech presentation at term. International Journal of Gynecology and Obstetrics, 112(1):48–51.

45.  Salzer L, Nagar R, Melamed N. et al. 2015. Predictors of successful external cephalic version and assessment of success for vaginal delivery. Journal of Maternal-Fetal and Neonatal Medicine, 28(1):49–54.

46.  Simm A. 2007. Fetal malpresentation. Obstetrics, Gynaecology and Reproductive Medicine, 17(10):283–288.

47.  Burgos J, Cobos P, Rodriguez L. et al. 2013. Is external cephalic version at term contraindicated in previous caesarean section? A prospective comparative cohort study. BJOG: An International Journal of Obstetrics and Gynaecology, 121(2):230–235.

48.  Burgos J, Cobos P, Rodriguez L. et al. 2011. External cephalic version: A review of the evidence. Current Women’s Health Reviews, 7(4):405–415.

49.  Cohain JS. 2007. Turning breech babies after 34 weeks: A review. MIDIRS Midwifery Digest, 17(3):373–375.

50.  Walker S, Perilakalathil P, Moore J. et al. 2015. Standards for midwife practitioners of external cephalic version: A Delphi study. Midwifery, 31(5):e79–e86.

51.  Vlemmix F, Kuitert M, Bais J. et al. 2013. Patient’s willingness to opt for external cephalic version. Journal of Psychosomatic Obstetrics and Gynecology, 34(1):15–21.

52.  Burgos J, Cobos P, Osuna C. et al. 2013. Nitrous oxide for analgesia in external cephalic version at term: Prospective comparative study. Journal of Perinatal Medicine, 41(6):719–723.

53.  Cardini F. 2005. A moxibustion story. Moxibustion for breech: Results of study on transferability of treatment to the context of some Western hospitals. MIDIRS Midwifery Digest, 15(2):S12–S16.

54.  Cardini F, Weixin H. 1998. Moxibustion for correction of breech presentation: A randomised controlled trail. Journal of the American Medical Association, 280(18):1580–1584.

55.  Coulon C, Poleszczuk M, Paty-Montaigne M-H, Gascard C, Gay C, Houfflin-Debarge V, Subtil D. 2014. Version of breech fetuses by moxibustion with acupuncture: A randomized controlled trial. Obstetrics and Gynecology, 124(1):32–39. doi:10.1097/AOG.0000000000000303.

56.  Manyande A, Grabowska C. 2008. Factors affecting the success of moxibustion in the management of a breech presentation as a preliminary treatment to external cephalic version. Midwifery, 25(6):774–780.

57.  Coyle ME, Smith CA, Peat B. 2012. Cephalic version by moxibustion for breech presentation. Cochrane Database of Systematic Reviews, (5). Art. No.: CD003928. doi:10.1002/14651858.CD003928.pub3.

58.  Weston M, Grabowska C. 2012. Moxibustion to turn the breech. Pract Midwife, 15(8):S3–S4.

59.  Tiran D. 2010. Complementary therapies in midwifery: A focus on moxibustion for breech presentation. In: Marshall JE, Raynor MD (Eds.). Advancing Skills in Midwifery Practice. Edinburgh: Elsevier, pp. 19–28.

60.  Tiran D. 2004. Breech presentation: Increasing maternal choice. Complementary Therapies in Nursing and Midwifery, 10:233–238.

61.  Founds SA. 2005. Maternal posture for cephalic version of breech presentation: A review of the evidence. Birth, 32(2):137–144.

62.  Hofmeyr GJ, Kulier R. 2012. Cephalic version by postural management for breech presentation. Cochrane Database of Systematic Reviews, (10). Art. No.: CD000051. doi:10.1002/14651858. CD000051.pub2.

63.  Kariminia A, Chamberlain ME, Keogh J. et al. 2004. Randomised controlled trial of effect of hands and knees posturing on incidence of occiput posterior position at birth. BMJ, 328(7438):490–493.

64.  Walmsley K. 2000. Managing the OP labour. MIDIRS Midwifery Digest, 10:61–62.

65.  Meehan H, Crowther S. 2015. Managing breech presentation in the absence of obstetric and paediatric support. In: Bates K, Crozier K (Eds.). Managing Childbirth Emergencies in the Community and Low-Tech Settings. 2nd ed. Basingstoke: Palgrave Macmillan, pp. 140–162.

66.  Banks M. 1998. Breech Birth Woman-Wise. Hamilton, New Zealand: Birthspirit.

67.  Cronk M. 1998. Midwives and breech births. Practising Midwife, 1(7/8):44–45.

68.  Reed B. 2003. A disappearing art: Vaginal breech birth. Practicing Midwife, 69:16–18.

69.  Burvill S. 2005. Managing breech presentation in the absence of obstetric assistance. In: Woodward V, Bates K, Young N (Eds.). Managing Childbirth Emergencies in Community Settings. Basingstoke: Palgrave Macmillan, pp. 111–139.

70.  Lewis P. 2012. Malpositions and malpresentations. In: Macdonald S, Magill-Cuerden J (Eds.). Mayes Midwifery. 14th ed. London: Elsevier.

71.  Jonsdottir F, Henriksen L, Secher NJ. et al. 2015. Does internal podalic version of the non-vertex second twin still have a place in obstetrics? A Danish national retrospective cohort study. Acta Obstetricia et Gynecologica Scandinavica, 94(1):59–64.

72.  Webster SNE, Loughney AD. 2011. Internal podalic version with breech extraction. Obstetrician and Gynaecologist, 13:7–14.

73.  Goffinet F, Carayol M, Foidart JM. et al. 2006. Is planned vaginal delivery for breech presentation at term still an option? Results of an observational prospective survey in France and Belgium. AJOG: American Journal of Obstetrics and Gynecology, 194(4):1002–1011.

74.  Royal College of Obstetricians and Gynaecologists (RCOG). 2014. Umbilical Cord Prolapse. Green-Top Guideline No. 50. London: RCOG.

75.  Talaulikar VS, Arulkumaran S. 2012. Malpositions and malpresentation of the fetal head. Obstetrics, Gynaecology and Reproductive Medicine, 22(6):155–161.

76.  Arya R, Whitworth M, Johnston TA. 2007. Abnormal labour: An evidence-based approach. Obstetrics, Gynaecology and Reproductive Medicine, 17(7):217–221.

77.  Gardberg M, Leonova Y, Laakkonen E. 2011. Malpresentations – Impact on mode of delivery. Acta Obstetricia et Gynecologica Scandinavica, 90(5):540–542.

78.  Eskandar O, Shet D. 2009. Risk factors for 3rd and 4th degree perineal tear. Journal of Obstetrics and Gynaecology, 29(2):119–122.

79.  Gardberg M, Stenwall O, Laakkonen E. 2004. Recurrent persistent occipitoposterior position in subsequent deliveries. BJOG: An International Journal of Obstetrics and Gynaecology, 111(2):170–171.

80.  Gardberg M, Laakkonen ES, Levaara M. 1998. Intrapartum sonography and persistent occipitoposterior position: A study of 408 deliveries. Obstetrics and Gynecology, 91(5/1):746–749.

81.  Sutton J. 2000. Occipito-posterior positioning and some ideas about how to change it. Practising Midwife, 3(6):20–22.

82.  Simkin P. 2010. The fetal occiput posterior position: State of the science and a new perspective. Birth, 37(1):61–71.

83.  Warren C. 2012. Helping or hindering occipito-posterior babies. Essentially MIDIRS, 3(5):17–22.

84.  Benavides L, Wu JM, Hundley AF. 2005. The impact of occiput posterior fetal head position on the risk of anal sphincter injury in forceps-assisted vaginal deliveries. American Journal of Obstetrics and Gynecology, 192(5):1702–1706.

85.  Wu JM, Williams KS, Hundley AF. 2005. Occiput posterior fetal head position increases the risk of anal sphincter injury in vacuum-assisted deliveries. American Journal of Obstetrics and Gynecology, 193(2):525–529.

86.  Hunter S, Hofmeyr GJ, Kulier R. 2007. Hands and knees posture in late pregnancy or labour for fetal malposition (lateral or posterior). Cochrane Database of Systematic Reviews, (4). Art. No.: CD001063. doi:10.1002/14651858.CD001063.pub3.

87.  Stremler R, Hodnett E, Petryshen P, Weston J, Willan A. 2005. Randomised controlled trial of hands-and-knees positioning for women labouring with a fetus in the occipitoposterior position in labour. Birth, 32(4):243–251.

88.  The Royal College of Midwives (RCM). 2012. Evidence Based Guidelines for Midwifery-Led Care in Labour: Persistant Lateral and Posterior Fetal Positions at the Onset of Labour. London: RCM Trust.

89.  Bhal PS, Davies NJ, Chung T. 1998. A population study of face and brow presentations. Journal of Obstetrics and Gynaecology, 18(3):231–235.

90.  Tapisiz OL, Aytan H, Altinbas SK. et al. 2014. Face presentation at term: A forgotten issue. Journal of Obstetrics and Gynaecology Research, 40(6):1573–1577.

7

Cord prolapse

ALISON MEINEL

Introduction

Risk factors and clinical issues

Diagnosis and outcomes

Management

Professional considerations

Summary of midwifery responsibilities

References

INTRODUCTION

Cord prolapse is defined once the membranes have ruptured and the cord lies in front of the presenting part (Figure 7.1). A loop of umbilical cord may descend through the cervix, either contained within the vagina (occult) or to become visible at the vulva (overt). Cord presentation is when any part of the cord lies in front of the presenting part within intact membranes. An occult presentation/prolapse can also mean the cord is lying alongside the presenting part but is not palpable on vaginal examination.1,2 The term funic is sometimes used within literature as this describes an origin from the umbilical cord.

Since the 1940s the incidence of cord prolapse in the United Kingdom has decreased from 6.4/1000 live births to 1.7/1000 live births.³ Suggestions for the reduction in incidence relate to changes in obstetric practices around breech birth and less multiparity in general. Societal changes are evident – for example due to lower parity in general, women are less likely to have an unstable lie. Better access to antenatal care hopefully leads to greater detection of an abnormal lie and women who are known to have a non-cephalic presentation in the later stages of pregnancy are more likely to have this confirmed on ultrasound scan as well as by palpation. Practices around obstetric advice for women whose babies are breech have changed dramatically in the last few decades. The Royal College of Obstetricians and Gynaecologists (RCOG) guidelines now recommend external cephalic version, and if this is unsuccessful, an elective caesarian section for all breech presentations at term.4,5 See Chapter 6 for a further discussion concerning breech presentation.

Current expectations are that babies of lower gestations are expected to have better outcomes than in previous years, and in addition those babies who formerly would not have survived now do, therefore care must reflect this, with antenatal admission a common response when any risk is identified.6,7 If an unstable lie is detected, women are advised to remain an inpatient or have greater access to outpatient services and be managed expectantly at home,⁸ which will optimise care if a cord prolapse does occur.

RISK FACTORS AND CLINICAL ISSUES

Risk factors

There are recognised risk factors for cord presentation and cord prolapse – most associated with malpresentation, smaller babies and multiparous women (see Box 7.1). If there is room for the cord to slip in front of the presenting part, there is the risk of a cord presentation or prolapse. Women who present with transverse/oblique or unstable lie or a footling breech presentation after 37 + 0 weeks of pregnancy are usually offered admission to an antenatal ward within an obstetric led unit that can accommodate an emergency caesarean section should the need arise. Any labour or SROM when the baby is an abnormal lie is an indication for urgent referral and probably emergency caesarean section.⁸

Figure 7.1  Umbilical cord prolapse.

Around half of all reported cases of cord prolapse have occurred after an intervention.⁹ Women who opt for external cephalic version of a breech presentation should be informed of all associated risks (see Chapter 6) and the midwife prepared for a cord prolapse, providing the appropriate environment accordingly.¹⁰ Induction of labour itself is cited as a possible risk factor; however, whether this is related to artificial rupture of membranes specifically is disputed.4,6,11

Clinical issues

When discussing place of birth with women, and providing them with information with which to make a decision, the position of the baby is one area of discussion during a risk assessment. If the woman is considering or requesting support to birth at home or in a midwife-led birth centre, she should be informed that the position of her baby will be an issue for further discussion should the lie of her baby become unstable, transverse and/or oblique, or a breech presentation (see Chapter 6 for further discussion of breech presentation).

BOX 7.1: Risk factors for cord prolapse⁸

MATERNAL

•  Multiparity

•  Polyhydramnios

•  Low-lying placenta

•  Unengaged presenting part

FETAL

•  Prematurity <37/40

•  Low birth weight <2.5 kg

•  Fetal congenital abnormalities

PROCEDURAL

•  Artificial rupture of membranes with high presenting part

•  External cephalic version

•  Vaginal manipulation of fetus with ruptured membranes

•  Internal podalic version

•  Stabilising lie: induction of labour

Before performing a vaginal examination (VE), if during the preliminary abdominal palpation the midwife finds any mobility of the presenting part, she should consider whether a VE could initiate a cord prolapse. Any high head should alert the midwife to inform other members of the team, ensuring the ability to respond in case an inadvertent rupture of membranes (ROM) during the VE causes a cord prolapse during the procedure.

It is normal midwifery practice to assess fetal well-being after spontaneous rupture of membranes (SROM). It is also pertinent to consider the merits of performing a VE in all women known to have a non-engaged presenting part as, if the head remains high, there may be a cord prolapse without immediate compromise to the fetal condition.

DIAGNOSIS AND OUTCOMES

During auscultation or cardiotocograph (CTG) monitoring, any instances of fetal heart abnormality should be suspected as having an origin in malpresentation of the cord.

Cord presentation is diagnosed on vaginal examination when the cord is felt behind intact membranes. It can also sometimes be seen on ultrasound.

Cord prolapse is diagnosed either visually by observing loops of cord at the vagina or during a vaginal examination when cord can be felt in front of or beside the presenting part.

Once the position of the cord becomes compromised, and especially when out of the vagina, the fetal blood supply is obstructed. This is either because of the drop in temperature and spasm of the vessels, or compression between the bony pelvis and the presenting part, therefore the amount of time from prolapse to birth determines the level of injury to the baby. This starts as fetal hypoxia, in varying degrees, and if delivery is not imminent may be followed by fetal or neonatal death. However, less than 3% of babies suffering from a prolapsed cord will die if birth is expedited.¹² The condition of the baby at the moment of prolapse and subsequent asphyxia is predicative of outcome, therefore low birth weight premature babies and those suffering anomalies are likely to have less successful outcomes.¹³ Outcomes for the baby do depend on where the mother is when the prolapse takes place and availability of an obstetric theatre and relevant staff.

Cord prolapse, although potentially fatal for the baby, is not associated with increased morbidity for the mother providing due care and attention is paid to preparing her for emergency surgery. Despite the extremely rapid delivery needed by the fetus, the maternal physical and psychological risks are that of an emergency caesarean and potential psychological disturbance.¹⁴

MANAGEMENT

See Table 7.1 for a summary.

Regardless of location, whether in hospital or in a community setting, if a cord presentation or prolapse is suspected or diagnosed, assistance must be called and pressure from the cord relieved. In hospital this would usually necessitate an emergency response – or crash call – in order to mobilise the necessary staff to potentially facilitate an emergency caesarean delivery. In a community situation, during either a planned or unplanned home birth, this is an emergency situation. The midwife should provide immediate support measures as detailed below and instruct the woman, her birth partner or any other person present to call emergency services (dial 999 in the UK) for an immediate transfer to hospital. The instructions to the operator must be clear and concise. Local policies and procedures may prescribe the wording for such emergencies.

Current evidence does not recommend attempting to replace the cord or wrapping warm swabs around the prolapsed cord; in fact these procedures may delay delivery.15–17 However, although evidence is insufficient to support this practice, midwives in an emergency situation outside of an obstetric unit will utilise every skill available to them and gentle replacement of the cord to within the vagina while awaiting the emergency services may help to keep it warm and viable. However, it must be remembered that handling may also cause the cord to spasm, and extreme care must be paramount.

Procedures must not inflict any time delay towards delivery – if the cord has prolapsed, the aim is delivery:

1.  To alleviate cord compression the presenting part is elevated – In the first instance use fingers to push the head away from the cord then, if a delay before delivery is anticipated, fill the bladder (see Box 7.2). In hospital, it would be pertinent to call for help then digitally elevate the presenting part while others assist. At home, once assistance has been called, the bladder can be filled and/or digital manipulation continued.

2.  Maternal position – Either knee-chest position (Figure 7.2) or exaggerated Sims (Figure 7.3) until birth is imminent. If transferring from home to hospital the knee-chest position is not safe in an ambulance; therefore the midwife should change the woman to exaggerated Sims while maintaining pressure off the cord, either with digital elevation or with the bladder still full. In a hospital, the woman is usually transferred to the operating theatre on her bed – the midwife can sit on the bed maintaining elevation of the fetal head during the transfer.

Table 7.1  Management: Hospital and home

BOX 7.2: Filling the bladder following a cord prolapse

To fill the bladder, a Foley urinary catheter is sited and 500–750 mL of sterile saline solution is inserted and the tubing is then clamped. With the clamp still in place, drainage tubing and a drainage bag are attached ready for the clamp to be removed when the caesarean section commences.¹³ If available, an IV/blood giving set can be inserted into the catheter to expedite filling.¹⁸ There is controversy concerning whether it is necessary to digitally displace the presenting part once the bladder has been filled as this has not been proven to improve neonatal outcomes.¹⁸

Catheterisation and other necessary equipment must be available at a planned home birth.

Figure 7.2  Knee-chest position.

3.  Ensure patent IV access.

4.  Provide facial oxygen if available at 8 L/min.

5.  Stop any oxytocin infusion.

6.  A tocolytic may be considered if there is an unavoidable delay and if there is enough assistance available, provided this does not delay the procedures needed to expedite delivery.

In hospital the fetal heart is not usually monitored until after the emergency call for help and transfer to labour ward/theatre, as this could delay delivery. Then auscultation and/or continuous fetal monitoring will display if fetal bradycardia or any pathological heart rate patterns are present which will indicate an immediate caesarean. An emergency caesarean section should be performed with the aim of delivering the baby within 30 minutes or less.⁸

However at home after the initial responses, and while waiting for the emergency services and during transfer from home to hospital, the midwife should endeavour to continue to monitor the fetal heart. If heart rate abnormalities occur it may be pertinent to alter maternal position and/or management. If digital displacement has moved the presenting part above the pelvic brim, a midwife may consider continuous suprapubic pressure upwards.¹⁹ Midwives should always put the women at the centre of care, and therefore they will decide on an individual basis if they feel the extra manipulations would be of benefit in the context.

Figure 7.3  Exaggerated Sims position.

Mode of delivery

When at home or in a midwifery-led birth centre, if the woman’s cervix is fully dilated the midwife must make a judgement as to whether the baby can be delivered quickly vaginally (by maternal effort and perhaps with the aid of an episiotomy) or whether the insult to the baby would be better alleviated by undertaking the measures described previously and transfer to obstetric care. Regardless of her decision, emergency help must be called for, as even after a successful vaginal delivery, the baby will likely need resuscitation.

In hospital, assessment of fetal viability will determine the course of action.

Once fetal viability has been confirmed, the stage of labour needs to be established. If the cervix is fully dilated it may be possible to expedite delivery either with maternal effort (more likely if multiparous), ventouse or forceps if the head is fully engaged and the requirements for instrumental delivery are met. If vaginal delivery is not likely to be swift, then early resort to caesarean section is necessary.

If the woman’s cervix is not fully dilated and no CTG abnormalities are detected, continuous electronic fetal monitoring should be maintained and preparation for surgery instigated. The speed of this preparation will be defined by the fetal condition, with the emphasis on minimising any insult and long-term effects for the baby. Women should provide verbal consent and the bladder must be emptied prior to incision. At all times, communication is paramount to inform the woman and her birth companions of events.

If there is any fetal heart activity then emergency procedures must be followed to expedite delivery. If an ultrasound scan confirms no heartbeat is present then the sequence of events is not an emergency situation.

Prognosis for the baby is generally very good if accessibility to a fully staffed obstetric theatre is available. Outcomes for the baby when prolapse occurs outside of hospital or in a lower resourced setting are less predictable. Perinatal mortality is increased by more than 10-fold when cord prolapse occurs outside hospital when compared to inside.2,20,21 The length of time to delivery – with the emergency procedures described in place – appears to predict outcomes. If more than 30 minutes pass from prolapse until delivery then the outcomes for the baby are less favourable (Table 7.2).²²

Table 7.2  Management flowchart

Consider

Assess risk – Malpresentation, high presenting part

At every VE in labour

At every fetal heart rate anomaly, particularly after SROM

After SROM with risk factors

Call for help

At home: Emergency services (999 in United Kingdom)

In hospital: Emergency crash call

Relieve

Pressure from cord:

  Maternal position

  Digital displacement

  Full bladder

Birth

Emergency transfer

By quickest means

PROFESSIONAL CONSIDERATIONS

As with all obstetric emergencies, actions must be accompanied by communication with the woman and her birth partners. Sudden onset changes, such as necessitating emergency management techniques, need to be communicated calmly and sensitively in order to minimise distress and still keep the woman informed.

It is vital to document a clear chain of events, not only to provide evidence for peer reflection and risk management review, but to provide the family with a transparent review of the care they have received. Some hospital Trusts have developed a proforma with which to document the chain of events, and if not, then usual midwifery standards apply. As discussed in Chapter 1, documentation should be clear, concise, factual and as contemporaneous as possible.23,24

In order to improve practice it is necessary to reflect on what has worked well and what needs improvement. In a review of a multidisciplinary team working in responding to obstetric emergencies, it is evident that the ability to communicate events relies not only on the documentation, but on the ability of all members of the multidisciplinary team to function effectively.25,26 Simulation training for cord prolapse is often omitted from multidisciplinary team training, despite large amounts of evidence that it should be included alongside other obstetric emergencies.²⁷ It possibly is dependent on whether midwives or doctors are responsible for delivering the programme, as midwives report more than doctors that training improves their practice.²⁵

Each Trust or organisation will have its own procedures to report such incidents for further investigation, either a clinical incident form or other. A midwife involved in the case should liaise with the team to ensure this has been completed.

The ongoing care that midwives provide must revolve around sensitively debriefing women and communicating events to them, as described in Chapter 14.

SUMMARY OF MIDWIFERY RESPONSIBILITIES

•  Call for help

•  In hospital use the ‘crash call system’ – The senior midwife, senior obstetric team, anaesthetic team and neonatologists – are needed. An emergency caesarean section is the most likely outcome.

•  In a home/community environment – Stay with the woman and get someone else to call the emergency services (dial 999 in the UK); immediate transfer to the nearest obstetric unit will most likely be needed. If the woman is delivering, then paramedics may be helpful for neonatal resuscitation as well as subsequent transfer.

•  Management procedures

•  Maternal – Reposition to relieve cord compression, and relieve pressure on cord digitally, consider filling the bladder.

•  Fetal – Auscultate the fetal heart, ensuring maternal heart rate is differentiated, when above actions are in place but do not delay transfer to operating theatre.

•  Communicate: With the woman and her birth companions.

•  Document: Use a proforma if available, if not ensure a concise, streamlined and factual chain of events.

•  Reflect: With peers and/or the Supervisor of Midwives.

•  Risk management: Explore any risk factors that were present. Any multidisciplinary team training issues following emergency procedures should be identified. Complete the incident report for Trust or organisation for clinical governance purposes.

•  Debrief: Offer the woman and any birth companions who were present the opportunity to discuss and debrief.

REFERENCES

1.  Arulkumaran S. 2013. Management of Labour. In: Symonds I, Arulkumaran S, Symonds EM [Emeritus Ed.] (Eds.). Essential Obstetrics and Gynaecology. 5th ed. Edinburgh: Churchill Livingstone Elsevier.

2.  Murphy DJ, MacKenzie IZ. 1995. The mortality and morbidity associated with umbilical cord prolapse. British Journal of Obstetrics and Gynaecology, 102(10):826–830.

3.  Gibbons C, O’Herlihy C, Murphy JF. 2014. Umbilical cord prolapse – Changing patterns and improved outcomes: A retrospective cohort study. BJOG: An International Journal of Obstetrics and Gynaecology, 121(13):1705–1708.

4.  Boyle JJ, Katz VL. 2005. Umbilical cord prolapse in current obstetric practice. Journal of Reproductive Medicine, 50(5):303–306.

5.  Hofmeyr GJ Prof, Impey, LWM, on behalf of the Royal College of Obstetricians and Gynaecologists (RCOG). 2006. The Management of Breech Presentation. Green-Top Guideline 20b. London: RCOG. Available at http://www.rcog.org.uk (accessed October 1, 2015).

6.  Obeidat N, Zayed F, Alchalabi H. 2010. Umbilical cord prolapse: A 10-year retrospective study in two civil hospitals, North Jordan. Journal of Obstetrics and Gynaecology, 30(3):257–260.

7.  Phelan JP, Boucher M, Mueller E, McCart D, Horenstein J, Clark SL. 1986. The nonlabouring transverse lie. A management dilemma. Journal of Reproductive Medicine, 31:184–186.

8.  Chebsey CS, Bristol BS, Fox R, Draycott TJ, Siassakos D, Winter C, on behalf of the Royal College of Obstetricians and Gynaecologists (RCOG). 2014. Umbilical Cord Prolapse. Green-Top Guideline No. 50. Available at http://www.rcog.uk (accessed October 1, 2015).

9.  Cohain, JS. 2013. Amniotomy and cord prolapse. Midwifery Today, Winter (108):32–33.

10.  Usta IM, Mercer BM, Sibai BM. 1999. Current obstetrical practice and umbilical cord prolapse. American Journal of Perinatology, 16:479–484.

11.  Silver RM. 2014. Umbilical Cord Prolapse – Progress! British Journal of Obstetrics and Gynaecology, 121(13):1709.

12.  Hamilton-Fairley D. 2009. Lecture Notes: Obstetrics and Gynaecology. 3rd ed. Oxford: Wiley-Blackwell.

13.  Paterson-Brown S, Howell C. 2014. The MOET Course Manual: Managing Obstetric Emergencies and Trauma. 3rd ed. Cambridge: Cambridge University Press.

14.  Hanretty KP. 2003. Obstetrics Illustrated. 6th ed. Edinburgh: Churchill Livingstone.

15.  Advanced Life Support in Obstetrics (ALSO). 2012. American Academy of Family Physicians (AAFP) Advanced Life Support in Obstetrics (ALSO) Instructor Manual. 5th ed. Washington, DC: AAFP.

16.  Barrett JM. 1991. Funic reduction for the management of umbilical cord prolapse. American Journal of Obstetrics and Gynaecology, 165:654–657.

17.  Cox C, Grady K, Howell C (Eds.). 2006. Managing Obstetrics Emergency and Trauma, The MOET Course Manual. London: RCOG Press.

18.  Bord I, Gemer O, Anteby EY, Shenhav S. 2011. The value of bladder filling in addition to manual elevation of the presenting fetal part in cases of cord prolapse. Archives of Gynecology and Obstetrics, 283:989–991.

19.  World Health Organisation (WHO), United Nations Population Fund (UNFPA), UNICEF, World Bank. 2007. Managing Complications in Pregnancy and Childbirth: A Guide for Midwives and Doctors, WHO, Geneva: WHO.

20.  Enakpene CA, Odukogbe AT, Morhason-Bello IO, Omigbodun AO, Arowojulu AO. 2010. The influence of health seeking behaviour on the incidence and perinatal outcomes of umbilical cord prolapse in Nigeria. International Journal of Women’s Health, 2:177–182.

21.  Koonings PP, Paul RH, Campbell K. 1990. Umbilical cord prolapse. A contemporary look. Journal of Reproductive Medicine, 35:690–692.

22.  Wassawa EW, Nakubulwa S, Mutyaba T. 2014. Fetal demise and associated risk factors following umbilical cord prolapse in Mulago hospital, Uganda: A retrospective study. Reproductive Health, 11(1):12.

23.  Nursing and Midwifery Council (NMC). 2013. Nursing and Midwifery Council (Midwives) Rules and Standards 2012. [Online]. Available at http://www.nmc-uk.org (accessed February 20, 2015).

24.  Nursing and Midwifery Council (NMC). 2015. Midwives Rules and Standards – The Revised Code [Online] effective March 31, 2015. Published January 29, 2015. Available at http://www.nmc-uk.org (accessed January 10, 2015).

25.  Calvert KL, McGurgan PM, Debenham EM. 2013. Emergency obstetric simulation training: How do we know where we are going, if we don’t know where we have been? Australian and New Zealand Journal of Obstetrics and Gynaecology, 53(6):509–551.

26.  Rogers C, Schiavone N. 2008. Cord prolapse audit: Recognition, management and outcome. British Journal of Midwifery, 16(5):315–318.

27.  Chebsey C, Siassakos D, Draycott T. 2012. A review of umbilical cord prolapse and the influence of training on management. Fetal and Maternal Medicine Review, 23(2):120–130.

8

Shoulder dystocia

JUDITH ROBBINS

Introduction

Predisposing and risk factors

Potential complications: Fetus/neonate and mother

Issues around management of shoulder dystocia

Professional considerations

Summary of midwifery responsibilities

References

INTRODUCTION

Shoulder dystocia is a largely unpredictable obstetric event with the potential for severe infant and maternal complications, both of which may be exacerbated by inappropriate management. The consequences for those involved, whether physical, psychological, emotional or financial – are serious.

Politi et al.¹ describe shoulder dystocia as ‘the nightmare of obstetricians’. Yet as midwives are often the lead clinicians at birth, the same may equally well apply to them. The potential for significant maternal and/or neonatal morbidity in the event of a shoulder dystocia makes this one of the leading causes of obstetric malpractice claims.²

Definition

It is suggested that there are several definitions of shoulder dystocia to be found in the literature and it may be that practitioners use the term in a general sense to describe a range of difficulties encountered with the delivery of the shoulders. This lack of an accepted definition probably accounts for a wide variation in reported incidence. An early definition by Spong et al.³ describes shoulder dystocia in a complex way: as a bony problem, which occurs when the anterior or, less commonly, the posterior, and rarely, both fetal shoulders impact on the maternal symphysis pubis and/or the sacral promontory. However, the Royal College of Obstetricians and Gynaecologists (RCOG)⁴ chose to adopt Resnick’s⁵ more simple definition and state that shoulder dystocia is defined as

vaginal cephalic delivery that requires additional obstetric manoeuvres to deliver the fetus after the head has delivered and gentle traction has failed

A retrospective analysis of risk factors associated with 56 cases of shoulder dystocia identified in a 1-year period by Mahran et al.⁶ found failure by clinicians to apply the clinical diagnostic criteria set down by the RCOG,⁴ which made shoulder dystocia susceptible to overdiagnosis.

Gibb⁷ describes three degrees of shoulder dystocia in order of severity as follows:

•  A tight squeeze of a big baby with the normal mechanism of rotation present

•  Unilateral dystocia where the posterior shoulder has entered the pelvis but the anterior is stuck above the symphysis pubis

•  Bilateral dystocia where both shoulders are arrested above the pelvic brim

With the second two types, downward traction will only further impact the shoulders.

The key diagnostic signs for the midwife are failed external rotation of the fetal head and the visible ‘turtle sign’, whereby the fetal head, after what is usually a prolonged/difficult birth, retracts hard against the perineum. If care is based on the definition proposed by the RCOG,⁴ then any additional manoeuvres that are used to facilitate delivery of the shoulders (including the use of McRoberts position) mean that a shoulder dystocia has occurred.⁸

Incidence

Olugbile and Mascarenhas⁹ state that the incidence of shoulder dystocia is difficult to calculate given the problems in defining it. Evidence suggests that the incidence rate of shoulder dystocia varies between 0.58% and 0.7%⁴ and can result in significant neonatal mortality and morbidity.10,11

A particularly interesting finding from Walsh et al.¹² was that despite increased training in the management of shoulder dystocia and a rising caesarean section rate, the incidence of Erb’s palsy or brachial plexus injuries has remained unchanged when compared with the previous 10 years. This could be due to a rise in the number of shoulder dystocias, which despite improved care, keeps complication rates stable. The rise in maternal obesity and gestational diabetes¹³ particularly in resource-rich areas has increased the potential for cases of shoulder dystocia.

PREDISPOSING AND RISK FACTORS

Baskett and Allen¹⁴ note that antenatal prediction is difficult since 48% of cases occur in normal birth weight babies (less than 4 kg). However, it is recognised that larger babies are at increased risk of shoulder dystocia; therefore, pre-labour risk factors such as maternal diabetes, raised body mass index (BMI), or fetal macrosomia10,15,16 should heighten clinicians’ awareness. Birth weight, by its definition, can only be confirmed at birth. Estimating fetal weight during pregnancy is not an exact science, and is subject to individual clinician’s assessment. The use of third trimester ultrasound scans have at least a 10% margin of error for actual birth weight and detect only 60% of infants weighing over 4500 g. In an overview of three studies examining the incidence of shoulder dystocia, Baxley and Gobbo¹⁰ report that it increases from 5% to 9% among fetuses weighing over 4 kg born to mothers without diabetes and with equal frequency in primigravid and multigravid women, although it is more common in infants born to women with diabetes.¹⁷ Overland et al.¹⁸ demonstrated that the recurrence rate where women have a previous history of shoulder dystocia varies widely following a retrospective cohort study aiming to estimate the relative and absolute risk of shoulder dystocia in the second birth according to a history of shoulder dystocia and the older child’s birth weight. Their study included all women in Norway with two consecutive singleton vaginal births with the fetus in cephalic presentation during the period 1967–2005. They found that in the second delivery, shoulder dystocia occurred in 0.8% of all women. In women with a prior shoulder dystocia delivery the recurrence risk was 7.3%. However, they found that most incidences of shoulder dystocia in the second birth were in women without such history – 96.2%. They found that the elder child’s birth weight was the most important risk factor for shoulder dystocia in the second birth (see Box 8.1).

POTENTIAL COMPLICATIONS: FETUS/NEONATE AND MOTHER

Fetus and neonate adverse outcomes

The major concern during shoulder dystocia is fetal hypoxia, which can result from compression of the neck and central venous congestion, compression of the umbilical cord, or reduction of the placental intervillous flow from prolonged increased intrauterine pressure, combined with secondary fetal bradycardia.

Box 8.2 lists potential fetal/neonate outcomes.

BOX 8.1: Predisposing and risk factors for shoulder dystocia

ANTENATAL

•  Gestational or pre-existing diabetes

•  Obesity (BMI >30)

•  Short stature

•  Abnormal pelvic anatomy

•  Suspected fetal macrosomia

•  Post-dates pregnancy

•  Previous shoulder dystocia

INTRAPARTUM

•  Protracted active phase of first stage of labour

•  Labour augmentation

•  Prolonged second stage of labour

•  Assisted vaginal delivery (forceps or vacuum)

It may be that a combination of risk factors multiply the likelihood of shoulder dystocia and can be predictive in individual cases but identification remains easier with the benefit of hindsight.

Many studies have focused on the importance and relationship between a long head to body delivery interval and low Apgar score.¹⁹ Umbilical cord compression between the fetal body and the maternal pelvis is a potential danger¹⁰ and is associated with an increase in acidosis, hypoxic ischaemic encephalopathy (HIE) and an increase in neonatal morbidity.19,20 While it is logical to suppose that prolonged head-to-shoulder delivery interval thresholds may be associated with permanent central neurologic dysfunction, there is no clear consensus in the clinical literature on the amount of time allowed for the safe resolution of shoulder dystocia as there are no conclusive data available, but there appears to be a very low rate of hypoxic ischaemic injury up to 5 minutes.²⁰ All findings demonstrate that timing is crucial to minimise adverse outcomes, especially long-term neurological damage and potential morbidity or mortality. Ensuring that neonatal support is present at the birth will assist in immediate resuscitative management.

BOX 8.2: Potential fetal/neonate complications

•  Brachial plexus injury

•  Phrenic nerve injury

•  Fracture of the clavicle and/or humerus

•  Neonatal asphyxia with or without permanent neurological damage

•  Fetal or early neonatal death

The litigation costs for shoulder dystocia predominantly relate to brachial plexus injuries.²¹ Brachial plexus injuries are most commonly encountered, occurring in 4%–15% of infants.¹⁰ It has been suggested that brachial plexus injury may occur regardless of the procedure used to dis-impact the shoulder.22,23 Gherman et al.¹⁶ concluded that there has not been a well-designed, population-based study, which allows for the determination of the exact amount of force, which is required to assist in a normal spontaneous vaginal delivery. The RCOG⁴ are clear in their current guidance that axial traction (gentle traction on the baby’s head in line with the fetal spine) should be used instead of ‘traditional’ downward, lateral flexion, although this has been criticised by Melendez et al.²⁴ who feel this could be subject to clinician bias. The important point for midwives to take from this discussion is that during shoulder dystocia, traction needs to be no more than the amount of traction applied during a spontaneous vaginal delivery.

Studies have questioned the accepted supposition that congenital brachial plexus injuries are invariably caused by overzealous neck traction when managing shoulder dystocia, which causes damage to the anterior shoulder or the anterior arm.25,26 However, Gonik and Grimm²⁷ concluded that endogenous forces of labour (maternal pushing and uterine contractions) may contribute substantially to brachial plexus injuries and that up to one-third of all brachial plexus injuries occur in births not associated with a recognised shoulder dystocia. Gherman et al.²⁸ go on to suggest that brachial plexus palsy and bone fracture may arise as a result of the labour process itself or as an intrauterine event. However, Gurewitsch et al.²⁹ found in their retrospective study of 23,273 deliveries over a 10-year period, 135 brachial plexus injuries occurred (5.8 per 1000) and concluded that such injuries were rare without the birth complication of shoulder dystocia. They also found that brachial plexus injuries in neonates whose births were not complicated by shoulder dystocia seemed temporary, whereas more than 90% of permanent brachial plexus injuries were associated with births complicated by shoulder dystocia.

In terms of neurological damage, Erb’s palsy is the result of trauma to the fifth and sixth cervical nerves and manifests with absent biceps and Moro reflex on the affected side. Clinically, there is internal rotation and adduction of the shoulder, an unequal Moro reflex, extension and pronation of the elbow and weak wrist extension or the ‘waiter’s tip’ position.³⁰ Klumpke palsy concerns the lower trunk lesion at the eighth cervical and first thoracic vertebrae, generally affecting the intrinsic muscles of the hand leading to a claw hand, which cannot be closed to make a fist. Horner syndrome may be present on the affected side due to the involvement of the sympathetic fibres that cross the first thoracic vertebra.³¹ Rarely, a severe injury will involve the entire plexus and cause complete paralysis of the arm. Another rare injury concerns the fourth cervical root, which involves trauma to the phrenic nerve and would present with features of respiratory distress with paralysed hemidiaphragm.¹¹

Neonatal clavicular fractures are among the most common injuries associated with shoulder dystocia and may frequently occur in infants weighing less than 4000 g.¹¹

Potential maternal complications

Women who experience shoulder dystocia have an 11% chance of developing a postpartum haemorrhage (PPH) (see Chapter 10) due to the increased risk of uterine atony¹⁰ and there is also an increased risk of third-or fourth-degree tears (3.8%).³² Other consequences include vaginal and cervical lacerations, bladder and uterine rupture and spontaneous symphyseal separation.³³ Women who have experienced traumatic births also report post-traumatic stress disorder and postnatal depression (see Chapter 14), often as a result of the way they were ‘cared’ for, and how they were spoken to.³⁴

BOX 8.3: Potential maternal complications

•  Postpartum haemorrhage

•  Third- or fourth-degree perineal tears (including extended episiotomies)

•  Uterine rupture

•  Bladder damage

•  Symphyseal separation or diathesis, with or without transient femoral neuropathy

•  Rectovaginal fistula

•  Psychosocial effects

See Box 8.3, which lists potential maternal adverse outcomes.

ISSUES AROUND MANAGEMENT OF SHOULDER DYSTOCIA

It is important to acknowledge that Hope et al.³⁵ found that the midwife was the lead professional at 65% of births compromised by shoulder dystocia by the time the body was delivered. MacKenzie et al.³⁶ concurs with this with their review of 514 shoulder dystocia cases, where 264 (51%) were managed by midwives alone. In addition, they emphasised effective management of shoulder dystocia relies on prompt recognition in order to minimise the delay in head-to-body birth interval and is aided by a clear understanding of the mechanism that is causing the dystocia. Staff training in the management of shoulder dystocia has been shown to reduce the incidence of adverse outcomes such as brachial plexus injury.37,38 Buerkle et al.³⁹ conducted a randomised controlled trial with midwives to compare the skills of performing a shoulder dystocia algorithm after hands-on training compared with a demonstration and found that the assessment of technical skills was significantly higher after the hands-on training. However, limitations to the study concluded that performance may be different in real-life situations and training success may only be in part transferable to actual emergencies.

In the United Kingdom, pioneering education in emergency training began in June 1996, with the first Advanced Life Support in Obstetrics (ALSO)⁴⁰ course, which was a systematic, mnemonics-based programme in the management of obstetric emergencies.⁴¹ This gathered momentum, with the mnemonic of ‘HELPERR’ (as shown in Table 8.1) becoming central to shoulder dystocia guidelines in many obstetric units, and rapidly expanding courses for skills and drills training were being introduced to assist in the management of shoulder dystocia.

Table 8.1  The ALSO HELPERR mnemonic⁴⁰

H

Call for Help

E

Evaluate for episiotomy

L

Legs (McRoberts manoeuvre)

P

Suprapubic Pressure

E

Enter-to commence internal manoeuvres

R

Remove the posterior arm

R

Repeat/Roll-onto all fours

The mnemonic was originally recommended and gained popularity because it encouraged clinicians to move away from ineffective, and potentially dangerous, practices such as applying fundal pressure and excessive traction. Fundal pressure is known to increase the risk of maternal morbidity⁴² by causing uterine rupture and severe haemorrhage⁴³ and neonatal morbidity may be increased by the clinician applying excessive traction to the baby’s neck increasing the risk of brachial plexus injury and further impacting the fetal shoulders.⁴⁴

A further advantage of the ALSO approach was the use of the mnemonic as an aide memoir for the provision of systematic care. However, by 2012 the RCOG⁴ identified some common difficulties observed in shoulder dystocia training drills using the ALSO HELPERR mnemonic: namely not calling the neonatologist; failing to state the problem; inability to gain appropriate internal vaginal access; and confusion over the internal manoeuvres.⁴⁵ The latest ALSO courses have incorporated a subsidiary mnemonic, to identify help needed, known as SOAPS (Senior midwives, Obstetricians, Anaesthetist, Paediatricians and Someone to support and scribe).⁴⁶ ALSO’s multiprofessional programmes have directly led to, and stimulated, the development of other similar structured programmes such as PRactical Obstetric Multi-Professional Training (PROMPT) (PROMPT Maternity Foundation³⁷) and Managing Obstetric Emergencies and Trauma (MOET) (Advanced Life Support Group⁴⁷).

The RCOG⁴ recently modified their guideline, departing from the use of the ALSO mnemonic and instead recommending the use of an algorithm detailing escalating manoeuvres to resolve shoulder dystocia. These are divided into three levels and escalate in both the skill required by the practitioner and the invasiveness of the manoeuvre for the woman. First-line manoeuvres are initially attempted and only if they are unsuccessful in resolving the shoulder dystocia should the clinician move onto second-and finally third-line manoeuvres. The other change to the ALSO approach is that the midwife should attempt a manoeuvre and if unsuccessful, move on, rather than persisting for 30 seconds.

The PROMPT manual⁴⁸ has become standard practice for many National Health Service (NHS) Trusts in the United Kingdom. It may be important to note that either HELPERR or PROMPT may be applied dependent on the environment and the experience of the clinician. It is usual for each maternity unit to have established a protocol, and it is imperative for all clinicians to be working to the same protocol to provide seamless multi-professional care for the woman.

PROMPT provides the measures to be taken as a step-by-step approach moving from the initial manoeuvres (such as McRoberts and suprapubic pressure) to the more invasive. They essentially require the midwife to undertake the same interventions as HELPERR, they are just presented in a different way. There is no evidence that one intervention is superior to another.³⁷ Although various mnemonics have been used to describe the different manoeuvres taught to manage shoulder dystocia, it should be noted that the manoeuvre of choice will depend on the specific clinical situation, for example; at a home birth ‘all-fours’ may be the first choice, whereas if the woman has a high BMI and may be less mobile with an epidural, in hospital this may not be possible. First-line manoeuvres can be easily implemented by a midwife faced with a shoulder dystocia and are generally very effective but need to be commenced immediately following recognition of this emergency.¹⁰

Calling for help remains a fundamental tenet of the management of any obstetric emergency, however, a recurring theme identified from MBRRACE⁴⁹ in the United Kingdom is the failure of early referral to senior staff, and the need to act on such referrals seriously and promptly. Clearly stating the problem in any obstetric emergency is good practice; therefore the midwife should announce ‘shoulder dystocia’ as help arrives. In addition, the help the midwife is calling for must be appropriate to the situation. For example, a midwife attending a home birth will be aware that her help will be the attendance of the paramedic team who can help with resuscitation and transfer into hospital. In a hospital setting, it is important that the midwife is clear about who she is requesting in attendance; a senior obstetrician and neonatologist at the very least.

Communication with the woman throughout the delivery is paramount, with explanations given during the manoeuvres. Importantly, when shoulder dystocia is recognised she is told clearly to stop pushing⁵⁰ and any oxytocic infusion running should also be stopped immediately.

First-line manoeuvres

First-line manoeuvres commence after alerting others to assist by calling for help (‘H’ in HELPERR mnemonic). Evaluation (‘E’ in the HELPERR mnemonic) for an episiotomy is the second element of the HELPERR mnemonic but the stress is on the evaluation, not the episiotomy (see Box 8.4).

McROBERTS MANOEUVRE

The McRoberts manoeuvre describes the sharp flexion of the maternal thighs against the abdomen to achieve pelvic tilt and straightening of the lumbosacral joint (‘L’ in HELPERR mnemonic). The McRoberts manoeuvre (Figure 8.1) is generally simple to perform, non-invasive and effective as a first response to shoulder dystocia.⁵¹ This will achieve delivery of the shoulders in approximately 90% of cases due to the sliding of the sacral promontory upwards. It allows the rotation of the pelvis and has been suggested to increase the anterior-posterior diameter by flattening the sacral promontory.10,52 However, this is challenged by Gherman et al.,⁵³ who in a statistically significant trial analysed the McRoberts manoeuvre by x-ray pelvimetry on 36 pregnant women and found that it does not change the actual dimension of the maternal pelvis, but that it does straighten the sacrum relative to the lumbar spine and may enable the symphysis pubis to rotate superiorly and slide over the fetal shoulder. Nevertheless, caution is recommended against lengthy and aggressive hyperflexion and abduction of the maternal thighs onto the abdomen⁵⁴ because this situation is often associated with increased traction that may lead to increased risk of brachial plexus injury12,26 and the potential of maternal damage such as a rare case of symphyseal separation and transient femoral neuropathy reported by Gherman et al.⁵⁴

BOX 8.4: Episiotomy

Shoulder dystocia is a ‘bony problem’. It is not a soft tissue problem, and undertaking an episiotomy is usually to give extra space at the introitus for the clinician to attempt any direct manoeuvres or manipulation of the fetus.

It may be that damage to the perineum is lessened in the long term; however, with the correct technique there is almost always enough room to gain internal access without performing an episiotomy.⁴⁷

The mother is assisted to lie flat, with any pillows removed from under her back, and if possible she is brought to the end of the bed. The mother’s legs are then hyperflexed against her abdomen so that her knees are upwards towards her ears. The midwife will generally need assistance with this manoeuvre, and if in the home environment this could be provided by the second midwife, paramedic and/or the woman’s birth partner. The woman herself can help adopt this position; when standing she can be encouraged to squat and if she is on the bed, encouraged to move her buttocks to the edge of the bed. If the anterior shoulder is not released with the McRoberts position, the midwife should move on to the next manoeuvre. The clinician must not continue to apply traction to the baby’s head if no movement is felt.

SUPRAPUBIC PRESSURE

Suprapubic pressure (‘P’ in HELPERR mnemonic) externally on the posterior aspect of the anterior fetal shoulder may reduce the bisacromial diameter (the diameter of the shoulders) and help to turn the fetus into the oblique. The method advocated is to apply gentle pressure with the palm or the heel of the hand against the fetal back, directing the pressure towards the fetal midline (Figure 8.2).⁴⁷ Clearly, it is important to know the position of the fetus beforehand because pressure in the wrong direction will cause the bisacromial diameter to increase and further exacerbate the situation.

Figure 8.1  McRoberts manoeuvre.

Once again the midwife is going to require assistance from another midwife, and when suprapubic pressure is combined with the McRoberts position efficacy is increased.48,55 The pressure is applied first in a continuous motion for 30 seconds and later in a ‘rocking’ motion – although the time spent on each manoeuvre may be reduced if no movement is felt. If movement is felt, the midwife should attempt to deliver the shoulders with routine axial traction but if there is no advance of the shoulders she should move onto the next manoeuvre.

‘HANDS AND KNEES’/’ALL-FOURS’ POSITION/GASKIN’S MANOEUVRE

Both PROMPT and HELPERR (the second ‘R’ in the HELPERR mnemonic) include the ‘hands and knees’ technique as part of their algorithm. First described by Gaskin in 1976, the ‘hands and knees’ position has been evaluated as resolving 83% of shoulder dystocias recorded in a ‘birth registry’ series of 4452 births (with 82 cases of shoulder dystocia).⁵⁶ A small study by Bruner et al.⁵⁷ reported that as well as a high rate of resolution (83% success rate without the need for other manoeuvres), ‘hands and knees’ was associated with a low rate of maternal complications with a 60% intact perineum rate with no third-or fourth-degree tears and only one case of postpartum haemorrhage. Both Walsh⁵⁸ and Kovavisarach⁵⁹ were enthusiastic in their appraisal of this manoeuvre but make it clear that the ‘hands and knees’ position does not preclude the performance of internal manoeuvres. By its nature it is also dependent on the woman’s ability to move into this position. Depending on what position the mother is in when the shoulder dystocia is diagnosed, if the McRoberts manoeuvre is not the most appropriate initial response then women and midwives may find the ‘hands and knees’ or ‘all fours’ position beneficial. It is non-invasive and the movement alone may reduce the impaction of the shoulder.⁵⁸ The ‘hands and knees’ position exploits the effects of gravity and increases space in the hollow of the sacrum to facilitate delivery of the posterior shoulder and arm.⁵⁹ Once the woman is repositioned, gentle downward traction may be used to deliver the posterior shoulder. The ‘hands and knees’ position is compatible with all internal manipulations for shoulder dystocia.¹⁰ For a mobile woman without epidural anaesthesia the ‘hands and knees’ position may be the most appropriate.

Figure 8.2  Suprapubic pressure.

Second-line manoeuvres

Most cases of shoulder dystocia will have resolved with the use of first-line manoeuvres; however, in rare cases this is not achieved. Since they are part of an escalating algorithm of care, by their nature, second-line manoeuvres are more invasive than the first-line manoeuvres. Second-line manoeuvres (internal manoeuvres) involve manipulating the fetus by entering the vagina (the second ‘E’ in the HELPERR mnemonic), and for this an episiotomy may be necessary (see Box 8.4).

There are two categories of internal vaginal manoeuvres: internal rotational manoeuvres and delivery (removal) of the posterior arm (the first ‘R’ in the HELPERR mnemonic). Recent recommendations suggest attempting to remove the posterior arm first. The strength of this recommendation predominantly lies with the large comparative study by Hoffman et al.⁶⁰ involving data from a cohort of 206,969 women where 2018 (1.5%) babies incurred a shoulder dystocia, and 101(5.2%) of these sustained a neonatal injury. Delivery of the posterior shoulder was associated with the highest rate (84.4%) of successful delivery when compared with other manoeuvres (24.3%–72.0%). However, the RCOG⁴ guidelines suggest the internal manoeuvre tried first is dependent on clinical judgment, and the clinician will make a decision probably based on which manipulation feels easiest when they are feeling the baby and can assess its position. All internal manoeuvres start with the same action, inserting the whole hand posteriorly into the sacral hollow which is the most spacious part of the pelvis.

Withdrawing (‘removing’) the posterior arm of the fetus involves the clinician’s hand inserted along the front of the fetus, feeling for the antecubital fossa and applying pressure that will cause the fetus to flex the posterior arm.⁶¹ As it does so, the forearm of the fetus can be grasped and swept across its face to remove it from the vagina. Once the posterior arm is delivered, the anterior shoulder should dis-impact and delivery can continue with routine axial traction (Figure 8.3).

Internal rotational manoeuvres were originally described by Woods⁶² and Rubin⁶³ who applied the principles of physics to the management of shoulder dystocia. It is these principles, when recognised and understood by the practitioner, which will enable the midwife to manually rotate the fetal shoulders out of the anterior-posterior diameter (the narrowest diameter at the brim of the pelvis) and into the wider oblique/transverse diameter, so that the fetal shoulder will enter the pelvic brim and thereby descend through the pelvis to the pelvic outlet (Figure 8.4).

Entering via the sacral hollow, the midwife can slide her hand to the posterior aspect of the posterior shoulder, and apply pressure to move the fetus into the oblique diameter of the pelvis, which is wider than the anterio-posterior diameter. As with all manoeuvres, if she feels movement, she can attempt to deliver the shoulders with gentle axial traction.

If there is no movement, the midwife can slide her hand upwards to the posterior aspect of the anterior shoulder and try to move the baby ‘forward’. This can be aided by another midwife applying suprapubic pressure. If there is still no movement, the practitioner can then, with her other hand, enter the vagina and apply pressure to the anterior aspect of the posterior shoulder to move the baby, using both her hands. She may need to continue the rotation through 180 degrees to achieve delivery.

Figure 8.3  Release of the posterior arm.

In community settings where immediate referral is not possible, the practitioners should repeat (the final “R” in the HELPERR mnemonic) the manoeuvres until transfer to an obstetric unit is possible; however, since the incidence of HIE increases with head-to-body birth interval the outcome is likely to be poor if this delay occurs.

Third-line manoeuvres

CLEIDOTOMY

Third-line manoeuvres are not usually the province of the midwife, but will require referral to obstetric colleagues. The most common third-line manoeuvre in the United Kingdom is cleidotomy; anecdotally this was part of midwives’ routine training until the early 1990s.⁶⁴ This involves applying upward digital pressure on the midportion of the fetal clavicle which decreases the bisacromial diameter; conflicting opinions suggest that this can significantly increase the risk of brachial plexus injury and compromise pulmonary vasculature⁶⁵; however, Backe et al.⁶⁶ consider the opposite and postulate a protective and successful effect against obstetric brachial plexus injury. Both of these studies are of a small scale however, and carry minimal significance.

SYMPHYSIOTOMY

This is the surgical division of the fibrocartilage junction of the symphysis pubis to enlarge the bony pelvis and has been practised for many years in areas of the world where caesarean section is difficult to perform. The procedure is not widely practised in the United Kingdom or the United States, possibly due to operator inexperience and maternal morbidity. Three case studies were published concerning the use of this procedure. In all cases the infants died, although it should be remembered that all the standard manoeuvres including cephalic replacement had already been performed to no avail and symphysiotomy was performed in extremis. There is a high incidence of serious maternal morbidity and poor neonatal outcome.⁶⁷

CEPHALIC REPLACEMENT: ZAVANELLI MANOEUVRE

The Zavanelli manoeuvre involves replacing the fetal head into the pelvis for extraction by caesarean section. The head is rotated to a direct occipitoanterior or occipitoposterior position and flexed. Then pressure is applied to the vertex to push the head upwards.68–70 Various case studies have been published concerning this manoeuvre but success rates vary.⁷⁰ Severe injuries associated with the Zavanelli manoeuvre, though not necessarily as a result, include neonatal Erb’s palsy, seizures, brain damage, delayed motor development, quadriplegia, cerebral palsy, and neonatal death. Reported maternal complications have included paresis of the lower extremities with pressure necrosis of the skin of the thigh, uterine infection requiring hysterectomy, vaginal ‘rupture’, laceration of the lower uterine segment and uterine rupture.⁷¹

Figure 8.4  Internal rotational manoeuvre.

PROFESSIONAL CONSIDERATIONS

As stated by the Nursing and Midwifery Council (NMC)⁷² accurate and contemporaneous recordkeeping by midwives helps to improve accountability and shows how decisions related to patient care were made. This is difficult in an emergency, but a scribe’s record of events (perhaps using a proforma) such as the timing of calls for help and of manoeuvres undertaken can aid the retrospective completion of the notes. When an emergency situation happens documentation supports effective clinical judgements and decisions, which in turn promote communication and teamwork.⁷³ In the evaluation by Stohl et al.⁷⁴ of 66 clinicians’ delivery notes, they found that many lacked the critical elements required for comprehensive documentation. Despite being a small study the generalisability of their findings is important, together with their recommendation in the use of standardised forms for shoulder dystocia delivery. See Box 8.5 for a suggestion of critical points to include within record-keeping.

Midwives have a clear obligation to recognise that it is their personal responsibility to ensure they are competent in their practice and that their knowledge and skills are always up to date. While the majority of maternity units provide a range of ‘skill training’, positive high-grade evidence to support simulation is evident in the works by Draycott et al.⁷⁵ who compared 15,908 eligible pre-training births with 13,117 births occurring after the introduction of training of the management of shoulder dystocia in their observational study. Pre-training, they found that none of the recommended manoeuvres for the resolution for shoulder dystocia were used in the delivery of 50% of the babies that suffered serious morbidity to include brachial plexus damage. After simulation training, at least one of the recommended manoeuvres was utilised in more than 90% of the cases of shoulder dystocia and the risk of neonatal injury decreased significantly from 9.3% to 2.3%. However, Morgan et al.⁷⁶ and Merien et al.⁷⁷ would argue that simulation is poorly supported by the evidence base and has yet to demonstrate clinical or economic benefits in obstetrics. Nevertheless, there is also evidence to suggest simulation can facilitate the development of non-technical skills, such as communication, decision making, and teamwork.78,79 It is suggested that it may be advisable to introduce the subsidiary mnemonic SOAPS (senior midwife, obstetrician, anaesthetist, paediatrician and someone to support the mother and scribe) with live skill training.⁷⁵

BOX 8.5: Critical points to include within record-keeping during shoulder dystocia

•  Time of delivery of the head and time of delivery of the body

•  Position of fetal head at delivery

•  Anterior shoulder at the time of the dystocia

•  Manoeuvres performed, their timing and sequence

•  Degree of axial traction applied

•  Maternal perineal and vaginal examination

•  Estimated blood loss

•  Assessment of the mother

•  Staff in attendance and the time they arrived

•  General condition of the baby (Apgar score and cord bloods)

•  Neonatal assessment of the baby

SUMMARY OF MIDWIFERY RESPONSIBILITIES

•  Remember that shoulder dystocia can occur with any birth. All practitioners, delivering babies in any healthcare setting, need to anticipate shoulder dystocia at every delivery.

•  Assess for risk factors (both antenatal and intrapartum) and refer and escalate concerns appropriately.

•  Early recognition means swifter response.

•  Enact the HELPERR mnemonic, PROMPT guidelines or variation according to local policy.

•  Note the time of the delivery of the fetal head.

•  Traction applied should be routine and the current recommendation⁴⁸ is that it is in an axial direction.

•  Ensure a scribe is assigned to maintain accurate records.

•  Communicate with the mother and her birth partner. Help her/them debrief later if appropriate (see Chapter 14 for further discussion).

•  Practise the manoeuvres and attend ‘skill drills’ whenever possible.

•  Reflect on your experiences with peers and/or Supervisor of Midwives.

•  Consider risk management issues.

REFERENCES

1.  Politi S, D’emidio I, Cignini P. 2010. Shoulder dystocia: An evidence-based approach. Journal of Prenatal Medicine, 4(3):35–42.

2.  National Health Service Litigation Authority (NHSLA). 2013. Summary of substandard care in cases of brachial plexus injury. NHSLA Journal, 2:ix–xi.

3.  Spong CY, Beall M, Rodrigues D, Ross MG. 1995. An objective definition of shoulder dystocia: Prolonged head-to-body delivery intervals and/or the use of ancillary obstetric manoeuvres. Obstetrics and Gynecology, 86:433–436.

4.  Royal College of Obstetricians and Gynaecologists (RCOG). 2012. Shoulder Dystocia: Greentop Guideline No. 42. RCOG: London.

5.  Resnick R. 1980. Management of shoulder dystocia girdle. Clinical Obstetrics and Gynaecology, 23:559–564.

6.  Mahran MA, Sayed AT, Imoh-Ita F. 2008. Avoiding overdiagnosis of shoulder dystocia. Journal of Obstetrics and Gynaecology, 28(2):173–176.

7.  Gibb D. 1995. Clinical focus: Shoulder dystocia: The obstetrics. Clinical Focus, 1:49–54.

8.  Crofts JF, Ellis D, Draycott TJ, Winter C, Hunt LP, Akande VA. 2007. Change in knowledge of midwives and obstetric emergency training: Randomised controlled trial of local hospital, simulation centre and teamwork training. British Journal of Gynaecology, 114:1534–1541.

9.  Olugbile A, Mascarenhas L. 2000. Review of shoulder dystocia at the Birmingham Women’s Hospital. Journal of Obstetrics and Gynaecology, 20(3):267–270.

10.  Baxley EG, Gobbo RW. 2004. Shoulder dystocia. American Family Physician, 69(7):1707–1714.

11.  Nocon JJ, McKenzie DK, Thomas LJ, Hansell RS. 2000. Shoulder dystocia: An analysis of risks and obstetric manoeuvres. American Journal of Obstetrics and Gynaecology, 168:1732–1737.

12.  Walsh JM, Kandamany N, Ni Shuibhne N, Power H, Murphy JF, O’Herlihy C. 2011. Neonatal brachial plexus injury: Comparison of incidence and antecedents between 2 decades. American Journal of Obstetrics and Gynaecology, 204:234.

13.  Carolan M, Steele C, Margetts H. 2010. Attitudes towards gestational diabetes among a multiethnic cohort in Australia. Journal of Clinical Nursing, 19:2446–2453.

14.  Baskett TF, Allen VM, O’Connell CM, Allen AC. 2007. Fetal trauma in term pregnancy. American Journal of Obstetrics and Gynaecology, 197(499):36–37.

15.  Athukorala C, Crowther CA, Willson K. 2007. Women with gestational diabetes mellitus in the ACHOIS trial: Risk factors for shoulder dystocia. Australian and New Zealand Journal of Obstetrics and Gynaecology, 47(1):37–41.

16.  Gherman RB, Chauhan S, Ouzounian JG, Lerner H, Gonik B, Goodwin TM. 2006. Shoulder dystocia: The unpreventable obstetric emergency with empiric management guidelines. American Journal of Obstetrics and Gynecology, 195(3):657–672.

17.  Mocanu EV, Greene RA, Byrne BM, Turner MJ. 2000. Obstetric and neonatal outcomes of babies weighing more than 4.5 kg: An analysis by parity. European Journal of Obstetrics and Gynaecology Reproductive Biology, 92:229–233.

18.  Overland EA, Spydslaug A, Nielsen CS, Eskild A. 2009. Risk of shoulder dystocia in second delivery: Does a history of shoulder dystocia matter? American Journal of Obstetrics and Gynaecology, 200(5):506.

19.  Stallings SP, Edwards RK, Johnson JW. 2001. Correlation of head-to-body delivery intervals in shoulder dystocia and umbilical artery acidosis. American Journal of Obstetrics and Gynaecology, 185(2):268–274.

20.  Leung TY, Stuart O, Sahota DS, Suen SS, Lau TK, Lao TT. 2010. Head-to-body delivery interval and risk of fetal acidosis and hypoxic ischaemic encephalopathy in shoulder dystocia: A retrospective review. British Journal of Obstetrics and Gynaecology, 118(4):474–479.

21.  Clements RV. 1994. Safe Practice in Obstetrics and Gynaecology. Edinburgh: Churchill Livingstone.

22.  Lerner HM, Salamon E. 2008. Case Report: Permanent brachial plexus injury following vaginal delivery without physician traction or shoulder dystocia. American Journal of Obstetrics and Gynaecology, 7(8):21–29.

23.  McFarland MB, Langer O, Piper JM, Berkus MD. 1996. Perinatal outcome and the type and number of manoeuvres in shoulder dystocia. International Journal of Obstetricians and Gynaecologists, 55:219–224.

24.  Melendez V, Forson V, Yoong W. 2009. Letter to the editor: Re: Mahran, M.A., Sayed, A.T. Imoh-Ita, F. (2008). Avoiding over diagnosis of shoulder dystocia. Journal of Obstetrics and Gynaecology, 28(2):173–176.

25.  Gherman RB, Ouzounian JG, Miller DA. 1998b. Spontaneous vaginal delivery: A risk factor for Erb’s palsy. American Journal of Obstetrics and Gynaecology, 178:423–427.

26.  Sandmire HF, DeMott RK. 2009. Controversies surrounding the causes of brachial plexus injury. International Journal of Gynaecology and Obstetrics, 104:9–13.

27.  Gonik B, Walker A, Grimm M. 2000. Mathematic modelling of forces associated with shoulder dystocia: A comparison of endogenous and exogenous sources. American Journal of Obstetrics and Gynaecology, 182:689–691.

28.  Gherman RB, Goodwin TM, Ouzounian JG. 1997. Brachial plexus palsy associated with cesarean section: An in utero injury? American Journal of Obstetrics and Gynaecology, 177:1162–1164.

29.  Gurewitsch ED, Johnson E, Hamzehzadeh S, Allen RH. 2006. Risk factors for brachial plexus injury with and without shoulder dystocia. American Journal of Obstetrics and Gynaecology, 194:486–492.

30.  Ubachs JMH, Slooff ACJ, Peeters LLH. 1995. Obstetric antecedents of surgically treated obstetric brachial plexus injuries. British Journal of Obstetrics and Gynaecology, 102:813–817.

31.  Medlock MD, Hanigan WC. 1997. Neurologic birth trauma. Intracranial, spinal cord, and brachial plexus injury. Clinical Perinatology, 24(4):845–857.

32.  Gherman RB, Goodwin TM, Souter I. 1997b. The McRoberts’ Manoeuvre for the alleviation of shoulder dystocia: How successful is it? American Journal of Obstetrics and Gynaecology, 176(3):656–661.

33.  Gherman RB, Joseph G, Ouzounian JG, Murphy Goodwin T. 1998. Obstetric manoeuvres for shoulder dystocia and associated morbidity. American Journal of Obstetrics and Gynaecology, 178(6):1126–1130.

34.  Robinson J. 2007. Post traumatic stress disorder. AIMS Journal, 19(1):7–12.

35.  Hope P, Breslin S, Lamont L, Lucas A, Martin D, Moore I. 1998. Fatal shoulder dystocia: A review of 56 cases reported to the confidential enquiry into stillbirths and deaths in infancy. British Journal of Obstetrics and Gynaecology, 105:1256–1261.

36.  MacKenzie IZ, Shah M, Lean K, Dutton S, Newdick H, Tucker L. 2007. Management of shoulder dystocia: Trends in incidence and maternal and neonatal morbidity. Obstetrics and Gynaecology, 110:1059–1068.

37.  Draycott T, Winter C, Crofts J, Barnsfield S (Eds.). 2008. PROMPT: Practical Obstetric Multiprofessional Training Course Manual. London: Royal College of Obstetricians and Gynaecologists (RCOG).

38.  Grobman WA, Miller D, Burke C, Hornbogen A, Tam K, Costello R. 2011. Outcomes associated with introduction of a shoulder dystocia protocol. American Journal of Obstetrics and Gynaecology, 205:513–517.

39.  Buerkle B, Pueth J, Hefler LA, Tempfer-Bentz E, Tempfer C. 2012. Objective structured assessment of technical skills evaluation of theoretical compared with hands-on training of shoulder dystocia management: A randomized controlled trial. Obstetrics and Gynecology, 120(4):809–814.

40.  Advanced Life Support in Obstetrics (ALSO). 2007. Provider Manual. Leawood, KS: American Academy of Family Physicians (AAFP).

41.  American Academy of Family Physicians (AAFP). 1996. Advanced Life Support in Obstetrics. Leawood, KS: AAFP.

42.  Gross SJ, Shime J, Farine D. 1987. Shoulder dystocia: Predictors and outcome: A five year review. American Journal of Obstetrics and Gynaecology, 156(2):334–336.

43.  Al-Najashi S, Al-Suleiman SA, El-Yahia A. 1999. Shoulder dystocia – A clinical study of 56 cases. Australian and New Zealand Journal of Obstetrics and Gynaecology, 29:129–131.

44.  Baskett TF, Allen AC. 1995. Perinatal implications of shoulder dystocia. Obstetrics and Gynaecology, 86:14–17.

45.  Crofts JF, Winter C, Sowter M. 2011. Practical simulation training for maternity care – Where we are and where next. British Journal of Gynaecology, 118(3):11–16.

46.  Lewis P. 2014. Discourse on dystocia: A much needed professional dialogue. British Journal of Midwifery, 22(6):390–392.

47.  Hinshaw K. 2003. Shoulder dystocia. In: Johanson R, Cox C, Grady K, Howell C (Eds.). Managing Obstetric Emergencies and Trauma. The MOET Course Manual. London: Advanced Life Support Group, Royal College of Obstetricians and Gynaecologists (RCOG), pp. 165–174.

48.  Winter C, Crofts J, Laxton C, Barnfield S, Draycott T. 2012. PROMPT – Practical Obstetric Multi-Professional Training Course Manual. 2nd ed. Cambridge, UK: Cambridge University Press.

49.  MBRRACE-UK. 2015. Maternal, newborn and infant clinical outcome review programme. Perinatal mortality surveillance report. Leicester: Department of Health Sciences, University of Leicester.

50.  Gonik B, Zhang N, Grimm MJ. 2003. Prediction of brachial plexus stretching during shoulder dystocia using a computer simulation model. American Journal of Obstetrics and Gynaecology, 189(4):1068–1072.

51.  Gurewitsch ED, Johnson TL, Allen RH. 2007. After shoulder dystocia: Managing the subsequent pregnancy and delivery. Seminars in Perinatology, 31:185–195.

52.  Allen RH. 2007. On the mechanical aspects of shoulder dystocia. Clinical Obstetrics and Gynaecology, 50(3):607–623.

53.  Gherman RB. 2002. Shoulder dystocia: An evidence-based evaluation of the obstetric nightmare. Clinical Obstetric Gynecology, 45:345–362.

54.  Gherman RB, Ouzounian JG, Incerpi MH. 1998. Symphyseal separation and transient femoral neuropathy associated with the McRoberts’ manoeuvre. American Journal of Obstetrics and Gynaecology, 178:609–610.

55.  Athukorala C, Middleton P, Crowther CA. 2009. Intrapartum interventions for preventing shoulder dystocia (Intervention Review). Cochrane Database of Systematic Reviews. Issue 4. Art. No.: CD005543. doi:10.1002/14651858.CD005543.pub2.

56.  Gaskin IM. 1988. Shoulder dystocia: Controversies in management. Birth Gazette, 5(1):14–17.

57.  Bruner JP, Drummond SB, Meenan AL. 1998. All-fours manoeuvre for reducing shoulder dystocia during labour. Journal of Reproductive Medicine, 43(5):439–443.

58.  Walsh D. 2007. Managing shoulder dystocia; ‘on your back’ or ‘all fours’. British Journal of Midwifery, 15(5):23.

59.  Kovavisarach E. 2006. The ‘all-fours’ manoeuvre for the management of shoulder dystocia. International Journal of Gynaecology and Obstetrics, 95(12):153–154.

60.  Hoffman MK, Bailit JL, Branch DW, Burkman RT, VanVeldhusien P, Lu L. 2011. A comparison of obstetric manoeuvres for the acute management of shoulder dystocia. Obstetrics and Gynaecology, 117:1272–1278.

61.  Kung J, Swan AV, Arulkumaran S. 2006. Delivery of the posterior arm reduces shoulder dimensions in shoulder dystocia. International Journal of Gynecology and Obstetrics, 93:233–237.

62.  Woods CE. 1943. A principle of physics as applicable to shoulder delivery. American Journal of Obstetrics and Gynaecology, 45:796–804.

63.  Gurewitsch ED, Kim EJ, Yang JH, Outland KE, McDonald MK, Allen RH. 2005. Comparing McRoberts’ and Rubin’s maneuvers for initital management of shoulder dystocia: An objective evaluation. American Journal of Obstetrics and Gynecology, 192:153–160.

64.  Silverton L. 1994. The Art and Science of Midwifery. Edinburgh: Prentice Hall.

65.  Amy G, Gottlirb H, Galan L. 2007. Shoulder dystocia: An update. Obstetrics and Gynecology Clinics of North America, 34:501–531.

66.  Backe B, Magnussen EB, Johansen OJ, Sellaeg G, Russwurm H. 2008. Obstetric brachial plexus palsy: A birth injury not explained by the known risk factors. British Journal of Obstetrics and Gynaecology, 87(10):1027–1032.

67.  Murphy Goodwin T, Banks E, Millar LK. 1997. Catastrophic shoulder dystocia and emergency symphysiotomy. American Journal of Obstetrics and Gynecology, 177:463–464.

68.  Namis NN. 1995. Cephalic replacement (The Zavanelli Manoeuvre): A desperate solution for severe shoulder dystocia. Society of Obstetricians and Gynaecologists Canada, 17:1017–1020.

69.  Sandberg EC. 1985. The Zavanelli maneuvre: A potentially revolutionary method for the resolution of shoulder dystocia. American Journal of Obstetrics and Gynaecology, 152:479–484.

70.  Vaithilingam N, Davies D. 2005. Cephalic replacement for shoulder dystocia: Three cases. British Journal of Obstetrics and Gynaecology, 112:674–675.

71.  Spellacy WN. 1995. The Zavanelli maneuver for fetal shoulder dystocia. Three cases with poor outcomes. Journal of Reproductive Medicine, 6767(40):543–544.

72.  Nursing and Midwifery Council (NMC). 2009. Record Keeping: Guidance for Nurses and Midwives. London: NMC. Available at http://www.nmc-uk.org (accessed September 9, 2015).

73.  Crofts JF, Bartlett C, Ellis D. 2008. Documentation of simulated shoulder dystocia: Accurate and complete? British Journal of Gynaecology, 115(10):1303–1308.

74.  Stohl HE, Granat A, Ouzounian J, Miller DA, Jaque J. 2014. Comprehensiveness of delivery notes for shoulder dystocia. Obstetrics and Gynecology, 123(Suppl 1):25S.

75.  Draycott TJ, Crofts JF, Ash JP, Wilson LV, Yard E, Sibanda T, Whitelaw A. 2008. Improving neonatal outcome through practical shoulder dystocia training. British Journal of Obstetricians and Gynecologists, 112:14–20.

76.  Morgan PJ, Cleave-Hogg D, Lam-McCulloch J. 2006. Applying theory to practice in undergraduate education using high fidelity simulation. Medical Teacher, 28(1):10–15.

77.  Merien AE, Mol BW, Houterman S, Oei SG. 2010. Multidisciplinary team training in a simulation setting for acute obstetric emergencies: A systematic review. Obstetrics and Gynaecology, 115:1021–1031.

78.  Arundell F, Cioffi J. 2005. Using a simulation strategy: An educator’s experience. Nurse Education in Practice, 5(5):296–301.

79.  Cioffi J, Purcal N, Arundell F. 2005. A pilot study to investigate the effect of a simulation strategy on the clinical decision making of midwifery students. Journal of Nurse Education, 44(3):131–134.

9

Uterine complications

MARIE HALL

Uterine rupture

Uterine inversion

References

UTERINE RUPTURE

Uterine rupture is a serious complication of pregnancy and labour in which the wall of the uterus tears. It is classified as either being complete (full) or incomplete (partial). A complete rupture of the uterus is defined as a defect involving the full thickness of the uterine wall (myometrium) and uterine serosa, with or without expulsion of the fetus into the abdominal cavity. A complete rupture of the uterus represents a potential catastrophic event that can result in severe maternal morbidity and mortality as well as possible fetal death. When occurring in pregnancy it is more likely to be after 32 weeks’ gestation and predominantly where there is an existing classical (longitudinal) uterine scar.

Incomplete uterine rupture or partial rupture occurs when the tear does not extend through the full thickness of the uterine wall and the peritoneum remains intact. In those with a scarred uterus it may result in scar dehiscence. This is a more common event and rarely results in extensive maternal or fetal complications due to the intact visceral peritoneum and clinically less significant bleeding from the edges of the preexisting uterine scar.¹ It generally presents with less acute symptoms and may well be found inadvertently. The fetus, placenta and umbilical cord remain inside the uterine cavity. It is vital that these two events are distinctly differentiated as the clinical management and outcomes are considerably different.

Spontaneous uterine rupture happens most often during labour in the context of a scarred uterus. Nonetheless it can occur in an unscarred uterus and even with no discernible associated risk factors, although this is extremely rare. There are several risk factors that predispose to a uterine rupture. Familiarity and understanding of these features may assist midwives to not only be aware of them but also to anticipate, through correct interpretation of the signs and symptoms, so ensuring appropriate and timely escalation.

It has been reported that the number of women attempting vaginal birth after cesaerean (VBAC) delivery is decreasing in many countries with an associated increase in the caesarean section rates.2–4 This has fundamentally been driven by reports implying the compounded risk of maternal and fetal complications related to VBAC, including uterine rupture. On the contrary, a recent study by Knight et al.⁵ ascertained that from 143,970 women who had their first baby by caesarean section between 2004 and 2011, just over half (52%) attempted a VBAC for their second baby with approximately two-thirds (63%) having a successful vaginal delivery.

Rupture of the unscarred pregnant uterus is a rare event, estimated to occur in 1/5700 to 1/20,000 pregnancies.6–8 Not surprisingly rupture of the unscarred uterus seems to occur more frequently in resource-poor countries, possibly associated to higher parity, longer labours, operational practices and a higher frequency of contracted pelves in these areas, together with poor access to emergency obstetrical facilities.⁹ A population-based survey in Norway conducted by Al-Zirqi et al.¹⁰ concluded that the incidence of rupture of both scarred and unscarred uteri over four decades appears to be on the increase with obstetric interventions contributing to this increase.

The incidence of uterine rupture varies extensively throughout the literature. In the United Kingdom a national case-control study over a 1-year period estimated the incidence of uterine rupture was 0.2 per 1000 maternities overall. Consistent with previous studies it was found to be higher in those women with a previous caesarean delivery who were planning vaginal or repeat elective caesarean section quoting the estimated incidence as 2.1 and 0.3 per 1000 maternities, respectively.¹¹ This risk was increased when associated with labour induction, the use of oxytocin and increased number of previous caesarean sections. In the unscarred uterus it is extremely rare at 0.5–2.0 per 10,000 maternities.¹² In resource-poor countries it is a more serious problem with an overall rate of 0.1%–1% with reports indicating that 75% of uterine ruptures occurred on an unscarred uterus. Maternal mortality was in the region of 1%–13% and perinatal mortality between 74% and 92%.⁹

Risk/predisposing factors

The vast majority of documented evidence in the literature identifies previous caesarean section as the predominant risk factor to uterine rupture. Other factors have been attributed to its occurrence (see Box 9.1).

PREVIOUS CAESAREAN SECTION

It is widely accepted in the literature that a woman has an increased possibility of sustaining a uterine rupture if she has a scarred uterus.1,9,11,13 This will arise predominantly from a previous caesarean section, however, other forms of uterine surgery such as myomectomy must also be taken into account. A scarred uterus is regarded as the main cause of uterine rupture in resource-rich countries,1,9 and it is also substantially prevalent in poorer countries.

BOX 9.1: Risk/predisposing factors for uterine rupture

•  Pharmacological induction of labour/augmentation of labour

•  Parity/multiple gestation

•  Previous uterine surgery (including minimally invasive procedures)

•  Previous uterine rupture

•  Abnormal placentation

•  Certain medical conditions

•  Congenital uterine anomalies

•  Trauma to the abdomen

•  Intrauterine manipulation or interventional procedures

•  Obstructed labour

The consequence of previous caesarean delivery on the risk of uterine rupture has been studied extensively yet it is difficult to precisely measure the risk it has as evidence within the literature varies considerably. It has been documented that the possibility of uterine rupture in labour ranges from 3 to 7 per 1000 pregnancies. The risk of perinatal death or severe morbidity should uterine rupture happen is higher with trial of vaginal delivery than with elective repeat caesarean section (ERCS) delivery.¹⁴ A systematic review by Guise et al.¹⁵ established that maternal mortality was increased significantly with ERCS compared with planned VBAC (1.34 versus 0.38 per 10,000). In contrast perinatal mortality was significantly increased with planned VBAC (13 per 10,000) compared with ERCS (5 per 10,000). These findings complicate the decision-making process as clinicians and women try to weigh-up the risks involved. As maternal morbidity is also significantly increased with ERCS when compared to planned VBAC the evidence, on balance, advocates that VBAC is a reasonable and safe option for most women. In the United Kingdom, around 10%–15% of the obstetric population has experienced previous caesarean delivery. It is fundamental that antenatal counselling should comprise an individualised assessment of the risks and benefits of ERCS and planned VBAC¹⁶ so that women are fully informed with the most up-to-date evidence. The Royal College of Obstetricians and Gynaecologists (RCOG)¹² state that planned VBAC carries a risk of uterine rupture of 22–74/10,000. There is virtually no risk of uterine rupture in women undergoing ERCS. Perhaps a scoring tool to assess individual risk may be considered with a proforma checklist as introduced by the American Congress of Obstetricians and Gynecologists (ACOG)¹⁷ in antenatal assessments to evaluate women’s suitability for either VBAC or ERCS.

Previous classical (longitudinal) incision

The incidence of uterine rupture occurring when the scar from a previous caesarean section is in the lower segment is relatively low as this is the segment of the uterus that does not contract.¹⁴ However, although caesarean delivery with a classical (longitudinal) incision is relatively uncommon in the modern era (representing 0.3%–0.4% of deliveries), it does pose a significant risk of rupture with subsequent pregnancies (1%–12% on the basis of published reports). Available data recommend that planned caesarean at 36–37 weeks optimises both maternal and fetal outcomes in these cases¹⁸ as there is an increased risk for antenatal uterine rupture.

PREGNANCY INTERVAL

A short interpregnancy interval increases the risk for uterine rupture and other major morbidities two-to threefold in those women having a VBAC.¹⁹ The timing between pregnancies has recently become an interesting predictor linked to VBAC.²⁰ A study by Bujold and Gauthier²¹ found that the risk of uterine rupture was significantly higher in women with an interdelivery interval less than 18 months than in women with an interval of 24 months or longer, but not in women with an interval between 18 and 23 months, inclusively. The rates of uterine rupture for an interval of 24 months or more were 1.3%, between 18 and 24 months 1.9% and for those with an interval less than 18 months 4.8%.

PREVIOUS LABOUR OR VAGINAL DELIVERY

It appears that those women who have had a prior vaginal delivery are at a considerably lower risk of uterine rupture than women without a previous vaginal delivery.²²

NUMBER OF PREVIOUS CAESAREAN SECTIONS

The more caesareans a woman has seems to increase the risk of uterine rupture⁵ but there remains uncertainty within the literature as to the number. A study by Fitzpatrick et al.¹¹ did find that women with two or more previous caesarean sections had an increased risk of uterine rupture compared to those with only one previous caesarean. Ruptures were also found to occur more frequently during latent activity in those who had multiple or unusual uterine scars.¹⁰

PREVIOUS WOUND CLOSURE

There is no quality evidence to suggest that the types of uterine closure methods, either single or double layer, have any impact on the rates of uterine rupture.23,24 A study by Durnwald and Mercer²⁵ did not find an increased uterine rupture rate with single-layer closure; uterine rupture rate for singlelayer closures was 0% and for double-layer closures was 0.8%.

PREVIOUS WOUND HEALING

Delayed wound healing with or without associated sepsis at the time of caesarean delivery may increase the risk of uterine rupture in subsequent pregnancies as there may be a weakness in the scar due to the poor wound healing secondary to the infection.20,26

PREVIOUS SURGICAL PROCEDURE

It is possible that any previous surgical intervention on the uterus such as myomectomy, dilatation and curettage (D&C) or hysteroscopy may cause weakness to the uterus and predispose to uterine rupture.²⁷ Studies have suggested that uterine rupture following laparoscopic myomectomy is rare as long as women meet certain criteria.²⁸

PARITY

It has been suggested that multiparity is considered a contributing factor for uterine rupture,²⁹ however, studies on the incidence of this vary widely. It was a customary belief within obstetrics that a ‘primigravida did not rupture’ – although only exceptional cases have been reported due to various causes, nonetheless it is important to be aware that uterine rupture in primiparous women can occur even when no contributory risk factors have been identified.27,30 There is a higher rate of mortality for primiparous women who sustain a uterine rupture compared to the multiparous. This has been identified as a mortality rate of 26% compared to 11.7%, respectively, with a higher rate of hysterectomy also noted in primiparous women.²⁷ It has been cited that diagnosis and therefore treatment are instigated far more quickly in the multiparous woman as suspicion is greater. It is therefore paramount that clinicians are aware that uterine rupture can occur in primiparous women and the outcome can be catastrophic.

ABNORMAL PLACENTATION

The incidence of abnormal placenta implantation such as accreta and percreta is rising due to the increase in caesarean sections within modern-day obstetric practice.³¹ One of the most severe complications of placenta percreta is uterine rupture with a haemoperitoneum. It has been documented that uterine rupture from percreta can occur in the early trimester periods. The contributing factor is thought to be a weakness in the decidua basalis allowing chorionic villus invasion of the myometrium.³² Once the woman has been diagnosed with abnormal placentation, careful and frequent monitoring must be undertaken with a concise plan of management in her notes.

MEDICAL CONDITIONS

There are no direct links associated with medical conditions and uterine rupture. Hypertensive disorders have been previously linked to uterine rupture but there is no contemporaneous evidence to support this.³³ There has been a suggested association with women who have a connective tissue disorder such as Ehlers-Danlos syndrome as well as those with ongoing steroid use.30,34 There has also been some indication that women who have had either an intrapartum or postpartum fever in the course of their caesarean delivery may have an increased risk of uterine rupture in subsequent pregnancies.²⁶ More quality studies are however required to confirm this premise.

PHARMACOLOGICAL INDUCTION/AUGMENTATION: OXYTOCIN AND/OR PROSTAGLANDIN

The use of prostaglandin E2 gel and intravenous Syntocinon for women with a previous caesarean section is listed as a contraindication in use by the manufacturer’s guidelines of both agents. Despite this both are used for either the induction or augmentation of labour for women with a previous caesarean scar.³⁵ Surveys of obstetricians globally have found that there was a willingness to use both prostaglandins and oxytocin in women with a previous caesarean section.35–37 It is well documented in the literature that the induction of labour for women with a previous caesarean section has an increased risk of uterine rupture.8,11,37 This risk is higher if prostaglandin agents are used when compared to mechanical methods and/or the use of oxytocin.10,38,39 It has been estimated that the risk of uterine rupture increases sixfold in women who have their labour induced with use of hormonal agents.⁴⁰ It is also worth remembering that induction of labour following a vaginal delivery with an unscarred uterus can double the risk of uterine rupture.³⁹ In today’s practice the use of prostaglandin and oxytocin is routine, however, caution should always be displayed when using these drugs for all women.

TRAUMA TO ABDOMEN

Uterine rupture is reported to occur in up to 0.6% of blunt abdominal trauma in pregnancy.⁴¹ Motor vehicle crashes, domestic violence, and falls are the most common causes of blunt trauma in pregnancy. Trauma can also occur through obstetric interventions such as external cephalic version, internal podalic version, mid to high instrumental vaginal delivery, manual removal of the placenta, manoeuvres performed in shoulder dystocia⁴² as well as unstable lies and fetal malpresentation. Penetrating trauma to the abdomen is usually sustained through either gunshot wounds or stabbing with a sharp instrument such as a knife. However, these types of injuries are uncommon. In a retrospective analysis, penetrating trauma accounted for 9% of all pregnancy trauma admissions. Of those, 73% were gunshot, 23% stab wounds and 4% shotgun related. Overall penetrating trauma in pregnancy is associated with a low maternal mortality of 3.9%–7% but fetal mortality is as high as 73%.⁴³

Signs and symptoms

The initial signs and symptoms of uterine rupture are typically nonspecific and can vary vastly, which makes the diagnosis difficult and sometimes delays fundamental therapy. It largely depends on the timing, site, and degree of the uterine defect. Uterine rupture at the site of a previous uterine scar is typically less harrowing than a spontaneous or traumatic rupture because of its relatively reduced vascularity.¹ The warning signs and symptoms of uterine rupture can be inconsistent, and may have similarities with those of a concealed abruption.²⁷ It is also worth bearing in mind that some signs and symptoms may be concealed due to medical conditions (such as pre-eclampsia) or certain prescribed drugs masking a tachycardia, as well as use of epidural infusions.⁴²

FETAL HEART RATE ABNORMALITIES

The most consistent early indicator of uterine rupture is an abnormal fetal heart rate pattern with bradycardia being the most common fetal heart rate abnormality especially if it is profound, persistent and prolonged.1,15,44 It is therefore understandable why the majority of hospitals, in conjunction with RCOG¹² and ACOG,¹⁷ recommend in their guidelines and policies that women labouring with a previous caesarean section scar have continuous fetal heart monitoring. Studies have noted that in up to 87% of uterine rupture cases abnormal fetal heart rates were the most frequent sign.15,21,45

DIMINISHED OR SLOWING OF UTERINE CONTRACTILITY

The slowing down or sudden cessation of previously effective uterine contractions is often an indication that there is a problem. No particular pattern of uterine activity is pathognomonic of uterine rupture.⁴⁶ However, there has been one case report describing the ‘staircase sign’ as characteristic of uterine rupture. This sign classically illustrates on the CTG monitor a stepwise gradual decrease in amplitude of the contraction succeeded by the sudden onset of profound and prolonged fetal bradycardia.⁴⁷ Uterine contractility pattern may vary depending on the presence or absence of a pre-existing scar or with the location and direction of rupture.⁴⁴ The RCOG do not recommend the use of intrauterine pressure catheters as they have no added significance over clinical or cardiotocograph (CTG) observation.

PAIN

Sudden or atypical maternal abdominal pain occurs less frequently than abnormal fetal heart abnormalities; however, the onset of severe continuous abdominal pain should never be ignored and gives rise to suspicion of uterine rupture.⁴⁸ The pain is usually of sudden onset and above and beyond that of normal labour pain and the abdomen will be tender to touch. In the scarred uterus, tenderness in the abdomen may be apparent before the rupture takes place. Chest pain or shoulder tip pain (Kehr sign) has also been observed in some cases. These are valuable signs of intraperitoneal blood in the sub-diaphragmatic region, although it is important to appreciate that it may take up to 24 hours or longer after the bleeding has occurred for the blood to track up under the diaphragm – however referred pain can be of great diagnostic significance.⁴⁸ Any woman postdelivery (either vaginal or by caesarean section) who has severe pain not relieved by opiate analgesia should be investigated for possible uterine rupture if all other sources have been ruled out.

BLEEDING

Vaginal bleeding during uterine rupture is a rare occurrence; a recent case-controlled study of 159 cases of uterine rupture reported only 29% presented with vaginal bleeding.¹¹ As bleeding is usually behind the presenting part it may not be visualised until after the delivery as a postpartum haemorrhage. Bleeding into the abdomen can be profuse especially if the tear is longitudinal rather than transverse with the woman displaying signs of shock or even sudden collapse. Haematuria is often seen especially if a urinary catheter is present, as the bladder may be adherent to a previous uterine scar and be the first indication of a rupture. It is worth being vigilant for those women who have fluctuating haemoglobin levels that require regular blood transfusion with no obvious signs of bleeding. This may be a sign of a silent bleed posterior of the uterus.⁴⁹

ABDOMINAL PALPATION

A Bandl ring is a pathological retraction ring and may be palpable – it is described as a late warning sign of impending rupture.⁴⁵ Following a uterine rupture, on examination a loss of uterine contour may be identified and two swellings may be prominent; one is the fetus lying in the abdominal cavity and the other is the contracted and retracted uterus. The fetal parts may then be easily palpable.⁴⁴ Examination will also be very painful for the woman.

MATERNAL VITAL SIGNS

Changes in vital signs from tachycardia to hypovolaemic shock may be the first indication of uterine rupture.⁴⁸ The changes that may be observed are dependent on the extent of rupture. The woman may initially be restless before any visual signs of shock are evident. The necessity of midwives using all of their senses to create a general assessment of the woman is vital. A previously fit and healthy woman who states she feels unwell must never be ignored and tachypnoea and breathlessness are frequently the first signs of acute illness.⁴² In most cases of maternal collapse, the cause is usually apparent but concealed haemorrhage from a ruptured uterus should not be ruled out.¹² The majority of cases will however see a progressive deterioration in basic but vital observations.

Incomplete rupture

Incomplete rupture is also referred to as uterine dehiscence whereby the uterine muscular layer is lost but the uterine serosa is preserved. This can occur in the unscarred primigravid uterus even without aetiological or risk factors.⁵⁰ An incomplete rupture can be asymptomatic and possibly will initially only show quite subtle signs; it may be diagnosed during the process of caesarean section or other surgical intervention for bleeding.⁵¹

Management

PREDICTION

It has been proposed that thinning of the lower uterine segment (LUS) measured by ultrasonography could be a potential predictor of uterine rupture.⁵² A meta-analysis assessed LUS thickness and risk if a uterine scar defect illustrated a strong correlation between the degree of LUS thinning and risk of uterine defect,⁵³ however, they were unable to define an ideal cut-off value usable within clinical practice. Before this process can be implemented routinely in antenatal care further studies to confirm reliability and validity need to be performed.

Management in hospital

•  Summon urgent help immediately. Like all obstetric emergencies this should include teamwork with a senior obstetrician, anaesthetist and midwife in attendance.

•  If oxytocin infusion is in use stop and disconnect infusion.

•  Administer facial oxygen and begin resuscitative treatment for the management of shock: cannulation, blood for crossmatch, intravenous fluids and monitoring of vital signs.

•  Prepare for surgical delivery or laparotomy – gaining consent in whatever is an appropriate method at the time of the emergency.

Management at home

•  Early recognition of the signs and symptoms is paramount.

•  Summon urgent help. Call the emergency response team (in the United Kingdom dial 999) and arrange for immediate transfer into hospital. Ensure the nearest obstetric-led maternity unit is notified of the transfer.

•  Commence resuscitation and treatment of shock while waiting for the emergency services to arrive (see Chapter 2).

Outcome

Careful consideration and planning must be undertaken with regard to subsequent pregnancies and indeed a planned caesarean section may be recommended. Repair of the uterus is by and large possible in the majority of women, however, it does carry an increased risk of recurrence.⁴⁹ In others, haemorrhage from extension of the rupture into the broad ligament or extensive damage to the uterus requires hysterectomy. It may be that hysterectomy is required to save the woman’s life.⁴⁸ No difference has been noted in the rates of hysterectomy in pregnancies with uterine rupture in women with scarred and unscarred uterus.⁵⁴ A study in Scandinavia reported that the rate of peripartum hysterectomy following uterine rupture was 3.5/10,000 deliveries.⁵⁵

Conclusion

The incidence of uterine rupture is extremely rare but when it occurs it is a catastrophic event that can be life threatening to both mother and fetus.

Uterine rupture can occur in the unscarred uterus as well as the primiparous woman. Healthcare professionals therefore need to be vigilant with respect to those women with potential risk factors, longer labour and the prolonged use of oxytocin infusions.

However, as women with pre-existing uterine scars are the group most at risk and careful consideration must be given to not only future pregnancies but how these women will deliver their baby. The old belief ‘once a caesarean always a caesarean’ is no longer the order of practice in modern maternity units.

It is essential that hospitals have evidence-based guidelines and policies that staff are familiar with and these are adhered to. The safety of women who choose to have a vaginal birth after a previous caesarean section is ensured by increased vigilant observation, careful monitoring in labour and the implementation of strict interventional criteria standards.

Women choosing to have a VBAC need to be carefully selected, therefore it is paramount that information relating to the previous caesarean both intrapartum and postpartum is carefully reviewed by the obstetrician. Likewise and just as important is the assessment of risk factors for uterine rupture antenatally, these if any should be documented clearly in the maternity notes.

Women should be encouraged to make informed choices regarding the mode of their delivery after they have been made fully aware of best practice guidelines and possible risks associated with their preferred choice,¹² hence it would not be unrealistic to suggest that women with a previous caesarean section could labour and aim for a vaginal delivery – as long as the following measures are in place:

•  Early antenatal counseling should be undertaken by a senior obstetrician or midwife.

•  Appropriate referral to a VBAC clinic should be made.

•  Women should be educated on the signs and symptoms of scar tenderness.

•  Senior input from obstetricians and anaesthetists is vital within the maternity unit.

•  Women with risk factors should be identified. These women should have an agreed plan of care documented in their notes relating to the management of labour plus whether the use of prostaglandins and or oxytocin is to be considered. This should include the point in time when to proceed to an emergency caesarean section – prolonged labour, scar tenderness, fetal distress or any sign that may indicate imminent scar dehiscence or uterine rupture.

•  Caution should be applied during oxytocin augmentation, especially in slow progressing multiparous women and those with a history of previous caesarean section.

•  Women who have been advised against VBAC but still wish to proceed with a vaginal delivery continue to require support and careful management from senior obstetricians and midwives including the Supervisor of Midwives. At no time should their choice be met with disapproval as this may only drive them away from care and a setting that can provide safe treatment in the event of an emergency.

Summary of midwifery responsibilities

•  Maintain an up-to-date knowledge of risk factors and management of uterine rupture.

•  Identify women at risk of uterine rupture as soon as possible and make appropriate referral.

•  Be aware of how to summon help in both the hospital and community settings.

•  Ensure knowledge and skills of induction of labour (IOL) and augmentation are maintained including understanding of drug doses and potential side effects.

•  Be proficient in basic life support attending mandatory skills and drills updates.

•  In a uterine rupture situation, work effectively within the multidisciplinary team.

•  If a uterine rupture occurs, ensure excellent record-keeping.

•  Ensure psychological support is provided for both mother and her family.

•  Communicate with the woman and her family, during and after the event, and arrange longterm access to relevant agencies if necessary.

UTERINE INVERSION

Uterine inversion is a rare but extremely serious obstetric emergency with the most common reported cause being fundal placentation with excessive cord traction in the third stage of labour.⁴² Uterine inversion is described as the passage of the uterine fundus through the endometrial cavity and cervix, turning the uterus inside out. It can occur either spontaneously, through mismanagement of the third stage, or in the postpartum period. It requires rapid diagnosis with immediate clinical intervention to prevent maternal morbidity and mortality.⁵⁶

The incidence of uterine inversion occurring varies within the literature. It has been cited as between 1:1500 to 1:20,000.57–59 This variation is likely due to geographic location, reporting of incidence and how the third stage of labour is managed.⁶⁰

Uterine inversion can be classified according to either timing of the inversion or degree (anatomical severity).

Timing

•  Acute uterine inversion: Occurs either at the third stage of labour or within 24 hours of delivery

•  Subacute inversion: Occurs after 24 hours and within 4 weeks after delivery

•  Chronic inversion: Occurs after 30 days postpartum and is rare

Severity

The severity of uterine inversion is classified in either stages or degrees60–62:

•  First degree: (Also referred to as incomplete:) The inverted fundus extends to, but not through the cervix.

•  Second degree: The inverted uterus extends through the cervix but remains within the vagina.

•  Third degree (Complete): The inverted uterus extends down outside the vagina to the introitus.

•  Fourth degree (Total): The vagina and uterus are inverted.

All types of uterine inversion denote a need for rapid diagnosis and correction since large volumes of blood loss with accompanying shock may ensue.⁴²

Aetiology

Several risk factors/causes have been linked to uterine inversion (see Box 9.2) but often there is no obvious cause identified, with no suggestion of mismanagement of the third stage of labour.60,63,64 It is therefore in essence regarded as unpredictable.

BOX 9.2: Risk/predisposing factors for uterine inversion

•  Mismanagement of third stage of labour

•  Fundal implantation of the placenta

•  Connective tissue disorders

•  Congenital abnormalities of the uterus (e.g. bicornuate/unicornuate uterus)

•  Retained placenta and abnormal adherence of the placenta

•  Short umbilical cord

•  Excessive fundal pressure

•  Fetal macrosomia

•  Primigravida

•  Multipara

•  Overstretched uterus

•  Certain drugs, such as those promoting tocolysis

The most common reported iatrogenic factor associated with uterine inversion is mismanagement of the third stage of labour that involves

•  Excessive and/or premature controlled cord traction (CCT) before signs of placental separation

•  Carrying out controlled cord traction on a relaxed uterus

•  Use of fundal pressure with or without cord traction

Controlled cord traction (CCT) must never be carried out on a relaxed uterus. At the time of uterine contraction, CCT with counter-traction must be applied to support and stabilise the uterus. It is worth noting that CCT is not intended to separate the placenta from the uterine wall but to facilitate its removal only. Midwives need to be mindful of this when managing the third stage of labour as well as the dangers of combining active and physiological third-stage management.⁶⁵ Active management of the third stage of labour done correctly is currently deemed best-practice and is now potentially perceived as the worldwide standard of care. It has been documented that active management of the third stage of labour has reduced the incidence of uterine inversion.66,67 There is, however, some suggestion that with more women in the United Kingdom delivering in the community in the future, hypothetically there could be an increase in the incidence of uterine inversion as these women are more likely to have a physiological third stage of labour.⁶⁰

The high incidence of uterine inversion in resource-poor areas is believed to be associated with the absence of active management of the third stage of labour and the lack of skilled or trained birth attendants. Suitable education and training regarding the third stage of labour specifically focussing on safe physiological management of the third stage, as well as diagnosis and management of uterine inversion, should be made available to traditional birth attendants and family physicians, so that this potentially life-threatening emergency can be avoided.⁶⁸

Other factors that may be associated with uterine inversion56,59,63 are shown in Box 9.3.

BOX 9.3: Factors associated with uterine inversion

•  Fundal implantation, abnormal placental adherence

•  Decompression of an overstretched uterus as in the case of a macrosomia or multiparity

•  Retained placenta

•  Vacuum extraction

•  Uterine structure anomaly

•  Short umbilical cord

•  Antenatal use of magnesium sulphate (can promote tocolysis, however lacks evidence)

•  Precipitate labour

•  Connective tissue disorders such as Marfan syndrome, Ehlers-Danlos syndrome

•  VBACs (although risk is minimal)

Signs and symptoms

The main fundamental signs of uterine rupture are shock, severe pain and bleeding along with clinical findings.69,70 Other clinical indications include lumps, masses and tenderness.⁶⁰

Signs

Symptoms

Lump in the vagina

Abdominal tenderness

Severe abdominal pain

Sudden cardiovascular collapse: shock

Absence of uterine fundus on palpation

Postpartum haemorrhage

Polypoidal red mass in the vagina with placenta attached

PAIN

Pain is usually in the pelvic region and can be described as severe cramping or lower back pain accompanied by a bearing-down sensation. This is due to the traction on the infundibulopelvic ligaments, round ligaments and the ovaries.⁷¹

SHOCK

Shock occurs in approximately 40% of cases with the signs usually sudden and acute and may be inconsistent to the amount of blood loss visualised. This is generally thought to be due in part to the parasympathetic response to traction of the uterine suspensory ligaments and is often accompanied by profound bradycardia.⁷² Ultimately shock will be as a result of haemorrhage and therefore inversion should always be eliminated in cases of acute postpartum collapse with or without haemorrhage.⁶³

Diagnosis

Uterine inversion is rare, and therefore may not be immediately considered; as a result healthcare professionals must be vigilant as it can be a life-threatening obstetric emergency. The clinical presentation and diagnosis depend on the classification and severity with obesity making the diagnosis slightly more difficult. A first-degree inversion is also more difficult to diagnose and can be missed as the fundus of the uterus is not visible or palpable at the cervix. Abdominal examination however may demonstrate dimpling of the uterine fundus and a bimanual examination will aid in confirming the diagnosis.⁷³ Further diagnostic tools such as imaging studies may be considered.

The diagnosis in both second-and third-degree inversion is clinical in nature with clear signs of the uterine fundus in the vagina or beyond.⁵⁶ In a third-degree uterine inversion, the uterine endometrium with or without the attached placenta may be visible.⁷³ On abdominal palpation there is an absence of the uterine fundus or existence of a noticeable defect. These findings require immediate intervention.

Differential diagnosis

As shock is a prime indication of an acute event it is necessary to eliminate any other clinical conditions. Differential diagnosis includes pulmonary embolism, uterine rupture, amniotic fluid embolism and acute myocardial infarction or marked uterine atony.70,74 A prompt vaginal examination will confirm the presence of uterine inversion and once confirmed it is crucial to take action immediately to minimise maternal morbidity and mortality. Delayed treatment will cause the uterus to become swollen and congested and may also lead to the formation of a contraction ring, all of which will impede replacement of the uterus and compromise the overall clinical status of the woman.⁵⁶

Immediate management

It is vital that management is based upon contemporaneous evidence and each unit should have evidence-based guidelines and protocols on both management of the third stage of labour and uterine inversion. All midwives should have knowledge and skills in both the active and physiological management of the third stage of labour.

IMMEDIATE MANAGEMENT IN HOSPITAL

As with all obstetric emergencies assistance is required and this is activated with the emergency call system specific to each unit. This ensures all relevant intra-professional team members including a consultant obstetrician and anaesthetist are present. The management consists of two vital components: the immediate treatment of shock and the replacement of the uterus.56,75 Any oxytocin infusion must be stopped immediately once inversion has been confirmed and withheld until correction has taken place. Replacement of the uterus is the quickest way to treat neurogenic shock.⁷²

Replacement of the uterus

This should be attempted whether the placenta has separated or not. Gentle manipulation is instigated to try and return the uterus to the vagina if it has prolapsed outside the introitus – no attempt should be made to manually remove the placenta if it has not separated. This would only exacerbate clinical shock and contribute to further massive haemorrhage.74,76 It is thought that the attached placenta prevents bleeding because the uterine sinuses are not exposed.

Manual repositioning of the uterus

If the uterine fundus can be felt or indeed is visible then the uterus should be replaced manually. This procedure is commonly referred to as the Johnson manoeuvre. The midwife or obstetrician inserts their hand into the vagina and cups the fundus of the uterus in the palm of their hand. Pressure is then applied back up and along the long axis of the vagina towards the posterior fornix of the vagina.60,77 When feeding the uterus back through the cervix it is fundamental to reposition the last section of the uterus that inverted first, to avoid overlapping tissue at the cervix which would further compound the oedema and congestion. Counter-support must also be applied as the uterus is put back by placing the other hand over the abdomen. Once the uterus is reverted it is essential that the clinician’s hand remains inside the uterine cavity for several minutes until contraction takes place to ensure the uterus remains in the pelvis. Uterotonic drugs such as intravenous oxytocin should be administered to promote uterine tone and prevent recurrence of the inversion. If this procedure is performed before oedema and development of a contraction ring, then it should be successful and allows the cervix to re-form.60,74,78

In some circumstances the clinician will use myometrial relaxant medication to assist with replacement of the uterus. Magnesium sulphate, terbutaline and salbutamol are the most commonly prescribed drugs due to their availability and frequent administration. There have been reports of good results with the use of nitroglycerin, with benefits cited as quicker onset of uterine relaxation and quick dissipation of the effect, obviating the need for reversal, as well as less effect on haemodynamics than with magnesium sulphate. These medications will not only relax the uterus but will also relax a cervical contraction ring.56,79

Once the uterus has been successfully replaced manual removal of the placenta is necessary – this will generally take place in theatre under a general anaesthetic due to the risk of postpartum haemorrhage.

Hydrostatic methods

If manual replacement fails, the hydrostatic method should be used as recommended by the World Health Organization.⁸⁰ Before this method is attempted, uterine rupture must be excluded. The procedure is performed in the operating theatre with the woman in the lithotomy position. The hydrostatic pressure involves warm sterile water or isotonic sodium chloride solution being rapidly instilled into the vagina via a rubber tube or intravenous giving set, while the clinician’s hand blocks the introitus. The fluid flows into the posterior aspect of the vagina and pushes the fundus upwards into its natural position by hydrostatic pressure. The bag of fluid should be elevated approximately 100–150 cm above the level of the vagina to ensure sufficient pressure. A problem associated with this method is the intricacy in maintaining a tight seal at the introitus. However, there are reports that this can be overcome by the use of a silastic ventouse cup positioned just inside the vagina, with tubing connected to the fluid, although a hand may still be necessary to ensure a tight seal. Despite large volumes of fluid being used there has been no reported incidence of embolus or pulmonary oedema.60,68,70,81

There is some evidence in the literature that the use of a Bakri balloon has been successful in preventing recurrence once the uterus has been manually repositioned. The Bakri balloon method is used to maintain the structural integrity of the uterine body following reposition. The balloon insertion ensures that the balloon conforms to the contours of the uterine cavity to prevent reinversion of the uterus as a spherical body exerting pressure to the cavity. When inserting the balloon it should be lifted up as much as possible into the cavity using placental forceps so ensuring that the uterine supporting ligaments are then extended, thus creating a combination of both Johnson’s method and hydrostatic pressure. In addition, this method also has a haemostatic effect against haemorrhage, which is the primary role of the Bakri balloon.82–85

If immediate replacement is not possible, the woman’s condition should be stabilised and she must be taken to theatre for a general anaesthetic. Manual replacement may then be possible and if not, then surgical intervention in the form of a laparotomy will be required.

IMMEDIATE MANAGEMENT IN THE HOME

No attempt should be made to remove the placenta for the reasons stated above.

Assistance

Call the emergency services (in the United Kingdom dial 999) and arrange for an immediate transfer to hospital by ambulance. The nearest consultant-led obstetric unit should be contacted and made aware of transfer and acuteness of situation. While awaiting the emergency services the following procedures should be carried out.

Resuscitation and treatment of shock

Even though a woman may not display signs of shock initially, IV cannulation and fluid replacement must be commenced as these women can deteriorate suddenly.

Replacement of the uterus

An attempt to replace the uterus using the Johnson manoeuvre described above should be undertaken by the attending clinician at home. If this is unsuccessful and the uterus is inverted outside the vulva, efforts should be made to gently return it into the vagina to prevent further shock. If this is not deemed possible then the uterus should be covered in sterile gauze that is soaked with either warm saline or water. It is useful to place a plastic bag over the gauze to retain the heat and moisture. This can then be further wrapped in a towel to preserve warmth and potentially delay the onset of shock. Reassurance and support must be given to the woman at all times.

Ongoing management

Following a uterine inversion, women need to be managed in either an intensive care environment or obstetric high dependency unit depending on the amount of intervention they required. It is vital that they have adequate antibiotic cover and close observation of haemoglobin and clotting levels is necessary in the immediate hours postpartum. Regular checking of the uterine fundus and blood loss is crucial and a senior obstetrician must have regular input into care. A referral to physiotherapy is also required. Debriefing of the events must take place with the woman and her family at a suitable time. The midwife involved in the case should be included in this meeting.

The woman will also require some counselling regarding the possibility of recurrence of uterine inversion in a subsequent labour. It is fundamental that discussion of this and recommended place and mode of delivery for future pregnancies are undertaken by a consultant obstetrician.

Professional issues

The midwife should be given the opportunity to reflect and discuss the events, in particular the management of the third stage of labour, with her Supervisor of Midwives.

It is paramount that all documentation is recorded contemporaneously and illustrates the course of events that took place and all interventions that were initiated. As with all obstetric emergencies, if notes are written retrospectively then this fact must be clearly recorded, including date and time of events. Patient safety and risk management documentation must also be completed for these clinical circumstances so that management and treatment can be investigated. This then allows constructive criticism, appraisal or changes to policies and guidelines to be made where deemed appropriate.

Summary of midwifery responsibilities

•  Ensure management of the third stage is always exemplary.

•  Maintain up-to-date knowledge of signs, symptoms and actions necessary for uterine inversion.

•  Be aware of local policies and guidelines related to management of uterine inversion.

•  If uterine inversion is suspected, call for help immediately if in hospital, or arrange emergency transfer if at home.

•  Maintain knowledge of Johnson manoeuvre for replacing the uterus, as speed of replacement is vital.

•  Be aware of hydrostatic methods of replacement of the uterus to enable efficient assistance to be given to the obstetrician.

•  Ensure clear and contemporaneous documentation is maintained.

•  Communicate with the woman and her family throughout and after the emergency.

REFERENCES

1.  Nahum GG. 2015. Uterine Rupture in Pregnancy Medscape. Available at http://reference.medscape.com/article/275854-overview (accessed May 25, 2015).

2.  MacDorman M, Declerq E, Menacker F. 2011. Recent trends and patterns in cesarean and vaginal births after C(VBAC) deliveries in the United States. Clinics in Perinatology, 38(2):179–192.

3.  Black C, Kaye JA, Jick HC. 2005. Cesarean delivery in the United Kingdom: Time trends in the general practice research database. Obstetrics and Gynecology, 106:151–155.

4.  Homer CSE, Johnson R, Foureur M. 2011. Next birth after caesarean section: Changes over a nine-year period in one Australian state. Midwifery, 27(2):165–169.

5.  Knight HE, Gurol-Urganci I, van der Meulen JH, Mahmood TA, Richmond DH, Dougall A, Cromwell DA. 2014. Vaginal birth after caesarean section: A cohort study investigating factors associated with its uptake and success. BJOG: An International Journal of Obstetrics and Gynaecology, 121(2):183–192.

6.  Dow M, Wax J, Pinette M, Blackstone J, Cartin A. 2009. Third-trimester uterine rupture without previous caesarean: A case series and review of the literature. American Journal of Perinatology, 26(10):739–744.

7.  Porreco R, Clarke S, Belfort M, Diddy G, Meyers J. 2009. The changing spectre of uterine rupture. American Journal of Obstetrics and Gynecology, 200(3):269–270.

8.  Zwart JJ, Richeters JM, Ory F, de Vires JI, van Roosmaien J. 2009. Uterine rupture in the Netherlands: A nationwide population-based cohort study. BJOG: An International Journal of Obstetrics and Gynaecology, 116(8):1069–1078.

9.  Hofmeyer GJ, Say L, Gülmezoglu A. 2005. WHO systematic review of maternal mortality and morbidity: The prevalence of uterine rupture. BJOG: An International Journal of Obstetrics and Gynaecology, 112(9): 1221–1228.

10.  Al-Zirqi I, Stray-Perdersen B, Forsén L, Daltveit LK, Vangen S. 2015. Uterine rupture: Trends over 40 years [Epub ahead of print]. BJOG: An International Journal of Obstetrics and Gynaecology. doi:10.1111/1471-0528.13394. (accessed June 3, 2015).

11.  Fitzpatrick KE, Kurinczuk JJ, Alfirevic Z, Spark P, Brocklehurst P, Knight M. 2012. Uterine rupture by intended mode of delivery in the UK: A national case-control study. Available at http://www.ncbi.nlm.nih.gov/pmc/articles/pmc3302846/ (accessed June 2, 2015).

12.  Royal College of Obstetricians and Gynaecologists (RCOG). 2007. Birth after Previous Caesarean Birth. Green-Top Guideline No 45. London: RCOG.

13.  UK Obstetric Surveillance System (UKOSS). 2012. Surveillance of Uterine Rupture Available at https://www.npeu.ox.ac.uk/ukoss/current-surveillance/topfph (accessed May 25, 2015).

14.  Talaulikar VS, Arulkumaram S. 2015. Vaginal birth after caesarean section. Obstetrics, Gynaecology and Reproductive Medicine. Available at http://dx.doi.org/10.1016/j.ogrm.2015.04.005 (accessed June 1, 2015).

15.  Guise JM, Eden K, Emeis C, Denman MA, Marshall N, Fu RR, Janik R, Nygren P, Walker M, McDonagh M. 2010. Vaginal birth after cesarean: New insights. Evidence Report Technology Assessment, March (191): 1–397.

16.  Mitali D, Varman R. 2012. Vaginal birth after caesarean section: A practical evidence-based approach. Obstetric and Gynaecology Reproductive Medicine, 22(7):177–185.

17.  American Congress of Obstetricians and Gynecologists. 2010. Vaginal Birth after Cesarean Section: Practice Bulletin Clinical Management Guidelines for Obstetricians – Gynecologists. Available at http://www.acog.org/Resources-And-Publications/Practice-Bulletins/Committee-on-Practice-Bulletins-Obstetrics/Vaginal-Birth-After-Previous-Cesarean-Delivery (accessed May 25, 2015).

18.  Landon MB, Lynch CD. 2011. Optimal timing and mode of delivery after cesarean with previous classical incision or myomectomy: A review of the data. Seminars in Perinatology, 35(5):257–261.

19.  Stamilio DM, DeFranco E, Paré E, Odibo AO, Peipert JF, Allsworth JE, Stevens E, Macones GA. 2007. Short interpregnancy interval: Risk of uterine rupture and complications of vaginal birth after cesarean delivery. Obstetrics and Gynecology, 110(5):1075–1082.

20.  Caughey AB. 2013. Vaginal birth after cesarean delivery. Medscape. Available at http://emedicine.medscape.com/article/272187-overview (accessed May 15, 2015).

21.  Bujold E, Gauthier RJ. 2010. Risk of uterine rupture associated with an interdelivery between 18 and 24 months. Obstetrics and Gynecology, 115:1003–1006.

22.  Zelop CM, Shipp TD, Repke JT, Cohen A, Lieberman E. 2000. Effect of previous vaginal delivery on the risk of uterine rupture during a subsequent trial of labour. American Journal of Obstetrics and Gynecology, 183(5):1184–1186.

23.  Humphries G. 2014. The Suture Debate ICAN (International Caesarean Awareness Network). Available at http://www.ican-online.org/wp-content/uploads/2014/06/The-Suture-Debate.pdf (accessed May 25, 2015).

24.  Roberge S, Demers S, Berghella V, Chaillet N, Moore L, Bujold E. 2014. Impact of single-vs double layer closure on adverse outcomes and uterine scar defect: A systematic review and meta-analysis. AJOG, 211(5):453–460.

25.  Durnwald C, Mercer B. 2003. Uterine rupture, preoperative and perinatal morbidity after single-layer and double-layer closure at cesarean delivery. AJOG, 189(4):925–929.

26.  Shipp T, Zelop C, Cohen A, Repke J, Lieberman E. 2003. Post-cesarean delivery fever and uterine rupture in a subsequent trial of labor. Obstetrics and Gynecology, 101:136–139.

27.  Walsh CA, O’Sullivan RJ, Foley ME. 2006. Unexplained prelabor uterine rupture in a term primigravida. Obstetrics and Gynecology, 108(3):725–727.

28.  Kumakiri J, Takeuchi H, Itoh S, Kitade M, Kikuchi I, Shimanuki H, Kumakiri Y, Kuroda K, Takeda S. 2008. Prospective evaluation for the feasibility and safety of vaginal birth after microscopic myomectomy. Journal of Minimally Invasive Gynecology, 15(4):420–424.

29.  Neilson JP, Lavender T, Quenby S, Wray S. 2003. Obstructed labour. British Medical Bulletin, 67:191–204.

30.  Mizutamari E, Honda T, Ohba T, Katabuchi H. 2014. Case report: Spontaneous rupture of an unscarred uterus in a primigravid woman at 32 weeks of gestation. Case Reports in Obstetrics and Gynecology. Available at http://dx.doi.org/10.1155/2014/209585 (accessed July 17, 2015).

31.  Khong TY. 2008. The pathology of placenta accreta, a worldwide epidemic. Journal of Clinical Pathology, 61(12):1243–1246.

32.  Langer J. 2011. Emergency Ultrasound: An Issue of Ultrasound Clinics. New York: Elsevier.

33.  Ronel D, Wiznitzer A, Sergienko R, Zlotnik A, Sheiner E. 2012. Trends, risk factors and pregnancy outcome in women with uterine rupture. Archives Gynecology and Obstetrics, 285(2):317–321.

34.  Elbmann CM, Kollinger M, Gmeinwieser J, Leser HG, Holstege A, Scholmerich J. 1997. Spontaneous rupture of liver in a patient with Ehlers Danlos disease type IV. Digestive Diseases and Science, 42:1724–1730.

35.  Dodd JM, Crowther CA. 2006. Elective repeat caesarean section versus induction of labour for women with a previous caesarean birth. The Cochrane Collaboration Review. Available at http//:onlinelibrary.wiley.com/doi/10.1002/14651858.cd004906.pub2/epdf/standard (accessed July 17, 2015).

36.  Brill Y, Kingdom J, Thomas J, Fraser W, Milne JK, Thomas M, Windrim R. 2003. The management of VBAC at term: A survey of Canadian obstetricians. Journal of Obstetrics and Gynaecology Canada, 25:300–310.

37.  Oladipo A, Syed A. 2008. The views of obstetricians in the south-west of England on the use of prostaglandins and syntocinon in VBAC. Journal of Obstetrics and Gynaecology, 28(2):177–182.

38.  Buhimschi CS, Buhimschi IA, Patel S, Malinow AM, Weiner CP. 2005. Rupture of the uterine scar during term labour: Contractility or biochemistry? BJOG: An International Journal of Obstetrics and Gynaecology, 112:38–42.

39.  Kaczmarczyk M, Sparen P, Terry P, Cnattingius S. 2007. Risk factors for uterine rupture and neonatal consequences of uterine rupture: A population based study of successive pregnancy in Sweden. BJOG: An International Journal of Obstetrics and Gynaecology, 114:1208–1214.

40.  Dekker GA, Chan A, Luke CG, Priest K, Riley M, Halliday J, King JF. et al. 2010. Risk of uterine rupture in Australian women attempting vaginal birth after one prior caesarean section: A retrospective population based cohort study. BJOG: An International Journal of Obstetrics and Gynaecology, 117:1358–1365.

41.  Tang A, Bellal J, Coc C, Rhee P. 2013. Trauma. In: van de Velde M, Schofield H, Plante LA (Eds.). Maternal Critical Care: A Multidisciplinary Approach. New York: Cambridge University Press.

42.  Francois K. 2011. Postpartum haemorrhage. In: Foley MR, Storng TH, Gartie TJ (Eds.). Obstetric Intensive Care Manual. 3rd ed. New York: McGraw-Hill Medical.

43.  Petrone P, Talving P, Browder T, Teixeira PG, Fisher O, Lozornio A, Chan LS. 2011. Abdominal injuries in pregnancy: A 155-month study at two level 1 trauma centres. Injury, 42(1):47–49.

44.  Manoharan M, Wuntakal R, Erskine K. 2011. Review uterine rupture: A revisit. Obstetrician and Gynaecologist, 12:223–230.

45.  Guiliano M, Closset E, Therby D, LeGoueff F, Deruelle P, Subtil D. 2014. Signs, symptoms and complication of complete and partial uterine rupture during pregnancy and delivery. European Journal of Obstetric and Gynaecology Reproductive Biology, 179:130–134.

46.  Phelan JP, Korst LM, Settles DK. 1998. Uterine activity patterns in uterine rupture: A case control study. Obstetrics and Gynaecology, 92:394–397.

47.  Matsuo K, Scanlon JT, Atlas RO, Kopelman JN. 2008. Staircase sign: A newly described uterine contraction pattern seen in rupture of unscarred gravid uterus. Journal of Obstetric Gynaecology Research, 34:100–104.

48.  Harris CM. 2011. Trauma and pregnancy. In: Foley MR, Storng TH, Gartie TJ (Eds.), Obstetric Intensive Care Manual. 3rd ed. New York: McGraw-Hill Medical.

49.  Augustin G. (Ed.). 2014. Spontaneous uterine rupture. In: Acute Abdomen during Pregnancy. Chapter 16. Switzerland: Springer.

50.  Matsubara S, Shimada K, Kuwata T, Usui R, Suzuk M. 2011. Thin anterior wall with incomplete uterine rupture in a primigravida detected by palpation and ultrasound: A case report. Journal of Medical Case Reports, 5(14):1752–1947.

51.  Ahmadi F, Siahbazi S, Akhbari F. 2013. Incomplete cesarean scar rupture. Journal of Reproductive Infertility, 14(1):43–45.

52.  Kok N, Wiersma IC, Opmeer IC, De Graaf IM, Mol BW, Paikrit E. 2013. Sonographic measurement of lower uterine segment thickness to predict uterine rupture during a trial of labor in women with previous cesarean section: A meta-analysis. Ultrasound Obstetrics and Gynecology, 42(2):132–139.

53.  Jastrow N, Chaillet N, Roberge S, Morency AM, Lacasse Y, Bujold E. 2010. Sonographic lower uterine segment thickness and risk of uterine scar defect: A systematic review. Obstetrics, April: 321–327.

54.  Ofir K, Sheiner E, Levy A, Katz M, Mazor M. 2004. Uterine rupture: Differences between a scarred and unscarred uterus. AJOG, 191(2):425–429.

55.  Colmorn LB, Petersen KB, Jakobsson M, Lindqvist PG, Klungsoyr K, Källen K, Bjarnadottir RI. et al. 2015. The Nordic Obstetric Surveillance Study: A study of complete uterine rupture, abdominal invasive placenta, peripartum hysterectomy and severe blood loss at delivery. Acta Obstetricia et Gynecologica Scandinavia, 94(7):734–744.

56.  Leal RFM, Luz RM, Branco RCC. 2014. Total and acute uterine inversion after delivery: A case report. Journal of Medical Case Reports, 8: 347.

57.  Hussain M, Jabeen T, Liaquat N, Noorani K, Bhutta SZ. 2004. Acute puerperal uterine inversion. Journal of the College of Physician and Surgeons–Pakistan, 14(4):215–217.

58.  Milenkovic M, Khan J. 2005. Inversion of the uterus: A serious complication at childbirth. Acta Obstetricia et Gynecologica Scandinavica, 84:95–106.

59.  Witteveen T, van Strsken G, Zwart J, van Roosmalen J. 2013. Puerpal uterine inversion in the Netherlands: A nationwide cohort study. Acta Obstetricia et Gynecologica Scandinavia, 92(3):334–337.

60.  Bhalla R, Wuntakal R, Odejinmi O, Khan RU. 2009. Review: Acute inversion of the uterus. Obstetrician and Gynaecologists, 11:13–18.

61.  Coates T. 2009. Midwifery and obstetric emergencies. In: Fraser DM, Ma C (Eds.). Myles Textbook for Midwives. 15th ed. London: Churchill Livingstone.

62.  Doumouchtsis S. 2011. Uterine inversion. In: Arulkumaran S, Regan L, Papageorghiou AT, Monga A, Farquharson DIM (Eds.). Oxford Desk Reference Obstetric and Gynaecology. New York: Oxford University Press, pp. 426–428.

63.  Majid H, Nawaz L, Ismail L, Luker R, Kalla S. 2008. Acute uterine inversion as a cause of major post-partum haemorrhage: A case report and review of the literature. Internet Journal of Gynaecology and Obstetrics, 12(1):1–9.

64.  Keriakos R, Chaudhuri SR. 2011. Managing major postpartum haemorrhage following acute inversion with Rusch balloon catheter. Case Reports in Critical Care, 1–3. Available at http://dx.doi.org/10.1155/2011/541479 (accessed July 27, 2015).

65.  Ganges F, Beck D, Engelbrecht M. 2007. Prevention of postpartum haemorrhage: Implementing active management of the third stage of labour. In: Armbustor D. et al. (Eds.) A Reference Manual for Health Care Providers. Seattle: Path, pp. 27–29.

66.  Kadkol RA, Lakshmi KS. 2015. Critical care management of third stage complication: Acute puerperal uterine inversion. Journal of Evidence Based Medicine and Healthcare, 2(5):566–568.

67.  Baskett T. 2002. Acute uterine inversion: A review of 40 cases. Journal of Obstetrics and Gynaecology Canada, 24:953–956.

68.  Ojabo OA, Adesiyun AG, Ifenne DI, Hember-Hilekan S, Umar H. 2015. Acute uterine inversion: A case report and literature review. Archives of International Surgery, 2015(5):52–55.

69.  Mirza FG, Gaddipati S. 2009. Obstetric emergencies. Seminars in Perinatology, 2009(33):97–103.

70.  Beringer RM, Patteril M. 2004. Puerperal uterine inversion and shock. British Journal of Anaesthesia, 92(3):423–441.

71.  Kean LH. 2000. Other problems of the third stage. In: Kean LH, Baker PN, Edelstone DI (Eds.). Best Practice in Labour Ward Management. Edinburgh: Churchill Livingstone.

72.  Clyburn P. 2010. Shock. In: Clyburn P, Collis R, Harris S (Eds.). Obstetric Anaesthesia for Developing Countries. New York: Oxford University Press.

73.  Saxena R. 2014. Postpartum haemorrhage. In: Saxena R (Ed.). Bedside Obstetrics and Gynecology. India: Jaypee Medical.

74.  Davis G. 2015. Collapse in the puerperium. In: Hollingworth T (Ed.). Differential Diagnosis in Obstetrics and Gynaecology. 2nd ed. Boca Raton, FL: CRC Press.

75.  Ihama Y, Fukasawa M, Ninomiya K, Miyazaki T. 2014. Acute puerperal uterine inversion. Forensic Science Medical Pathology, 10:272–274.

76.  Arulkumaran S. 2006. Emergencies in Obstetrics and Gynaecology. Oxford: Oxford University Press.

77.  Holmes D, Baker P. 2014. Midwifery by Ten Teachers. Boca Raton, FL: CRC Press.

78.  Johnson AB. 1949. A new concept in replacement of the inverted uterus and report of nine cases. AJOG, 57:557–562.

79.  Malik R, Sangwan V, Jain S, Jain N. 2015. Management of acute subacute puerperal uterine inversion with intravenous nitroglycerin. Journal of Gynecologic Surgery, 31(2):104–106.

80.  World Health Organisation (WHO). 2000. Correcting uterine inversion. Available at http://www.who.int/reproductive-health/impact/correcting_p91_p94>html (accessed August 3, 2015).

81.  Ogueh O, Ayida G. 1997. Acute uterine inversion: A new technique of hydrostatic replacement. BJOG: An International Journal of Obstetrics and Gynaecology, 104:951–952.

82.  Ida A, Ito K, Kubota Y, Nosaka M, Kato H, Tsuji Y. 2015. Successful reduction of acute puerperal uterine inversion with the use of a Bakri postpartum balloon. Case Reports in Obstetrics and Gynecology, Article ID 424891.

83.  Gupta P, Sahu R, Huria A. 2014. Acute uterine inversion: A simple modification of hydrostatic method of treatment. Annuls of Medical and Health Research, 4(2):264–267.

84.  Grönvall M, Tikkaneen M, Tallberg E, Paavonen J, Stefanovic V. 2013. Use of Bakri balloon tamponade in the treatment of postpartum hemorrhage: A series of 50 cases from a tertiary hospital. Acta Obstetricia et Gynecologica Scandinavia, 92(4):433–438.

85.  Majid HS, Pilsniak A, Reginald PW. 2009. Recurrent uterine inversion: A novel treatment approach using SOS Bakri balloon. BJOG: An International Journal of Obstetrics and Gynaecology, 116(7):999–1001.

10

Intrapartum and primary postpartum haemorrhage

HELEN CRAFTER

Introduction

Incidence of severe obstetric haemorrhage

Diagnosis and management of intrapartum haemorrhage

Management of haemorrhage after delivery of the placenta

Conclusion

Summary of midwifery responsibilities

References

INTRODUCTION

When the usually joyous event of birth is accompanied by excessive bleeding in the mother, the atmosphere in the birth room can change very quickly from being one of calm supportiveness to one of bustling intensity. Yet if the midwife and other health professionals are knowledgeable, well equipped and confident in their skills, most cases of haemorrhage can be prevented from causing long-term physical damage or emotional trauma to the mother. However, there is no place for complacency. Severe obstetric haemorrhage can be lethal and if it does not kill, it can leave the woman physically damaged and all the family deeply distressed for a very long time. This chapter aims to equip midwives with the knowledge and confidence to prevent and deal with excessive bleeding at and around the time of birth.

Intrapartum haemorrhage (IPH) and primary postpartum haemorrhage (PPH) are commonly defined as excessive blood loss from the genital tract during labour, or in the 24 hours following it, respectively, amounting to 500 mL or more, or of any amount that compromises the well-being of the mother. However, these definitions require challenge.

Well-nourished pregnant women may lose significantly more blood than 500 mL with no ill effects and before they notice the light-headedness which accompanies acute anaemia. This is hardly surprising given that before pregnancy women have a circulating plasma volume of approximately 4 L and by 32 weeks of gestation this has risen on average by 40%–50%.¹ The definition is perhaps more appropriate to the less well-nourished women of previous decades in the Western world and of women living in poverty today, particularly in resource-poor areas. Most health professionals would argue that it is the woman’s overall condition that should indicate to her midwife whether she has lost an excessive amount of blood, and this will be dictated by her haematological status prior to labour and the events that occur during labour. Another problem of defining intrapartum and postpartum blood loss by amount is that estimation of blood loss at delivery by health professionals is highly inaccurate, and becomes more inaccurate the more blood a woman loses.2,3 In the latest UK Confidential Enquiries into Maternal Deaths and Morbidity⁴ it is noted that due to the increase in circulating blood volume in pregnancy to 100 mL/kg, blood loss estimates should take a woman’s stature into account. In addition, blood often remains concealed as a retroplacental clot, or occasionally as intra-abdominal bleeding. Finally, a good midwife does not wait for 500 mL of blood to trickle or gush from the vagina at birth before she acts. If she sees the potential for excessive blood loss unfolding, she acts promptly to try to prevent a haemorrhage or reduce the blood loss. The most important part of the definition of IPH and primary PPH above is therefore ‘any amount of blood loss that compromises the well-being of the mother’. However, it should always be borne in mind that compromise to the mother’s condition may not be apparent until she has lost a dangerous amount of blood (see Table 10.1). This chapter concentrates more on contemporaneous evidence about which actions are effective when a woman bleeds excessively. The Cochrane Database of Systematic Reviews advises that treatment for primary PPH needs further research, particularly where women fail to respond to uterotonic therapy such as oxytocin.⁵

Table 10.1  Maternal symptoms of primary PPH by amount of blood loss

Average proportion lost of total blood volume (=6 L) of a pregnant woman

Amount of blood lost

Degree of shock in a woman with BMI 20–25

Physiological effects

Signs and symptoms a health professional will notice

20%

1200 mL

Mild

Decreased perfusion of non-vital organs and tissues, e.g. bone, fat and skeletal muscle

Pale and cool skin

Woman starts to complain of thirst

Clamminess

Possible mild tachycardia and small drop in blood pressure

20%–40%

1200–2400 mL

Moderate

Decreased perfusion to vital organs and tissues, e.g. gut, liver and kidneys

Skin on legs starts to mottle

Tachycardia more noticeable and further drop in blood pressure

Oliguria and/or anuria

40% and more

2400 mL +

Severe

Reduced perfusion to heart and brain

Agitation, restlessness, coma

Echocardiogram and electrocardiogram abnormalities. Metabolic acidosis and finally cardiac arrest

Source:  Adapted from Mukherjee S, Arulkumaran S. 2009. Obstetrics, Gynaecology and Reproductive Medicine, 19(5):121–126; Winter C et al. 2012. Practical Obstetric Multi-Professional Training PROMPT: Module 8 Major Obstetric Haemorrhage. Cambridge: Cambridge University Press.

INCIDENCE OF SEVERE OBSTETRIC HAEMORRHAGE

Worldwide, 140,000 women die of PPH each year, most within 24 hours of birth, and a further 20 million new mothers report significant morbidity from postnatal blood loss.⁸ Postpartum haemorrhage of 500 mL or more affected 13% of childbearing women in England in 2011–2012.⁹ Severe, life-threatening obstetric haemorrhage, in which women lose 1500 mL of blood or more, or require at least four units of blood by transfusion, remained steady at 6–6.7 per 1000 births from 1997 to 1998 in a study of women in South East Thames¹⁰ and in Scotland.¹¹ The term obstetric haemorrhage used in the latter studies above refers to both antepartum and postpartum haemorrhage, and although PPH is the more common of the two, APH often leads into a PPH due to the woman being already haemodynamically compromised when she gives birth.

In the 2014 Confidential Enquiries into Maternal Deaths⁴ 14 deaths were reported from 2009 to 2012 primarily due to postpartum haemorrhage, seven cases being attributed to atony and seven to genital tract trauma (including four ruptured uteri; this condition is discussed in Chapter 9). Of the women who died primarily from haemorrhage due to uterine atony, three had had spontaneous vaginal births and four had delivered by caesarean section (CS). Three of the women who died following CS weighed below 60 kg despite normal body mass index (BMI) measurements, hence the guidance from Mothers and Babies: Reducing Risk through Audits and Confidential Enquiries across the UK (MBRRACE-UK) that a woman’s stature should be taken into account when assessing the severity of PPH; small women having less circulating blood volume and therefore a lower tolerance of blood loss.

Confidential Enquiries over the last two decades have also suggested that some risk factors for haemorrhage are becoming more common, for instance

•  The increasing mean age of childbearing women

•  The increasing number of women with complex medical disorders choosing to become pregnant

•  An increase in the number of multiple pregnancies following assisted reproduction

•  An increasing caesarean section rate leading to subsequent placenta praevia and accreta

Causes and predisposing factors

Any combination of the causes (see Box 10.1) or predisposing factors (see Box 10.2) will increase the risk of IPH and early PPH.

Postpartum haemorrhage can also be classified in terms of ‘the four Ts’, and some women will develop more than one of these:

Tone – atony (poor uterine contraction), the most common cause

Trauma – to the uterus (rupture), cervix (tear), or vagina/perineum (haematoma, tear or episiotomy)

BOX 10.1: Causes

•  Placental abruption

•  Placenta praevia

•  Ruptured uterus

•  Cervical or vaginal lacerations

•  Atonic uterus, with or without retained products (placenta, membrane and/or blood clot)

•  Haematoma

Note: The woman could display signs of haemorrhage with a less usual site of bleeding, such as subcapsular liver rupture seen in pre-eclampsia and haemolysis, elevated liver enzymes and low platelets (HELLP) syndrome.¹²

Also beware of vasa praevia which presents with vaginal bleeding through fetal blood loss.

BOX 10.2: Physiological/medical predisposing factors

Small stature (even with a normal BMI)

Previous caesarean section

Raised blood pressure (more than 140/90 mm Hg)

Anaemia

Hydramnios or multiple pregnancy

APH or placenta praevia in current pregnancy

Prolonged labour

Precipitate labour

Injudicious use of Syntocinon

Genital infection

Obesity

Supine or semi-recumbent birth

Instrumental delivery

Caesarean delivery, especially as an emergency procedure

Mismanagement of the third stage of labour

Retained placenta

Morbidly adherent placenta

Clotting disorder

Amniotic fluid embolism

Tissue – retained placental tissue, membrane or blood clots

Thrombin – coagulation abnormalities

Some of the main causes of IPH and PPH in Box 10.1 are discussed in other chapters, so are not addressed here. However, the medical predisposing factors also warrant attention because contemporary evidence is increasingly becoming available as to how they can affect haemostasis before and after the third stage of labour, and how individual conditions should best be managed. Each of these is discussed separately here.

ATONIC UTERUS

Uterine atony remains the most common cause of postpartum haemorrhage with or without retained placental tissue.3,7

The uterus literally lacks muscle tone because the myometrium fails to contract and retract as or after the placenta separates. The ruptured blood vessels at the placental site, a key physiological feature of normal third stage of labour, are not compressed by the living ligature action of the myometrial fibres and bleeding is not controlled. In pregnancy at least 600–700 mL of blood crosses the placenta every minute¹³ and so atony can lead to rapid, heavy blood loss if efficient uterine action is not quickly achieved. Uterine atony is most commonly associated with incomplete separation of the placenta, retained cotyledon, membrane or blood clot, precipitate or prolonged labour, placenta praevia or abruption, general anaesthesia or mismanagement of the third stage. Sometimes its aetiology is unknown.

HAEMATOMA

A haematoma is a collection of blood in the tissues which cannot escape – literally, a large bruise. Haemotomas, when they occur, tend to form in the broad ligament or the lower genital tract during and immediately after birth. A haematoma which forms around the time of birth may occur as a result of a ruptured uterus in labour, or ruptured vulval varicose vein in the second stage of labour (see also Chapter 13).

SMALL STATURE

Women of small stature have a lower circulating blood volume than women of generous stature, reduced by up to 2 L of circulating blood volume.³ This may not be apparent from their BMI, which may be proportionate at 20 or above.

PREVIOUS CAESAREAN SECTION

Rising recent caesarean section rates are leading to questions about the effects on future pregnancy of a uterine scar. Two previous Confidential Enquiries into Maternal Deaths (2004 and 2007)¹⁴,¹⁵ and Royal College of Obstetricians and Gynaecologists (RCOG) Green-Top Guideline Number 27¹⁶ acknowledge that in England and Wales there is a rise in cases of placenta praevia and placenta accreta almost certainly due to the rise in caesarean section rates. While awaiting further research, both mothers and birth attendants need to be aware of this risk factor. Caesarean section should therefore be seen in the context of having risk factors for future pregnancies, not just for the present one.

RAISED BLOOD PRESSURE

Pre-eclampsia and gestational hypertension are known to be risk factors for postpartum haemorrhage.³ Importantly, for the management of maternal haemorrhage either before or after the birth, pre-eclampsia can progress rapidly,¹⁷ so a woman presenting with a primary diagnosis of acute haemorrhage may have undiagnosed pre-eclampsia and/or HELLP syndrome. Pre-eclampsia may make her blood pressure soar; haemorrhage may make it plummet. One condition may mask the other so different vital signs must be diligently monitored to effect accurate diagnosis and treatment. For all women presenting in labour with haemorrhage these should include a history of pregnancy and present symptoms, general appearance and condition, pulse, respiratory rate, blood pressure reading, blood oxygen saturation level, urinalysis and a haematological pre-eclampsia screen (see Chapter 5).

ANAEMIA

Women become anaemic in pregnancy due to poor diet, poor iron absorption or bleeding. Low haemoglobin level and iron stores predispose to intolerance of blood loss. Iron deficiency anaemia may also contribute to uterine atony due to depletion of uterine myoglobin levels³ (myoglobin is an iron- and oxygen-binding protein which accelerates oxygen perfusion and function in muscle cells).

HYDRAMNIOS, FETAL MACROSOMIA AND MULTIPLE PREGNANCY

When the membranes rupture in labour in cases of polyhydramnios, or following the birth of a very large baby or the first baby in a multiple pregnancy, the sudden and large reduction in the uterine cavity may precipitate placental separation. Where the uterus is overstretched in pregnancy, the muscle cells become less able to contract and retract efficiently in the third stage of labour. The cause of PPH is therefore atonic uterus (lacerations may also play a part when the fetus is macrosomic).

ANTEPARTUM HAEMORRHAGE IN CURRENT PREGNANCY

Both placental abruption and placenta praevia lead to anaemia from bleeding in pregnancy, and the reduction in red blood cells reduce the woman’s tolerance to blood loss at and following birth. See also Chapter 3.

PROLONGED LABOUR

Prolonged labour is characterised by weak and incoordinate contractions. Dehydration, ketosis and fatigue may play a part and ultimately uterine muscle will become exhausted. The resulting inertia can lead to uterine atony.

INJUDICIOUS USE OF PROSTAGLANDIN AND SYNTOCINON

Prostaglandins and the drug Syntocinon should be used with great caution. While useful in inducing labour, preventing excessively long labour and reducing the caesarean section rate when used wisely, imprudent overuse can damage both the mother and the baby. The use of both prostaglandins and Syntocinon has been implicated in cases of uterine rupture in labour, sometimes when the uterus has been scarred from previous birth or surgery.

After the birth PPH may occur when a Syntocinon infusion is stopped as soon as the infant is born and, in the absence of enough naturally produced oxytocin, the relaxed uterine muscle fibres allow excessive passage of blood from the recently separated placental vessels. Therefore Syntocinon should be discontinued quickly in labour if its use causes problems, however, it should not be discontinued abruptly after the birth of the baby and placenta when uterine muscle relaxation is undesirable.

INSTRUMENTAL DELIVERY

Some of the factors which predispose to Ventouse and forceps delivery will also predispose to PPH, such as multiple pregnancy, previous caesarean section and prolonged labour, thereby multiplying the risk. Instrumental delivery is also probably a risk factor in itself, as the natural rhythm of labour is countered by an unnaturally expedited birth and the necessity for the uterus to contract and retract immediately. Furthermore, women who have an instrumental delivery will frequently have an episiotomy and/or genital tract lacerations.

CAESAREAN DELIVERY

Caesarean birth is almost inevitably associated with a relatively high blood loss because of the amount of tissue incised to reach the baby. In elective surgery maternal oxytocin levels will be low, thereby increasing the risk of atonic uterus, although intravenous Syntocinon is routinely given to counteract this.

MISMANAGEMENT OF THE THIRD STAGE AND RETAINED PLACENTA

A full bladder in late labour, ‘fundus fiddling’ (where a health professional applies frequent, irregular pressure to the uterine fundus usually in order to check for good contractility), overstrong cord traction on an unseparated placenta and an inappropriate combination of techniques, all contribute to a raised incidence of PPH and/or a retained placenta. All interfere with the normal rhythmic contractions which are designed to exactly coordinate muscle contraction and retraction with placental separation, with or without administration of an oxytocic drug. A retained placenta following administration of an oxytocic is a risk factor for PPH in itself, because it can prevent the uterus from maintaining strong contractility. However, avoiding, observing for and managing excessive blood loss should be prioritised whichever way the third stage is managed.

MORBIDLY ADHERENT PLACENTA

This refers to placenta accreta, where the placental villi have attached through the decidua into the muscle layer of the uterus; placenta percreta where they have attached through the muscle layer; and the even rarer placenta increta, with attachment right through the muscle layer and encroaching into the perimetrium. PPH occurs when there is partial separation of the placenta, often because only part of the placenta is morbidly adherent, preventing the uterus from contracting adequately.

CLOTTING DISORDER

An idiopathic clotting disorder may be present in the mother during pregnancy and its existence may become apparent during routine blood tests, thereby alerting health professionals to an increased risk of bleeding.

Disseminated intravascular coagulopathy (DIC) is an acute condition that occurs when there is a large area of tissue damage, for instance following placental abruption, as a result of pre-eclampsia, following intrauterine fetal death or as a complication of PPH or haemorrhage from another cause. A massive release of thromboplastins from the damaged cells into the bloodstream causes widespread clotting throughout the circulation. Clotting factors are used up.¹⁸ Fibrinolysis is triggered and the production of fibrin degradation products (FDPs) further interferes with the process of normal clotting. When no further clotting can take place, uncontrolled bleeding occurs from any site in the body from where blood can escape. (See Box 10.7 for information about management and diagnosis of DIC.)

AMNIOTIC FLUID EMBOLISM

This rare condition tends to occur in labour, accompanied by DIC. The condition is discussed in Chapter 11.

SUPINE BIRTH

From a physiological perspective, if a woman gives birth in an upright position, her abdominal organs will naturally compress her uterus against her pelvic floor as the baby is born. However, if she gives birth in a supine or semi-recumbent position, she is not afforded this advantage. This is one of many choices available to the mother and midwife in aiming to prevent maternal haemorrhage from atony occurring.

NOTE ON THE CONDITION ‘VASA PRAEVIA’

Vasa praevia is present when there is a velamentous insertion of the umbilical cord into a low-lying placenta. The unprotected fetal blood vessels therefore lie in the lower segment of the uterus, and in front of the presenting part of the fetus. When the membranes rupture, a fetal vessel may also rupture giving rise to severe fetal bleeding which escapes through the woman’s vagina. This is not a maternal haemorrhage; it is the fetus that can exsanguinate, and differentiation between maternal and fetal blood can be difficult.

Vasa praevia is a rare condition, and it is even rarer for a vasa praevia to tear and bleed. A skilled midwife may diagnose the condition with keen, knowledgeable observation and fetal heart rate surveillance. Fetal bleeding starts when the membranes rupture spontaneously or more commonly after their artificial rupture. The midwife will note that the mother will not show any signs of shock but, unless a speedy diagnosis is made and the fetus delivered within minutes, it will die through excessive blood loss.

Although uncommon, occurring in 1:6000 pregnancies, fetal death occurs in 44% of undiagnosed cases. If diagnosed on ultrasound, there is a 97% survival rate for the fetus,⁷ however, this pre-labour diagnosis is not always available.

DIAGNOSIS AND MANAGEMENT OF INTRAPARTUM HAEMORRHAGE

Vaginal bleeding in the first stage of labour may be due to a show (which can be quite heavy in late labour), placental abruption, undiagnosed placenta praevia (see Chapter 3) or rarely, a ruptured uterus (see Chapter 9) or vasa praevia.

Resuscitation if required, and diagnosis and management of the cause of bleeding must be the first priorities in dealing with IPH. It is good practice for protocols to be in place which give clear instructions about how to deal with major obstetric haemorrhage.3,4 Resuscitation and the presence of a second midwife, consultant obstetrician and consultant anaesthetist should be immediately sought to prevent severe collapse in the mother.

Undiagnosed bleeding in labour

On no account should vaginal examinations be done or pessaries, suppositories or enemas be given until placenta praevia has been categorically ruled out by a new ultrasound scan. These procedures can precipitate torrential haemorrhage.

Initial assessment and management of intrapartum haemorrhage

A woman who starts to bleed heavily per vaginam in labour will be extremely concerned both for her own safety and that of her baby. As the midwife deals with the situation, either at home or in hospital, her manner and communication skills will be crucial in enlisting the woman’s trust and co-operation. Her partner must also be taken into consideration.

Having excluded a normal heavy show in advanced labour, bleeding from haemorrhoids, and vasa praevia the midwife must decide whether the blood loss is trickling or gushing (bearing in mind a trickle can quickly become a gush), and on the likely cause. The physiology and management of placental abruption, placenta praevia and ruptured uterus are discussed in Chapters 3 and 9.

As she collects this information the midwife must also carry out observations of the woman. These may include general condition (including pallor, level of consciousness and pain), amount of blood loss, pulse, respirations, blood pressure, oxygen saturation, the nature of any contractions, abdominal girth, abnormal pain (present in between the contractions and a possible indication of Couvelaire and/or ruptured uterus) and the condition of the fetus. The midwife will be aware that IPH is unpredictable in its course and the woman’s condition may deteriorate rapidly with little or no warning. The midwife must therefore decide, while talking to the woman, how urgent the need is for a medical or paramedic presence.

In all cases of IPH at home or in a midwifery-led unit, it is prudent to agree and arrange immediate transfer to hospital, preferably to a maternity unit with an on-site, 24-hour haematology unit and blood bank. The midwife should undertake basic life support if necessary, site an intravenous infusion to access a vein and replace lost fluids, in the first instance with a crystalloid solution. Fluid balance recordings should be commenced. Paramedic assistance may be vital in helping with any necessary resuscitation and/or treatment of shock, as well as transfer to hospital.

BOX 10.3: Preparation for immediate delivery by caesarean section

•  Maintain resuscitation procedures until surgery.

•  Explain to the woman and her partner what is happening and why.

•  Maintain frequent observations of mother and fetus, record them and share them.

•  Inform and involve appropriate personnel, including obstetricians, midwives, anaesthetists, theatre staff, paediatricians and haematologists.

•  Group and crossmatch blood.

•  Make routine preparations for surgery, including consent, removal of jewellery and make-up, catheterisation and appropriate local skin care.

When in hospital, or on arrival in hospital, after summoning urgent medical aid, management of the labour must continue with basic life support if required, resuscitation, appropriate pain relief and a plan for care. If birth is not imminent, caesarean section will be considered (see Box 10.3). Needless to say such women must be prioritised for one-to-one or two midwives’ full attention and care. A modified early obstetric warning score (MEOWS) chart should be used to record observations which should be acted on appropriately and the SBAR (situation, background, assessment and recommendation) communication tool is ideal for structured communication and handover to other health professionals.¹⁹

Management of haemorrhage after the birth and before delivery of the placenta

Intrapartum haemorrhage after the birth of the baby, but before delivery of the placenta is often a midwifery emergency and although medical and senior midwifery aid must be summoned (or emergency services if at home), the situation must be dealt with immediately, even while waiting for help. Bleeding may be from the placental site (uterine atony) where the placenta has wholly or partially separated, or from a cervical or vaginal laceration.

The most common predisposing factors for a partially separated placenta include incoordinate action caused by ‘fundus fiddling’ or prolonged labour. Partial placenta accreta or percreta are also possibilities, although these conditions are rare. Lacerations may complicate any birth, and may be associated with compound presentation, a large baby and/or instrumental delivery.

Bleeding from a laceration is often obvious. If a vessel can be seen spurting or oozing blood it should be immediately clamped and sutured as soon as possible. Occasionally it is difficult to tell if bleeding is from the uterus, a laceration or both. If the bleeding vessel cannot be located and ligated, and heavy bleeding from the placental bed is suspected, it is prudent to get the placenta delivered as quickly as possible.

Partial separation should be suspected if there is vaginal bleeding with no apparent lengthening of the umbilical cord. Diagnosis is by vaginal examination. If the placenta can be felt just inside the uterine cavity it has separated and should be delivered by controlled cord traction so the cause of the bleeding can be quickly diagnosed and brought under control. However, if the fingers can be easily moved into and up the uterus, partial separation is the most likely cause of bleeding; this is a potentially dangerous situation.

If the woman has not recently passed urine, the bladder should be emptied. If she does not have an intravenous infusion with Syntocinon in place, a bolus of 10 units of intravenous Syntocinon should be administered and nipple stimulation considered, either by putting the baby to the breast or perhaps by the mother rolling her nipples herself. This will encourage natural oxytocin release within seconds and help the mother to feel she is involved in her own recovery.

The third stage should be actively managed; if the drug of choice is Syntometrine and has been given with the birth of the baby, the placenta and membranes should be delivered within 5–7 minutes before the ergometrine component closes the os. However, if the placenta remains partially attached and cannot be removed by controlled cord traction even with the addition of intravenous Syntocinon the birth attendants will need to proceed quickly to a manual removal of the placenta (see Box 10.4) to prevent blood loss becoming excessive. See Box 10.5 for a summary of pharmacological management.

Having carried out initial emergency procedures, the midwife should reassess ongoing bleeding and separation of the placenta. If an emergency situation persists and the baby has been born at home, transfer to hospital must be arranged. It is prudent to call for this help as soon as a complication is suspected. However, it is always preferable to deliver the placenta before transferring a woman by ambulance and every effort should be made to do so. It is highly dangerous to move a woman who is bleeding heavily from a partially separated placenta.

If it has not already been done, the midwife should now site an intravenous infusion. This must be done before accessible veins in the arms collapse, which would make the procedure more difficult and more time consuming. Community and free-standing birth centre midwives should be proficient in intravenous cannulation and hospital-based midwives will also find it advantageous to have this skill. A continuous intravenous route can then be used to replace lost fluid and administer drugs and blood products as necessary.

BOX 10.4: Manual removal of retained placenta (performed by an obstetrician if the woman is in hospital)

If the placenta is retained and there is no bleeding, it is likely that the placenta is still completely attached, as logically only a partially separated placenta will lead to uterine bleeding. A woman has a prolonged third stage of labour if the placenta has not delivered within 30 minutes of birth if actively managed, and an hour in a physiologically managed third stage.²² Before manual removal of the placenta is attempted intravenous access should be secured; oxytocic drugs should be given only if the woman is bleeding excessively; the woman should be offered analgesia in advance of the procedure (or anaesthetic in hospital), and offered a vaginal examination to assess the need to undertake the procedure.¹⁹ A retained placenta without heavy uterine bleeding is less of an obstetric emergency, but it may become one if not managed appropriately.

Procedure:

•  Observe strict aseptic technique.

•  Use elbow-length gloves.

•  Insert a whole hand (extended) through the os following the cord (if it is still attached to the placenta), while the other hand supports the fundus to prevent it being pushed upwards.

•  Slip the internal hand between the separated portion of the placenta and the wall of the uterus and gently scoop the placenta off with a spatula-like movement, moving the hand smoothly back and forth.

•  Once it has been separated, manually sweep all fragments of placenta from the placental site.

•  Grasp the placenta and manually remove it from the uterus.

•  Once the removal has been completed, the uterus should be vigorously massaged to rub up a contraction. Intravenous oxytocin is also indicated.

BOX 10.5: Common pharmacological methods of managing atony

INTRAMUSCULAR, INTRAVENOUS BOLUS OR INTRAVENOUS INFUSION (IVI) OF SYNTOCINON

Given intramuscularly Syntocinon takes 2½ minutes to act on the uterus and given intravenously, within 45 seconds. In acute primary PPH, 10 international units (IU) should be given by slow intravenous injection, followed up by 5–20 more units added to 500 mL intravenous solution and run into the vein at a rate sufficient to control uterine atony. This is the manufacturer’s recommended dose but in practice women may be given up to 50 units in 500 mL of intravenous fluid as maternity units each have their own slightly differing protocol. Fluid overload must be avoided as this has inherent dangers, particularly acute (formerly adult) respiratory distress syndrome (ARDS). Stronger concentrations can be given if there are specific concerns about fluid overload, for example in women with pre-eclampsia. High doses of Syntocinon can cause nausea, vomiting, arrhythmias, rash and anaphylactic reactions including hypotension.

INTRAMUSCULAR SYNTOMETRINE (5 UNITS OXYTOCIN AND 0.5 MG ERGOMETRINE)

Syntometrine is a drug of choice in British obstetrics as it can be prescribed by the midwife and has a more sustained action than Syntocinon alone. It will act on the uterus within 2½ minutes causing a prolonged contraction. Syntometrine should not be repeated without medical involvement, and no more than two doses in total should be administered because the ergometrine component can cause severe peripheral vasoconstriction, a sharp rise in blood pressure and pulmonary hypertension. For these reasons it should never be administered to women with high blood pressure or severe asthma. It is also contraindicated in women with heart, liver and renal disease and some other medical disorders. Side effects include nausea and vomiting.

INTRAMUSCULAR, INTRAVENOUS BOLUS OR INTRAUTERINE INJECTION OF ERGOMETRINE (0.25–0.5 MG)

Ergometrine can be given intramuscularly, intravenously or directly into uterine muscle. Given intramuscularly, ergometrine takes from 2½ minutes to act and given intravenously, up to 45 seconds. If it is injected into uterine muscle it will take effect almost immediately although this route of administration is rarely seen in practice. A single 0.5-mg dose is recommended for treatment of uterine atony, although this may be split between intramuscular and intravenous administration. The same contraindications as for Syntometrine apply.

CARBOPROST TROMETHAMINE (HEMABATE) (250 μG IN 1 ML)

Carboprost is a type of prostaglandin which causes contraction of the myometrium to treat atony. It is often given when Syntometrine and/or Syntocinon have been ineffective and up to eight doses can be given, no closer than 15 minutes apart and more usually with an hour and a half between doses. It can potentiate the effect of oxytocin and when both have been used, the woman should be closely monitored. Carboprost should never be given intravenously or to women with hypertension, severe asthma, pelvic inflammatory disease, cardiac, pulmonary, renal or hepatic disease. This drug is not normally accessible at a home birth.

MISOPROSTOL (CYTOTEC) (200 MICROGRAM ORAL TABLETS, 400 MICROGRAMS RECTAL, SUBLINGUAL; CAN BE GIVEN VAGINALLY)

Misoprostol is seen on some British delivery suites, and is likely to become increasingly commonly used worldwide as it is relatively safe, inexpensive, and easy to administer. It tends to be administered rectally at a dose of 400–1000 micrograms for prevention or treatment of PPH, and its efficacy is said to be similar to that of oxytocin, although it can also cause nausea.

MORE RECENT PHARMACOLOGICAL AND MEDICAL ADDITIONS TO TREATMENT

Tranexamic acid (10 mg/kg intravenously immediately after delivery)

Tranexamic acid has been used extensively in medical conditions involving heavy blood loss but its use in preventing PPH is relatively recent. Trials of its effectiveness and side effects continue. It works by potentiating the blood clotting system as it is a fibrinolysis inhibitor.

Cell salvage

This is a process whereby blood lost during a caesarean section is collected, filtered, washed and transfused back into the woman’s circulation. It is particularly useful for women who haemorrhage and decline blood or blood products although contamination with amniotic fluid can be a problem, and anti-D immunoglobulin should be administered to Rhesus-negative women in case fetal cells are present in the transfusion.

Recombinant factor VIIa (40–90 mcg/kg following confirmation that platelet and fibrinogen levels are adequate)

rFVIIa achieves haemostasis by enhancing thrombin formation; however, it puts women at risk of thromboembolitic events so the presence of a senior haematologist is required. It only works if the woman has adequate platelets and fibrinogen, also necessary for clot generation.

If bleeding continues, manual removal of the placenta should now be considered (see Box 10.4 and Figure 10.1). Although a very simple procedure, it is a painful one for the mother and carries a risk of uterine rupture and infection. Accordingly the procedure is only suitable in an emergency, although the Midwives Rules and Standards²⁰ refer to the Standards for Pre-registration Midwifery Education (2009)²¹ which state that

‘Emergency procedures the midwife must be proficient in include

•  Manual removal of the placenta

•  Manual examination of the uterus

•  Managing postpartum haemorrhage

•  Resuscitation of the mother and/or baby’

The course of action must be explained to the parents and the partner given the opportunity to leave the room, perhaps to care for the baby, if desired.

Syntocinon should be given, preferably by continuous intravenous infusion, as soon as the placenta is out and this will be continued for a few hours. If the woman is still at home, it may be more appropriate to give ergometrine to aid contraction of the uterus before transfer to hospital. The placenta is quickly examined for completeness, and if there is any doubt, an evacuation of the uterus (ERPC) should be considered in hospital. Blood loss must be measured and recorded, and contemporaneous notes made. If she is still at home, the woman should be transferred to hospital whether or not she shows signs of shock, in case of uterine muscle relaxation in the next 24 hours. The placenta should also be taken to hospital with the woman, so the obstetricians can make their own decision about its completeness and suggest future management for the woman. She will almost certainly be offered a full blood count to check for anaemia and antibiotics because of her increased risk of uterine infection. Close observation of both the mother and the baby should be continued during this time.

Figure 10.1  Manual removal of placenta (a) Stage 1: separation. (b) Stage 2: removal.

Occasionally a partially separated placenta cannot be completely removed manually because it is morbidly adherent to the uterine wall. If the midwife suspects this is the case at a home birth, she should administer an oxytocic if there is any blood loss, with the aim of minimising it while transfer to hospital is made.

MANAGEMENT OF HAEMORRHAGE AFTER DELIVERY OF THE PLACENTA

The slow, steady trickle of blood after delivery of the placenta can be the most dangerous of all if it is not closely monitored. Changes of shift, failure to add up the total blood loss and frequent changes of the bed sheets may lead midwives to underestimate the situation and the woman may slowly sink into unconsciousness while the midwife completes her record-keeping.

The causes of excessive bleeding after delivery of the placenta tend to be the same as for bleeding before its delivery, namely atonic uterus or lacerations. If there is a continuous gush of blood, the midwife must immediately diagnose the cause of the heavy bleeding. There may or may not have been excessive bleeding before the delivery of the placenta and the present cause of bleeding may or may not remain the same. Continual assessment of the situation is therefore necessary.

Lacerations incurred during the birth of the baby may only now become apparent as a significant cause of bleeding, as expeditious delivery of the placenta may have preoccupied the midwife until now. If the uterus is well contracted, haemostasis needs to be quickly achieved and lacerations sutured. If the woman is at home, the midwife must consider how best to position her and how to achieve optimal lighting, especially if she has not had the opportunity to do this during the woman’s pregnancy (for instance in a case of unplanned home birth). This may require some ingenuity on the midwife’s part. However, it is vital that the apex of the laceration is identified and repair is undertaken speedily and adequately before the blood loss compromises the well-being of the woman.

If atonic uterus is diagnosed its cause may remain unknown. However, of the known causes, retention of placental tissue, membrane or blood clot interfering with contraction of the myometrium are the most likely. Retained products can sometimes be diagnosed from examination of the expelled placenta and membranes, but this is by no means foolproof. Clots in the uterus should be suspected if the placenta and membranes appear to be complete, the uterus feels enlarged and a little soft, and a slow trickle of blood after placental delivery gradually increases. A full bladder should also be considered if the bladder has not been emptied recently.

Many predisposing factors to PPH, such as multiple birth, polyhydramnios, antepartum haemorrhage or instrumental delivery will have already led to the attendance of an obstetrician. However, if uterine atony is diagnosed and a doctor is not present, the midwife should immediately summon medical aid, explain what is happening to the woman and her birth partner, tell them briefly what she is going to do and ask for their co-operation. The woman needs to get into a semi-recumbent or recumbent (flat supine) position preferably on a bed and given high-flow facial oxygen.⁷ The uterus should be made to contract as soon as possible by the following means:

•  Rub up a contraction (see Box 10.6 and Figure 10.2). This should also express retained blood clots.

BOX 10.6: Rubbing up a contraction

•  Gently feel for the fundus with the pads of the fingertips (a manoeuvre similar to palpation of the fundus in pregnancy) and assess uterine contraction.

•  Cup the hand around the uterus and massage it firmly but gently (this action should not be overly painful for the woman) with a smooth, circular movement until its soft texture starts to become firmer with an oncoming contraction.

•  Hold the hand still and do not recommence massage unless the uterus starts to relax again.

•  Catheterise the bladder. The midwife needs to know that the bladder is empty and kept empty until the bleeding is brought under control (a partially full bladder can interfere with strong uterine contraction).

Figure 10.2  Rubbing up a contraction.

Figure 10.3  Internal bimanual compression.

•  Consider a (further) dose of Syntocinon as an intravenous bolus or by infusion, or Syntometrine intramuscularly (if not contraindicated).

•  Misoprostol is a midwifery exemption drug in some maternity units, in which case it may be administered.

•  If the woman is in the delivery suite the multidisciplinary team may give additional drugs (see Box 10.5).

These measures will bring most cases of haemorrhage from atony speedily under control. However, if excessive bleeding continues, the midwife should perform bimanual compression (Figure 10.3).

To achieve bimanual compression, one hand is coned (Figure 10.3), inserted into the anterior fornix of the vagina and clenched, while the other hand massages the fundus, thereby pressing the walls of the uterus together. Alternatively, bimanual compression can be done externally by grasping the uterus with both hands and squashing the uterus between them but this is less likely to be effective. It should be noted that internal bimanual compression in particular is extremely painful for the woman and should only be performed if other procedures are not effective, while awaiting medical action. All this should be explained clearly to the woman and her partner before the procedure is attempted, as great distress will be caused if either is unprepared for the extreme discomfort which will ensue.

If these procedures do not work a blood coagulation problem should be considered. By this time the woman should be under the maternity unit’s Major Obstetric Haemorrhage (MOH) protocol, with senior clinicians in attendance. Urgent blood tests will be done to enable diagnosis and the correct management, including full blood count and coagulation studies including fibrinogen. HemoCue is a useful bedside test for haemoglobin level to prevent delay in blood transfusion. The mother is now likely to be shocked and should be treated with intravenous fluids (2–4 L of crystalloids) and appropriate drugs. A central venous and/or arterial line may be indicated and a blood transfusion ordered; meanwhile O-negative blood from the delivery suite fridge can be given if the haemorrhage is life threatening. The doctors may also consider administration of fresh frozen plasma (FFP), cryoprecipitate or platelet concentrate, preferably warmed and delivered through a rapid infuser pressure bag. Bimanual compression will need to be continued until the bleeding is brought under control (see Box 10.7).

A blood coagulation problem is relatively easy to diagnose because bleeding continues either in a steady stream or a gush and does not clot where it collects. Once medical diagnosis has been made and haematological results are known to ascertain the extent of the problem, it can be treated accordingly.

In cases of continued bleeding, uterine packing (tamponade) may be considered.3,23 Dry sterile gauze is used, which can be moistened with saline. Analgesia is required during the procedure and antibiotic cover is suggested. A urinary catheter should remain in situ for 24–36 hours until the pack is removed on the delivery suite, with operating theatre facilities at the ready in case bleeding restarts. A danger is that an obstetrician may pack the uterus to arrest the bleeding when unable to diagnose the cause; in such a case laparotomy, to discover and then treat the actual cause, may be safer. However, uterine packing can be a useful measure while a woman is transferred to an operating theatre for more intensive investigation and treatment.

Less common treatments, which have been attempted with varying success in the control of PPH and in which the midwife may be called upon to assist the medical practitioner, include giving IV tranexamic acid at delivery to prevent haemorrhage, bilateral internal iliac artery ligation, bilateral uterine artery ligation, bilateral ovarian and uterine artery ligation, arterial occlusion or embolisation, applying haemostatic (compression: brace or B-Lynch) sutures, or insertion of a balloon catheter into the uterus (balloon tamponade).3,23 Hysterectomy is a final resort.

Uterine artery embolisation appears to be an increasingly adopted procedure in the UK and although this appears to be an effective way of avoiding hysterectomy in intractable haemorrhage with a more than 95% success rate,²³ the necessity of performing the procedure under radiological guidance makes it impractical in many maternity units.

Ongoing observations and documentation of pulse, respirations, blood pressure, blood loss, oxygen saturation monitoring and consciousness level should continue every 5 minutes until bleeding and the woman’s condition are under control; fluid balance must also be carefully monitored to prevent overload.

Unusually, a postpartum haemorrhage may present as a haematoma, concealed in the broad ligament or the vaginal wall. Symptoms include pain at the site, collapse and shock, and it can usually be seen on ultrasound. The woman should be transferred to the operating theatre where the haematoma should be drained and haemostasis achieved under spinal or epidural anaesthesia. Blood replacement may be required, and antibiotics should be given (see also Chapter 13).

Once the bleeding has been controlled the woman must be observed, and her recovery carefully managed, possibly in either a high-dependency unit on the delivery suite or in an intensive care unit. The needs of all the family should also continue to be met.

As with all midwifery actions, record-keeping is important and notes should be kept as contemporaneously as possible. Where a scribe has taken notes these must be transcribed into the woman’s obstetric notes.

Following incidents of major obstetric haemorrhage, the maternity team may wish to consider meeting to debrief and consider non-judgemental reflection on what went well and what could be improved on, and consider further training and development to promote learning and team cohesion.

CONCLUSION

Peripartum haemorrhage in the mother is the obstetric emergency the midwife is most likely to face in her career. Many potential cases can be and are avoided by skilled support of women throughout pregnancy and in labour. Some cases can be predicted from women’s histories and with the appropriate use of technology, but most cases are unforeseen and their course is unpredictable. For this reason all women who may refuse blood products should be identified antenatally as soon as possible³ (see Chapter 3 for further discussion on this subject).

BOX 10.7: Diagnosis and management of disseminated intravascular coagulopathy

Prompt diagnosis and management are vital for maternal survival.

Diagnosis

•  An acute history of a predisposing condition (e.g. placental abruption).

•  Bleeding from orifices, e.g. nose, mouth, venapuncture site, haematuria.

•  Blood loss that does not immediately clot.

•  Torrential haemorrhage.

•  Signs of circulatory obstruction, e.g. cyanosis in fingers, cerebrovascular accident (stroke) or renal failure.

•  Blood test results: Low haemoglobin, abnormal clotting study results (prothrombin time, abnormal levels of platelets, fibrinogen and FDPs).

Management

•  Give ongoing explanations and emotional support to the woman and her partner as necessary.

•  Refer to the local protocol, which should include how DIC should be managed.

•  Request urgent medical attendance when DIC is suspected.

•  Look for the underlying cause if it is not known (DIC is never a primary disease) although the woman’s condition will need to be stabilised before the condition is treated (or the baby delivered, when the condition occurs in pregnancy).

•  Urgent blood test results will dictate the course of management, including full blood count, clotting studies and time taken to group and crossmatch blood. Replacement of blood cells and clotting factors will be required with fresh frozen plasma, platelet concentrates and ultimately, with red blood cells.

•  Maintain frequent and accurate observations of the woman’s vital signs. Invasive monitoring with a central venous pressure and/or arterial line may be necessary. The bladder should be catheterised and fluid balance vigilantly monitored. Any sign of renal failure must be reported to the team immediately.

•  Note that transfer to the intensive-care unit (ICU) is likely.

Wherever possible, management options should be discussed with the woman to ensure that she is involved in decision making about her care. As most cases of obstetric haemorrhage occur without warning, the midwife, along with the multiprofessional obstetric team, needs to be continually vigilant, and equipped to deal with these situations whether at home, in a birth centre or in hospital.

With prompt and skilful management, the majority of intrapartum and early postpartum haemorrhages can be brought under control with a minimum of interventions. However, the latest Confidential Enquiries⁴ concluded that ‘improvements in care which may have made a difference to outcome were noted in all deaths’; this suggests that we all still have many lessons to learn.

SUMMARY OF MIDWIFERY RESPONSIBILITIES

•  Encourage an iron-rich, balanced diet in pregnancy and consider checking haemoglobin levels through later pregnancy in order to avoid/treat anaemia as birth approaches.

•  Discuss risk and management issues of the third stage of labour in pregnancy and document the woman’s wishes (including whether or not she would consent to a blood transfusion – see Chapter 3).

•  Ensure in particular that women who have had a previous caesarean section are offered a timely ultrasound scan for placental localization.

•  Know the history of each woman supported in labour (however, primary PPH is often unpredictable, and risk assessment in pregnancy does not accurately predict women who will have a PPH).5,6

•  Know where all equipment is, especially for emergency procedures.

•  Thoroughly understand the pathophysiology of the different causes of bleeding, the signs and symptoms, and the most effective treatments.

•  Keep labour as normal as possible by offering good psychological support, non-pharmacological pain relief, information, explanations and a listening ear, and encourage the woman to be as upright and active as she is able.

•  Where a woman is likely to benefit from intervention, discuss the benefits and risks with her and her partner and listen to her ideas and concerns, to enhance her feeling of emotional well-being and control.

•  Be aware of the dangers inherent in using prostaglandin, Syntocinon and mismanaging the third stage of labour.

•  Consider the use of a trigger system such as the modified early obstetric warning score (MEOWS) to record all maternal observations¹⁹; involve the multiprofessional team as indicated and refer appropriately.⁴

•  Be on good terms with your multiprofessional team. Encourage and if necessary lead the dialogue in decision making. Be prepared to state a case and be an advocate for the woman. Consider the use of a structured communication enhancement tool such as SBAR (situation, background, assessment, recommendation) as standard practice.¹⁹

•  Ensure that all clinicians are aware of the maternity unit’s protocol for severe obstetric haemorrhage, and ensure it is regularly updated by a multidisciplinary team with obstetric, midwifery, anaesthetic, haematological, radiological and managerial representation.

•  Practice ‘skills drills’ regularly, preferably with the multiprofessional team.

•  Do not leave a woman at the end of a shift without ensuring that a suitable ‘handover’ has been achieved, and there is continuation of optimal care.⁴

Summary of immediate action when an intrapartum/postpartum haemorrhage occurs

Note that many of the following actions will be done simultaneously.

•  Assess the cause and amount of bleeding while talking to the woman and her partner, aiming to keep them calm and co-operative.

•  Call for help from appropriate colleagues.

•  Start resuscitation (including siting an IV) as soon as it is indicated by the woman’s condition.

•  Arrest the bleeding:

•  Actively manage the delivery of the placenta, by manual removal if necessary.

•  Ligate spurting vessels in the vagina (and proceed to perineal suturing if bleeding is now under control).

•  If haemorrhage continues:

•  Administer a 10-unit bolus of Syntocinon, or if IVI in situ give 10 units Syntocinon mixed with IV fluid.

•  Catheterise and empty the bladder.

•  Rub up a contraction.

•  Consider a second bolus of 10 units of Syntocinon.

•  Administer bimanual compression.

If bleeding is still not under control, hand over management to medical colleagues who will consider coagulation problems, alternative drug treatment, uterine/vaginal tamponade, artery ligation or occlusion, and then hysterectomy as a final resort.

Other considerations at various points during management include transfer to an obstetric unit, maternal observations and recording on a MEOWS chart, taking blood (for a full blood count, clotting studies, and other tests as necessary), fluid balance recording, pain relief, continual reassessment of maternal condition and bleeding, and documentation and care planning. In addition, ongoing psychological support of the woman and partner should be maintained.

REFERENCES

1.  Murray I, Hassall J. 2014. Change and adaptation in pregnancy. In: Marshall J, Raynor M (Eds.). Myles Textbook for Midwives. Chapter 9. 16th ed. Edinburgh: Elsevier, pp. 143–178.

2.  Davies K, Rucklidge M. 2007. Management of Obstetric Haemorrhage. Anaesthesia UK. Available at http://www.frca.co.uk/article.aspx?articleid=100758 (accessed September 25, 2015).

3.  Royal College of Obstetricians and Gynaecologists (RCOG). 2009. Prevention and Management of Postpartum Haemorrhage. Green-Top Guideline No. 52. London: RCOG. Available at https://www.rcog.org.uk/globalassets/documents/guidelines/gt52postpartumhaemorrhage0411.pdf (accessed September 25, 2015).

4.  Knight M, Kenyon S, Brocklehurst P et al. (Eds.), on behalf of MBRRACE-UK. 2014. Saving Lives, Improving Mothers’ Care – Lessons Learned to Inform Future Maternity Care from the UK and Ireland Confidential Enquiries into Maternal Deaths and Morbidity 2009–2012. Oxford: National Perinatal Epidemiology Unit, University of Oxford.

5.  Mousa H, Blum J, El Senoun et al. 2014. Treatment for primary postpartum haemorrhage. Cochrane Database of Systematic Reviews. Volume 2. Available at http://onlinelibrary.wiley.com/doi/10.1002/14651858.CD003249.pub3/full (accessed March 4, 2016).

6.  Mukherjee S, Arulkumaran S. 2009. Postpartum haemorrhage. Obstetrics, Gynaecology and Reproductive Medicine, 19(5):121–126.

7.  Winter C, Crofts J, Laxton C, Barnfield S, Draycott T. 2012. Practical Obstetric MultiProfessional Training PROMPT: Module 8 Major Obstetric Haemorrhage. Cambridge: Cambridge University Press.

8.  Duncan A, Von Wildkind C. 2012. Bleeding from the lower genital tract. In: Arulkamarans S, Karoshi M, Keith LG, Lalonde AB, B-Lynch C (Eds.). A Comprehensive Textbook of Postpartum Haemorrhage: An Essential Clinical Reference for Effective Management. London: Sapiens, pp. 193–198.

9.  Health and Social Care Information Centre. 2012. NHS Maternity Statistics England 2011–2012. Available at http://www.hscic.gov.uk/searchcatalogue?productid=10061&q=maternity+statistics&sort=Relevance&size=10&page=1#top (accessed September 25, 2015).

10.  Waterstone M, Bewley S, Wolfe C. 2001. Incidence and predictors of severe obstetric morbidity: Case control study. BMJ, 322:1089–1094.

11.  Lennox C, Marr L. 2013. Scottish Confidential Audit of Severe Maternal Mortality. 9th Annual Report 2011. Available at http://www.scottishpatientsafetyprogramme.scot.nhs.uk/Media/Docs/MCQIC/Maternity%20Care/2013-08-09%20Final%209th%20annual%20SCASMM%20report.pdf (accessed September 25, 2015).

12.  Williamson C, Girling J. 2011. Hepatic and gastrointestinal disease. In: James D, Steer PJ, Weiner CP (Eds.). High Risk Pregnancy Management Options. St. Louis, MO: Elsevier Saunders, pp. 839–860.

13.  Wang Y, Zhoa S. 2010. Vascular Biology of the Placenta. San Rafael, CA: Morgan and Claypool Life Sciences.

14.  Lewis G, Drife J (Eds.). 2004. Why Mothers Die 2002–2004 the Sixth Report of Confidential Enquiries into Maternal Deaths in the United Kingdom. London: RCOG.

15.  Lewis G (Ed.). 2007. Saving Mothers Lives 2003–2005. Seventh Report on Confidential Enquiries into Maternal Deaths in the United Kingdom. London: CEMACH.

16.  Royal College of Obstetricians and Gynaecologists (RCOG). 2011. Placenta Praevia, Placenta Praevia Accrete and Vasa Praevia: Diagnosis and Management. Green-Top Guideline No. 27. London: RCOG. Available at https://www.rcog.org.uk/globalassets/documents/guidelines/gtg_27.pdf (accessed September 25, 2015).

17.  Boyce T, Dodd C, Waugh J. 2008. Hypertensive disorders. In: Robson SE, Waugh J (Eds.). Medical Disorders of Pregnancy: A Manual for Midwives. Chichester: Blackwell, pp. 19–26.

18.  Crafter H, Brewster J. 2014. Common problems associated with early and advanced pregnancy. In Marshall J, Raynor M (Eds.). Myles Midwifery. 16th ed. Edinburgh: Churchill Livingstone, pp. 221–242.

19.  National Institute of Health and Care Excellence. 2007. CG 50 Acutely Ill Patients in Hospital, Recognition of and Response to Acute Illness in Adults in Hospital. Available at http://www.nice.org.uk/guidance/cg50 (accessed September 25, 2015).

20.  Nursing and Midwifery Council. 2013. Midwives Rules and Standards. Available at http://www.nmc.org.uk/standards/additional-standards/midwives-rules-and-standards/ (accessed September 25, 2015).

21.  Nursing and Midwifery Council. 2009. Standards for Pre-Registration Midwifery. London: NMC. Available at https://www.nmc.org.uk/standards/additional-standards/standards-for-pre-registration-midwifery-education/ (accessed March 4, 2016).

22.  National Institute of Health and Care Excellence. 2014. CG 190 Intrapartum Care: Care of Healthy Women and Their Babies During Childbirth. Available at http://www.nice.org.uk/guidance/cg190 (accessed September 25, 2015).

23.  Bedfort MA, Dildy GA. 2011. Postpartum haemorrhage and other problems in the third stage. In: James D, Steer PJ, Weiner CP, Gonik B (Eds.). High Risk Pregnancy Management Options. St Louis, MO: Elsevier Saunders, pp. 1283–1311.

11

Amniotic fluid embolism: Anaphylactoid syndrome of pregnancy

MAUREEN BOYLE

Introduction

Pathophysiology

Clinical features

Predisposing/risk factors

Management

Complications and potential long-term effects

Conclusion

Summary of midwifery responsibilities

References

INTRODUCTION

Amniotic fluid embolism (AFE) is a rare obstetric emergency that is impossible to predict, offers few, if any, warning signs and frequently has a tragic outcome. It usually includes a sudden cardiovascular collapse, DIC (disseminated intravascular coagulation) and hypoxia, often manifesting as an altered mental state.

When assessing the rates of maternal deaths, it is difficult to make comparisons between countries as there are variations in the methodology of data collection¹ as well as in definitions. However, in all countries that keep comprehensive records, AFE is identified as one of the most significant contributors to maternal mortality.

In the United Kingdom, recent research² covering 2005–2014 demonstrated AFE being diagnosed in 1.7:100,000 births, with a case fatality rate of 19%. In the four years 2009–2012, 11 women died in the United Kingdom and Ireland, making AFE the fifth most common cause of maternal mortality. Although the rates of death have fluctuated over the years, there has been no statistically significant change since 2003.³ Of the 23 women who died from 2005 to 2014 in the United Kingdom,² the median time of death was 1 hour and 42 minutes after presentation of AFE.

Alongside the mortality rate, significant longterm morbidity is frequently associated with AFE survivors.⁴ In the 2015 Fitzpatrick et al. study² 7% of the survivors were left with permanent neurological injury, and a further 17% experienced other major morbidities. For those babies who were undelivered when their mothers suffered AFE, high levels of mortality and morbidity were also noted, with a perinatal mortality rate of 67:1000.²

For all women with the diagnosis of AFE, 53% presented before or at the time of birth, the remainder presenting a median of 19 minutes after delivery.² A number of previous studies has demonstrated that on average, about 70% occurrences of AFE happen during labour.⁵ The majority of those presenting following birth had an instrumental delivery (20%) or caesarean section (71%). It is of course possible that these women had their deliveries expedited because of symptoms which were later diagnosed as AFE. There have been reports of AFE occurring considerably later than would be expected, for example following caesarean section rather than during the procedure. It is suggested that such a delayed reaction may occur following a spinal anaesthesia if the amniotic fluid is present in dilated uterine veins and this is displaced when the block wears off and the venous tone is allowed to return.⁶

Although many definitions involve the timing of AFE restricted to occurrence in labour and immediately post delivery, there are cases that have been reported in the second trimester,⁷ after trauma⁸ and postnatally.⁹ Also, rarely, cases have been reported antenatally,¹⁰ after first-trimester termination and following amniocentesis.¹¹

In the most recent Confidential Enquiries report,³ all the women who died collapsed before or within minutes of delivery: seven during labour, three during caesarean section and one after vaginal delivery. Two of these women had an intrauterine fetal death.³

Epidemiology

AFE was first mentioned in 1926, however, the description in 1941 by Steiner and Lushbaugh of ‘maternal pulmonary embolism by amniotic fluid’, after finding amniotic fluid in the pulmonary vessels at autopsy following a collapse during delivery with symptoms mimicking pulmonary embolism, is seen as the first publication in English acknowledging its importance.¹² Knowledge of the condition has only developed slowly since then, due to its rarity. However in 1988, a central registry recording women suffering from amniotic fluid embolism in the United States was set up and reports from this group have contributed to awareness.⁸ In the United Kingdom, a similar registry was set up in 2000.¹³ The collection of data is now undertaken by UKOSS (UK Obstetric Surveillance System), their latest report on AFE being in 2012,¹ although UKOSS data were used in a study by Fitzpatrick et al.² more recently in 2015.

Much knowledge of AFE worldwide continues to be from the review of case reports, or case studies, and due to the differences in reporting these events, analysis may be challenging. Agustin Conde-Agudelo and Roberto Romero⁵ have identified the need for a worldwide registry based on uniform diagnostic criteria and reports.

In the United Kingdom all cases of suspected AFE are submitted to UKOSS,¹ and deaths from AFE continue to be reported on, with the analysis contributing to clinical recommendations by the Confidential Enquiries into maternal deaths, now under the umbrella of MBRRACE-UK³ (Mothers and Babies: Reducing Risk through Audits and Confidential Enquiries across the UK).

PATHOPHYSIOLOGY

Amniotic fluid can enter the maternal circulation through the endocervical veins and it is suggested that it may do so frequently without damage.¹⁴

However, although it may be possible that amniotic fluid may be able to enter the maternal circulation without causing problems, in some women it seems an inflammatory response can develop, causing a rapid collapse similar to anaphylaxis or septic shock.¹⁵ Once amniotic fluid enters the maternal circulation there are thought to be a number of haemodynamic, humoral and coagulopathic changes that may occur and lead to the signs and symptoms of AFE, and there is much evidence for the theory that an immunological mechanism is the major cause.¹⁶

It is suggested that fetal antigens in the amniotic fluid could stimulate a cascade of endogenous immune mediators, producing a reaction similar to anaphylaxis.¹⁷ Benson¹⁸ proposed that the immune reaction, when triggered, could result in activation of the complement system, generated by fetal antigens. Others have suggested that bioactive chemicals present in the amniotic fluid cause these reactions directly. It is possible that it is the amount, the chemical composition or the individual woman’s susceptibility that causes the AFE, or perhaps a combination of these or other unknown factors.

Obvious times of risk for entry of amniotic fluid and its constituents are during caesarean section or uterine rupture, but since amniotic fluid embolism can occur without these scenarios, it is also suggested that there may be small injuries during labour that allow the fluid access to maternal circulation. Amniotomy is an intervention that may cause injury and it has been reported in an American study of 3 million births¹⁹ 78% of women with amniotic fluid embolism had ruptured membranes (two-thirds being artificial rupture of membranes) and in the most recent UK analysis² 91% of women had ruptured membranes at or before AFE presentation. A recent finding that placenta praevia and placenta abruption may be predisposing factors for AFE¹⁹ is a further indication that the breakdown of the maternal/fetal barrier may be significant. However, it is clear that in some cases the damage may occur spontaneously.

It has been observed that women with clinical signs of AFE have mucin, lanugo, vernix and perhaps meconium present in blood from their pulmonary circulation, and these are often coated with leukocytes, which could indicate this fetal debris caused a maternal reaction. Other substances such as zinc coproporphyrin-1, sialyl Tn antigen (STN), complement C3, C4 and interleukin-8 have also been used as serum markers of AFE.²⁰

As AFE is now seen as a maternal response to the amniotic fluid and/or fetal debris in her circulation, rather than the fluid itself causing a blockage, this is represented in the suggested new name: anaphylactoid syndrome of pregnancy (various other names have also been suggested in the literature, such as ‘anaphylactoid lung of pregnancy’ and ‘sudden obstetric collapse syndrome’).

CLINICAL FEATURES

Signs and symptoms

Although the exact underlying pathophysiology and the reasons why any individual woman might be susceptible are not completely understood, the physical effects are clear. The pulmonary circulation is compromised, and ventricular failure and coronary artery vasospasm causing myocardial ischaemia are involved.21,22 As in acute sepsis or anaphylaxis, decreased coronary perfusion and ischaemic injury to the myocardium can cause devastating consequences.

The first symptoms seen may be shortness of breath and altered mental status, followed by cardiovascular collapse and DIC.²³ However, haemorrhage may be the first symptom, or in some cases fetal bradycardia. Seizures are a less common presenting symptom.

Secondary coagulation problems affect about 80% of those developing AFE.²⁴ It has been noted by the UK Confidential Enquiries report³ that the small number of women who did not demonstrate DIC all died quickly, suggesting that the coagulopathy effect perhaps had not yet commenced. In a French study, it was reported that 10 of the 11 women diagnosed with AFE had DIC necessitating massive blood and blood products transfusion.²⁵ The cause of this coagulopathy is not well understood. It is known that amniotic fluid is a procoagulant²⁶ but this may not be enough to cause the often catastrophic haemorrhage. The coagulopathy may also be a result of complement system activation.¹⁸ It has been noted that there may be increased coagulation pathology when meconium is present.²⁷ The DIC is likely to be consumptive rather than fibrinolytic (amniotic fluid contains active coagulation factors II, VII and X).¹⁶

The analysis of the American Registry showed that the symptoms of women diagnosed with amniotic fluid embolism were as follows, given in the order in which they most commonly occurred⁸:

•  Hypotension

•  Fetal distress

•  Pulmonary oedema

•  Cardiopulmonary arrest

•  Cyanosis

•  Coagulopathy

•  Respiratory distress

•  Convulsions

•  Uterine atony

•  Bronchospasm

These symptoms can appear alone, in combination, and in any order. Hypotension, hypoxia, DIC, altered mental status present in 80%–100% of affected women.¹⁷

Women may present with vague ‘predominary’ signs and symptoms such as breathlessness, chest pain, light-headedness, nausea/vomiting, distress or panic immediately or up to 4 hours prior to AFE.²⁸ Many women, especially in advanced labour, become agitated and commonly display non-specific symptoms, especially related to hyperventilation, which often occurs at this time. It is difficult to see how these suggested ‘predominary signs’ can translate to normal midwifery care in labour, however, it could be that early recourse to oxygen saturation monitoring would be minimally disruptive to the labour, reassuring to the midwife, and serve to identify a woman with hypoxia in the rare circumstances where this occurs.

Diagnosis

Traditionally diagnosis of amniotic fluid embolism has only been made on postmortem examination when fetal cells or debris have been found during histological analysis of the maternal lungs.²⁹ Diagnosis has also been made in women who have survived, for example, following special staining of blood from the mothers’ pulmonary vessels³⁰ or after finding fetal squames in the sputum. However, these cells may be due to contamination and adult and fetal squames often cannot be distinguished histologically.5,11,27 Of course these tests are usually carried out only when the mother’s physical condition is compromised. It should also be noted that evidence of fetal debris in maternal lungs may not be present at autopsy if she had survived for several days.¹¹

The finding of squamous cells is considered more significant if they are present in large numbers, are coated with neutrophils and/or are accompanied by other fetal debris.5,17 It is a difficult diagnosis as fetal squames may be found in maternal circulation in those who do not die, or in fact are not unwell.³

Diagnosis has been accepted on clinical symptoms, after exclusion of other possible causes, since 1991 by the Confidential Enquiries³¹ reports. UKOSS,¹ who have been monitoring AFE occurrences since 2005, define AFE clinically using set criteria for diagnosis (see Box 11.1).

Most authorities agree that the sudden onset of a triad of severe symptoms, namely hypotension, hypoxia and coagulopathy are highly suspicious. These can involve8,27

•  Acute hypotension or cardiac arrest

•  Acute hypoxia (cyanosis, dyspnoea or respiration arrest)

•  Coagulopathy

BOX 11.1: UKOSS¹ case definition for AFE

Either: Clinical diagnosis, such as maternal collapse with one or more of the following features: cardiac arrest, acute hypotension, acute hypoxia, cardiac arrhythmias, seizures, haemorrhage/coagulopathy, premonitory symptoms, sudden fetal compromise.

Or: Pathological diagnosis.

The presence of fetal squames or hair in the lungs.

In the absence of any other potential explanation for the signs and symptoms.

•  Onset during labour or within 30 minutes of delivery

•  No other clinical conditions or possible diagnoses for signs and symptoms

Amniotic fluid embolism should always be suspected if a previously asymptomatic healthy woman develops cardiac or respiratory failure during labour, caesarean section or immediately after.

Investigations

Investigations which may aid diagnosis by excluding other possible conditions include

•  Chest x-rays (usually non-specific in AFE but may show diffuse lung opacity).

•  12-lead ECG (which may show changes from right ventricular strain), echocardiograms (may confirm right or left ventricular failure or severe pulmonary hypertension), transoesophageal echocardiograms.

•  Lung V/Q scan (may show non-specific perfusion defects).

•  Blood tests (a fall in haemoglobin, a rise in the white cell count, prolonged prothrombin and partial thromboplastin, a fall in fibrinogen, elevated cardiac enzymes). Sialyl (fetal glycoprotein) may be elevated, complement levels may be decreased.

•  ABG to assess ventilation and degree of hypoxemia.

However, no tests should delay basic, comprehensive and ongoing resuscitation: a previous Confidential Enquiries²⁸ report noted substandard care in two cases where resuscitation was delayed as women were sent for unnecessary diagnostic scans.

PREDISPOSING/RISK FACTORS

Associations with labour, delivery, immediate postnatal period, caesarean section, amniocentesis, removal of placenta, therapeutic abortion, abdominal trauma, cervical suture removal, ruptured uterus or intrapartum amnioinfusion have all been reported in the literature.¹⁷ Cell salvage has been previously thought to lead to fetal debris in maternal circulation, and so to AFE, however, this has not been found to be the case.¹⁶

Some reports have also noted a significant number of women had a medical history of allergy or atopy.³¹ Risk factors in two large population-based cohort studies in the United States¹⁹ and Canada³² identified maternal age >35, caesarean section, assisted vaginal delivery, placenta praevia, abruption, eclampsia and fetal distress (see Box 11.2).

In the current Confidential Enquiries³ report, 11 women died with a median age of 30, five multiparous, all had appropriate antenatal care and most had an uncomplicated pregnancy. There was one twin pregnancy, two women with uterine scars, and most delivered at term. The body mass index (BMI) median was 26 (only two >30), none with an allergy/atopy history, three women smoked, and all were UK or Irish citizens speaking English. Labour care showed that six of the women had induction of labour (IOL)/augmentation (including inappropriate use of drugs). However, two women developed hyperstimulation and collapse after a single vaginal prostaglandin.

BOX 11.2: Possible risk factors for AFE11,19

•  ‘Tumultuous’ contractions

•  Age (especially ‘elderly primiparous’)

•  Multiple pregnancy/large fetus (uterine overdistension)

•  Meconium

•  Long labour

•  Abruption/placenta praevia

•  Multiparity

•  Induction/augmentation

•  Invasive interventions in labour

IOL with prostaglandins or oxytocin, or augmentation with oxytocin or artificial rupture of membranes (ARM), are often considered to be associated with amniotic fluid embolism and UKOSS¹ identified induction as a significant risk factor. Medical induction has been said to increase the risk of AFE.³³ However, in a former Confidential Enquiries²⁸ report of the 17 women who died, only eight had received uterine stimulation (three oxytocin, five prostaglandins), and two had received artificial rupture of membranes. The role of induction and augmentation is therefore far from clear.

‘Tumultuous’ labour was described in 28% of women in one American report,³⁴ and abnormally strong contractions have also been noted by previous Confidential Enquiries in the United Kingdom.²⁹ If the strength of contractions is considered to have influence over the occurrence of amniotic fluid embolism, multiparous women could be assumed to frequently have very strong contractions and therefore be at increased risk. Multiparity has been found to be a factor in 75%–88% of cases in American studies,8,9 however, not in others.³⁴

It is also possible that the reported tumultuous contractions are not the cause of the AFE, but a reaction to it. It is a common characteristic of mammals when a sudden threatening pathophysiological event occurs, for the body to make a desperate attempt to rid itself of the pregnancy in order to survive. This could be a normal reaction of the woman’s body to try and survive the acute insult of the AFE.

Multiple pregnancy has not been identified as a risk factor in Confidential Enquiries reports in the United Kingdom, however, it has been noted in American studies.⁹

Amniotic fluid embolism appears more common with increasing age, and was found to be a risk factor in large American studies.5,34 Interestingly, in a large (almost 3 million hospital records over 5 years reviewed) recent study, age and in particular ‘elderly primiparous’ women were significantly more likely to suffer AFE.¹⁹ However, there were no deaths in this category. This is particularly relevant as it is assumed this group would be more likely to have induction of labour, caesarean section and other interventions. Could it be increased surveillance led to quicker recognition and treatment, and therefore a better outcome?

Identification of risk factors is common throughout the literature, however, these are not yet specific enough to allow AFE to be predicted, or even anticipated. When interpreting risk factors from reports, caesarean section/instrumental delivery are usually high on the list, but analysis of the studies should be made as frequently the intervention was a result of the signs and symptoms of AFE, rather than the signs and symptoms occurring for the first time following the delivery. Although the roles of different risk factors are uncertain, they do serve to highlight the range of women who may suffer AFE, and the necessity for the midwife to keep the possibility of an occurrence in mind.

MANAGEMENT

Since it is not yet possible to clearly identify those women who are at risk of amniotic fluid embolism, or to prevent it, the focus must be on providing those women who collapse with prompt and competent first aid prior to a speedy transfer to where they can receive expert support and care, usually in an intensive care unit. This can improve their chances not only of survival, but also of a complete recovery.

Management of sudden unexpected collapse and haemorrhage is key to a successful outcome (Figure 11.1).

Initial care

This will be the same whether at home or in hospital and includes the following:

•  Call for emergency help

•  Intravenous access and fluids

•  Ventilation: Oxygen administration, manual ventilation with an ambubag or intubation, depending on the site and availability of equipment or personnel

•  Chest compressions as necessary

Figure 11.1  Flowchart of management. (Adapted from Tuffnell D, Slemeck E. 2014. Obstetrics, Gynaecology and Reproductive Medicine, 24(5):148–152, with kind permission.)

(See Chapter 2 for further details of basic CPR resuscitation.)

Ongoing care

Following the arrival of help in hospital or the woman’s arrival at hospital, the priorities of care in response to treatment aims (see Box 11.3) continue, many occurring simultaneously:

SUPPORT RESPIRATION

•  Note that early endotrachael intubation is recommended.

•  Maintain oxygenation via intermittent positive pressure ventilation (IPPV) as required.

•  Deliver the baby if necessary to enable efficient resuscitation.

•  Trigger major obstetric haemorrhage (MOH) protocol at the same time as decision to proceed to perimortum caesarean section is made, or earlier if any indication.³

MAINTAIN CIRCULATION

•  Administer fluids to maintain circulation (may be blood, fresh frozen plasma, cryoprecipitates, crystalloids or platelets depending on availability and the woman’s need).

•  Give fluids to maintain blood pressure and respond to haemorrhage – note that there is a danger of overload, leading to pulmonary oedema, so careful fluid balance and renal assessment (including inserting an indwelling urinary catheter) is necessary.

TREAT COAGULOPATHY

•  Maintain uterine tone – initially with the usual drugs (oxytocics, ergometrine, prostaglandins) and/or surgically (packing, tamponade, balloon, brace suture), including bimanual compression.

BOX 11.3: Treatment aims

•  Circulatory support

•  Respiratory support

•  Correct coagulopathy

•  Note that hysterectomy may be necessary, and it has been reported that about one-quarter of women may need a hysterectomy to stop the bleeding.¹⁴

•  Anticipate coagulation abnormalities and maternal haemorrhage – blood and blood product transfusions with fresh frozen plasma, cryoprecipitate and platelets are often required as indicated by laboratory results and advised by the haematologist.³⁵

•  Monitor clotting and correct coagulopathy.

•  Use uterine artery embolization, to inhibit coagulopathy, if available.

•  Keep in mind that recombinant factor VIIa has been used but this is a controversial treatment.4,36

Ongoing monitoring

•  Initial blood tests should include a full blood count, group and crossmatch, electrolytes, coagulation studies including prothrombin time, partial thromboplastin time, fibrin degradation products, D-dimer and antithrombin III levels, plus arterial blood gases.

•  Maternal condition should be monitored, initially with pulse oximetry to assess the respiratory system, continuous cardiac telemetry to detect arrhythmias and frequent blood pressure monitoring (or continuous with arterial line).

•  Central venous pressure, arterial lines or pulmonary artery catheters as appropriate may be used to guide therapy but coagulopathy may restrict the ability to use invasive monitoring.

•  The effect of blood/fluid replacement and supportive treatment should be continuously monitored by signs and symptoms of adequate O₂ delivery and tissue perfusion.³

Drugs

•  Drugs such as epinephrine, dopamine, milrinone or noradrenaline may be used to support the cardiovascular system.¹⁷

•  Treatment of anaphylaxis with adrenaline, salbutamol, aminophylline and hydrocortisone may be appropriate.³⁵

Additional treatments

Several ongoing treatments have been suggested, but are not currently in widespread use. The use of heparin, either unfractionated or low molecular weight, has been reported but is not yet established as recommended care.³⁷ Pulmonary vasodilators, for example inhaled nitric oxide, intralipids and cardiopulmonary bypass have all been suggested as potential treatments in some circumstances.³ Plasma exchange transfusion may be used, in theory to remove cellular debris, coagulation byproducts and cytokines, and may also help correct acidosis.¹⁴ Therapeutic hypothermia has been reported, with the aim of maintaining a normal neurological outcome.³⁸

Psychosocial care

Support and care for partners and others must not be neglected (see Chapter 14 for further discussion on this important matter) and consideration of psychological support for women who survive this life-threatening situation is necessary.

COMPLICATIONS AND POTENTIAL LONG-TERM EFFECTS

The highest mortality in women is immediately following the initial collapse in the acute stage, and chances of survival may be good with appropriate ongoing supportive care.¹⁴

In the report from Clark et al.’s national American registry⁸ a rate of 61% for persisting neurological impairment was demonstrated in the survivors. However, in the more recent UKOSS report¹ only 7% of survivors had serious permanent neurological damage. Although these reports were from different countries, and different times, it is more likely that better and more timely care around the time of the initial occurrence may be responsible for the improved outcomes. The difficulties around identification and diagnosis, especially of those women who may not present with particularly catastrophic symptoms, may also influence these results.

If the woman is still pregnant when suffering the amniotic fluid embolism, the fetus may not survive, and a perinatal mortality rate of 67:1000 is quoted.² Although it has been suggested in the past that surviving infants commonly have neurological damage,⁸ it is likely that better care is decreasing this number.²

Although there are limited numbers to base this on, there are indications that recurrence of AFE is very unlikely in subsequent pregnancies.4,39

CONCLUSION

It is not possible to identify how to prevent amniotic fluid embolism. However, it seems clear that care needs to be taken in the use of prostaglandins and oxytocins, particularly in those women with other possible risk factors, for example age, parity and obstetric complications, and that other obstetric interventions, such as amniotomy, should be used only when necessary.

In the past Confidential Enquiries reports have recommended that better treatment for those women who survive the initial event may help improve the outcome. In the most recent report,³ out of the 11 women who died, it was felt that in four cases improvements to care could have been made which might have made a difference to the outcome.

SUMMARY OF MIDWIFERY RESPONSIBILITIES

•  If a woman collapses at home or in hospital, prompt effective emergency support can improve her chance of complete recovery.

•  The resuscitation trolley should contain equipment (pre-mounted scalpel blade and two cord clamps at a minimum) to undertake perimortem caesarean section wherever necessary.

•  All maternity units should have regular ‘skills drills’ and it should be mandatory for all those working within midwifery and obstetrics to update regularly – emergencies happen too infrequently for any midwife or doctor to be complacent about their abilities. It is also particularly useful (although admittedly challenging to arrange) if at least some of these ‘skills drills’ take place on the labour ward itself. This can help to ensure all personnel know how to access relevant drugs and equipment and that the emergency (arrest) team can gain easy access through security doors, etc.

•  Labour, and especially transition, is often a time of mood change and uncharacteristic maternal behaviour, and midwives are very familiar with this scenario. However, given that confusion and/or behavior/mood change can be the first sign of hypoxia, it would be useful if the midwife can assess this quickly with a O₂ saturation reading, so she can be reassured – or in the unlikely event hypoxia is present – summon help immediately ensuring as early action as possible is obtained. Until there is further knowledge of the meaning and reliability of these noted ‘predominary’ signs, there seems little else the midwife can do other than ensure she remains alert.

•  Use midwifery skills to augment slow labour (e.g. support, mobilisation, comfort strategies, etc.) to avoid amniotomy and oxytocin use. Despite their common use, always treat prostaglandin and oxytocin with respect and monitor all women receiving these drugs carefully to avoid overstimulation. Use particular care when administering to older women, multiparous women or those with other complications.

•  Following collapse/suspected AFE:

•  Commence resuscitation, call for emergency help, transferring into hospital if necessary. Summon team (major obstetric emergency).

•  Cannulate (two large-bore cannulae if possible) and catheterise.

•  Commence pulse oximetry and three-lead ECG monitoring.

•  Be able to access all emergency drugs and equipment.

•  Assist anaesthetist in respiratory support as necessary.

•  Liaise with blood bank and haematologist.

•  Administer drugs and fluids including all blood products as prescribed.

•  Effective resuscitation may depend on the delivery of the baby (see Chapter 2) and the midwife may be the member of the team who is ‘free’ to assess times and remind those undertaking resuscitation of the time scales. It is noted in the current MBRRACE report³ that no woman received perimortem caesarian section within 5 minutes. The midwife may also need to call the neonatal team.

•  If the baby was born before the collapse, ensure appropriate care for the infant.

•  Ensure partner and other family/friends present are informed and given support as appropriate (see Chapter 2).

REFERENCES

1.  Knight M, McClymont C, Fitzpatrick K et al. 2012. United Kingdom Obstetric Surveillance System (UKOSS) Annual Report 2012. Oxford, National Perinatal Epidemiology Unit.

2.  Fitzpatrick KE, Tuffnell D, Kurinczuk JJ, Knight M. 2015. Incidence, risk factors, management and outcomes of amnioticfluid embolism: A population-based cohort and nested case–control study. BJOG: An International Journal of Obstetrics and Gynaecology, 123(1):100–109. doi:10.1111/1471-0528.13300.

3.  Harper A, Wilson R. 2014. On behalf of the MBRRACE-UK Amniotic Fluid Embolism chapter writing group. Caring for women with amniotic fluid embolism. In: Knight M, Kenyon S, Brocklehurst P, Neilson J, Shakespeare J, Kurinczuk JJ (Eds.), on behalf of MBRRACE-UK. Saving Lives, Improving Mothers’ Care – Lessons Learned to Inform Future Maternity Care from the UK and Ireland Confidential Enquiries into Maternal Deaths and Morbidity 2009–12. Oxford: National Perinatal Epidemiology Unit, University of Oxford, pp. 57–63.

4.  McDonnell N, Percival V, Paech M. 2013. Amniotic fluid embolism: A leading cause of maternal death yet still a medical conundrum. International Journal of Obstetric Anesthesia, 22:329–336.

5.  Conde-Agudelo A, Romero R. 2009. Amniotic fluid embolism: An evidence-based review. American Journal of Obstetrics and Gynecology, 201(5): 445, e1–13.

6.  Margarson M. 1995. Delayed amniotic fluid embolism following cesarean section under spinal anaesthesia. Anaesthesia, 50(9):804–806.

7.  Kelly M, Bailie K, McCourt K. 1995. A case of amniotic fluid embolism in a twin pregnancy in the second trimester. International Journal of Obstetric Anesthesia, 4:195–197.

8.  Clark S, Hankins G, Dudley D et al. 1995. Amniotic fluid embolism: Analysis of the national registry. American Journal of Obstetrics and Gynecology, 172(4:1):1158–1169.

9.  Gilbert W, Danielsen B. 1999. Amniotic fluid embolism: Decreased mortality in a population-based study. Obstetrics and Gynecology, 93(6):973–977.

10.  Powie R, Levy M. 2008. Acute lung injury and acute respiratory distress syndrome. In: Rosene-Montella K, Keely E, Borbour L, Lee R (Eds.). Medical Care of the Pregnant Patient. 2nd ed. Philadelphia: ACP Press, pp. 383–394.

11.  Kocarev M, Lyons G. 2007. Amniotic fluid embolism. In: Dob D, Cooper G, Holdcroft A (Eds.). Crises in Childbirth – Why Mothers Survive. Oxford: Radcliffe. pp. 159–167.

12.  Benson M. 2014. Amniotic fluid embolism: The known and not known. Obstetric Medicine, 7(1):17–21.

13.  Tuffnell D, Johnson H. 2000. Amniotic fluid embolism: The UK register. Hospital Medicine, 61(8):532–534.

14.  Tuffnell D, Slemeck E. 2014. Amniotic fluid embolism. Obstetrics, Gynaecology and Reproductive Medicine, 24(5):148–152.

15.  Clark S. 1997. Amniotic fluid embolism: Current concepts. Contemporary Reviews in Obstetrics and Gynaecology, 9(4):297–301.

16.  Tuffnell D, Slemeck E. 2014. Amniotic fluid embolism. Obstetrics, Gynaecology and Reproductive Medicine, 24(5):148–152.

17.  Rudra A, Chatterjee S, Sengupta S, Nandi B, Mitra J. 2009. Amniotic fluid embolism. Indian Journal of Critical Care Medicine, 13(3):129–135.

18.  Benson M. 2007. A hypothesis regarding complement activation and amniotic fluid embolism. Medical Hypotheses, 68(5):1019–1025.

19.  Abenhaim H, Azoulay L, Kramer M, Leduc L. 2008. Incidence and risk factors of amniotic fluid embolisms: A population-based study on 3 million births in the United States. American Journal of Obstetrics and Gynecology, 199(49): e1–8.

20.  Kanayama N, Tamura N. 2014. Amniotic fluid embolism: Pathophysiology and new strategies for management. Journal of Obstetrics and Gynaecology Research, 40(6):1507–1517.

21.  McDonnell N, Chan B, Frengley R. 2007. Rapid reversal of critical haemodynamic compromise with nitric oxide in a parturient with amniotic fluid embolism. International Journal of Obstetric Anesthesia, 16:269–273.

22.  Shechtman M, Ziser A, Markovits R, Rozenberg B. 1999. Amniotic fluid embolism: Early findings of transesophageal echocardiography. Anesthesia and Analgesia, 89:1456–1458.

23.  Stafford I, Sheffield J. 2007. Amniotic fluid embolism. Obstetrics and Gynecology Clinics of North America, 34(3):545–553.

24.  Clark S. 2014. Amniotic fluid embolism. Obstetrics and Gynecology, 123:337–348.

25.  Guillaume A, Sananes N, Akladios CY, Boudier E, Diemunsch P, Averous G, Nisand I, Langer B. 2013. Amniotic fluid embolism: 10-year retrospective study in a level III maternity hospital. European Journal of Obstetrics, Gynecology, and Reproductive Biology, 169:189–192.

26.  Lockwood CJ, Bach R, Guha A, Zhou XD, Miller WA, Nemerson Y. 1991. Amniotic fluid contains tissue factor, a potent initiator of coagulation. American Journal of Obstetrics and Gynecology, 165(5:1): 1335–1341.

27.  Patterson Brown S, Howell C (Eds.). 2014. Amniotic fluid embolism. In: Managing Obstetric Emergencies and Trauma: The Moet Course Manual. 3rd ed. Cambridge: Cambridge University Press, pp. 121–128.

28.  Lewis G (Ed.). 2007. The Confidential Enquiry into Maternal and Child Health (CEMACH). Saving Mothers’ Lives: Reviewing maternal deaths to make motherhood safer 2003–2005. The Seventh Report on Confidential Enquiries into Maternal Deaths in the UK. London: CEMACH.

29.  Department of Health. 1998. Why Mothers Die: Report on Confidential Enquiries into Maternal Deaths in the United Kingdom 1994–1996. London: The Stationery Office.

30.  Locksmith G. 1999. Amniotic fluid embolism. Obstetrics and Gynecology Clinics of North America, 26(3):435–444.

31.  Hikiji W, Tamura N, Shigeta A et al. 2012. Fatal amniotic fluid embolism with typical pathohistological, histochemical and clinical features. Forensic Science International, 226: e16–19.

32.  Kramer M, Rouleau J, Baskett T, Joseph K, Maternal Health Study Group of the Canadian Perinatal Surveillance System. 2006. Amniotic-fluid embolism and medical induction of labour: A retrospective, population-based cohort study. Lancet, 368:1444–1448.

33.  Tuffnell D, Hamilton S. 2008. Amniotic fluid embolism. Obstetrics, Gynaecology and Reproductive Medicine, 18(8):23–26.

34.  Abenhaim H, Azoulay L, Kramer M, Leduc L. 2008. Incidence and risk factors of amniotic fluid embolisms: A population-based study of 3 million births in the United States. American Journal of Obstetrics and Gynecology, 199(49):49–52.

35.  Scottish Multiprofessional Maternity Development Programme. 2011. Scottish Core Obstetric Teaching and Training. In: Magowan B and the SCOTTIE Working Group on behalf of the Scottish Multiprofessional Maternity Development Group (Eds.). Emergencies “SCOTTIE” Course Manual. Available at http://www.scottishmaternity.org (accessed February 13, 2015).

36.  Prosper S, Goudge C, Lupo V. 2007. Recombinant factor VIIa to successfully manage disseminated intravascular coagulation from amniotic fluid embolism. Obstetrics and Gynecology, 109(2 part 2): 524–525.

37.  Uszynski M, Uszynski W. 2013. Heparin and other anticoagulants in amniotic fluid embolism (AFE): Literature review and concept of the therapy. Open Journal of Obstetrics and Gynecology – Electronic Document, 3(7):573–598.

38.  Barriuso V, Pombar X, Bankowski H. 2013. The use of therapeutic hypothermia in the management of amniotic fluid embolism. Obstetric Medicine, 6(2):92–93.

39.  Abecassis P, Benhamou D. 2006. Is amniotic fluid embolism likely to recur in a subsequent pregnancy? International Journal of Obstetric Anesthesia, 15(1): 90.

12

Serious infection

JUDY BOTHAMLEY AND MAUREEN BOYLE

Introduction

Sepsis

Influenza (flu)

Pneumonia

References

INTRODUCTION

Although infection is not rare around the time of childbirth, it is usually easily resisted by the woman’s own immune system and/or treatment with antibiotic therapy. However, in recent years serious infection has become more widespread and is now one of the most common causes of death in women around the time of childbirth.¹ The physiology of pregnancy and the interventions of childbirth make women more susceptible to serious complications of infection. A particularly worrying feature of many of these cases of infection is the frequently vague symptoms of initial presentation and also the speed in which they move through the woman’s body,2,3 potentially causing death within hours. For that reason some infections can be considered an ‘emergency’ and midwives need to be able to recognise, refer and carry out appropriate treatment for these women as a matter of urgency. Midwives need to maintain up-to-date knowledge of the signs and symptoms of infection, in particular the subtle symptoms of sepsis, that may rapidly escalate to life-threatening disease.

Of particular concern is the number of women who may develop an infectious condition when in the community, and with the current restricted community midwife contact, midwives will need to ensure women know when and how to self-refer.

SEPSIS

[E]very medical, [midwifery] and nursing practitioner working with pregnant or recently delivered women should be aware of the cost of delay in this devastating condition. It may reach the point of being irreversible before the women can access appropriate levels of care if there is any delay on the part of the women themselves, the primary care teams or the hospital staff.⁴

Puerperal sepsis, formerly known as ‘childbed fever’, was responsible for around two-thirds of deaths of women in the eighteenth and nineteenth centuries. Handwashing, aseptic techniques, improved general health and antibiotic treatment have all contributed to a dramatic improvement in safety for mothers during childbirth,⁵ although in resource-poor settings, poverty and health inequality continue to contribute to maternal deaths from infection.⁶ However, in the United Kingdom, after many years of very low levels of maternal deaths from sepsis, the rate of maternal mortality from sepsis has doubled in the last 20 years.⁷

In 2011, a report of the Confidential Enquiries into Maternal Deaths in the UK for 2006–2008,⁸ stated that sepsis had become the leading direct cause of maternal deaths. More recently sepsis has decreased to the number-two direct cause of maternal death¹; however, many issues remain to be addressed concerning effective diagnosis and treatment.

A virulent organism, Lancefield group A betahaemolytic streptococcus (GAS) was responsible for the majority of maternal deaths from sepsis from 2009 to 2012.¹ Deaths occurred during pregnancy as well as in the postnatal period. It must also be remembered that figures for maternal death reflect a much larger incidence of morbidity and it is estimated that approximately 50 women have life-threatening morbidity for each woman who dies.⁹

Definitions and course of the disease

Sepsis, severe sepsis and septic shock are terms used to describe the progress of disease following infection. Sepsis involves a systemic inflammatory reaction that triggers pathophysiological changes that can lead to septic shock. Box 12.1 lists definitions in relation to the development of septic shock.

Pathophysiology of the development of septic shock

Inappropriate fluid shift and vasodilation are the key pathophysiological features of systemic infection.¹⁰ Vasodilation and reduced systemic resistance are normal physiological features of pregnancy. In response to invading pathogenic bacteria, the immune system activates macrophages and neutrophils as well as other factors such as cytokines, tumour necrosis factor and interleukins. This is usually effective at controlling the spread of infection. However, if the infection does spread, the inflammatory response increases and this can have a serious impact on the cardiovascular system.

Compensatory mechanisms such as an increased heart rate and an increased respiratory rate aim to increase cardiac output and correct acidosis, but as these fail to work, underperfusion to the organs occurs. As organs start to fail, renal damage occurs and coagulation disorders further compromise organ function.

BOX 12.1: Stages of clinical response to severe infection

Infection: Invasion by pathogenic organisms that reproduce and multiply, which then generate an immune response

Bacteraemia: The presence of bacteria in the blood; this presence may be sustained or transient.

Systemic inflammatory response syndrome (SIRS): The presence of any two of the following features:

•  Temperature: >38°C or <36°C

•  Tachycardia: Heart rate >90 beats per minute

•  Tachypnoea: Respiratory rate >20 breaths per minute

•  White blood cell count: Raised (>12 × 10⁹ cells/L) or low (<4 × 10⁹ cells/L)

•  Sugar: Blood glucose >7.7 mmol/L in the absence of diabetes

Sepsis: Arises from the systemic response to infection and is defined as the presence of a number of the clinical signs of SIRS (listed earlier) alongside an identifiable infection. It is challenging to treat and it is life threatening.

Severe sepsis—Multiple organ dysfunction syndrome: Sepsis is considered severe when associated with organ dysfunction, hypoperfusion or hypotension. The generalised inflammatory response and procoagulant changes lead to organ dysfunction. Neurological impairment, lactic acidosis and acute renal, liver, heart or respiratory failure may occur.

Septic shock: Includes the characteristics of multiple organ dysfunction syndrome listed earlier and the persistence of hypoperfusion and hypotension despite adequate fluid replacement.

The inflammatory mediators act on the endothelial lining of blood vessels, causing an increased production of the powerful vasodilator, nitric oxide. The blood vessels dilate and cause a significant drop in blood pressure. The heart rate will increase in an effort to compensate for the drop in blood pressure. In addition, activation of the coagulation system can result in disseminated intravascular coagulation. The tendency to clot formation on top of already-existing pro-coagulation of pregnancy predisposes pregnant and postpartum women with sepsis to microvascular clot formation. The combination of ischaemia from low blood pressure and clot formation can result in organ dysfunction. Fluid shifts can be dangerous. Pregnant women are at greater risk of developing pulmonary oedema due to the pregnancy-induced changes in colloid osmotic pressure, which governs the fluid shift in the lungs. As sepsis progresses there will be reduced blood flow to the uterus, with consequent reduced oxygenation to the fetus.¹¹

The two phases recognised in the progress of septic shock are warm shock followed by cold shock. Box 12.2 lists the features of the progressive stages of septic shock.

Sites of infection

Sepsis can arise from many sources and is not limited to infections beginning in the genital tract. However, genital tract infection is common, and postpartum the uterus and birth canal remain susceptible to invasion by organisms for several days following birth. Sepsis occurs when these organisms invade the lining of the uterus, adjacent structures, the lymphatics and the bloodstream. Caesarean section (CS) is a significant risk factor for serious puerperal infection and yet sepsis can occur following uncomplicated vaginal delivery.⁶ Confidential Enquiries⁸ highlighted the potential risk of sepsis following contact with young children who had a sore throat or upper respiratory tract infection.

Risk factors for the development of infection and sepsis

Although risk factors have been identified, it must be remembered that sepsis can occur in previously healthy women following uncomplicated pregnancy and vaginal birth (see Box 12.3).

Assessment and diagnosis

The early warning signs of sepsis should trigger a rapid response with immediate transfer to hospital and/or appropriate referral to a senior obstetrician and anaesthetist.8,11,12 The potential speed of the condition must be acknowledged. In a recent report⁹ for half of women with GAS, severe sepsis was diagnosed within 2 hours of the first signs of a systemic inflammatory response.

BOX 12.2: Features of septic shock

INITIAL: WARM SHOCK

•  Warm peripheries (peripheral vasodilation)

•  Low blood pressure

•  Raised and bounding heart rate

•  Temperature instability

•  Increased respiratory rate

•  Altered mental state

LATE STAGES: COLD SHOCK

•  Cold peripheries (peripheral vasoconstriction)

•  Sweating

•  Weak, thready pulse

ORGAN DYSFUNCTION

•  Impaired renal function: Oliguria, anuria, electrolyte imbalance, raised creatinine

•  Neurological compromise: Confusion, agitation and possibly coma

•  Cardiopulmonary impairment: Cyanosis and adult respiratory distress syndrome

•  Haematological changes: Reduced platelet count, disseminated intravascular coagulation

•  Metabolic acidosis with raised serum lactate

•  Liver impairment: Increased serum bilirubin and increased alkaline phosphatase

•  Gastrointestinal signs (paralytic ileus) 196 Serious infection

BOX 12.3: Risk factors for development of infection and sepsis

FEATURES OF THE WOMAN

•  Obesity

•  Impaired glucose tolerance or diabetes

•  Impaired immunity, for example human immunodeficiency virus, immunosuppressive medication

•  Anaemia or sickle cell disease

•  Women from poor socio-economic groups

•  Black or minority ethnic group origin

•  History of pelvic infection or vaginal discharge

•  History of group B Streptococcus infection

•  Intravenous drug misuse

FACTORS RELATED TO PREGNANCY AND CHILDBIRTH

•  Septic miscarriage or termination of pregnancy

•  Cervical cerclage

•  Prolonged spontaneous rupture of membranes

•  Amniocentesis and other invasive procedures

LABOUR AND PUERPERIUM

•  Induction of labour

•  Preterm birth

•  CS

•  Instrumental vaginal delivery

•  Prolonged rupture of membranes or chorioamnionitis

•  Prolonged labour with multiple (more than five) vaginal examinations

•  Retained products of conception

•  Urinary tract infection or catheterisation

•  Mastitis

•  GAS infection among family members

Identifying a woman who is unwell involves

•  Assessment of physical signs

•  Assessment of her current condition and history

•  Intuition that the woman is ‘not quite right’

A quick assessment of airway, breathing and circulation (ABC) is fundamental to midwifery assessment,¹³ but in most cases there will be no obvious compromise in these areas and the midwife will need to elicit more subtle features of deteriorating condition.

Intuition arises from tacit knowledge, where patterns are observed from previous experiences, and should be followed up with more objective assessment. Midwifery assessment will include the four classic vital observations: (1) temperature, (2) pulse, (3) respiratory rate and (4) blood pressure.

Midwives should observe the woman generally, enquire how she is feeling and carry out these observations. Assessment of oxygen saturation, pain, neurological function, skin perfusion and urine output are further important aspects of assessment.¹⁰ The identification and treatment of the source of infection are paramount, and a general history and examination should be carried out to try to identify the source of the infection.³ Abdominal pain, offensive lochia and diarrhoea are particular features to be identified.¹⁴

MEOWS (modified early obstetric warning system) charts provide a standard to record maternal observations with the aim of identifying serious illness early and activating appropriate referral and management. They provide a template to record basic observations of heart and respiratory rate, temperature, blood pressure, level of consciousness and other observations, enabling recognition of subtle changes as well as being effective in providing some continuity when the woman is cared for by different caregivers.¹⁵ To enable this, the chart should follow the woman if she moves from area to area.

However, these charts should not replace, but rather supplement, effective ongoing clinical assessment of the mother by the midwife. To enable prompt care, midwifery assessment will aim to detect early signs that the woman is developing illness and make prompt referral.¹⁴

Box 12.4 lists signs and symptoms midwives should readily identify, if present, during their assessment of a woman. They include general signs and symptoms and those that relate to determining the focus of the infection. Box 12.5 highlights ‘red flag’ features that warrant urgent referral. If the woman is at home and appears seriously unwell, then transfer by emergency ambulance may be appropriate. The Managing Obstetric Emergencies and Trauma (MOET)⁴ manual emphasises the need for speed.

BOX 12.4: Signs and symptoms of sepsis that midwives should identify during assessment³

SIGNS

•  Pyrexia (although may not be present)

•  Hypothermia

•  Tachycardia

•  Tachypnoea

•  Hypoxia

•  Hypotension

•  Oliguria

•  Abdominal or pelvic pain

•  Impaired neurological state

SYMPTOMS

•  Fever or rigors

•  Diarrhoea

•  Vomiting

•  Generalised rash

SYMPTOMS RELATED TO FOCUS OF INFECTION

•  CS or perineal wound infection

•  Symptoms of urinary tract infection

•  Delay in involution, heavy lochia, offensive vaginal discharge

•  Productive cough

•  Mastitis

•  Signs of fetal compromise

Following on from basic observations, a range of secondary assessments includes the testing, and assessing, of urine, swabs, blood tests, and use of ultrasound, x-ray, and other investigative tools according to symptoms (see Box 12.6).

Depending on the stage of pregnancy or puerperium, the usual fetal assessment, antenatal examination or postnatal checks should be done.

BOX 12.5: ‘Red flag’ features that would prompt urgent referral for medical assessment3,4

•  Pyrexia of >38°C or hypothermia <36°C

•  Sustained tachycardia more than 90 beats per minute

•  Breathlessness (respiratory rate more than 20 breaths per minute)

•  Hypotension

•  Abdominal or chest pain

•  Diarrhoea and/or vomiting, dehydration

•  Spontaneous rupture of membranes with offensive liquor

•  Persistent vaginal bleeding

•  Uterine or renal angle pain and tenderness

•  Clear signs of sepsis, for example, a broken-down perineal wound

•  The woman is generally unwell or seems unduly anxious or distressed

Clinical features

SIGNS AND SYMPTOMS2,5

Signs and symptoms of the initial infection will depend on the source of the infection, and identification of that source is an important part of diagnosis and management.

BOX 12.6: Investigations for sepsis3,4,16

•  Blood culture

•  Serum lactate

•  Full blood count (including detailed white cell count), urea and electrolytes, and C-reactive protein

•  Consider group and save and clotting studies

•  Samples and swabs taken as indicated by clinical suspicion of the focus of infection, also considering the less common (e.g. malaria) where appropriate

•  Imaging: Chest x-ray, pelvic ultrasound scan, computed tomography

One of the earliest signs of sepsis is an increased respiratory rate. The respiratory rate will go up in response to pyrexia and lactic acidosis, and is a result of cytokine-mediated (immune response) effects on the respiratory centre. Pyrexia is common when infection is present, but in sepsis a normal temperature or hypothermia can be found.

Constant severe abdominal or perineal pain and tenderness that is disproportionate to that which would normally be expected, and which is not relieved by usual analgesic medication, should be a warning sign. Diarrhoea in addition to unexplained pain is characteristic of sepsis.

An abnormal fetal heart rate pattern or intrauterine fetal death may indicate maternal disease.

CAUSATIVE ORGANISMS ASSOCIATED WITH SEPSIS

Toxic shock syndrome caused by staphylococcal or streptococcal exotoxins can produce an array of confusing symptoms including nausea, vomiting, diarrhoea, severe pain due to necrotising fasciitis, watery vaginal discharge and a generalised maculopapular rash.

GAS is a community-acquired infection that has significantly contributed to the recent rise in rates of maternal mortality.1,8 It is a particularly serious organism, as it produces a virulent exotoxin A, which causes a rapid skin and soft tissue necrosis known as necrotising fasciitis. Although Escherichia coli causes the largest number of infections, outcomes are significantly worse with GAS.⁹ The genital and renal tracts are predominant sites of infection, and all modes of instrumental and operative deliveries carry significant risks.

The natural reservoir for GAS is the nasopharynx and it is a cause of pharyngitis (‘strep throat’) and scarlet fever as well as genital tract sepsis. Approximately 5%–30% of the population are asymptomatic carriers of the organism. Transmission is via aerosolised droplets and occurs more frequently in the winter months. Women may acquire the infection from family members, particularly children. Colonisation of the genital tract may occur via incomplete handwashing with subsequent contamination of the perineum.⁶

The damage caused by GAS progresses rapidly to septic shock and multi-organ failure and it has a mortality rate of up to 25%.¹⁷ A concerning feature of GAS infections is that initially the infection has few symptoms but can progress rapidly to fulminant infection and multi-organ involvement. The Confidential Enquiries report gives examples of the rapid progression of the infection. Even where health professionals recognised the illness and acted promptly, sadly some women still died, despite excellent care.⁸

Management

[T]he key to management of sepsis is early recognition, aggressive resuscitation, antibiotic administration and source control.¹⁸

All Trusts will have their own protocol, based on the ‘Surviving Sepsis Campaign’¹⁹ and guidelines on management of sepsis issued by the Royal College of Obstetricians and Gynaecologists.2–4 Key elements are summarised in Box 12.7. Box 12.6 lists suggested investigations for suspected sepsis.

MONITORING THE FETUS AND CONSIDERATIONS REGARDING THE TIMING OF DELIVERY

CTG monitoring of the fetus is advised although this will depend on the gestation. Changes to the CTG may prove sensitive indicators of deteriorating maternal condition and therefore should prompt reassessment of both mother and baby.²

Delivery may be beneficial to the woman or to the baby or to both. The decision will be made in consultation with other members of the multidisciplinary team involved, and with the woman, although this may be difficult where she is critically unwell. Attempting delivery when the mother is haemodynamically unstable is unsafe for both mother and baby, but delivery of the baby will aid recovery of the mother where the fetus, placenta and membranes are the source of infection and will be an essential part of management in the context of a mother’s deteriorating condition.² Where there is respiratory compromise, delivery of the baby will improve respiratory function in the mother.

BOX 12.7: Key elements of management of sepsis

•  Provide ABC resuscitation as necessary (see Chapter 2).

•  Note that early recognition and prompt management are critical.

•  Provide multidisciplinary management with senior clinical leadership to direct care; the team in addition to senior maternity unit staff may include an intensive care specialist, general surgeon, microbiologist and haematologist. If available, a critical outreach team should be involved at an early stage.

•  Obtain two blood cultures and other appropriate swabs and specimens prior to commencement of antibiotics.

•  Measure serum lactate (repeat as necessary if raised or condition worsens).

•  Provide prompt treatment with adequate dose(s) of appropriate intravenous antibiotics – the aim is that antibiotics should start within 1 hour of suspecting sepsis and after samples have been obtained for culture.

•  Restore haemodynamic status to ensure adequate oxygen delivery to tissues; this may include fluid replacement and use of medication to maintain blood pressure – careful management of fluid balance is required to prevent fluid overload.

•  Provide facial mask oxygenation or ventilation, oxygen saturation monitoring.

•  Ensure clear and detailed documentation of signs and treatment; use MEOWS charts/fluid balance chart/pain scoring system and/or a specific chart designed for use in high-dependency care.

•  Admit to intensive care unit as indicated by condition.

•  Consider continuous cardiotocography (CTG).

•  Deliver the baby or perform surgery to remove the focus of infection; hysterectomy may be required as a life-saving measure.

Outcome, follow-up and other considerations

Multiple organ failure may complicate some cases of severe sepsis, including DIC, myocardial dysfunction and failure, hepatic encephalopathy and renal failure, and for some women, these complications may cause death.15 It is thought that of those who die from sepsis, about one-third die from refractory hypotension and two-thirds die from multiple organ failure.

Many infections progress even following antibiotic treatment; therefore midwives obtaining treatment for women should ensure they also monitor the effects. In their study, UKOSS⁹ found more than 40% of women with severe sepsis had previously had a pyrexia or had been prescribed antibiotics before presentation, and this suggests at least some were not adequately diagnosed or followed up. Consultation with the microbiologist may be helpful.

Some women will have a slow course of improvement and careful observation may need to be maintained for some time. Antimicrobial treatment may need to be reassessed and changed if necessary.

Follow-up after discharge from hospital will be important for both the physical and the psychological aspects of recovery following sepsis.

Whatever the cause of the infection, but in particular where invasive GAS is identified, midwives need to take measures to protect themselves, ensure they do not pass the organism to others and provide information and instruction to other staff, such as maternity care assistants and domestic staff and to the woman’s friends and family. Healthcare workers have been identified as a source of hospital-acquired GAS infection. The particular strain of GAS can be identified and if more than one case of GAS puerperal sepsis occurs in the same unit within 6 months, and has the same strain, there is a possibility that a birth attendant has been the source of infection.²⁰

Specific guidelines for the control and prevention of the spread of GAS infection in healthcare settings, including maternity units, are available.²¹ The key recommendations are summarised in Box 12.8. The infection prevention and control team will need to provide specialist advice for the woman’s close community contacts such as her family.

BOX 12.8: Summary of recommendations from GAS guideline Development Working Group on the control and prevention of spread of GAS infection in acute healthcare settings²¹

•  Cases of GAS should be referred to the infection prevention and control team, and the local health protection specialist informed.

•  The woman should be isolated and healthcare workers should wear disposable protective equipment, including gloves and aprons, when in contact with the woman and in the vicinity of where she is located.

•  Strict hand hygiene is essential.

•  Visitors will need instruction and supervision so they follow the required procedures, including vigilant handwashing.

•  Prophylaxis should be considered for healthcare workers who sustain needlestick injury with potentially infectious material.

•  Healthcare workers in contact with a case of GAS should be alert to symptoms including a sore throat, skin infection or lesion or vaginitis. If these symptoms appear around this time, they should present to occupational health for screening with a view to antibiotic treatment.

Summary of midwifery responsibilities

•  Conduct regular assessment of all women that includes basic observations when indicated.

•  Note early recognition of the features of infection and/or sepsis and any indication of deteriorating illness.

•  Ensure prompt and effective referral of women with signs of sepsis and/or deteriorating illness.

•  Work alongside the multidisciplinary team to instigate the elements of the ‘Surviving Sepsis Campaign’ in a timely manner.

•  Keep accurate documentation of the ongoing assessment of the woman.

•  Attend to elements of infection control.

•  Provide psychological support for the woman and her family.

INFLUENZA (FLU)

Influenza is a contagious respiratory illness caused by influenza viruses. Outbreaks of influenza occur seasonally and more serious pandemic flu occurs periodically. Clinical symptoms of influenza are usually mild (most cases of H1N1 – swine flu – were mild) but can be severe, as was seen with avian flu in 2004. Morbidity and mortality from influenza vary according to the viral strain but with all influenza, pregnant women and their newborn offspring are more vulnerable to serious complications.22–24 In the United Kingdom during the period 2009–2012, 36 women died from ‘flu’, 32 of which were believed to be from the H1N1 strain.¹

Although pregnant women are not more likely than non-pregnant women to contract a respiratory infection, when they do it is more likely to lead to serious complications including pneumonia. This is due to a number of anatomical, physiological and immune changes of pregnancy, such as increased cardiac output, decreased lung capacity and greater oxygen (O₂) demand. However, in particular, it is due to fluid shifts that increase pulmonary oedema and restriction to the ventilation of the lungs, contributing to more serious complications of influenza, including pneumonia and adult respiratory distress syndrome.²⁵ This risk seems more pronounced in the second and third trimesters.²⁶

Pregnant women have been found to be seven times more likely to die from influenza than nonpregnant women in the same age group.⁴ Clinical comorbidities or conditions contribute to the risk, however, problems can occur in previously healthy women. It is considered that delays in recognition, diagnosis and treatment contributed to many of those who died.⁴

BOX 12.9: Highest-risk categories for complications of respiratory infection²⁷

•  Smoking

•  Substance abuse

•  Poor nutrition

•  Pre-existing conditions including asthma, diabetes, cardiac disease, anaemia and renal disease

•  Morbid obesity

•  Those with immune suppression including human immunodeficiency virus, immunosuppressive medication

•  Pregnancy

Every year there is an outbreak of seasonal flu in winter that affects approximately 5%–15% of the population, and recently pregnant women have been included as an at-risk group. Midwives need to be conversant with the care of women with flu and with public health measures to prevent spread of influenza including the vaccination of pregnant women.

Assessment of the respiratory system

The use of modified early obstetric warning system (MEOWS) charts is recommended,⁸ and has been widely adopted in practice as an aid to ensure timely referral. Observations of respiratory rate, pulse, blood pressure, temperature and O₂ saturations need to be put in context and interpreted as part of a more detailed assessment of mother and fetus. Compensatory mechanisms will attempt to maintain homeostasis in the presence of disease. Breathlessness (increased respiratory rate), tachycardia and changes in blood pressure all indicate deteriorating respiratory function. Box 12.10 lists some specific features the midwife may note in her assessment of respiratory function. The doctor, or midwife with advanced practitioner skills, will also perform a chest examination involving percussion and auscultation. A chest x-ray will provide valuable information for respiratory assessment and should be arranged without delay. Chest x-rays are not contraindicated in pregnancy, although shielding of the uterus is still advised.²⁸

BOX 12.10: Assessment of respiratory function by the midwife

In addition to the usual set of basic observations, the midwife should observe for the following features.

•  Stridor, cough, wheeze

•  Verbal response (Is the woman able to complete a sentence in one breath?)

•  Central or peripheral cyanosis

•  Decreased capillary refill

•  Signs of respiratory distress such as sitting upright and leaning forward, use of accessory muscles when breathing

•  Production of sputum – blood-stained/green sputum

•  Change to the rate, depth and symmetry of breathing

•  Level of consciousness and degree of orientation

Box 12.11 lists the features of deteriorating respiratory function. One of the challenges of assessment of the respiratory system in pregnancy is distinguishing between the physiological breathlessness experienced by up to 75% of pregnant women and breathlessness of a more serious cause. Normal breathlessness comes on gradually over a number of weeks and is not associated with other adverse signs or symptoms. The woman may notice it when she is talking and it can get worse with exercise. A recent Confidential Enquiries report⁸ identified ‘red flag’ features useful in identifying a more serious cause of breathlessness (see Box 12.12). This report⁸ also recommended that pulmonary oedema be considered as a possible cause of a ‘wheeze’ in a pregnant woman, especially in those not known to have asthma.

BOX 12.11: Features of deteriorating respiratory function²⁹

•  Increased respiratory rate (above 20 breaths per minute – assess for a full minute following pulse assessment)

•  Dropping O₂ saturation

•  Increased supplemental O₂ required to keep O₂ saturation within normal range

•  Increased MEOWS chart score

•  Carbon dioxide (CO₂) retention (as indicated by arterial blood gas levels)

•  Abnormalities of the CTG may reflect deterioration in the mother

•  Drowsiness

•  Headache

•  Flushed face

•  Tremor

Clinical features and complications of influenza

Influenza may be confused with the common cold but it is a more serious illness and is caused by a different virus. Cold symptoms come on gradually and include having a stuffy or runny nose and a sore throat. Flu symptoms come on more suddenly and severely (see Box 12.13). Midwives and other healthcare providers need to educate women about the symptoms of influenza (see Box 12.13) and advise them to seek medical advice promptly so that antiviral treatment (if indicated) can be started as early as possible. Ideally, this would be within 48 hours of the onset of symptoms.³⁰

The mean duration of illness is 7 days, although 50% of people take up to 10 days or longer to recover.27,31,32 The influenza virus has a 1- to 4-day incubation period and a person is infectious for a day preceding and 3 days after symptoms are evident.³³ For most, influenza is a relatively mild illness but for some it may cause considerable morbidity and even death.

BOX 12.12: ‘Red flag’ features of serious breathlessness in pregnancy⁸

•  Breathlessness of sudden onset

•  Breathlessness associated with chest pain

•  Orthopnoea (difficulty breathing when lying flat) or paroxysmal nocturnal dyspnoea (a sensation of shortness of breath that wakes the woman up at night)

BOX 12.13: Common symptoms of influenza31,32

•  Chills

•  Sudden onset of fever (temperature of 38°C or above)

•  Cough and sore throat

•  Generalised muscle aches and pains (especially in the back and legs)

•  Severe headache

•  Weakness or fatigue

•  Loss of appetite

•  Gastrointestinal symptoms (nausea, vomiting, diarrhoea and abdominal pain) are a feature of swine flu in children and adults requiring admission to hospital

A primary viral or secondary bacterial pneumonia can complicate the recovery from influenza.³³ Reviews of pregnant women admitted to hospital with H1N1 flu indicated a rapid progression of illness requiring admission to the intensive therapy unit (ITU) and ventilation. Complications, in addition to pneumonia, included sepsis, haematological disorders, pneumothorax, cardiac arrhythmias, renal failure and encephalopathy.²⁷,³⁴,³⁵

Transmission of influenza viruses is via direct contact with respiratory secretions and through airborne droplets generated by coughing, sneezing and talking. Infection can be acquired through contact with contaminated surfaces. Box 12.14 summarises general advice to prevent the spread of influenza.

A systematic review by Jefferson et al.³⁷ of interventions to reduce the spread of respiratory viruses in healthcare settings showed that wearing masks, gloves, gowns and frequent hand washing were all beneficial in minimising the spread of infection associated with flu.

Pregnant women and influenza

Pregnancy is considered an independent risk factor for the development of serious complications of influenza. Many pregnant women died during influenza pandemics of the twentieth century³⁶ and during the 2009 H1N1 flu pandemic, pregnant women were four to seven times more likely to be admitted to hospital with complications of flu compared to the non-pregnant population.23,26,38–40 They were also seven times more likely to require admission to intensive care units.¹ Although women in the ‘high-risk’ category (see Box 12.9) are more likely to have severe complications, a systematic review of studies of H1N1 flu found that many pregnant women (almost 70%) who were admitted to hospital with flu did not have any other high-risk pre-existing factors, apart from pregnancy, that would have complicated their recovery.²⁴

BOX 12.14: General advice to prevent the spread of influenza³⁶

•  Cover your nose and mouth when you cough or sneeze, using a tissue where possible

•  Dispose of used tissues quickly and sensibly (i.e. bag and bin them)

•  Wash hands often with hot water and soap

•  Clean frequently touched hard surfaces (e.g. door handles and kitchen surfaces) using normal cleaning products

•  Make sure children follow these hygiene rules

Babies of mothers with influenza

During the influenza pandemic, the babies of mothers with serious complications of H1N1 flu were much more likely to be delivered prematurely, although very few of them tested positive for H1N1 flu.²⁴,⁴¹ It is generally thought that seasonal flu virus does not affect the fetus. However, a severe or sustained pyrexia during pregnancy has been associated with an increased risk for birth defects, including neural tube defects,⁴² and for this reason the midwife should advise measures to ensure women do not develop a high temperature.

Recommendations for management of influenza in pregnancy

At the time of the H1N1 flu outbreak, the Department of Health and Royal College of Obstetricians and Gynaecologists published joint guidelines on the management of pregnant women entitled Pandemic H1N1 2009 Influenza: Clinical Management Guidelines for Pregnancy.⁴³ They were published only in an electronic version, with the intention to update them online as any new information emerged. They were only for use during the pandemic and clinicians were urged to keep up to date with emerging information. They have now been archived. In the event of another pandemic, readers should access information provided by these organisations. Midwives will have a key role in keeping up to date with such recommendations and providing information to women. The guidance here is also useful in outlining principles of care during the annual flu season. Box 12.15 provides general information for the care of women in the community at the time of a flu outbreak. It will be important that women know when they should seek additional advice (see Box 12.16). Midwives will need to identify features of deteriorating health and ensure prompt referral and admission to hospital (see Box 12.17).

BOX 12.15: Influenza: Summary of key recommendations for care of women in the community43–45

•  Women who think they have flu are advised to stay at home and phone their general practitioner, midwife or helpline for advice. Midwives may arrange home visits, where required.

•  Pregnant women with uncomplicated influenza should be expected to make a full recovery.

•  Women should be given clear information about when to re-consult their general practitioner or midwife and when to seek emergency medical help (see Box 12.16).

•  Women with flu should stay at home, drink plenty of fluids and use paracetamol to control high temperature.

•  Antibiotics may be prescribed as indicated for secondary bacterial infection.

BOX 12.16: Influenza: When women should seek further medical help44,45

Women should be advised to seek emergency medical help should they experience any of the following factors:

•  Difficulty breathing

•  Pain or pressure in chest or abdomen

•  Sudden dizziness or confusion

•  Severe or long-lasting vomiting

•  Blood-stained sputum

•  Decreased fetal movements

•  High temperature not controlled by paracetamol

In cases where a woman does become critically ill, involvement of a wider multidisciplinary team is vital and will include consultant level obstetrician, respiratory physician, obstetric anaesthetist, haematologist, the intensive care team and the infection prevention and control team. The midwife should remain involved providing an important link for ongoing psychological support for the woman and her family alongside physical care.

BOX 12.17: Criteria for urgent hospital referral of suspected swine flu in a pregnant woman according to guidance given at time of the 2009 swine flu outbreak45*

•  Signs of respiratory distress – dyspnoea, tachypnoea (respiratory rate >30 breaths per minute)

•  Peripheral O₂ saturation ≤94% in air

•  Dehydration or shock

•  Any signs of sepsis

•  Altered conscious level

•  Seizures

* List is not exclusive.

A summary of recommendations for the management of a woman with influenza based on guidance given at the time of the 2009 swine flu pandemic included the following points44,45:

•  Admission should be made to a single room with respiratory isolation.

•  A multidisciplinary decision needs to be made with regard to the best place to manage women admitted with influenza. Intensive care unit admission will be indicated if there are signs of respiratory distress, pneumonia, persistent tachycardia (>100 beats per minute) or altered level of consciousness.

•  Multidisciplinary assessment is necessary for exclusion of other pathology or obstetric complications including pre-eclampsia, chorioamnionitis, urinary tract infection and pulmonary embolism.

•  An early warning tool (MEOWS chart) should be used to facilitate identification of women whose condition is deteriorating. Tachycardia and hypoxia were clear signs of severe disease as identified in the Centre for Maternal and Child Enquiries (CMACE)⁸ report.

•  Appropriate bacteriological investigations are performed including blood and sputum cultures.

•  Chest x-ray is a useful diagnostic test and should be used when indicated to aid diagnosis of respiratory disorders in pregnant women.

•  Antiviral medication may possibly be used.

•  Careful fluid monitoring and assessment are important.

•  Pulse oximetry and arterial blood gas are monitored.

•  Maternal pyrexia is controlled to prevent complications including fetal abnormality and preterm delivery.

•  Corticosteroids to promote fetal lung maturity may be used with caution. Specialist guidance should be sought.

•  Multidisciplinary decision should be made regarding timing and mode of delivery. Preterm delivery may be indicated to improve ventilation of a very ill mother.

•  Assessment is made by the medical team regarding the need for antibiotics.

•  Be aware of potential complications including disseminated intravascular coagulation, cognitive impairment, venous thromboembolism and psychological morbidity.

•  Implement appropriate infection control measures: notify infection prevention and control team, hand washing, women should be cared for in isolation, women should wear a surgical mask and staff should wear surgical mask, plastic apron, gloves and eye protection (where risk of eye splash).

•  Women should be offered appropriate psychological support.

Vaccination

Influenza vaccination is the best way to prevent the spread of influenza. It is recommended to reduce the possibility of complications of flu in the mother with the added benefit of providing immunity to the neonate.46–48 The recommendation of a healthcare provider has been identified as a key factor in improving the uptake of vaccination by pregnant women.⁴⁹ The Royal College of Obstetricians and Gynaecologists and the Royal College of Midwives⁴³ suggest midwives facilitate women’s decision making with regard to flu vaccination by informing women of their higher risk of complications from flu, that the vaccines have been licensed as safe for use in pregnancy and that side effects are minimal. This has been endorsed by the MBRACCE report¹ which stated that the deaths of more than half of the women who died from flu could have been prevented if they had been vaccinated.

Summary of midwifery responsibilities

COMMUNITY

•  Serve as the point of contact for pregnant women with regard to knowledge of prevention, symptoms and spread of influenza providing written and verbal advice.

•  Provide information and administration of flu vaccination.

•  Provide detailed information on infection control measures including cough etiquette and hand washing.

•  Provide information regarding self-care at home for women with flu symptoms ensuring women know when and how to seek emergency care if required.

•  Identify any women with deteriorating health and instigate appropriate referral.

•  Facilitate a home visit if indicated during the time the woman needs to avoid contact with other pregnant women, although it may be prudent to postpone regular antenatal care.

WOMEN ADMITTED TO HOSPITAL WITH INFLUENZA

•  Perform and document a range of regular observations; record on MEOWS chart and refer any abnormal findings to appropriate medical staff

•  Monitor usual signs of maternal and fetal well-being.

•  Monitor O₂ saturation

•  Check fluid balance and administration of fluid regimen as per medical instructions.

•  Administer prescribed medication, which may include antiviral medication, antibiotics and medication to bring down a maternal temperature.

•  Observe strict isolation and infection control measures.

•  Observe for signs of labour.

•  Provide assistance with the establishment and maintenance of breastfeeding.

•  Provide psychological support to the woman and her family.

PNEUMONIA

Pneumonia is an inflammation of the lungs caused by microorganisms, usually bacteria or viruses. The inflammation produces fluid and the small air sacs (alveoli) of the lungs become filled with fluid exudate, impairing gaseous exchange. The affected area can be confined to one portion of the lungs (lobar pneumonia) or it can be more widespread (bronchopneumonia).⁵⁰ Pneumonia does not occur more often in pregnant women than in the nonpregnant population but it can be more virulent and mortality is higher.⁵¹ Pneumonia accounts for nearly 20% of admissions to ITU of women who are currently pregnant.⁵²

Clinical features of pneumonia

The classic features of pneumonia include a dry cough, breathlessness (increased respiratory rate) and chest pain. There may also be fever, agitation and confusion.⁵³ Ventilation and perfusion are likely to be compromised, resulting in reduced O₂ saturation. An examination of the chest may note that lung expansion is reduced on the affected side. Percussion will note dullness over the consolidated area and bronchial breathing may be heard. There may be production of purulent or ‘rusty’ sputum as the pneumonia clears.⁵⁰

Blood cultures should be taken and a chest x-ray will confirm diagnosis.⁵¹ There may be a delay in the diagnosis of pneumonia in pregnancy and this may contribute to increased morbidity. The normal breathlessness of pregnancy may mask developing disease. Breathlessness is experienced by nearly 75% of women in the third trimester. The feature of this ‘physiological’ breathlessness is that it does not interfere with daily activity and rarely occurs at rest. A woman may also normally experience a degree of chest discomfort due to the mechanical effects of the enlarged uterus on the diaphragm.8,27 A distinction between these normal findings and disease can be made by detailed assessment and a chest x-ray as indicated.

Management of pneumonia in pregnancy

Key elements of the treatment for pneumonia will include O₂ therapy, rehydration, and antibiotic therapy and/or antiviral medication as indicated. It is important to remember the fetus and to include monitoring of the fetus when treating pregnant women. Blood flow and oxygenation to the placenta are entirely dependent on the mother’s haemodynamic state and thus fetal well-being requires effective treatment of the mother.⁵³ The woman may be cared for in a high-dependency maternity care setting, but if her condition is poor or deteriorating and/or she requires ventilation, she is likely to be transferred into a critical care unit.⁵⁴ The consultant anaesthetist and/or the critical outreach team will facilitate and monitor the transfer.

When the woman is being cared for in a maternity setting the midwifery responsibilities will include basic observations and respiratory assessment, positioning, O₂ therapy, monitoring fluid balance, fetal assessment, administration of medication, effective infection control measures and psychological care. When a woman is experiencing difficulty in breathing it will help to maximise ventilation by encouraging her to adopt a high side-lying position. This promotes aeration and perfusion of any healthy lung tissue.⁵⁰ This position also avoids any aortocaval compression by the uterus, which would be detrimental to mother and baby.⁵⁵ Continuous CTG monitoring may be indicated. O₂ therapy is recommended when there is evidence of hypoxaemia, with the aim of maintaining O₂ saturation levels at or above 95%. In cases of severe hypoxaemia, high-concentration O₂ (15 L/min) via a non-rebreathing reservoir mask should be commenced. For those with milder hypoxaemia, O₂ can be administered via nasal cannulae at 2–6 L/min or via a simple face mask at 5–10 L/min.²⁹ Humidification is not usually necessary for low-flow O₂ therapy but may be required when using high-flow O₂ for longer than 24 hours.⁵⁰

Fluid replacement may be indicated. An increase in insensible water loss associated with an increased respiratory rate and fever may lead to dehydration, which can cause secretions to become more sticky. Regular sips of water where possible is advocated. A fluid balance chart should be used.⁵⁰

Summary of midwifery responsibilities

•  Effective assessment of respiratory function to enable early detection and prompt referral of women developing critical illness.

•  Interventions to maximise respiratory function that will include upright positions to expand the chest, and avoidance of aortocaval compression.

•  Timely and appropriate use of supplemental O₂ therapy when indicated.

•  Ongoing assessment of mother and fetus, clear documentation including accurate fluid balance and clear communication with appropriate members of the multidisciplinary team.

•  Timely administration of prescribed medication.

•  Psychological support for the woman and her family.

REFERENCES

1.  Knight M, Kenyon S, Brocklehurst P, Neilson J, Shakespeare J, Kurinczuk J (Eds.), on behalf of MBRRACE-UK. 2014. Saving Lives, Improving Mothers’ Care – Lessons Learned to Inform Future Maternity Care from the UK and Ireland Confidential Enquiries into Maternal Deaths and Morbidity 2009–2012. Oxford: National Perinatal Epidemiology Unit, University of Oxford, pp. 57–63.

2.  Royal College of Obstetricians and Gynaecologists (RCOG). 2012. Bacterial Sepsis in Pregnancy. Green-Top Guideline 64a. London: RCOG.

3.  Royal College of Obstetricians and Gynaecologists (RCOG). 2012. Bacterial Sepsis following Pregnancy. Green-top Guideline 64b. London: RCOG.

4.  Paterson-Brown S, Howell C. (Eds.) 2014. Sepsis. In: The MOET Course Manual: Managing Obstetric Emergencies and Trauma. 3rd ed. Cambridge: Cambridge University Press.

5.  Lucas DN, Robinson PN, Nel MR. 2012. Sepsis in obstetrics and the role of the aneasthetist. International Journal of Obstetric Anesthesia, 21(1): 56–67.

6.  Acosta CD, Knight M. 2013. Sepsis and maternal mortality. Current Opinion in Obstetrics and Gynecology, 25(2):109–116.

7.  Acosta CD, Bhattacharya S, Tuffnell D, Kurinczuk JJ, Knight M. 2012. Maternal sepsis: A Scottish population-based case-control study. BJOG: An International Journal of Obstetrics and Gynaecology, 119(4):474–483.

8.  Centre for Maternal and Child Enquiries (CMACE). 2011. Saving Mothers’ Lives: Reviewing maternal deaths to make motherhood safer: 2006–2008. The eighth report of the confidential enquiries into maternal deaths in the United Kingdom. BJOG: An International Journal of Obstetrics and Gynaecology, 118(Suppl. 1): 1–203.

9.  Acosta C, Kurinczuk J, Lucas D, Tuffnell D, Sellers S, Knight M, UK Obstetric Surveillance System. 2014. Severe sepsis in the UK, 2011–2012: A national case-control study. PLoS Medicine, 11(7):e1001672. doi:10.1371/journal.pmed.101672.

10.  Ferns T. 2007. Shock and the critically ill woman. In: Billington M, Stevenson M (Eds.). Critical Care in Childbearing for Midwives. Oxford: Blackwell, pp. 140–166.

11.  Hayes M. 2007. Sepsis. In: Dob D, Cooper G, Holdcroft A (Eds.). Crisis in Childbirth: Why Mothers Survive; Lessons from the Confidential Enquiries into Maternal Deaths. Abingdon: Radcliffe, pp. 168–186.

12.  Raynor M. 2012. Sepsis. In: Raynor M, Marshall J, Jackson K (Eds.). Midwifery Practice: Critical Illness, Complications and Emergencies Case Book. Maidenhead: McGraw-Hill, pp. 175–192.

13.  Bothamley J, Boyle M. 2015. Infections Affecting Pregnancy and Childbirth. London: Radcliffe.

14.  Bick D, Beake S, Pellowe C. 2011. Vigilance must be a priority: Maternal genital tract sepsis. Practising Midwife, 14(4):16–18.

15.  Lack N, Ugwumadu A. 2012. Sepsis and septic shock in pregnancy. In: Chandraharan E, Arulkumaran S (Eds.). Obstetrics and Intrapartum Emergencies. Cambridge: Cambridge University Press, pp. 41–47.

16.  Burke K, Gupta M. 2013. Puerperal sepsis: A traveller’s tale. Acta Obstetricia et Gynecologica Scandinavica, 92(11):1335.

17.  Gourlay M, Gutierrez C, Chong A, Robertson R. 2001. Group A streptococcal sepsis and ovarian vein thrombosis after an uncomplicated vaginal delivery. Journal of the American Board of Family Practice, 14(5):375–380.

18.  Arulkumaran N, Singer M. 2013. Puerperal sepsis. Best Practice and Research. Clinical Obstetrics and Gynaecology, 27(6):893–902.

19.  Dellinger RP, Levy MM, Rhodes A et al. 2013. Surviving Sepsis Campaign: International guidelines for management of severe sepsis and septic shock: 2012. Critical Care Medicine, 41(2):580–637.

20.  Palaniappan N, Menezes M, Wilson P. 2012. Group A streptococcal puerperal sepsis: Management and prevention. Obstetrician and Gynaecologist, 14(1): 9–16.

21.  Steer JA, Lamagni T, Healy B et al. 2012. Guidelines for prevention and control of group A streptococcal infection in acute healthcare and maternity settings in the UK. Journal of Infection., 64(1): 1–18.

22.  Dodds L, McNeil SA, Fell DB et al. 2007. Impact of influenza exposure on rates of hospital admissions and physician visits because of respiratory illness among pregnant women. Canadian Medical Association Journal, 176(4):463–468.

23.  Jamieson DJ, Honein MA, Rasmussen SA et al. 2009. H1N1 2009 Influenza virus infection during pregnancy in the USA. The Lancet, 374(9688):451–458.

24.  Mosby LG, Rasmussen SA, Jamieson DJ. 2011. 2009 pandemic influenza A (H1N1) in pregnancy: A systematic review of the literature. American Journal of Obstetrics and Gynecology, 205(1): 10–18.

25.  Hegewald M, Crapo R. 2011. Respiratory physiology in pregnancy. Clinics in Chest Medicine, 32(1):1–13.

26.  Louie J, Acosta M, Jamieson D et al. 2010. Severe 2009 H1N1 influenza in pregnant and postpartum women in California. New England Journal of Medicine, 362(1):27–35.

27.  Lim BH, Mahmood TA. 2010. Pandemic H1N1 2009 (swine flu) and pregnancy. Obstetrics Gynaecology and Reproductive Medicine, 20(4):101–106.

28.  Brent R. 2011. The pulmonologist’s role in caring for pregnant women with regard to the reproductive risks of diagnostic radiological studies or radiation therapy. Clinics in Chest Medicine, 32(1):33–42.

29.  O’Driscoll BR, Howard LS, Davidson AG. 2008. BTS Guideline for Emergency Oxygen Use in Adult Patients. London: British Thoracic Society. Available at https://www.brit-thoracic.org.uk/document-library/clinical-information/oxygen/emergency-oxygen-use-in-adult-patients-guideline/emergency-oxygen-use-in-adult-patients-guideline/ (accessed September 28, 2014).

30.  Ramussen SA, Kissin DM, Yeung LF et al. 2011. Preparing for influenza after 2009 H1N1: Special considerations for pregnant women and newborns. American Journal of Obstetrics and Gynecology, 204(6):S13–S20.

31.  Department of Health (DH). 2013. Influenza. In: Immunisation against Infectious Disease: The Green Book [online]. Available at www.gov.uk/government/uploads/system/uploads/attachment_data/file/239268/Green_Book_Chapter_19_v5_2_final.pdf (accessed November 23, 2013).

32.  Panda B, Panda A, Riley LE. 2010. Selected viral infections in pregnancy. Obstetrics and Gynecology Clinics of North America, 37(2):321–331.

33.  Gillespie S, Bamford K. 2012. Medical Microbiology and Infection at a Glance. 4th ed. Oxford: Wiley.

34.  Ellington S, Hartman LK, Acosta M et al. 2011. Pandemic 2009 influenza A (H1N1) in 71 critically ill women in California. American Journal of Obstetrics and Gynecology, 204(6):S21–S29.

35.  Pratt R. 2009. The global swine flu pandemic 1: Exploring the background to influenza viruses. Nursing Times, 105(34):18–21.

36.  Pratt R. 2010. Pandemic A (H1N1) 2009 influenza: An enhanced hazard during pregnancy. Midwifery, 26(1):13–17.

37.  Jefferson T, Del Mar C, Dooley L et al. 2009. Physical interventions to interrupt or reduce the spread of respiratory viruses: Systematic review. British Medical Journal, 339:1–10.

38.  Creanga AA, Johnson TF, Graiter SB et al. 2010. Severity of 2009 Pandemic Influenza A (H1N1) virus infection in pregnant women. Obstetrics and Gynecology, 115(4):717–726.

39.  Jain S, Kamimoto L, Bramley AM et al. 2009. Hospitalized patients with 2009 H1N1 influenza in the United States, April–June 2009. New England Journal of Medicine, 361(20):1935–1944.

40.  Jalfari A, Langen ES, Aziz N et al. 2010. The effects of respiratory failure on delivery in pregnant patients with H1N1 2009 influenza. Obstetrics and Gynecology, 115(5):1033–1035.

41.  Mendez-Figueroa H, Raker C, Anderson BL. 2011. Neonatal characteristics and outcomes of pregnancies complicated by influenza infection during the 2009 pandemic. American Journal of Obstetrics and Gynecology, 204(6 Suppl. 1): S58–S63.

42.  Moretti ME, Bar-Oz B, Fried S et al. 2005. Maternal hyperthermia and the risk for neural tube defects in offspring: Systematic review and meta-analysis. Epidemiology, 16(2):216–219.

43.  Royal College of Obstetricians and Gynaecologists (RCOG), Royal College of Midwives (RCM). 2009. Guidance on Swine Flu (H1N1v) for Pregnant Mothers: A Joint Statement from the Royal College of Obstetricians and Gynaecologists and the Royal College of Midwives [online]. Available at www.rcm.org.uk/college/policy-practice/position-statement/swine-influenza-h1n1/#sthash.BrvGjAsm.dpufhttp (accessed April 1, 2014).

44.  Modder J. 2010. Review of Maternal Deaths in the United Kingdom Related to A/H1N1 2009 Influenza [online]. Available at https://www.rcm.org.uk/sites/default/files/Review-of-Maternal-Deaths~he-United-Kingdom-re.pdf

45.  Department of Health (DH), Royal College of Obstetricians and Gynaecologists (RCOG). 2009. Pandemic H1N1 2009 Influenza: Clinical Management Guidelines for Pregnancy. Updated December 10, 2009; now archived. Available at http://webarchive.nationalarchives.gov.uk/20130107105354/http://www.dh.gov.uk/prod_consum_dh/groups/dh_digitalassets/@dh/@en/documents/digitalasset/dh_107840.pdf (accessed September 28, 2014).

46.  Benowitz I, Esposito DB, Gracey KD et al. 2010. Influenza vaccine given to pregnant women reduces hospitalization due to influenza in their infants. Clinical Infectious Diseases, 51(12):1355–1361.

47.  Steinhoff MC, MacDonald N, Pfeifer D et al. 2014. Influenza vaccine in pregnancy: Policy and research strategies. Lancet, 383(9929):1611–1612.

48.  Tamma P, Ault K, del Rio C et al. 2009. Safety of influenza vaccination during pregnancy. American Journal of Obstetrics and Gynecology, 201(6):547–552.

49.  Steelfisher GK, Blendon RJ, Bekheit MM et al. 2011, Novel pandemic A (H1N1) influenza vaccination among pregnant women: Motivators and barriers. American Journal of Obstetrics and Gynecology, 204(6):S116–S123.

50.  Margereson C, Withey S. 2012. The patient with acute respiratory problems. In: Peate I, Dutton H (Eds.). Acute Nursing Care: Recognising and Responding to Medical Emergencies. London: Pearson, pp. 81–106.

51.  Stone S, Nelson-Piercy C. 2012. Respiratory disease in pregnancy. Obstetrics, Gynaecology and Reproductive Medicine, 22(10):290–298.

52.  Intensive Care and National Audit Research Centre (ICNARC). 2009. Female admissions (aged 16–50 years) to adult, general critical care units in England, Wales and Northern Ireland, reported as ‘currently pregnant’ or ‘recently pregnant’: 1 January 2007 to 31 December 2007. Available at http://www.oaa-anaes.ac.uk/assets/_managed/editor/File/Reports/ICNARC_obs_report_Oct2009.pdf (accessed February 19, 2013).

53.  Goodnight WH, Soper DE. 2005. Pneumonia in pregnancy. Critical Care Medicine, 33(10 Suppl.):S390–S397.

54.  Paruk F. 2008. Infection in obstetric critical care. Best Practice and Research. Clinical Obstetrics and Gynaecology, 22(5):865–883.

55.  Bamber JH, Dresner M. 2003. Aortocaval compression in pregnancy: The effect of changing the degree and direction of lateral tilt on maternal cardiac output. Anesthesia and Analgesia, 97(1):256–258.

13

Other causes of potential maternal collapse

ANDREA ARAS-PAYNE

Introduction

Presenting symptoms

Specific conditions

References

INTRODUCTION

This chapter considers the less common causes of maternal conditions which need emergency or urgent attention. It should be noted that all of these conditions fall outside the midwives’ remit and therefore their role is to provide a high standard of supportive care after summoning emergency assistance or organising urgent referral.¹ Although the outcome in several of these serious and life-threatening situations relies on prompt and effective resuscitation (see Chapter 2), many of these conditions are reversible with timely and appropriate treatment and effective teamwork and communication.2–4

For most of these conditions, prompt medical or surgical aid is the only treatment. However, it could be that an overview of the potential causes of the woman’s symptoms will help the midwife to decide how best to support her, especially in isolated situations, until assistance arrives. It is also possible that prior revision of these conditions will lead to earlier suspicion and referral of symptoms which might otherwise have progressed to an emergency situation. Updated knowledge is an important part of professional development.⁵

The overview given in this chapter is intended to be just a brief summary. It is hoped it will provide a starting point; further access to other resources for more in-depth information will be required. Further information may also be necessary in preparation for discussing and supporting women who have experienced any of these conditions.

The main presenting symptoms of maternal collapse are identified in the first part of this chapter, with the conditions that may be the potential cause listed alphabetically below each one. Many conditions manifest with various symptoms, depending on the degree of severity or just the individual aetiology and therefore may appear in more than one list. Some of these conditions are discussed in previous chapters. Others are briefly summarised later in this chapter, presented in alphabetical order. All require urgent care and referral.

A diagnosis of amniotic fluid embolism (see Chapter 11) should be strongly considered in cases of sudden unexplained maternal cardiorespiratory collapse.⁶

PRESENTING SYMPTOMS

Loss of Consciousness

The Glasgow Coma Scale has been developed to provide a standardised approach when assessing level of consciousness and severity of dysfunction (see http://www.glasgowcomascale.org for further information). Assessment using this scale allows for a quick and clear picture of responsiveness that can be conveyed alongside other clinical findings.⁷

COMMON CAUSES

•  Acute (formerly adult) respiratory distress syndrome (ARDS) (see section, this chapter)

•  Amniotic fluid embolism (see Chapter 11)

•  Anaphylaxis (see section, this chapter)

•  Aneurysm: Ruptured

•  Asthma (see section, this chapter)

•  Cerebrovascular accident or stroke (see section, this chapter)

•  Diabetic ketoacidosis (see section, this chapter)

•  Drug intoxication

•  Epidural: High block (see section, this chapter)

•  Eclampsia (see Chapter 5)

•  Gastric aspiration (see ARDS)

•  Haematoma: Paravaginal or paragenital (see section, this chapter)

•  Hyperventilation

•  Hypoglycaemia (see section, this chapter)

•  Hypotension

•  Local anaesthetic toxicity

•  Magnesium toxicity (see Chapter 5)

•  Myocardial infarction (see section, this chapter)

•  Peripartum cardiomyopathy (see section, this chapter)

•  Pulmonary embolism (see Chapter 4)

•  Thyroid crisis (see section, this chapter)

•  Uterine rupture (see Chapter 9)

Chest pain

Because heartburn is so common a complaint in pregnancy, chest pain may not be treated with the urgency it may need in some rare cases. However, life-threatening causes usually present with severe pain, unrelieved by common medicine, and are associated with other symptoms (e.g. dyspnoea, nausea, vomiting and altered consciousness). In a former Report on Confidential Enquiries into Maternal Deaths⁸ a woman of 33 weeks’ gestation who, after seeking repeat antacids from her general practitioner (for presumably ongoing ‘heartburn’) and seemingly with no other signs than proteinuria and some oedema, died suddenly at home from eclampsia.

COMMON CAUSES

•  Aortic dissection

•  Myocardial infarction (see section, this chapter)

•  Pericarditis

•  Peripartum cardiomyopathy (see section, this chapter)

•  Pleurisy

•  Pneumonia (see Chapter 12)

•  Pneumothorax

•  Pre-eclampsia: Fulminating (see Chapter 5)

•  Pulmonary embolism (see Chapter 4)

•  Sickle cell crisis (see section, this chapter)

Confusion

Confusion may manifest not only as inappropriate speech, but also as aggression or withdrawal of communication. The midwife must make a decision as to whether the cause could be a pathophysiological condition before deciding on the most appropriate action. However, it is worth noting that confusion can often be an early sign of hypoxia.

COMMON CAUSES

•  ARDS (see section, this chapter)

•  Asthma (see section, this chapter)

•  Cerebrovascular accident (see section, this chapter)

•  Drug intoxication or drug withdrawal

•  Hypoglycaemia (see section, this chapter)

•  Hypotension

•  Magnesium toxicity (see Chapter 5)

•  Permanent mental disability

•  Pre-eclampsia: Fulminating (see Chapter 5)

•  Psychiatric illness

•  Pulmonary oedema (see section, this chapter)

•  Sepsis (see Chapter 12)

•  Thyroid crisis (see section, this chapter)

Shock

See Chapter 2 for a full discussion on recognition of shock.

COMMON CAUSES

•  Amniotic fluid embolism (see Chapter 11)

•  Antepartum haemorrhage (see Chapter 3)

•  Appendicitis (see section, this chapter)

•  ARDS (see section, this chapter)

•  Ectopic pregnancy (see section, this chapter)

•  Postpartum haemorrhage (see Chapter 10)

•  Pulmonary embolism (see Chapter 4)

•  Sepsis (see Chapter 12)

•  Uterine inversion (see Chapter 9)

•  Uterine rupture (see Chapter 9)

Abdominal pain

Abdominal pain is probably the most common presenting symptom seen by midwives, and as women manifest contraction pain in various ways, it is tempting to assume most abdominal pain is labour. However, it is worth maintaining a degree of suspicion, and considering carefully where the pain is, if there is anything that makes it worse or better, and – most importantly – is it intermittent, with the uterus relaxing in between. It is also relevant whether gastric symptoms (such as diarrhoea) are present.

COMMON CAUSES

•  Antepartum haemorrhage (see Chapter 3)

•  Appendicitis (see section, this chapter)

•  Ectopic pregnancy (see section, this chapter)

•  Fibroids (see section, this chapter)

•  Haematoma: Rectus (see section, this chapter)

•  Pyelonephritis

•  Renal stones (unusual in pregnancy as the renal tract is dilated)

•  Sepsis (see Chapter 12)

•  Thyroid crisis (see section, this chapter)

•  Uterine inversion (see Chapter 9)

•  Uterine rupture (see Chapter 9)

Convulsion

Although the most common cause of a convulsion in pregnancy, labour or following birth is eclampsia, other more rare conditions can first present with a fit.

COMMON CAUSES

•  Amniotic fluid embolism (see Chapter 11)

•  Eclampsia (see Chapter 5)

•  Epilepsy (see section, this chapter)

•  Sickle cell crisis (see section, this chapter)

Trauma

It is always possible that a midwife may be the first person on the scene following a car accident, a violent incident or other injury to a pregnant woman. In these circumstances it is possible to do no more than provide skilled first aid, remembering that the best way to care for the fetus is to adequately resuscitate the mother (see Chapter 2). After calling for emergency help, initial assessment and action should include the emergency measures in Box 13.1.

If a woman is still pregnant during any of the situations discussed in this chapter, in addition to caring for the mother the midwife will also need to monitor fetal well-being, usually by cardiotocography (CTG). Non-reassuring or abnormal features on a CTG may resolve as the maternal condition improves, however, a deteriorating CTG trace may reflect deterioration in the woman’s condition, sometimes evident before other maternal signs and symptoms. Plans for delivery may be needed but will depend on maternal stability and fetal gestation and condition; timing will be made on an individual basis. The midwife will be working as part of a multidisciplinary team to help facilitate the best care while responding to the needs and circumstances of each individual woman.

BOX 13.1: Emergency care

Call for help. Follow ABCDE approach:

•  Airway: Maintain open. Ensure a lateral tilt or displace the uterus (see Chapter 2), while protecting the cervical and remainder of the spine.

•  Breathing: Assist if necessary.

•  Circulation: Control obvious bleeding if possible and give cardiac massage if necessary.

•  Disability: Assess level of consciousness by noting response to voice or pain.

•  Exposure: Keep warm and safe.

SPECIFIC CONDITIONS

Acute (formerly adult) respiratory distress syndrome

Most cases of acute respiratory distress syndrome (ARDS) result from one of the following causes:

•  Sepsis from pulmonary or non-pulmonary sources

•  Major trauma

•  Multiple transfusions

•  Aspiration of gastric contents

For childbearing women, causes associated with pregnancy need to also be considered including tocolytic-induced pulmonary oedema, preeclampsia, acute fatty liver of pregnancy, amniotic fluid embolism, placental abruption, haemorrhage, chorioamnionitis and retained products of conception.⁹ Although mortality rates have been quoted as high, for the survivors the long-term prognosis, even following prolonged ventilation,¹⁰ is good with lung function recovery back to normal in 4 to 6 months in many women. However, there is also the possibility of complications as a result of ventilation and admission to an intensive therapy unit.

Women will show signs of acute respiratory distress such as dyspnea, orthopnea, tachycardia, tachyapnoea and cyanosis. There will be lung crackles and/or wheezing, and bilateral interstitial infiltrates appear on chest x-ray.⁶ Diagnosis is by clinical signs, but the primary cause also needs to be diagnosed and treated concurrently.

Treatment is usually in an intensive care unit, which means good communication between the maternity and critical care teams is essential.¹¹ Care is aimed at treating the cause and supporting lung function until the lung heals. Optimum oxygenation must be maintained and acidosis, anaemia and hypothermia prevented. Careful fluid balance is necessary to prevent pulmonary oedema, and ventilation may be necessary in severe cases.⁹

Anaphylaxis

Anaphylaxis is a severe, life-threatening, systemic hypersensitivity reaction.¹² Airway and/or breathing and/or circulation problems rapidly develop typically with accompanying skin and mucosal changes. Anaphylaxis is an acute response, with multisystem involvement, resulting from the rapid release of inflammatory mediators to a substance to which the woman has become sensitised. Current estimates suggest an incidence of 1.5 per 100,000 maternities in the United Kingdom.¹³ Common triggers for anaphylaxis include food (most commonly nuts), drugs (muscle relaxants, antibiotics, NSAIDS and aspirin are the most common triggers) and stings/venom (such as wasp or bee). Latex can also cause a reaction, which is an important consideration when working in a healthcare environment where gloves, catheters, masks and other equipment may contain latex. Severe and sometimes fatal reactions to a trigger can begin rapidly; most reactions appear over several minutes; however, this can depend on the cause. A response to an IV medication administration may be significantly quicker than to orally ingested foods. Exposure to a known allergen (trigger) can support diagnosis but it is important to be aware that some women may present with no previous history or obvious trigger.4,14,15

Anaphylaxis is likely when the following criteria are met:

•  Sudden onset and rapid progression of symptoms (feels unwell, maybe anxious, ‘feels sense of impending doom’)

•  Life-threatening problems (use ABCDE approach to recognise these):

•  Airway: Throat and tongue swelling, difficulty swallowing, hoarse voice, stridor (high-pitched inspiratory noise) and/or

•  Breathing: Shortness of breath, wheezing, confusion (caused by hypoxia) tiredness, cyanosis and respiratory arrest and/or

•  Circulation problems: Pale, clammy, tachycardia, hypotension, dizziness, collapse, decreased level of consciousness, ECG changes, cardiac arrest often preceded by bradycardia

•  Disability problems: Confusion, agitation, and loss of consciousness

•  Exposure: Skin and/or mucosal changes, including erythema (patchy or generalised red rash), urticaria (welts or hives, may look like nettle stings often surrounded by a red flare and usually itchy), angioedema (swelling of deeper tissues, most commonly eyelids, lips and sometimes in the mouth and throat)

Additional symptoms may include vomiting, incontinence and abdominal pain.¹⁵

Once an anaphylactic reaction is recognised, urgent help needs to be summoned and assessment and treatment administered based on the ABCDE approach. The immediate treatment is to stop any drugs and infusions, remove any trigger (e.g. latex, sting). Intramuscular epinephrine (adrenaline) should be considered and given to all women with life-threatening symptoms. Assess the best position for the woman; sitting up may be easier if she is experiencing breathing difficulties, laying down if feeling faint or losing consciousness (left lateral if she is pregnant). Establish an airway and administer oxygen and monitor oxygen saturations, also monitor vital signs, obtain intravenous (IV) access and administer fluids to maintain blood pressure. Blood gases must be monitored and a full blood count, electrolyte assessment and clotting studies carried out. An electrocardiograph (ECG) and x-ray may be required. Intubation and ventilation for respiratory support may be necessary. CPR will need to be initiated (see Chapter 2) if the woman has a cardiorespiratory arrest following an anaphylactic reaction.

Further drug therapy is an important part of treatment and may include IV epinephrine (this should be administered only by those trained to do so), antihistamines, corticosteroids and bronchodilators.

Women may have a latex allergy, so need to be asked a specific question at booking regarding any previous reactions to other latex products such as condoms, balloons or household rubber gloves.¹⁶ Documentation of any allergy must be made clear within the woman’s maternity notes. If latex allergy is identified, great care is needed to avoid using equipment (such as tape, catheters, masks, as well as gloves), which contain latex. If a woman has had a suspected anaphylactic reaction, it needs investigating usually by a local allergy clinic.¹⁵

Appendicitis

Appendicitis is the most common surgical complication in pregnancy, occurring in approximately one in 1500 pregnant women (similar to that of the non-pregnant population).¹⁷ It is thought to be more common in the first and second trimester, but in the third trimester an infected appendix is more likely to rupture.18,19 A difficulty in diagnosis, a delay in treatment and a possible altered immunological response during pregnancy have all been attributed to this higher incidence of perforation.²⁰ Peritonitis and other adverse complications (including postoperative infections, sepsis, bowel obstruction and transfusion) are more common in pregnant women with appendicitis.¹⁷

Signs and symptoms may include acute abdominal pain, nausea, vomiting, alteration in bowel habits and possibly pyrexia. During pregnancy the appendix is displaced by the enlarging gravid uterus, so pain may be experienced higher and more laterally. Although tenderness may be elicited on examination, signs and symptoms may be altered in pregnancy leading to a delay in diagnosis.²⁰ Ultrasound is usually undertaken to help support the diagnosis but if this is inconclusive, computed tomography (CT) and magnetic resonance imaging (MRI) assessment may be used.²¹ Although medical management may be undertaken²² due to the serious adverse outcomes for pregnant women with an appendicitis, conservative management is usually avoided.¹⁷ Surgical treatment is justified with minimal delay due to increased maternal and perinatal morbidity and mortality when diagnosis is delayed or missed.²⁰

Asthma

Estimates suggest that asthma may affect up to 14% of pregnancies²³ and is the most common chronic medical disorder seen in pregnancy.²⁴ In the latest UK Confidential Enquiry report²⁵ three women were reported to have died from asthma, raising important key messages for clinicians to ensure all women with medical disorders in pregnancy receive coordinated multidisciplinary care and urgent assessment and referral if they present with acute respiratory compromise.

For women with asthma, pregnancy can be an unpredictable time. One-third of women experience deterioration in their condition, a third experience an improvement while the remaining third report no change at all.²⁶

A history of asthma can predispose women to complications during pregnancy, particularly women with moderate to severe asthma²⁷ and for those whose asthma is poorly controlled.23,28 During pregnancy the risks of taking medication may also be of concern to women²⁹; exacerbation of symptoms may therefore be caused by a reduction or cessation of prescribed treatment. However, if asthma in pregnancy is well controlled throughout, there is little or no increased risk of adverse outcomes.²⁶

Signs and symptoms of acute severe asthma may include increased respiration rate >25/min, tachycardia >110/min, peak expiratory flow rate (PEFR) <50%, coughing, wheezing, bronchospasm, the use of accessory muscles for breathing, chest tightness and noticeably when talking an inability to complete a sentence without taking a breath. As the attack worsens in severity, the woman may start to make only a poor respiratory effort, become exhausted, cyanosed, confused and finally bradycardic and comatosed. Life-threatening asthma is considered when an oxygen saturation is <92%, there is increasing cyanosis, hypotension is present and weak respiratory effort is being made.²⁴

Treatment of an asthma exacerbation includes the administration of humidified oxygen and ongoing assessment with pulse oximeter (saturation should be maintained at >94%); intravenous access will be required and fluid replacement as appropriate. Drug therapy will include nebulised β2 antagonists (e.g. salbutamol) and early administration of corticosteroids. An ECG and chest x-ray may be indicated (particularly if pneumonia or pneumothorax is suspected). Arterial blood gases and PEFR should be monitored. Intravenous drugs may be considered including β2 antagonists, aminophylline and magnesium sulphate. With a severe asthma attack that is difficult to treat (status asthmaticus) and progressing to respiratory failure, intubation and ventilation are needed.24,26 All women who present with acute respiratory compromise need to be urgently referred and assessed by a physician and an anaesthetist (or intensive care specialist).²⁵

Cerebrovascular accident

Although considered a condition of old age, strokes happen to childbearing women and in some cases can be fatal.³⁰ Women are more susceptible to stroke than men and this is further increased by the physiologic changes in pregnancy,³¹ with the puerperium seeming to be the most vulnerable period.32,33 Although stroke in pregnancy is rare, the rising prevalence of obesity, hypertension, cardiac disease and increasing maternal age means women continue to be at risk.32–34

A stroke may be either ischaemic or haemorrhagic and symptoms are similar although treatments will differ. An ischaemic stroke is caused by severe loss of blood flow to a specific part of the brain with tissue necrosis; causes include embolism and hypotension. Haemorrhagic stroke is triggered by a ruptured blood vessel causing blood to spread into the brain tissue (either intracerebral or subarachnoid). This may result from hypertension or traumatic injuries.³¹

Symptoms can range in severity from headache, neck stiffness, visual changes and mild muscle weakness to collapse and cardiac or respiratory arrest. Various investigations may be needed to determine a diagnosis, including CT scan, MRI, lumbar puncture, cerebral angiography and haematological testing.

Treatment of ischaemic stroke includes possible anticoagulation, while treatment of haemorrhagic stroke is usually surgical.³¹ Ongoing treatment needs will depend on the severity of the stroke.

The standard of care for a stroke should not be altered for pregnant women and as timely treatment is essential for attaining better outcomes, prompt referral and admission to a Hyperacute Stroke Unit should take place.³⁰

Diabetic ketoacidosis

Diabetic ketoacidosis (DKA) is a medical and obstetric emergency. Although rare, it is a serious potentially life-threatening complication affecting approximately 1%–3% of diabetic pregnancies.³⁵ It has serious consequences for both the mother and fetus, with increased morbidity and mortality rates³⁶; therefore effective prevention and management are key.³⁷

DKA normally affects only those with type I diabetes mellitus (T1DM), but it is not unknown in type II or even gestational diabetes;³⁵ deaths due to DKA were cited in the latest UK Confidential Enquiry report²⁵ and although most had longstanding T1DM, one woman did not have any clinical features of diabetes in her pregnancy or after, developing her first episode of DKA several months after birth.

Clinical features of DKA include nausea and vomiting, polydipsia or polyuria, weakness, abdominal pain, signs of dehydration (e.g. dry mucous membranes), tachycardia, hypotension, oliguria and changes in behaviour or emotional state, disorientation and finally coma. Tachypnea may also be present, with the woman’s breath often smelling ‘fruity’ due to acetone excretion via the lungs. As infection is a precipitating factor to ketoacidosis, women may present with pyrexia, however conversely, they may present with hypothermia.³⁵ During pregnancy, diabetic women are at increased risk of DKA, which can be more severe, rapid in onset and occur at lower blood glucose levels.36,38

Diagnosis is usually by serum and urinary (dipstick) assessment of ketones, arterial pH and plasma glucose levels (noting ketoacidosis can be present at lower glucose levels).35,36,38,39 Management includes appropriate resuscitation, treatment of dehydration, and lowering of blood glucose. Transfer to a high-dependency area is usual. Underlying causes need to be investigated and treated; these may include infection, hyperemesis, non-compliance with insulin and the use of cortiosteriods.³⁹

Ectopic pregnancy

An ectopic pregnancy occurs when a fertilised egg develops outside of the uterus.⁴⁰ They are reported to occur in 11/1000 pregnancies with 95% occurring within the fallopian tube.⁴¹ Women with an ectopic pregnancy are at risk of collapse following rupture of the fallopian tube, with the latest UK Confidential Enquiries report² showing women continue to die in early pregnancy from this cause.

Symptoms of ectopic pregnancy can be varied; commonly they include abdominal or pelvic pain, amenorrhoea or missed menstrual period and vaginal bleeding. Other reported symptoms include shoulder-tip pain, rectal pressure or pain on defecation, as well as urinary and gastrointestinal symptoms.⁴² Due to the fact that the signs and symptoms of ectopic pregnancy can appear similar to other conditions such as urinary tract infection and gastrointestinal upset, it is recommended health professionals consider offering a pregnancy test and assessment to all women of childbearing age who present with these symptoms.42,43 For diagnosis a transvaginal ultrasound scan is recommended.⁴⁰

Treatment involves resuscitation to stabilise the woman’s condition, including administering IV fluids (with blood transfusion as necessary) and laparoscopic or abdominal surgery. In an early and unruptured ectopic pregnancy, it may be possible to treat the condition medically.42,44

Epidural/spinal: High block

High regional blocks may occur as a result of an unexpected spread of local anaesthetic after a subarachnoid (spinal) injection or after an accidental subarachnoid injection of an epidural dose of local anaesthetic.⁴⁵ This may be due to too much medication, an exaggerated response or an inadvertent injection into the wrong space.³

Signs and symptoms are dependent on the height of the block but may include tingling (“pins and needles” in fingers and arms), weakness in hands, nausea, difficulty in breathing, speaking and swallowing, hypotension and/or bradycardia.³ With a total spinal block, loss of consciousness will occur due to the direct action of local anaesthetic on the brain.

Immediate treatment is to turn off the epidural if running as a continuous infusion, call for urgent help and commence resuscitation if necessary. Oxygen should be given and oxygen saturations continuously monitored; with respiratory rate, pulse and frequent blood pressure readings underpinning treatment. Anaesthetists will treat hypotension and bradycardia as appropriate.

Epilepsy

Epilepsy is the most common neurological disorder seen in pregnancy, approximately 0.5%–1% of women of childbearing age are affected.⁴⁶ Epilepsy is a high-risk condition in pregnancy, with 14 reported deaths attributed to epilepsy or seizures in the latest UK Confidential Enquiries report. Two women were reported to have drowned; therefore care must be taken to advise women not to bathe or sleep alone and they should not be accommodated alone in a single hospital room.³⁰ Many women have specific ‘triggers’ for their seizures (such as sleep deprivation, pain, stress, dehydration, non-compliance of medication) and care should be taken to avoid these when possible.⁴⁷ For women who do experience seizures during pregnancy, it can be hard to establish if the poorly controlled epilepsy is due to severe drug-resistant epilepsy, suboptimal disease management or noncompliance with medication due to the fear of its potential teratogenic side effects.¹³

A seizure can last for a varying amount of time. Compulsive status epilepticus, which represents a medical emergency, is a continuous prolonged seizure lasting for 30 minutes or more, or a series of seizures without full recovery of consciousness in between. Besides having serious potential maternal effects, this can result in premature labour, rupture of membranes, abruption or fetal death.⁴⁸

If a midwife observes or suspects a seizure, a call for urgent help should be made immediately and then the woman’s safety must be maintained (ensuring she does not hit her head, injure herself or fall). The woman should be placed in the recovery position with priority given to maintaining a patent airway and administering oxygen if available. If at home, transfer into hospital via ambulance needs to be made. The woman is given IV anticonvulsant drugs and ventilation may be required if the seizure is not controlled. Blood specimens are sent as required (to include toxicology and anti-epileptic drug levels). Her normal drug regime should be reviewed and changes to it may be made. If there is any question of eclampsia, then magnesium sulphate will be given (see Chapter 5).

Fibroids

Fibroids are common benign tumours which can be located in the uterus. The effect on pregnancy and birth can depend on certain characteristics including number, size and location of the fibroids.⁴⁹ Complications can include bleeding, preterm labour, placental abruption, malpresentation and high rates of caesarean section.⁵⁰

Although fibroids are not usually symptomatic in the antenatal period, women may present with acute abdominal pain due to degeneration, torsion or impaction. Diagnosis is usually by ultrasound and treatment is generally rehydration and analgesia.⁵⁰

Fibroids may contribute to postpartum haemorrhage (see Chapter 10).

Haematoma: Paravaginal or paragenital

If a woman collapses or shows signs of shock after the third stage of labour with no visible sign of haemorrhage, a concealed haemorrhage may be suspected.¹⁹

Although most severe genital tract trauma is likely to be caused by an instrumental delivery, a past Report on Confidential Enquiries into Maternal Deaths ⁵¹ included the case of a woman giving birth to a preterm baby unattended and subsequently dying from a vaginal wall haematoma, despite treatment. Visible trauma may not be evident – a paravaginal haematoma has been reported following a spontaneous vaginal delivery with no perineal or vaginal trauma⁵² and in another case a spontaneous intrapartum vulvar haematoma occurred.⁵³

Treatment is resuscitation as necessary, including siting an IV, and treating the cause. Depending on the site, the haematoma may be treated through the vagina or the woman may need a laparotomy. The haematoma will need to be evacuated and the bleeding stopped.

Haematoma: Rectus

This is a rare condition and occurs when a sudden spasm such as a sneeze ruptures the inferior epigastric veins and/or causes the rectus muscle to dehisce. This usually only takes place late in pregnancy when the abdominal wall is under pressure from a large uterus but a recent report has noted an occurrence resulting in an emergency caesarean section at 30 weeks.⁵⁴

Signs and symptoms include severe local pain and possible slight blood loss. Diagnosis is usually from symptoms, but ultrasound may be used. Management will depend on the severity and time of diagnosis and may be a conservative treatment with analgesia and bed rest, or surgery.¹⁸

Hypoglycaemia

In contrast to DKA, hypoglycaemia can cause rapid loss of consciousness and can be immediately life threatening. (This can occur when a woman has taken insulin but then not eaten.) Prior to loss of consciousness the woman may feel confused or lethargic or start behaving in an unusual way. Hypoglycaemia can present not only in diabetes mellitus, but also in Addison’s disease, hypopituitarism and hypothyroidism. Diagnosis is by measurement of the blood glucose level.

Treatment includes resuscitation as necessary and, following assessment of blood glucose, food/oral glucose should be given immediately (if the woman can tolerate and is conscious). If this is not possible, IV administration of 50% glucose or intramuscular or subcutaneous glucagon if IV access is not available.39,55 This should be accompanied by oxygen administration and oxygen saturation monitoring. Any insulin containing solution should be discontinued until further reassessment is made. Investigation as to the underlying cause needs to take place.⁵⁵

Myocardial infarction

Myocardial infarction (MI) (heart attack), resulting from coronary arterial disease, is a growing problem in women of childbearing age. Obesity, a sedentary lifestyle, smoking and a higher maternal age all contribute to this issue, as do pre-existing conditions such as diabetes and hypertension.13,56 Cardiac disease remains the largest single cause of indirect maternal deaths in the United Kingdom.² Physiological changes in pregnancy and the postpartum period can place an extra burden on the heart, this can be compounded if other risk factors for MI are present.⁵⁷

Traditionally, signs and symptoms of MI include chest pain (often described as ‘crushing’), pain in arm (usually left), neck, back and/or lower jaw, nausea and sweating. However, women often report different and more vague symptoms such as feeling light-headed or an overwhelming anxiety. As initially symptoms may be mild, midwives need to keep a degree of suspicion when a woman complains of chest pain, although the cause is usually the common pregnancy ailment of heartburn. Nevertheless, careful assessment will enable midwives to refer appropriately, where a diagnosis can be made usually by 12-lead ECG and blood tests. Oxygen should be administered if saturation levels fall below 95%. Cardiac surgery is performed only when there are complications.4,39

In the case of a cardiac arrest immediate resuscitation is required (see Chapter 2). Effective multidisciplinary management and rapid interventions are key to improved outcomes.3,13,57

Peripartum cardiomyopathy

Peripartum cardiomyopathy (PPCM) is defined as cardiac failure (left ventricular systolic dysfunction) occurring in the last month of pregnancy or up to 5 months post birth in women with no previous history of cardiac disease or any other identifiable cause. Approximately half of all women will recover after 6 months, however, women with PPCM are at risk of serious complications including severe heart failure, cardiopulmonary arrest and death. Women with a history of PPCM are at greater risk in subsequent pregnancies and need to be counselled appropriately.⁵⁸ Aetiology is unknown but may be due to factors including myocarditis caused by infection, genetic influences or an autoimmune response.⁵⁶

Risk factors include advanced maternal age, multiparity, twin pregnancy, obesity, hypertension, long-term tocolytic therapy and non-Caucasian ethnicity.⁵⁶ Delayed diagnosis can lead to further complications.⁵⁸

Presenting signs and symptoms may include dyspnoea, tachypnoea, cough, orthopnoea, palpitations, tachycardia, haemoptysis, chest pain, abdominal pain, ascites, peripheral oedema and/or confusion. Symptoms should prompt chest radiograph, ECG and echocardiography.³⁹ Treatment involves care by a cardiology team in a cardiac unit, with close monitoring and support of cardiac and respiratory function.

Pulmonary oedema

Pulmonary oedema is a potential complication of many conditions including pre-eclampsia, septicaemia, pulmonary embolism, amniotic fluid embolism, aspiration of gastric contents or it may be caused by fluid overload and/or tocolytic treatment for premature labour.⁶ Fluid may enter the alveoli of the lungs due to pulmonary capillary damage or may diffuse from the vessels due to a reduction in colloid oncotic pressure. This fluid will not only block effective oxygenation, but also damage the alveoli.

The woman will appear breathless, have a cough and may display agitation. Other signs are tachycardia, tachypnea, crackles and wheezing on chest auscultation and decreased oxygen saturations. Diagnosis will be made on clinical signs and by x-ray and ECG findings.⁵⁹ Treatment has three aims – to maintain oxygen saturations at >95%, to treat the cause and to relieve symptoms.⁶ Management and therapy will include assessment of the maternal condition, including identifying the underlying cause. Diuretics in particular will be used, blood pressure may need to be lowered, tocolytic therapy stopped and/or infection treated. Respiratory support may be required, especially if amniotic fluid embolism is suspected. Maternal observations and careful fluid balance monitoring is vital, which may include fluid restriction.⁵⁹ Pulmonary oedema must be effectively treated or it may progress to ARDS.

Sickle cell crisis

Women with sickle cell disease have a high rate of both maternal and fetal complications during pregnancy.⁶⁰ This includes sickle cell crisis which is more common in pregnancy because of increased hypercoagulability, occurring most often in the third trimester and postnatal period.⁶¹ A painful crisis in pregnancy may be caused by infection, dehydration, hypothermia, physical exertion and increased stress.⁶²

When a woman with sickle cell disease presents with pain a thorough investigation needs to take place and pain management initiated and closely monitored. Care must be taken to exclude other possible causes such as abruption, pulmonary embolism, or fulminating pre-eclampsia (pregnant women with sickle cell disease are at higher risk of pre-eclampsia).⁶³ Other signs of sickle cell crisis may include tachypnea, acute chest pain, cough, shortness of breath, severe anaemia and for some women acute neurological impairment.⁶⁴

Management will include the treatment of any pregnancy complications, as well as oxygen therapy, rehydration (with a strict fluid balance), appropriate analgesia, low molecular weight heparin (if pulmonary embolism is suspected) and possible transfusion or exchange transfusion. Assessment of blood results, a chest x-ray, ECG and an infection screen may be required as well as brain imaging for any woman with neurological impairment. All care should be managed within a multidisciplinary team including a haematologist.⁶⁵

Thyroid crisis (storm)

A thyroid storm is an obstetric emergency and may occur in a woman already being treated for thyrotoxicosis (hyperthyroidism) or in a woman where the disease has not yet been diagnosed. It can be caused by a failure to take prescribed antithyroid medication or be precipitated by events including infection, surgery, trauma, venous thromboembolism or diabetic ketoacidosis.⁵⁵ A thyroid crisis may be triggered by labour and birth in women with poorly controlled or untreated thyrotoxicosis.⁶⁶ Prompt recognition and treatment can significantly improve maternal and fetal outcome.⁵⁵

Signs and symptoms include extreme symptoms of hyperthyroidism, such as pyrexia, tachycardia, tachypnea, chest pains, palpitations, nausea and vomiting, abdominal pain and/or diarrhoea, agitation, anxiety and/or confusion, psychosis, seizures and coma. If the woman has not given birth there may be evidence of fetal tachycardia.⁶⁶ It is easier to suspect this condition if the woman has a goitre or known history of thyrotoxicosis. Care will involve gaining IV access, monitoring oxygenation, treatment of underlying cause (exclude or treat infection), and administration of specific thyroid therapies as well as treating any cardiac failure. The maternal condition should be stabilised prior to considering delivery.⁵⁵

REFERENCES

1.  Nursing and Midwifery Council (NMC). 2012. Midwives Rules and Standards. London: NMC.

2.  Knight M, Kenyon S, Brocklehurst P, Neilson J, Shakespeare J, Kurinczuk JJ (Eds.). 2014. On behalf of MBRRACE- UK. Saving Lives, Improving Mothers’ Care – Lessons Learned to Inform Future Maternity Care from the UK and Ireland Confidential Enquiries into Maternal Deaths and Morbidity 2009–12. Oxford: National Perinatal Epidemiology Unit, University of Oxford.

3.  Winter C, Crofts J, Laxton C, Barnfiled S, Draycott T (Eds.). 2013. PROMPT. Practical Obstetric Multi-Professional Training. Course manual. 2nd ed. Cambridge: Cambridge University Press.

4.  Royal College of Obstetricians and Gynaecologists (RCOG). 2011. Maternal Collapse in Pregnancy and the Puerperium. Green Top Guideline No. 56. London: RCOG.

5.  Nursing and Midwifery Council (NMC). 2015. The Code. Professional Standards of Practice and Behavior for Nurses and Midwives. London: NMC.

6.  Gibson P, Powrie R. 2011. Respiratory disease. In: James D, Steer P, Weiner C, Gonik B, Crowther C, Robson S. (Eds.). High Risk Pregnancy: Management Options. 4th ed. St. Louis, MO: Elsevier Saunders, pp. 657–682.

7.  Teasdale G. 2014. Forty years on: Updating the Glasgow Coma Scale. Nursing Times, 110(42):12–16.

8.  Department of Health. 1998. Why Mothers Die: Report on Confidential Enquiries into Maternal Deaths in the United Kingdom 1994–1996. London: Stationery Office London.

9.  Mehta N, Chen K, Hardy E, Powrie R. 2015. Respiratory disease in pregnancy. Best Practice and Research. Clinical Obstetrics and Gynaecology, 29(5):598–611.

10.  Catanzarite V, Willms D, Wong D et al. 2001. Acute respiratory distress syndrome in pregnancy and the puerperium: Causes, courses and outcomes. Obstetrics and Gynecology, 97(5) part 1:760–764.

11.  Duarte A. 2014. ARDS in pregnancy. Clinical Obstetrics and Gynecology, 57(4):862–870.

12.  Johansson SG, Bieber T, Dahl R et al. 2004. Revised nomenclature for allergy for global use: Report of the nomenclature review committee of the World Allergy Organization, October 2003. Journal of Allergy and Clinical Immunology, 113(5):832–836.

13.  O’Connor M, Smith A, Nair M, Fitzpatrick K, Peiregaele P, Kurinczuk JJ, Knight M. 2015. UKOSS Annual Report. Oxford: National Perinatal Epidemiology.

14.  National Institute for Health and Care Excellence (NICE). 2011. Anaphylaxis: Assessment to confirm an anaphylactic episode and the decision to refer after emergency treatment for a suspected anaphylactic episode. CG134. London: NICE.

15.  Resuscitation Council (UK). 2008. Emergency treatment of anaphylactic reactions. Guidelines for Healthcare Providers. London: Resuscitation Council (UK).

16.  Draisci G, Nucera E, Pollastrini E et al. 2007. Anaphylactic reactions during cesarean section. International Journal of Obstetric Anesthesia, 16(1): 63–67.

17.  Abbasi N, Patenaude V, Abenhaim HA. 2014. Management and outcomes of acute appendicitis in pregnancy – populationbased study of over 7000 cases. BJOG: An International Journal of Obstetrics and Gynaecology, 121:1509–1514.

18.  Mahomed K. 2011. Abdominal pain. In: James D, Steer P, Weiner C, Gonik B, Crowther C, Robson S (Eds.). High Risk Pregnancy: Management Options. 4th ed. St. Louis, MO: Elsevier Saunders, pp. 1013–1026.

19.  Patterson Brown S, Howell C (Eds.). 2014. Abdominal Emergencies in Pregnancy. Managing Obstetric Emergencies and Trauma. The Moet Course Manual. 3rd ed. Cambridge: Cambridge University Press, pp. 229–239.

20.  Devarajan S, Chandraharan E. 2011. Abdominal pain in pregnancy: A rational approach to management. Obstetrics, Gynaecology and Reproductive Medicine, 21(7):198–206.

21.  Kastenberg J, Hurley M, Luan A, Vasu-Devan V, Spain D, Owens D, Goldhaber-Fiebert G. 2013. Cost-effectiveness of preoperative imaging for appendicitis after indeterminate ultrasonography in the second and third trimester of pregnancy. Obstetrics and Gynecology, 122(4):821–829.

22.  Young B, Hamar B, Levine D et al. 2009. Medical management of ruptured appendicitis in pregnancy. Obstetrics and Gynecology, 114:2, part 2:453–456.

23.  Charlton R, Hutchison A, Davis K, de Vries S. 2013. Asthma management in pregnancy. PLoS ONE, 8(4):1–10.

24.  Nelson Piercy C. 2015. Respiratory disease. In: Handbook of Obstetric Medicine. 5th ed. Boca Raton, FL: CRC Press. pp. 63–84.

25.  Nelson Piercy C, MacKillop L, Williamson C, Griffiths M, on behalf of the MBRRACE-UK Medical complications chapter writing group. 2014. Caring for women with other medical complication. In: Knight M, Kenyon S, Brocklehurst P, Neilson J, Shakespeare J, Kurinczuk JJ (Eds.), on behalf of MBRRACE-UK. Saving Lives, Improving Mothers’ Care – Lessons Learned to Inform Future Maternity Care from the UK and Ireland Confidential Enquiries into Maternal Deaths and Morbidity 2009–12. Oxford: National Perinatal Epidemiology Unit, University of Oxford, pp. 81–87.

26.  British Thoracic Society/SIGN. 2014. British Guideline on the Management of Asthma. Edinburgh: Scottish Intercollegiate Guidelines Network, Healthcare Improvement Scotland.

27.  Wang G, Murphy V, Namazy J, Powell H, Schatz M, Chambers C, Attia J, Gibson P. 2014. The risk of maternal and placental complications in pregnant women with asthma: A systematic review and meta-analysis. Journal of Maternal Fetal and Neonatal Medicine, 27(9):934–942.

28.  Murphy V, Namazy J, Powell H et al. 2011. A meta-analysis of adverse perinatal outcomes in women with asthma. BJOG: An International Journal of Obstetrics and Gynaecology, 118:1314–1323.

29.  Bain E, Pierides K, Clifton VL, Hodyl N, Stark M, Crowther C, Middleton P. 2014. Interventions for managing asthma in pregnancy. Cochrane Database of Systematic Reviews, Issue 10, Art. No. CD010660. doi:10.1002/14651858.CD010660.pub2.

30.  Kelso A, Willis A, on behalf of the MBRRACE-UK neurology chapter writing group. 2014. Learning from neurological complications. In: Knight M, Kenyon S, Brocklehurst P, Neilson J, Shakespeare J, Kurinczuk JJ (Eds.), on behalf of MBRRACE-UK. Saving Lives, Improving Mothers’ Care – Lessons Learned to Inform Future Maternity Care from the UK and Ireland Confidential Enquiries into Maternal Deaths and Morbidity 2009–12. Oxford: National Perinatal Epidemiology Unit, University of Oxford, pp. 73–79.

31.  Crovetto F, Somigliana E, Peguero A, Figueras F. 2013. Stroke during pregnancy and pre-eclampsia. Current Opinion in Obstetrics and Gynecology, 25:425–432.

32.  Moatti Z, Gupta M, Yadava R, Thamban S. 2014. A review of stroke and pregnancy: Incidence, management and prevention. European Journal of Obstetrics and Gynecology and Reproductive Biology, 181:20–27.

33.  Foo L, Bewley S, Rudd A. 2013. Maternal death from stroke: A thirty year national retrospective review. European Journal of Obstetrics and Gynecology and Reproductive Biology, 171:266–270.

34.  Leffert L, Clancy C, Bateman B, Bryant A, Kuklina V. 2015. Hypertensive disorders and pregnancy-related stroke. Obstetrics and Gynecology, 12(1):124–131.

35.  de Veciana M. 2013. Diabetes ketoacidosis in pregnancy. Seminars in Perinatology, 37:267–273.

36.  Sibai B, Viteri O. 2014. Diabetic ketoacidosis in pregnancy. Obstetrics and Gynecology, 1(1):167–178.

37.  Gosmanov A, Gosmanovar E, Dillard-Cannon E. 2014. Management of diabetic ketoacidosis. Diabetes, Metabolic Syndrome and Obesity: Targets and Therapy, 7:255–264.

38.  Hawthorne G. 2011. Maternal complications in diabetic pregnancy. Best Practice and Research Clinical Obstetrics and Gynaecology, 25:77–90.

39.  Patterson Brown S, Howell C (Eds.). 2014. Cardiac, Diabetic and Neurological Emergencies in Pregnancy. Managing Obstetric Emergencies and Trauma: The Moet Course Manual. 3rd ed. Cambridge: Cambridge University Press, pp. 241–265.

40.  National Institute for Health and Care Excellence (NICE). 2014. Ectopic pregnancy and miscarriage. NICE Quality Standard 69. London: NICE.

41.  Kirk E, Bourne T. 2011. Ectopic pregnancy. Obstetrics, Gynaecology and Reproductive Medicine, 21(7):207–211.

42.  National Institute for Health and Care Excellence (NICE). 2012. Ectopic pregnancy and miscarriage: Diagnosis and initial management (CG154). NICE Clinical Guideline. London: NICE, p. 12.

43.  Patterson Brown S, Howell C (Eds.). 2014. Saving Mothers’ Lives: Lessons from the Confidential Enquiries. Managing Obstetric Emergencies and Trauma: The Moet Course Manual. 3rd ed. Cambridge: Cambridge University Press, pp. 7–21.

44.  Royal College of Obstetricians and Gynaecologists (RCOG). 2004. Tubal Pregnancy, Management. Green-Top Guideline No. 21. London: RCOG.

45.  Patterson Brown S, Howell C (Eds.). 2014. Anaesthetic Complications in Obstetrics. Managing Obstetric Emergencies and Trauma: The Moet Course Manual. 3rd ed. Cambridge: Cambridge University Press, pp. 437–449.

46.  Mohan A, Nelson-Piercy C. 2014. Neurological disease in pregnancy. Obstetrics, Gynaecology and Reproductive Medicine, 24(10):303–308.

47.  Hart L, Sibai B. 2013. Seizures in pregnancy: Epilepsy, eclampsia and stroke. Seminars in Perinatology, 37:207–224.

48.  Carhuapoma J, Tomlinson M, Levine S. 2011. Neurologic complications. In: James D, Steer P, Weiner C, Gonik B, Crowther C, Robson S (Eds.). High Risk Pregnancy: Management Options. 4th ed. St. Louis, MO: Elsevier Saunders, pp. 861–891.

49.  Lam S, Best S, Kumar S. 2014. The impact of fibroid characteristics in pregnancy outcome. American Journal of Obstetrics and Gynecology, 211:395, e1–e5.

50.  Lee H, Norwitz E, Shaw J. 2010. Contemporary management of fibroids in pregnancy. Reviews in Obstetrics and Gynecology, 3(1):20–27.

51.  Lewis G (Ed.). 2001. Why Mothers Die 1997–1999: The Fifth Report of the Confidential Enquiries into Maternal Deaths in the United Kingdom. London: RCOG Press.

52.  Singh J, Basu S, Aich A et al. 2008. Spontaneous ischiorectal and retroperitoneal haematoma after normal vaginal delivery. Journal of Obstetrics and Gynaecology, 28(8):798–799.

53.  Gurtovaya Y, Hanna H, Wagley A. 2013. Spontaneous intrapartum vulvar haematoma. Midwives Magazine, 16(5):48–49.

54.  Kundodyiwa T, Thomas A, Nwosu E. 2008. A case of spontaneous rectus sheath haematoma in pregnancy. Journal of Obstetrics and Gynaecology, 28:795–796.

55.  Sullivan S, Goodier C. 2013. Endocrine emergencies. Obstetric and Gynecology Clinics of North America, 40:121–135.

56.  Zöllner J, Curry R, Johnson M. 2013. The contribution of heart disease to maternal mortality. Current Opinion in Obstetrics and Gynecology, 25(2):91–97.

57.  Wuntakal R, Shetty N, Ioannou E, Sharma S, Kurian J. 2013. Myocardial infarction and pregnancy. Obstetrician and Gynaecologist, 15:247–255.

58.  Lewey J, Haythe J. 2014. Cardiomyopathy in pregnancy. Seminars in Perinatology, 38:309–317.

59.  Dennis AT, Solnordal CB. 2012. Acute pulmonary oedema in pregnant women. Anaesthesia, 67(6):646–659.

60.  Oteng-Ntim E, Ayensah B, Knight M, Howard J. 2015. Pregnancy outcome in patients with sickle cell disease in the UK – A national cohort study comparing sickle cell anaemia (HbSS) with HbSC disease. British Journal of Haematology, 169(1):129–137.

61.  Parrish M, Morrison J. 2013. Sickle cell crisis and pregnancy. Seminars in Perinatology, 37:274–279.

62.  Howard J, Oteng-Ntim E. 2012. The obstetric management of sickle cell disease. Best Practice and Research. Clinical Obstetrics and Gynaecology, 26:25–36.

63.  Oteng-Ntim E, Meeks D, Seed P, Webster L, Howard J, Doyle P, Chappell L. 2015. Adverse maternal and perinatal outcomes in pregnant women with sickle cell disease: Systematic review and meta-analysis. Blood, 125(21):3316–3325.

64.  Oteng-Ntim E, Nazir S, Singhal T, Howard J. 2012. Sickle cell disease in pregnancy. Obstetrics, Gynaecology and Reproductive Medicine, 22(9):254–263.

65.  Royal College of Obstetricians and Gynaecologists (RCOG). 2011. Management of Sickle Cell Disease in Pregnancy. Green-Top Guideline No. 6. London: RCOG.

66.  Kenyon A, Nelson-Piercy C. 2011. Thyroid disease. In: James D, Steer P, Weiner C, Gonik B, Crowther C, Robson S (Eds.). High Risk Pregnancy: Management Options. 4th ed. St. Louis, MO: Elsevier Saunders, pp. 813–825.

14

Psychological considerations for emergencies around childbirth

ELISABETH HALLEWELL

Introduction

Psychological health and childbirth: An overview

Antenatal care and pre-existing psychological factors

The psychological impact of a traumatic birth

Childbirth risk factors for PTSD

Postnatal support and care following a birth emergency

Conclusion

Summary of midwifery responsibilities

References

INTRODUCTION

Psychological care of the woman and her birth partner during a birth emergency is an important element of the management of a birth emergency. The previous chapters have focused on life-saving measures and professional considerations. The physical well-being of the woman and her baby is paramount, as is professional competence. The psychological well-being of the woman and her partner may not seem as crucial at the time of a birth emergency but occurrence of an emergency can result in long-lasting adverse effects, including flashbacks and nightmares, panic attacks and disrupted relationships with baby and partner.1 Emotional support needs to be provided during and after a birth emergency, as evidenced by the following quotes from qualitative research (Reference 1, p. 332):

Two months after experiencing a significant postpartum haemorrhage, ‘…the staff and care me and the babies received were excellent. Just the emotional side of the labour and birth still bothers me’²

… they do what is easiest to save your life but the care of the mind is not looked at, at all (p. 34).³

In addition, there has been concern that use of manikins for emergency skills training does not consider the patient’s viewpoint.3 Research clearly indicates that this area of care needs to be addressed.

Postnatal depression (PND) and post-traumatic stress disorder (PTSD) (see Box 14.1 for definitions) have been shown to be more common in women following a difficult birth such as emergency caesarean section (EmCS) or operative vaginal birth.4–6 A traumatic birth event can also result in PTSD in fathers.7–9 Depression and post-traumatic stress (PTS) have been shown to co-occur, and pre-existing depression, anxiety disorder and/or social isolation can increase susceptibility to PTS following a birth that is perceived as a traumatic event.10–12 The two disorders share some features including diminished interest, feelings of detachment, and difficulties with sleep and concentration.13,14 Verreault et al.¹⁵ state that the risk factors for postpartum PTSD symptoms ‘can be categorised into vulnerability-related, trauma related, and postpartum factors’ (p. 257). Awareness of these psychological disorders should be used to inform postnatal psychological care following a birth emergency/traumatic birth.

BOX 14.1: Definitions

•  Postnatal (postpartum) Depression (PND) refers to depression identified by the Edinburgh Postnatal Depression Scale¹⁶ or a modified version of the Beck Depression Inventory¹⁷ to take into account ante/postnatal factors.

•  Postnatal Stress refers to symptoms of postnatal distress where all the criteria for postnatal stress disorder may not have been measured or met. Only a small percentage of women are likely to experience all the criteria.

•  Postnatal Stress Disorder refers to the disorder reflecting the criteria in the American Psychiatric Association Diagnostic and Statistical Manual of Mental Disorders, 4th edition (DSM-IV)¹³ and 5th edition (DSM-V).¹⁴ The symptoms are mostly the same in the two editions, apart from the removal of an individual’s response to the event being intense fear, helplessness or horror in DSM-V. Much of the literature refers to DSM-IV.

•  PTS and PTSD are used somewhat interchangeably. In the literature and research there is no standardised scale used for PTSD across studies.¹⁸

Factors during a birth emergency shown to benefit psychological well-being and recovery following a traumatic birth should be implemented as part of the emergency management. Midwives should also take into account the body of evidence showing there is a relationship between antenatal and postnatal psychological well-being. This is reflected in the National Institute for Clinical Excellence (NICE) guidelines.¹⁹ The guidelines, in addition to recommendations relating to specific care for those women receiving treatment for a mental health problem, advocate routine screening of all women at their antenatal booking visit for depression and anxiety.¹⁹ NICE also provides guidelines for the postnatal period.¹⁹

It is clear that psychological care needs to be addressed by those providing maternity care commencing with the first contact and continued throughout the whole childbirth experience. Midwives have a particular responsibility in labour, as failure to address the woman’s psychological wellbeing during labour and a birth emergency could have long-term ramifications for the woman and her family. White et al.¹¹ suggest that symptoms of PTSD can persist for as long as 40 years after the event.

The main aim of this chapter is to equip midwives with knowledge of the factors shown by research to promote the psychological well-being of the woman and her partner when there has been an emergency during the birth of their baby. It is hoped that by implementing the recommendations indicated by research findings, women and their partners will be better able to cope with a traumatic birth and be able to enjoy parenthood. Psychological disorders associated with childbirth are also discussed to enhance midwives’ knowledge.

PSYCHOLOGICAL HEALTH AND CHILDBIRTH: AN OVERVIEW

Early descriptions of psychological disturbances following childbirth were associated with physical problems. Hippocrates, in his description of ‘milk fever’, mentioned symptoms of weeping and hysteria.²⁰ Louis Victor Marce (1828–1864), a Parisian physician, was one of the first to recognise the existence of mental distress specifically relating to childbirth²¹; however, toxemia and sepsis were common causes of puerperal psychoses around this time. Fears of complications of childbirth in the nineteenth and early twentieth century also led to maternal apprehension and depression. Shorter, in his chapter on pain and death in childbirth,²² includes a quote from a working class woman around 1914: ‘I always prepared myself to die, and I think this awful depression is common to most at this time’ (p. 70). Recognition in the 1930s that women may have psychological problems associated with childbirth and lactation was acknowledged by the Infanticide Acts of 1922 and 1938. These Acts considered that a woman who caused the death of her baby (up to 1 year) was deemed to have diminished responsibility as a result of her mind being disturbed. Altered mental states following childbirth were largely thought to be a result of the reproductive process; women were at the mercy of their problematic biology. Oakley²³ suggests menstruation and childbirth are beyond the understanding of men and this resulted in medical psychiatric diagnoses of premenstrual tension and PND. Thus unhappiness after childbirth, frequently a result of a defective social structure,²³ became more or less universally labeled as PND. Postnatal mental health needs to be considered in the social context rather than being seen as an individual psychological or biological problem, as may be the case in a biomedical approach, where ‘the women’s feelings are reduced to a matter of hormonal imbalance’²⁴ (p. 112). The positive effect of social support has been shown in studies of postnatal well-being.25,26

The main psychological problems associated with childbirth are PND, anxiety disorders and PTSD. Mild and moderate PND has been considered largely to have its roots in the biophysical and psychosocial domains and has been accepted as a postnatal illness since 1968, when it was described by Pitt.27,28 PND is relatively common, with an incidence of 8%–15%.²⁸ When it is transient, lasting no longer than a few days following childbirth, it is referred to as postpartum depression (or ‘baby blues’). If it lasts beyond a week and results in impairment in the woman’s ability to function it is known as PND. Postnatal depression may also occur in fathers and is estimated by Beck and Driscoll²⁹ to affect 10%–28%. The onset of postpartum depression appears to occur later in the postpartum period in fathers, and studies have shown it to be significantly correlated to postpartum depression in their partner/spouse.29,30

Postnatal psychosis is often considered with PND but it is much more severe and rare, affecting about 1:1000 new mothers.²⁸ Unlike depression, it is a psychotic disorder involving delusions, hallucinations and gross impairment in functioning usually requiring inpatient treatment.³¹

Postnatal anxiety may accompany PND. Mild and self-limiting anxiety symptoms are commonplace in the first few weeks after delivery,³² but these symptoms can be the early signs of something more serious such as PTSD in some women. NICE¹⁹ uses the term anxiety disorders to include ‘generalised anxiety disorder, panic disorder, obsessive-compulsive disorder, phobias, post-traumatic stress disorder and social anxiety disorder’ (p. 4). In DSM-V,¹⁴ PTSD has been moved into a new class of ‘trauma and stress related disorders’ to include conditions that require exposure to a stressful or traumatic event as a diagnostic criterion.

Unlike PND, PTSD was not accepted as result of childbirth until recently. This in part seems to be because the symptoms associated with PTSD in men were interpreted differently when seen in women. Women having these symptoms were at risk of being labelled emotional and/or neurotic; alternatively, the symptoms were seen as an adjunct to PND. This is discussed later when the evidence that PTSD can occur as a result of childbirth is examined. Another issue was that the DSM diagnosis and criteria for PTSD (prior to 1994) was more restricted and could less easily be applied to birth trauma.

PTSD was outlined following World Wars I and II. It was often described as ‘shell shock’ and the description of it in DSM-I (1952) and DSM-II (1968) was as reactions to traumatic events which were seen as temporary and having an endogenous aetiology.³³ As knowledge of the disorder increased, the diagnosis and criteria for PTSD included more stressors, and a more general picture of post-trauma anxiety appeared.³³ This meant that in DSM-III-R³⁴ the stressors extended more widely from military combat to include stressors such as rape, but there was still controversy about the stressors which could lead to a diagnosis of PTSD. The diagnostic criteria were restricted to events ‘outside the range of usual human experience’,³⁴ and childbirth did not fit comfortably with this. Even with further modifications in DSM-IV, which took into account that PTSD may occur in individuals who were not exposed to an unusual event or even to an acute stressor,¹³ controversy continued. However, this change was an important one in that it recognised that an individual’s perception of a threat and response to an event can affect the subsequent development of PTSD. The broadening of the diagnostic criteria has enabled consideration of PTSD as a consequence of childbirth by researchers and clinicians.³⁵ Subsequently this has been further endorsed by DSM-V, which includes exposure to actual or threatened death, serious injury or sexual violation as triggers for PTSD. (See Box 14.2 for diagnostic criteria.)

BOX 14.2: DSM-V diagnostic criteria for PTSD as applied to childbirth¹⁴

A.  The person has been exposed to a traumatic event, i.e. childbirth, which involved threatened or actual death, or serious injury, or violation to the woman or her baby. The exposure may be direct experience, witnessing or by learning of the event involving a close family member or friend.

B.  Following the traumatic birth one or more of the following intrusive symptoms are present: recurrent, involuntary distressing memories. Recurrent distressing dreams related to the birth event; dissociative reactions such as flashbacks in which the mother or relative/friend relives the traumatic birth; intense or prolonged psychological distress on exposure to cues such as sexual intercourse and anniversary of the birth; marked psychological reactions to internal or external cues that symbolise or resemble an aspect of the traumatic birth.

C.  Persistent avoidance of stimuli relating to the birth and including one or both of the following: efforts to avoid memories, thoughts or feelings associated with the traumatic birth; efforts to avoid external reminders (people, places, conversations, activities, objects, situations) that arouse distressing memories, thoughts or feelings about, or closely associated with, the traumatic birth, which may result in avoiding a subsequent pregnancy.

D.  The beginning or worsening of negative altercations and mood associated with the traumatic birth, such as inability to remember an important aspect of the trauma, negative beliefs or expectations, distorted beliefs about the cause or consequences of the trauma, negative emotional state such as fear, horror, anger, guilt or shame about the experience, marked diminished interest or participation in significant activities, feeling of detachment or estrangement from others, restricted range of feelings, sense of foreshortened future. All these criteria may affect the parents’ relationship and bonding with their baby.

E.  Persistent symptoms of increased arousal and reactivity such as angry outbursts and aggression, reckless behaviour, hypervigilance (of baby), exaggerated startle response, problems with concentration, sleep disturbances.

F.   Duration of criteria B, C, D and E is more than 1 month.

G.  The disturbance causes significant distress or impairment in social, occupational or other areas of functioning such as parenting.

H.  The disturbance is not attributable to the effects of substances (such as medication or alcohol) or another medical condition.

Ideas relating to the psychological sequelae of childbirth have moved from the perception that any problems were endogenous, being a result of the woman’s biology, to being largely a result of outside factors, which can be mediated to improve women’s postnatal psychological well-being. Thus midwives have a key mediation role to help facilitate an environment which promotes women’s mental health in childbirth. In order to do this, midwives also need to consider that the psychological effects of childbirth, as with any psychological response, are affected by numerous variables. Those relating to childbirth include:

•  The psychological type or personality of the individual

•  Previous life experiences and mental health

•  Social support available

•  Expectations of birth and becoming a parent

•  Antenatal well-being

•  The birth experience

•  Postnatal well-being and experience

These variables interact, with the result that women and their partners will respond differently to experiences the midwife may feel are similar. For example, Ryding et al.,³⁶ in their study of 25 women’s experiences of EmCS, found that positive expectations turning into disappointment resulted in the highest prevalence (two-thirds of the women) of post-traumatic intrusive stress reactions 6 weeks after the birth. In this study women identified as confident whatever happened had no signs of PTS, whereas women who had fears that were realised all perceived the birth as traumatic, and one third had signs of PTS. The research of O’Donovan et al.¹² exploring predictors of PTSD after birth concluded that helping women – especially those with a history of previous PTSD and affective disorders such as depression – develop realistic expectations may help them to not view their birth experience as traumatic and thereby reduce the incidence of postnatal PTS.

For the midwife to understand why women respond differently, risk factors for PTS and depression after birth need to be explored. The variables suggested above may provide some clues and will be considered further. These factors relate to what has happened before the pregnancy as well as what happens during the pregnancy and childbirth, thus providing a holistic view.

ANTENATAL CARE AND PREEXISTING PSYCHOLOGICAL FACTORS

Pre-existing factors which have been found to increase the risk of PTSD following childbirth¹⁰ include

•  Depression in (early) pregnancy

•  Fear of childbirth (severe)

•  Pre-traumatic stress

•  Anxiety disorders

•  Low stress coping (low self-esteem and self-efficacy)

•  Previous psychological problems

•  History of psychological counselling related to childbirth

Previous psychosocial problems such as domestic violence and sexual abuse are examples of factors that result in women being more vulnerable to further psychological problems. In a study undertaken by Menage³⁷ almost one third of women found to have diagnostic criteria for PTSD following obstetric and/or gynaecological experiences gave a prior history of sexual abuse or rape. Lev-Wiesel et al.³⁸ likewise found that childhood sexual abuse increased the risk of PTSD following childbirth. There is also a suggestion that people have different thresholds for trauma in the same way as people are thought to have for pain.³⁹ This may partly explain why women who appear similar respond differently to what appear to be similar situations. Midwives caring for women during birth emergencies should be aware that by providing evidence-based psychological care they may be able to reduce the incidence of adverse psychological sequelae but not eliminate it, due to the severity of the birth emergency, the woman’s psychosocial background and the woman’s threshold for trauma.

The importance of identifying mental health and psychosocial factors has been recognised as a key issue following findings of maternal mortality reports,32,40,41 which have shown that suicide is a leading cause of maternal death (although the rates are similar to the general female population). These findings have indicated that more attention needs to be paid to mental health issues when providing maternity care. The number of suicides during pregnancy up to and including 6 months postnatal was 29 in 2006–2008.³² Four of these were during pregnancy and 25 were postnatal. These deaths provide an indication to the prevalence of postnatal mental distress. Of these women, 66% had a previous psychiatric history. Midwives therefore need to be alert to all signs of maternal distress including PND and PTSD. If mental health problems are identified antenatally, informed efforts could be made to provide appropriate care throughout the maternity experience and potentially improve psychological well-being should a birth emergency occur. The strongest predictor for PND has been identified as prenatal depression.⁴²

The 2011 CEMACE³² report noted a non-significant increase in maternal suicide. As has been previously recommended by CEMACE’s earlier reports, this report re-emphasised that all women should be routinely asked, at their antenatal booking visit, about a previous history of mental illness as well as their current mental health. These recommendations are reflected in NICE guidelines¹⁹ that provide guidance for recognising mental health problems in pregnancy and the postnatal period, and the importance of referral. They recommend that all healthcare professionals communicate information on any past or present mental health problems when referring a woman to a maternity service, and that the range and prevalence of anxiety disorders and depression are recognised. The guidelines suggest that depression identification questions and two-item Generalised Anxiety Disorder scale (GAD-2) questions are asked as part of a general discussion about a woman’s mental health and well-being (see Box 14.3) at booking. These questions should be repeated during the early postnatal period, and all health professionals should consider asking these questions at all contacts with the woman during pregnancy and postnatally.¹⁹ If a woman responds positively to the depression identification questions or scores three or more on the GAD-2 scale there should be further assessment and referral to the general practitioner or mental health professional. All interventions for mental health symptoms should be delivered by competent practitioners. The guidelines include treatment for specific mental health problems such as tokophobia. The guidance for postnatal support following a traumatic birth will be considered later.

BOX 14.3: Antenatal mental health screening questions¹⁹

DEPRESSION IDENTIFICATION QUESTIONS

•  During the past month, have you often been bothered by feeling down, depressed or hopeless?

•  During the past month, have you often been bothered by having little interest or pleasure in doing things?

TWO-ITEM GENERALISED ANXIETY DISORDER SCALE¹⁹

•  During the past month, have you been feeling nervous, anxious or on edge?

•  During the past month have you not been able to stop or control worrying?

The issues of mental illness and pre-existing psychosocial problems are largely beyond the scope of this chapter except where they have a direct impact on the woman’s ability to cope with a traumatic birth. Women with a mental illness require specialist care, however, the principles of effective psychological care should be applied to all women and their partners. If women do have depression or PTSD following a previous traumatic birth and this has not been addressed it may have an adverse effect on any subsequent pregnancy. Midwives therefore need to be aware of care that supports women following a birth emergency and understand how to promote antenatal psychological well-being.

Pre-traumatic stress, general anxiety and fear of childbirth have been shown to be the factors most strongly related to PTS and depression one month after the birth.4,10 These antenatal factors may in some cases, as indicated above, be related to previous births. Zar et al.,⁴³ in a study on anxiety disorder and fear of childbirth in late pregnancy, found all six multiparous women with PTSD in their study had a previous birth as the traumatic event. These women had a phobic fear of childbirth. This symptom of PTSD may not be identified until a subsequent pregnancy when the woman expresses her fear of childbirth. A subsequent pregnancy can lead to panic and terror.3,44 Some of these women request an elective caesarean section (CS).45,46 As well as having a negative impact on subsequent pregnancies,33,44 fear of childbirth has also been shown to cause some women and/or their partners to avoid having subsequent children.3,9,47 Choosing not to have further children after a near-miss event (where the woman nearly lost her life) may be a normal response, but in some circumstances it may be related to inadequate support provided around and subsequent to the event.

In addition to pre-existing factors, midwives also need to be mindful of antenatal preparation that can assist a woman to cope mentally with a birth that does not go according to plan. As identified by Ryding et al.,³⁶ positive expectations turning into disappointment appears to be strongly associated with postnatal PTS. Women in a study by Somera et al. ⁶ of women’s experience of EmCS clearly indicated that women were not prepared for their birth to not be a normal or ‘beautiful experience’.

I didn’t prepare myself for the possibility of a c-section. I didn’t expect it at all.

It ended up being a medical emergency rather than this idyllic beautiful experience. It certainly wasn’t what I had pictured (p. 2828).

Antenatal preparation should also be considered for women’s partners to enable them to have realistic expectations and assist their ability to support women during labour and birth.⁴⁸ A survey of 140 fathers in New Zealand found that 100% valued a separate ‘dads group’ during the antenatal course and to be able to talk with ‘dads’ who had gone through the experience to prepare them for the birth.⁴⁹ Experiences of traumatic birth discussed later demonstrate that antenatal preparation can be expected to assist both pregnant women and their partners in coping with a traumatic birth and avoid descriptions of being ‘totally unprepared’.⁷

THE PSYCHOLOGICAL IMPACT OF A TRAUMATIC BIRTH

The woman’s perception of her birth being traumatic could be expected to lead to negative psychological repercussions. However, perceptions and the ability to deal with traumatic experiences are affected by variables (such as depression and anxiety) identified earlier. Midwives and others who provide care need to acknowledge that their perception of what happened may not be the same as the woman or her partner’s perception. For example, some aspects of labour care such as artificial rupture of membranes (ARM), or the ‘pulling’ involved in a LSCS when the baby is delivered, both considered routine by a midwife, can constitute a traumatic experience.⁵⁰ Also, hospital staff may view a ‘near miss’ as a positive outcome and not consider the perception by the woman and her close family of the potential for negative outcomes.⁹ Lack of awareness can lead midwives to be dismissive of such concerns. By being mindful of this, and by avoiding factors that have been identified as contributing to women’s psychological problems, midwives can make a positive contribution to the psychological well-being of the women for whom they provide care.

In the United Kingdom, providing care that promotes a positive birth experience has been highlighted in government policy for maternity care.51–54 Reports state that midwives and others providing care should work in partnership with women. A national strategy launched in 2012⁵⁴ introduced the six ‘Cs’ (care, compassion, competence, communication, courage and commitment; see Chapter 1), in relation to psychological care; compassion and communication are particularly of note. Midwifery 2020 indicates that midwives are responsible for providing both a physically and emotionally safe service.⁵⁵ Sadly, literature and research into PTSD indicates that some cases of PTSD may be wholly or partially a result of these government policies not being followed. The experience of undergoing a birth emergency could be expected to be traumatic for a woman and as such will create challenges for the team providing care to promote a positive experience. While their priorities are to the physical well-being of the mother and baby, a bit more consideration of the mother as a person may make a big difference to her and her partner.

Awareness of women’s traumatic experiences of childbirth and the resulting psychological problems increased when campaigners from organisations such as the Association for Improvement of Maternity Services (AIMS) and National Childbirth Trust (NCT) addressed women’s experiences. An example of this awareness is a letter written in 1985 by Beech and Robinson⁵⁶ to the editor of the British Journal of Psychiatry, concerning women suffering ‘severe nightmares’ a year or more following childbirth. The term PTSD was not used, but the symptom of ‘severe nightmares’ is one associated with PTSD. They also identified mediating factors including ‘excessively painful and traumatic deliveries’, ‘unsympathetic staff’, experience of ‘technological rape’ and the ‘impossibility to discuss criticism of previous care’. Several authors, including Kitzinger,57,58 describe quality of care factors such as poor communication and lack of control, causing subsequent distress. She provides graphic examples⁵⁷ in quotes from women: ‘They didn’t speak to me. Only about me’. ‘… felt like an oven-trussed turkey’ (p. 12). Poor communication and lack of control are described as key issues leading to PTS after childbirth. More recent studies echo these findings. Harris and Ayres,⁵⁹ in a survey of intrapartum ‘hot spots’ for traumatic labour and birth, concluded that interpersonal issues such as ‘being ignored, lack of support, [and] poor communication’ were the most common ‘hot spots’ identified. These were followed by obstetric events and pain, and then by events concerning the baby. An example of being ignored is provided by Beck⁶⁰: ‘The hospital discussed my baby’s possible death in front of me and argued in front of me just as if I weren’t there’ (p. 33).

Inhumane treatment is further described in a meta-ethnographic study,¹ together with other themes relating to women’s experiences of a traumatic birth. Women used phrases such as ‘barbaric’, ‘horrific’ and ‘degrading’ to describe their treatment by health professionals. They had thoughts of death to make their ordeal of pain and trauma end. Sadly, such examples of care associated with traumatic births occur all too frequently. Ayres et al.,⁵⁰ when discussing narratives relating to traumatic birth, state ‘The importance of negative interaction with staff is consistent with a large amount of research showing that interpersonal traumas, such as abuse are more pathogenic than non interpersonal traumas’. Ayres et al.⁵⁰ also state that meta-analyses have shown that lack of support is associated with PTSD.

The importance of relationship with the staff is also shown in a study of 825 women’s experiences of childbirth undertaken by Green et al.⁶¹ which explored women’s expectations and identified both positive and negative experiences. The issues they identified affecting women’s overall satisfaction with birth included the womens’ feelings about major/minor interventions, pain and pain relief, control, relationship with the staff, amount and accuracy of information, and ability to get into a comfortable position. When assessing ‘emotional well-being’ following birth, a relationship was found with having or not having interventions. This was not so much to do with whether they had the intervention but the context in which the decision was made. The woman’s perception of the ‘rightness’ of the intervention was seen to be more important for her emotional well-being than the intervention itself. Women who felt the right decision had been made were significantly happier. This again reflects the importance of good communication and involvement of women with their care.

A body of psychological research has provided further information and evidence regarding PTSD following a woman’s traumatic experience of childbirth. This research should increase knowledge and understanding to assist health professionals in developing interpersonal skills that support women and their partners, particularly when an emergency occurs.

The incidence of PTSD and PTS as a result of childbirth varies throughout studies depending on the methods used and whether all the DSM-IV criteria are met. Rates between 1% and 7% are described by Soderquist et al.⁶² A study undertaken by Alcorn et al.⁶³ using all the DSM-IV criteria found 3.1% of women had PTSD at 6 months after birth after controlling for previous traumatic events and clinically significant antenatal anxiety and depression. The number of women identifying aspect(s) of their birth as a traumatic event is much higher than this, at around 33%⁶⁴–45.5%,⁶³ but the majority of these women do not develop PTSD. The prevalence of a PTSD profile appears to be fairly stable over the first year, leading researchers to conclude women with PTSD do not all recover spontaneously.11,62 Although studies show some variation in research methods and findings, they consistently indicate that PTSD can occur as a result of childbirth and that it may not resolve spontaneously. However, there is some evidence that a larger proportion of women do spontaneously recover from postnatal PTSD compared with women experiencing PTSD after other traumatic events such as rape.⁶⁵

PTSD may also occur in fathers witnessing a traumatic birth involving their partner and/or baby.7–9,66 In Western society there is an expectation by partners, friends and family that the father attends the birth of his children, and while many fathers do this willingly, some are ambivalent and nervous. In a meta-synthesis of fathers’ experiences, midwives were identified as best placed to make a significant difference in how the fathers perceived labour and birth.⁴⁸ The key conclusions of this study indicated that while being committed to being involved, the men expressed overwhelming feelings and inadequacy. They often felt vulnerable, so being prepared and supported were essential elements of a positive experience and being able to support their labouring partner. For some fathers, being present at the birth can be ‘distressing and distasteful’⁶⁷ even if there are no complications. Ayers et al.’s⁶⁶ study of PTSD in couples after birth showed that 5% of men and women had severe symptoms of PTSD, other studies have shown rates for men to be approximately half that for women.68–70 The symptoms were found to be strongly associated within couples, and related to similar birth factors.

White⁷ investigated the experience of fathers witnessing a traumatic birth. All the participants had been distressed by their experience and had bad memories, although not all described symptoms of PTSD. Descriptions from the fathers included:

Our birthing experience was a traumatic one.

My single worst experience…

Took three days to get over the scene, shock, did not take it in I was a dad… I can describe everything in the room, smells, sounds, colours. I can still see the images…causes headaches…clinical smells get you going. I resigned from my hospital laboratory job.

These findings clearly show that partners can experience similar negative psychological outcomes as mothers following a traumatic birth.

In addition to PTSD, the incidence of PND may also increase as a result of a traumatic birth. PND has been reported to be present in a significant number of women with PTSD after childbirth.10,11,35,62,71,72 This has also been shown to be true with fathers.⁶⁸ The consistent findings of a high comorbidity of PND and PTSD appear to be associated with risk factors the two conditions share, and they show that pre-existing depression increases the risk of PTSD.¹⁰ It is important that the diagnosis is correct for appropriate treatment to be provided. White et al.¹¹ suggest that if there is a high degree of overlap between PND and PTSD, PTSD may be missed. They cite cases of women who experienced a traumatic birth and subsequent upsetting thoughts being diagnosed with PND by their general practitioners. Joseph and Bailham⁷³ point out that only routinely screening for PND can mean that PTSD is missed, and the treatment for these two conditions is different. Drug treatments may help PND, but psychological therapies are thought to be more appropriate for PTSD. This situation may improve if the guidelines introduced in the United Kingdom in 2014¹⁹ are implemented and if women are also routinely screened for anxiety disorders (see Box 14.3).

CHILDBIRTH RISK FACTORS FOR PTSD

As identified earlier, it is the woman’s perception of childbirth and the support she receives that are important for her psychological well-being. After investigating 40 women’s experiences of traumatic births, Beck⁶⁰ concluded a traumatic birth was ‘in the eye of the beholder’. From the women’s descriptions of their births Beck identified four main themes. These related to care, communication, trust and price of the outcome. She also listed the birth traumas identified by the 40 women in her sample.⁶⁰ The traumas she identified are largely similar to those identified in other studies. (See Box 14.4 for a summary of potential birth traumas.)

Women’s experiences of birth trauma include aspects of childbirth which may not have been recognised by midwives and other carers, for example ‘inadequate medical care’ and ‘degrading experience’. Ayers et al.⁶⁶ point out that research shows that subjective factors such as perceived support and control may be more important than objective factors such as type of delivery for the development of postnatal PTSD. Ayres et al.⁵⁰ state that a body of evidence shows interpersonal trauma during birth to be more pathogenic than non-interpersonal trauma.

Subjective factors (involving interpersonal care) as well as having a negative impact may also alleviate the effects of a complicated birth. In a study of the effects of EmCS, a woman was quoted concerning her experience of a second EmCS:

I really feel as though I was given every possible chance to achieve what I wanted. Nobody forced anything on me. I can only look back positively. Even though I ended up with an emergency caesarean section it was absolutely the right decision⁷⁴ (p. 46).

Creedy et al.⁶⁴ also found that women experiencing a high level of obstetric intervention were less likely to develop PTSD if they perceived their intrapartum care to have been adequate. Similarly, Boorman et al.,⁷⁵ in a study of 890 Australian women, found that only one third of those who had an EmCS reported a traumatic birth. Their findings indicated that factors such as a sense of control around decision making and adequate information from staff were protective. Another study⁷⁶ found that ‘support during birth was shown to be particularly important for women with a history of prior trauma or having a high levels of interventions during birth’ to protect against the development of PTS symptoms.

BOX 14.4: Summary of potential birth traumas

Stillbirth/infant death

Emergency caesarean section/fetal distress/fear for baby’s life

Fear for own life (maternal collapse/cardiac arrest)

Inadequate medical care/felt that staff did not know what they were doing

Fear of epidural/felt coerced into having an epidural

Inadequate pain relief

Postpartum haemorrhage/manual removal of placenta

Forceps/vacuum extraction

Severe pre-eclampsia/eclampsia

Premature birth

Separation from infant in neonatal intensive care unit (NICU)

Prolonged, painful labour

Rapid delivery

Degrading experience/unsympathetic staff

As indicated earlier, the incidence of PTSD has been shown to be higher where birth complications/interventions have occurred. Many of the birth traumas listed in Box 14.4 are associated with emergencies around childbirth. The majority of psychological research focuses on the prevalence of PTSD and the factors that are associated with it, and although this provides valuable information, the detail that may assist midwives and other carers is not always provided. A study that does provide detail in respect to obstetric emergencies is one undertaken by two research midwives.³ They studied 10 women’s experiences of obstetric emergencies that included cord prolapse, placental abruption, shoulder dystocia, uterine scar rupture, severe pre-eclampsia, and major obstetric haemorrhage. The interviews in their study highlight practice issues that need to be considered to improve the woman’s experience and recollection of the event.

The findings of Mapp and Hudson³ are directly related to emergencies around childbirth. The significant themes they identify include communication and the need to make sense of what happened. In regard to communication, the women were very aware of nonverbal cues such as fear being expressed in the facial expressions of the healthcare professionals. This was also expressed by women in the study by Thompson et al.² The women were aware that something was wrong without being told, and were frightened when they did not know what was happening. The women also commented on being reassured by receiving a smile. Touch was also identified as being important as it made the woman feel she was a human being. This contrasted with staff communicating with each other and ignoring the woman.

Information given during an emergency situation may not be understood and explanations may be required later. A mother illustrates this in a study undertaken by Calam et al.⁷⁷:

I had fulminating toxaemia. They took the trouble to explain everything. What they’d do, how they’d make the incision. Another doctor explained about premature babies and their chances. I felt supported. Even the anaesthetist bothered to see me. I was a person.

Did you understand?

No. I was too upset and involved.

The women in Mapp and Hudson’s³ study appreciated that the staff were probably shocked by the situation too, and needed to manage the emergency. They identified a variety of experiences. Positives included anaesthetists and midwives providing explanations and support. There were comments regarding communication with their partners, with instances of women thinking there was a problem relating to them when their partner was called aside to change out of theatre clothing. The positioning of the partner in theatre and the ‘green sheet’ impaired communication. They felt disorientated and restricted in theatre. The women recalled experiences such as staff running down a corridor and the air blowing on their face, inexplicable pain, drifting off and then feeling better when blood transfusions were up. In most cases the women felt the situation was in the medical domain and recognised they did not have the knowledge to influence the management or outcome.

The women felt fearful for their baby’s mortality but appeared to trust the healthcare professionals would help them, despite lack of explanations. They viewed continuity of carers and familiar faces positively, and felt secure when staff showed concern. However, there were instances described where the women did not feel listened to and false reassurances did not validate their situation and how they felt. The women were concerned that their partners were looked after and kept informed. They looked to their partners for support such as holding their hand and reassurance, but recognised that they would be frightened too.

The study by Thompson et al.² indicated similar findings in relation to women’s experiences, but it focused more on the negative aspects of interpersonal care. It sought to identify sources of distress for the women including gaps in the service and meeting informational needs following a significant primary postpartum haemorrhage (PPH). The study included a cohort of 204 women recruited from 17 major hospitals in Australasia. Quotes from the women provide graphic examples of inadequate information to help them understand what had happened, and lack of supportive care. One woman stated ‘I was incredibly frightened and I didn’t get any reassurance’ (p. 330). As identified in other studies,59,75 staff did not speak directly to the women at the time. Thompson et al.² provide statistics showing satisfaction of care following a PPH. These show that overall satisfaction is high – 96% were either very or somewhat satisfied. This figure may reflect that the women were relieved to have survived a significant PPH. When women were asked about the information they were given about their physical recovery, 62% said they had adequate information, and regarding their emotional recovery only 48% thought they had adequate information. Emotional support is discussed further in relation to postnatal care.

Further insight of women’s experiences is provided by a meta-ethnography of women’s perceptions and experiences of a traumatic birth in which 10 qualitative studies were examined.¹ The studies identified six major themes:

•  feeling invisible and out of control

•  to be treated humanely

•  feeling trapped: the reoccurring nightmare of my childbirth experience

•  a rollercoaster of emotions

•  disrupted relationships

•  strength of purpose: a way to succeed as a mother

The issues raised for midwives and other healthcare professionals include taking notice of women’s opinions and not making authoritarian decisions, not being ‘too busy’ to explain procedures and what is happening.

Further suggestions for midwives and other birth attendants are identified in research undertaken by Ayres. Ayres’⁷⁸ study aimed to explore issues that might be important in the development of PTS. It compared women with and without PTS following similar birth experiences. The sample had a high incidence of birth complications, due to this being the case for women with PTS, and those without PTS being matched. Twenty-five women in each group were interviewed about their experiences 3 months after giving birth to examine their thoughts and emotions during birth and their subsequent cognitive processing. Some themes identified from the interviews were common – for example poor understanding and feeling scared. Those with PTS felt more panicky, helpless, angry and discouraged, and had more thoughts of death, mental defeat and dissociation. The thoughts of death were not always in response to a life-threatening situation, showing that women can fear death without a medical reason or trigger. Midwives and other carers need to be sensitive to women’s fears and reassure women and their partners by preventing or minimising the perception of a threat to life as appropriate.

The theme of anger may relate to not being listened to and not being happy about the care given. However, in some cases, it may be due to the birth not going to plan despite the best efforts of the birth attendants. Anger appears to exacerbate and perpetuate PTS symptoms. Steps should be taken to recognise negative emotions to avoid mental defeat and dissociation, and when negative emotions are evident the woman should be supported as much as possible.

In the study of ‘hot spots’ undertaken by Harris and Ayres⁵⁹ interpersonal difficulties and obstetric complications were associated with a higher incidence of PTSD than complications with the baby. They suggested a reason for this could be that women receive more support from hospital staff, friends and family, recognising the upset involved with having a sick baby. This reinforces the importance of communication and support to reduce the risk of PTSD following all birth complications.

The experiences of fathers during birth emergencies also warrant consideration as they may be sidelined, with the focus being on the woman and her baby. The themes identified as encapsulating fathers’ traumatic experiences in White’s⁷ study related to being a spectator, not being included, feeling sexually scarred and having to ‘tough it out’. Fathers are under pressure to witness the birth of their baby but their role is not always clear. They are expected to be a support, a fetcher and carrier, and a spectator but not necessarily a participant. They felt alienated, excluded and disregarded. The following quotes from the study⁷ illustrate these feelings:

felt like an appendage in the way

not being given any information

I was rushed to the corner of the delivery suite and told not to interfere… it’s like you don’t count

evidence of midwife only working with the mother

These quotes clearly indicate that the fathers were not given information and support. Lack of support is further shown in the theme ‘toughing it out’, where fathers describe being fearful of losing their wife and unborn child, and coping by breaking down in private. They felt disempowered and unable to help their wife. The fathers in the study were all keen to be involved but the pressure to witness led a few to experience sexual scarring, affecting their ability to resume a sexual relationship with their partner. Three fathers declared they would never have any more children.

Further information of partners witnessing birth is provided by a qualitative study of 10 male partners’ and one lesbian partner’s experiences of life-threatening experiences in pregnancy undertaken by Hinton et al.⁹ Such experiences could be expected to be shocking and distressing. Their findings also showed that the partners’ experiences were characterised by powerlessness and exclusion. For example, Sally describes being asked to leave the room when her partner had a haemorrhage. She was left alone and no one provided any explanation while the emergency was being managed. Similarly, John was left for hours with no news of his wife’s condition when she haemorrhaged and doctors had to perform a hysterectomy to save her life. One husband recalled waiting without news and twice being told to go away when he approached the operating theatre doors. Another husband whose wife was taken to intensive care misunderstood the situation and thought his wife was dead. When he was taken to see her on a life support machine he stood with her for about an hour stroking her hand. No one explained to him that she would recover. Two other husbands described being shocked when seeing their critically ill partners, and no one provided information to assist their understanding.

Support from both family and staff was very important. Personal touches from individual staff have been shown to make a real difference in how partners cope. One husband whose baby was stillborn after his wife had an antepartum haemorrhage was comforted by a kind anaesthetist’s act of support. A year later he recalled when his wife was ‘out for the count’ and he was holding his daughter, the anaesthetist putting her arm around him and stroking his wife’s hair.⁹

Communication from medical staff that was clear and honest was highly valued. Partners appreciated it was difficult to communicate while dealing with an emergency. However, how well staff communicated during or after the emergency was important. One husband whose wife developed HELLP syndrome 11 weeks later stated, ‘I think they did a wonderful job of trying to explain it in a way that a medical dummy like me could sort of understand things’⁹ (p. 5).

Feelings such as being scared, fearful, helpless and angry were common to mothers and fathers7,78 experiencing PTS. Both mothers and fathers have shown awareness and concern about the support given to their partner during a birth emergency. A woman in Mapp and Hudson’s³ study commented about her partner’s experience, ‘He had a midwife with him making sure he was kept up to date’ (p. 32).

It is important that psychological care during childbirth is provided for both the woman and her partner. Fathers as well as mothers need to be psychologically supported for good postnatal outcomes. All the men in White’s⁷ study experienced subsequent marital difficulties. If midwives focus exclusively on ‘being with woman’ the outcome for the couple will not be optimal. NICE⁷⁹ advocates involvement of partners throughout pregnancy and childbirth, and there is evidence that involvement during labour and support postnatally have a positive effect on the subsequent health of the mother and baby.⁹

There is some evidence that worries and fears related to childbirth are more prevalent in women from different cultures. Redshaw and Heikkilä⁸⁰ found that compared with white women, twice as many ethnic minority women worried about pain and discomfort, length of labour, possible medical interventions and embarrassment. The research of Ternström et al.⁸¹ had similar findings. Their results showed foreign-born women were almost three times more likely to be fearful. Sociocultural factors related to emergencies around childbirth are not specifically discussed in the literature and research, but if women from different cultures have increased antenatal anxiety, it is likely that they will be more at risk of postnatal mental health problems should an emergency occur. Also, if a language barrier impairs communication, this may have a negative impact on the already traumatic experience of a birth emergency. For these women and their partners, nonverbal communication and continuity of carer are important strategies to reduce the emotional trauma of the situation. Interpreters should be used where possible.

The literature shows that midwives have a key role in minimising emotional trauma during a birth emergency. (See Box 14.5 for strategies.)

BOX 14.5: Strategies to minimise emotional trauma during a birth emergency

Communicate with the woman and her partner. If the doctors do not communicate directly, convey what they are saying to the woman and her partner.

Provide simple explanations of what is happening to both the woman and her partner and rationale for decisions.

Encourage the woman and her partner to express their feelings and ask questions when appropriate to the situation.

Listen and respond to anything the woman and/or her partner say.

Ensure adequate pain relief.

Avoid false reassurance.

Avoid inconsiderate comments, e.g. suggesting the baby is causing problems to the parents.

Encourage parents by focusing on positive aspects such as imminent birth of baby where appropriate and enhance any perception of control.

Use touch to support the woman and her partner if appropriate.

Position the partner where he/she can communicate with the woman where possible.

Positively acknowledge any support the partner provides.

Be aware of facial expression; try to show encouragement and that you care.

Try to provide continuity of carer.

Introduce staff to the woman and her partner.

BOX 14.6: Postnatal care following a birth emergency

Promote parental–baby bonding as appropriate.

Encourage and facilitate breastfeeding as desired by the mother.

Avoid leaving the woman alone in the initial period.

Ensure effective postnatal analgesia is provided for women experiencing pain.

Offer simple explanations and information as desired by the mother and father.

Offer sympathy and apologies where appropriate, do not justify or defend care given.

Take into account that women may not want too much information initially, but give information that is needed to facilitate recovery.

Routine ‘debriefing’ is not advised and if felt beneficial should be used with caution.

Provide opportunities and support for women wishing to talk about their experience, encourage use of support from family and friends.

Consider the effect on the partner and include in postnatal care.

Refer parents for specialist support, e.g. psychologist or bereavement counsellor when required.

Provide information concerning ongoing support available so parents can make contact when they want to.

POSTNATAL SUPPORT AND CARE FOLLOWING A BIRTH EMERGENCY

See Box 14.6 for a summary of postnatal care following a birth emergency.

Following a birth emergency, where possible and appropriate, skin-to-skin contact with the newborn baby and early breastfeeding should be encouraged and facilitated to promote parental-infant attachment, newborn thermoregulation and successful breastfeeding.⁸² Breastfeeding has been shown to empower the new mother and benefit mental as well as physical health in women choosing to breastfeed.⁸³ For some women breastfeeding provides an opportunity to overcome a birth trauma, and it can be a way of compensating for not having the birth they would have chosen. The close proximity of the baby can assist women in healing from their ordeal and promote their satisfaction and confidence.1,84

It is therefore particularly important that women experiencing a birth emergency should receive all the support they need to enable them to successfully breastfeed their babies. There are some reports of women choosing not to breastfeed to protect their equilibrium and avoid breastfeeding difficulties. There are also reports of women feeling alienated from their baby due to their experience and as a result are not keen to breastfeed.⁸⁴ Midwives need to be particularly mindful and empathetic with regard to women’s preferences after a traumatic birth, so that their support aids emotional recovery and does not add to the trauma.

If the mother is unwell, the baby’s skin-to-skin contact may be with the father if desired.⁸⁵ Parents with infants requiring intensive or special care will require additional support to promote parental bonding and cope with anxieties regarding the well-being of their baby, and these issues are addressed elsewhere.86–89

The experience of a traumatic birth can result in women feeling disconnected from their baby.¹ This inability to feel a closeness and develop a bond may be short-lived, but it can persist. Studies of women with postnatal psychopathology including PTSD have shown that the mother–infant bond⁹⁰ may be impaired, resulting in the mother either avoiding the baby or being overvigilant.⁶⁶ PND can also have a negative impact on the maternal–infant relationship. Beck and Driscoll²⁹ and Green et al.⁶¹ found that women’s descriptions of their babies were more negative if they had poor ‘emotional well-being’ postnatally. Midwives should support and encourage parents in getting to know their baby and in caring for their baby.

Mapp⁹¹ analysed women’s feelings following a birth emergency using evidence from 10 women interviewed for a study of their feelings and fears during a birth emergency. The women felt ‘shell shocked’ and emotional; they experienced nightmares and were frightened to be alone in the initial postnatal period. They were unable to process what had happened to them and lacked understanding of why the emergency had happened. This lack of understanding led two of the women not to be aware of how ill they had been and take appropriate care of their health postpartum. In the initial period the women felt ‘in a fog’ and were unsure of the amount of information they would have been able to take in. Thus midwives need to ensure any information given has been understood and repeat as required.

Postnatal factors such as additional stress, support and the meanings attached to birth events may influence the development of PTSD.⁶⁵ Postnatal support by the midwife should include the care recommended in NICE guidelines⁷⁹ for postnatal care and respond to individual needs to avoid any additional stress. For example, women experiencing a birth emergency may have had interventions resulting in postnatal pain, so midwives need to ensure analgesia is provided and effective. The experience of postnatal pain can be overwhelming and it has been shown to contribute to PTS symptoms.⁶⁴ As for all women, communication is important, but women who have experienced a birth emergency may require additional information and explanations to assist understanding. In a study by Thompson et al.,² a woman at 4 months postpartum said she had not been given any details about why she haemorrhaged or what was done to stop the bleeding. Another woman 2 months postpartum said she was not informed about the extra time it would take for her to recover after losing a lot of blood, she felt she was not coping compared with other women.

A way of assisting women to understand and come to terms with their birth experience may be by providing postnatal ‘debriefing’. NICE guidelines⁷⁹ state that women should be asked at each postnatal contact about their emotional well-being and support they have. They should be encouraged to report any concerns and health professionals should be aware of signs and symptoms such as unexplained sleeping difficulties. NICE also state that ‘women should be offered an opportunity to talk about their birth experiences and to ask questions about the care they received during labour’ (p. 9). NICE⁷⁹ do not recommend formal debriefing of the birth, as there is a lack of evidence to support the practice.

Ayers et al.⁹² identified that 94% of hospitals in the United Kingdom provided postnatal services for women who have had a difficult birth. Of these services 65% were debriefing services, and 13% ‘birth afterthoughts’ programmes provided by midwives, midwife-counsellors or doctors. The other 22% were psychotherapy (14%) and service based on individual needs (8%). It was reported that 5% of services were provided in response to research evidence and the remaining 95% in response to women’s perceived needs. It is possible that some services have been implemented as a damage limitation measure in response to concerns relating to litigation in obstetrics.92,93

The term debriefing is frequently used, but it is a broad term that has caused some confusion in literature and research. Baxter et al.⁹⁴ identified two main types, structured and unstructured, the former relating to more formal psychoanalytical forms and the latter to sessions commonly undertaken by midwives, but they comment that the type of service provided was not always clear in the studies. The need for clarity of terms has been identified by Alexander⁹⁵ and Rowan et al.⁹⁶ who concluded that the provision of a postnatal childbirth discussion as part of good midwifery care should be differentiated from a formal debriefing, which is not recommended (see Box 14.7).

There is little evidence that formal debriefing interventions are beneficial in improving mental health, and there is some evidence that such interventions could possibly increase the risk of developing PTSD and depression.97–101 However, it should be noted that despite no measurable benefit, women generally reported it to be helpful. The recent critical review of the literature by Baxter et al.⁹⁴ relating to current practice in offering a postpartum ‘debriefing’ (both structured and unstructured) service to women reached similar conclusions from examination of 20 papers – that women’s responses to the service were generally positive and the women valued the service, but there was no evidence that it reduced morbidity.

There is evidence that women who have had a traumatic birth experience welcome the opportunity to talk about their birth experience with a supportive health professional, feeling it facilitated their postnatal recovery and adjustment.102,103 NICE¹⁹ advises offering advice and support to women who wish to talk about their experience and encouraging the woman and her partner to accept support from family and friends. Gamble and Creedy¹⁰⁴ developed a counselling model for postpartum women after a traumatic birth. The results of their study suggest that women are more able to process events surrounding birth at 4–6 weeks postpartum rather than immediately, and that counselling offered too soon may interfere with the woman’s ability to process her experience. They identify key elements for counselling support that can be used by midwives, including showing kindness, listening with encouragement/prompting, clarifying misunderstandings, not justifying or defending care, gently challenging any self-blame, and identifying ways to enhance social support.

BOX 14.7: Postnatal interventions intended to reduce PTSD and PND

Counselling is an intervention intended to help the woman understand the cognitive processes that link the (birth) event with trauma reactions, with the intention of reducing her distress following a traumatic birth experience. Specialist training is required for this.

Debriefing is the most common term used and usually consists of one session within 4 weeks of a traumatic birth. The individual is encouraged to talk about his or her experience in order to promote emotional processing and understanding. The types of debriefing are as follows.

Psychological debriefing is a type of counselling.

Medical debriefing is provided by a midwife or doctor and may focus more on the medical events and explanations, and involves going through their notes.

Informal debriefing is similar to the interventions below.

Defusing is a term used by Alexander⁹⁵ to describe midwives giving women the opportunity to talk about their birth during the postnatal period.

Post-childbirth discussion as referred to in the literature is similar to ‘defusing’, or a listening and information service.

Listening service is similar to defusing and discussion but the emphasis is on listening. A listening and information service may be one that women can access to discuss unresolved issues in an unlimited time period postpartum.

‘Birth Afterthoughts’ programmes are where women meet with a midwife or midwife counsellor to go over the obstetric events of their birth and express their feelings. These programmes may be similar to listening and information services.

The problems related to ascertaining the effectiveness of debriefing and counselling may be due to inconsistency in the approaches used and the personal nature of this type of intervention.103,105 The research tends to focus on the provision of a specific session or sessions rather than providing opportunities for women to talk about their experience and have questions answered. Being able to recount what has happened to a sympathetic person has been shown to promote understanding and regaining of psychological equilibrium.¹⁰⁴ A formal session may result in women revisiting their experience at an inappropriate time and/or being provided with more information than they can cope with.

The opportunity for women to talk about their birth experience and gain the information they need may be provided during routine postnatal care or arranged later when the woman requests it. Women’s views of postnatal care have identified that they are frequently not encouraged to ask questions about their birth experience and how they felt about it, and that emotional support was often not provided.¹⁰³ Therefore midwives need to ensure they ask women if they have any concerns or questions regarding what happened during the birth of their baby and offer emotional support. Discussion should be led by the woman to avoid providing more information than she can take in, while providing information that will assist the mother in helping herself to recover. In this way women will be able to access the information they need when they want it. The 6-week postnatal check may be a more appropriate time for some women to discuss their birth, when they have sufficiently recovered from the emergency they experienced. However, only two out of the ten women in Mapp and Hudson’s³ study understood what had happened to them after their 6-week postnatal check with their general practitioner. For this reason Mapp⁹¹ suggests that it may be more appropriate for women who have experienced a birth emergency to have their appointment with a healthcare professional who had an understanding of the events.

Partners should also be included in postnatal care and provided with support and information. The woman and her partner may both develop PTSD, or less frequently only the partner.8,106 Partners are expected to provide support, understanding and consideration of the woman’s needs. However, a traumatic birth can sometimes negatively affect marital relationships and result in relationship breakdown.¹⁰⁷ The couple may have difficulty in expressing their feelings and emotions, resulting in a lack of understanding and inability to provide each other with affection and support. Women who feel violated by their experience may blame their partner and avoid intimacy. Also, women may avoid sex, fearing a subsequent pregnancy. The woman may feel guilty about not meeting the expectations of her partner. Partners have reported feeling rejected and frustrated,1,106 and they are often reluctant to seek help, as childbirth is viewed as a female event.⁹ If health professionals do not include them when providing care their emotional needs may be neglected.

If a woman or her partner show any signs of PTSD or PND it is important that they are referred for diagnosis and treatment. Cognitive behaviour therapy (CBT) has been shown to be effective for PTSD,⁶⁵ though it is not useful for all cases. Peeler et al.¹⁸ suggest that face-to-face counselling or structured writing (written emotional disclosure) may be used to reduce PTSD symptoms. NICE¹⁹ advises offering CBT or eye movement desensitisation and reprocessing (EMDR) for PTSD. In the case of PND, CBT and/or anti-depressant medication can be used according to the woman’s preference and condition.¹⁹

CONCLUSION

PTSD and PND are more common in women and their partners when a birth emergency occurs,4,5,7,64 and psychological considerations are an essential part of midwifery care at such a time. Some women are more at risk of PTSD and PND due to factors other than the birth emergency, and these need to be taken into consideration.³⁶ Information from women and their partners indicates that professionals may focus on the birth emergency and physical care,2,3 whereby the woman and her partner may not be listened to and not informed of what is happening, resulting in emotions such as anger, fear and loss of control, which in turn increase poor psychological outcomes. Working in partnership with the woman and including her partner may provide the support needed to help the couple cope psychologically when an emergency occurs. The risk of PTSD and PND is increased when women and their partners do not feel supported and have a poor relationship with those providing care. A traumatic birth is ‘in the eye of the beholder’⁶⁰ and information from parents clearly shows that it is important that caregivers communicate and show that they care. Feeling the care provided at the time was appropriate and ‘the right thing was done’⁶¹ improves the experience of the woman and her partner and facilitates a good psychological outcome.

Following a birth emergency it is important that psychological care is continued to support parent/infant bonding and assist the couple in coming to terms with what has happened. The couple may initially feel ‘shell shocked’ so information needs to be provided when they are physically and emotionally able to take it in. Information may need to be repeated with additional explanations to assist understanding and avoid unresolved issues.

Strategies need to be incorporated in emergency skills training so they can be rehearsed and implemented. Midwives have a key role in providing emotional support and consequently can make a big difference to a woman and her partner’s experience and memories of childbirth.

SUMMARY OF MIDWIFERY RESPONSIBILITIES

•  Antenatal considerations

•  Identify women with or at risk of mental ill health.

•  Ensure women requiring specialist care are appropriately referred and followed up.

•  Provide antenatal information that prepares women and their partners for birth ‘not going to plan’.

•  Provide care that supports the woman emotionally as well as her physical health.

•  Labour considerations

•  Use all appropriate strategies (see Box 14.5) to minimise emotional trauma during a birth emergency.

•  Ensure effective communication at all times (including non-verbal).

•  Include and support partners as appropriate.

•  Ensure appropriate pain relief.

•  Maintain continuity of caregivers wherever possible.

•  Postnatal considerations

•  Promote parental/baby bonding.

•  Ensure appropriate pain relief.

•  Provide opportunities and support for women wishing to talk about their experiences, following their lead as to the amount and sort of information which is appropriate.

•  Refer women for specialist support as necessary.

REFERENCES

1.  Elmir R, Schmied V, Wilkes L, Jackson D. 2010. Women’s perceptions and experiences of a traumatic birth: A meta-ethnography. Journal of Advanced Nursing, 66(10):2142–2153.

2.  Thompson J, Ford J, Raynes-Greenow C, Roberts C, Ellwood D. 2011. Women’s experiences of care and their concerns and needs following a significant primary postpartum hemorrhage. Birth, 38(4):327–335.

3.  Mapp T, Hudson K. 2005. Feelings and fears during obstetric emergencies – 1. British Journal of Midwifery, 13(1):30–35.

4.  Wijma K, Ryding EL, Wijma B. 2002. Predicting psychological well-being after emergency caesarean section: A preliminary study. Journal of Reproductive and Infant Psychology, 20(1):25–36.

5.  Gamble J, Creedy D. 2005. Psychological trauma symptoms of operative birth. British Journal of Midwifery, 13(4):218–224.

6.  Somera MJ, Feely N, Ciofani L. 2010. Women’s experience of an emergency caesarean birth. Journal of Clinical Nursing, 19:2824–2831.

7.  White G. 2007. You cope by breaking down in private: Fathers and PTSD following childbirth. British Journal of Midwifery, 15(1):39–45.

8.  Iles J, Slade P, Spilby H. 2011. Posttraumatic stress symptoms and postpartum depression on couples after childbirth: The role of partner support and attachment. Journal of Anxiety Disorders, 25:520–530.

9.  Hinton L, Locock L, Knight M. 2014. Partner experiences of “near-miss” events in pregnancy and childbirth in the UK: A qualitative study. PLoS ONE, 9(4):1–8 e91735. doi:10.1371/journal.pone.0091735.

10.  Solderquist J, Wijma B, Thorbert G, Wijma K. 2009. Risk factors in pregnancy for post-traumatic stress and depression after childbirth. BJOG: An International Journal of Obstetrics and Gynaecology, 116:672–680.

11.  White T, Matthey S, Boyd K, Barnett B. 2006. Postnatal depression and posttraumatic stress after childbirth: Prevalence, course and co-occurrence. Journal of Reproductive and Infant Psychology, 24(2):107–120.

12.  O’Donovan A, Alcorn KL, Patrick JC, Creedy DK, Dawe S, Devilly GJ. 2014. Predicting posttraumatic stress disorder after childbirth. Midwifery, 30:935–941.

13.  American Psychiatric Association (APA). 1994. Diagnostic and Statistical Manual of Mental Disorders. 4th ed. Washington, DC: APA.

14.  American Psychiatric Association (APA). 2013. Diagnostic and Statistical Manual of Mental Disorders. 5th ed. Arlington, VA: APA.

15.  Verreault N, Da Costa D, Marchand A, Ireland K, Banack H, Dritsa M, Khalife S. 2012. PTSD following childbirth: A prospective study of incidence and risk factors in Canadian women. Journal of Psychosomatic Research, 73:257–263.

16.  Cox JL, Holden JM, Sagovsky R. 1987. Detection of postnatal depression: Development of the 10-item Edinburgh Postnatal Depression Scale. British Journal of Psychiatry, 150:782–876.

17.  Beck A, Ward C, Mendelsohn M, Mock J, Earbaugh J. 1961. An inventory for measuring depression. Archives of General Psychiatry, 4:561–571.

18.  Peeler S, Chung M, Stedmon J, Skirton H. 2013. A review assessing the current treatment strategies for postnatal psychological morbidity with a focus on post-traumatic stress disorder. Midwifery, 29:377–388.

19.  National Institute for Clinical Excellence (NICE). 2014. Antenatal and Postnatal Mental Health: Clinical Management and Service Guidance: NICE Guideline 192. London: NICE.

20.  Littlewood J, McHugh N. 1997. Maternal Distress and Postnatal Depression: The Myth of the Madonna. London: Macmillan.

21.  Glangeaud-Freudenthal NM-C. 2003. Channi Kumar and the history of the Marce society. Archives of Women’s Mental Health, 6(Suppl. 2): s79–s82.

22.  Shorter E. 1991. Women’s Bodies. A Social History of Women’s Encounter with Health, Ill-Health, and Medicine. London: Transaction.

23.  Oakley A. 1993. Essays on Women, Medicine and Health. Edinburgh, UK: Edinburgh University Press.

24.  Radley A. 1994. Making Sense of Illness: The Social Psychology of Health and Disease. London: Sage.

25.  McCourt C. 2009. Social support and childbirth. In: Squire C (Ed.). The Social Context of Birth. 2nd ed. Oxford: Radcliffe Medical Press.

26.  Scheidner Z. 2002. An Australian study of women’s experiences of their first pregnancy. Midwifery, 18:238–249.

27.  Pitt B. 1968. Atypical depression following childbirth. British Journal of Psychiatry, 114:1325–1335.

28.  Murray L, Cooper PJ. 1997. Postpartum Depression and Child Development. London: Guilford Press.

29.  Beck CT, Driscoll JD. 2006. Postpartum Mood and Anxiety Disorders: A Clinician’s Guide. London: Jones and Bartlett.

30.  Paulson JF, Bazemore SD. 2010. Prenatal and postpartum depression in fathers and its association with maternal depression: A meta-analysis. Journal of the American Medical Association, 303(19): 1961–1969.

31.  Brockington IF, Cernick KF, Schofield EM, Downing AR, Francis AF, Keelan C. 1981. Puerperal psychosis: Phenomena and diagnosis. Archives of General Psychiatry, 38:829–833.

32.  Centre for Maternal and Child Enquiries (CEMACE). 2011. Saving mothers’ lives: Reviewing maternal deaths to make motherhood safer: 2006–08. The eighth report on confidential enquiries into maternal deaths in the United Kingdom. BJOG: An International Journal of Obstetrics and Gynaecology, 118(Suppl. 1): 1–203.

33.  Wijma K. 2006. Post-traumatic stress disorder and childbirth. In: Keane V, Marsh M, Seneviratne G (Eds.). Psychiatric Disorders and Pregnancy. London: Taylor & Francis, pp. 161–196.

34.  American Psychiatric Association (APA). 1987. Diagnostic and Statistical Manual of Mental Disorders. 3rd ed. – Revised. Washington, DC: APA.

35.  Leeds L, Hargreaves I. 2008. The psychological consequences of childbirth. Journal of Reproductive and Infant Psychology, 26(2):108–122.

36.  Ryding EL, Wijma K, Wijma B. 2000. Emergency cesarean section: 25 women’s experiences. Journal of Reproductive and Infant Psychology, 18(1):33–39.

37.  Menage J. 1993. Post-traumatic stress disorder in women who have undergone obstetric and/or gynaecological procedures. Journal of Reproductive and Infant Psychology, 11(4):221–228.

38.  Lev-Wiesel R, Daphna-Tekoah S, Hallak M. 2009. Childhood sexual abuse as a predictor of birth-related posttraumatic stress and postpartum posttraumatic stress. Child Abuse and Neglect, 33:877–887.

39.  Bowman ML. 1999. Individual differences in posttraumatic distress: Problems with the DSM-IV model. Canadian Journal of Psychiatry, 44:21–33.

40.  Lewis G (Ed.). 2007. Confidential Enquiry into Maternal and Child Health (CEMACH). Saving Mothers’ Lives: Reviewing Maternal Deaths to Make Motherhood Safer – 2003–2005. The seventh report on Confidential Enquiries into Maternal Deaths in the United Kingdom. London: CEMACH London.

41.  Knight M, Kenyon S, Brocklehurst P, Neilson J, Shakespeare J, Kurinczuk JJ (Eds.), on behalf of MBRRACE-UK. 2014. Saving Lives, Improving Mothers’ Care – Lessons Learned to Inform Future Maternity Care from the UK and Ireland Confidential Enquiries into Maternal Deaths and Morbidity 2009–12. Oxford: National Perinatal Epidemiology Unit, University of Oxford.

42.  O’Hara MW, Swain AM. 1996. Rates and risk of postpartum depression: A meta-analysis. International Review of Psychiatry, 8:37–54.

43.  Zar M, Wijma K, Wijma B. 2002. Relations between anxiety disorders and fear of childbirth during late pregnancy. Clinical Psychology and Psychotherapy, 9:122–130.

44.  Fenech G, Thomson G. 2014. Tormented by ghosts from their past: A meta-synthesis to explore the psychosocial implications of a traumatic birth on maternal well-being. Midwifery, 30:185–193.

45.  Nieminen K, Stephansson O, Ryding EL. 2009. Women’s fear of childbirth and preference for cesarean section – A cross-sectional study at various stages of pregnancy in Sweden. Acta Obstetricia Gynecologica Scandinavica, 88(7):807–813.

46.  Fenwick J, Toohill RM, Creedy D, Smith J, Gamble J. 2015. Sources, responses and moderators of childbirth fear in Australian women: A qualitative investigation. Midwifery, 31:239–246.

47.  Fones C. 1996. Post-traumatic stress disorder occurring after painful childbirth. Journal of Nervous and Mental Disease, 18:195–196.

48.  Johansson M, Fenwick J, Premberg A. 2015. A meta-synthesis of father’s experiences of their partner’s labour and the birth of their baby. Midwifery, 31:9–18.

49.  Mitchell D, Chapman P. 2002. Part of the Team or Warming the Bench? Nelson, NZ: Nelson Marlborough Institute of Technology, Nelson Marlborough District Health Board.

50.  Ayres S, Radoš SN, Balouch S. 2015. Narratives of traumatic birth: Quality and changes over time. American Psychological Association, 7(3):234–242.

51.  Department of Health. 1993. Changing Childbirth, Part 1: Report of the Expert Maternity Group. London: HMSO.

52.  Department of Health. 2004. National Service Framework for Children, Young People and Maternity Services. London: HMSO.

53.  Department of Health. 2007. Maternity Matters: Choice, Access and Continuity of Care in a Safe Service. London: HMSO.

54.  Department of Health. 2012. Compassion in Practice. Nursing Midwifery and Care Staff: Our Vision and Strategy. London: National Health Service Commissioning Board. Available at https://www.england.nhs.uk/wp-content/uploads/2012/12/compassion-in-practice.pdf (accessed Feb 24, 2016).

55.  Rogers J Associates (Ed.). 2010. Midwifery 2020: Delivering Expectations. Cambridge: Midwifery 2020 Programme.

56.  Beech B, Robinson J. 1985. Nightmares following childbirth. British Journal of Psychiatry, 147: 586.

57.  Kitzinger S. 2004. Flashbacks, nightmares and panic attacks after birth. British Journal of Midwifery, 12(1):12.

58.  Kitzinger S. 2005. The Politics of Birth. London: Elsevier.

59.  Harris R, Ayres S. 2012. What makes labour and birth traumatic? A survey of intrapartum ‘hotspots’. Psychology and Health, 27(10):1166–1177.

60.  Beck CT. 2004. Birth trauma in the eye of the beholder. Nursing Research, 53(1):28–35.

61.  Green JM, Coupland VA, Kitzinger JV. 1998. Great Expectations: A Prospective Study of Women’s Expectations and Experiences of Childbirth. 2nd ed. Hale Cheshire: Books for Midwives Press.

62.  Soderquist J, Wijma B, Wijma K. 2006. The longitudinal course of post-traumatic stress after childbirth. Journal of Psychosomatic Obstetrics and Gynaecology, 27(2):113–119.

63.  Alcorn K, O’Donovan A, Patrick J, Creedy D, Devilly GA. 2010. A prospective longitudinal study of the prevalence of posttraumatic stress disorder resulting from childbirth events. Psychological Medicine, 40:1849–1859.

64.  Creedy D, Shochet I, Horsfall J. 2000. Childbirth and the development of acute trauma symptoms: Incidence and contributing factors. Birth, 27(2):104–111.

65.  Ayers S, McKenzie-McHarg K, Eagle A. 2007. Cognitive behaviour therapy for postnatal post-traumatic stress disorder: Case studies. Journal of Psychosomatic Obstetrics and Gynaecology, 28(3):177–184.

66.  Ayers S, Wright DB, Wells N. 2007. Symptoms of post-traumatic stress disorder in couples after birth: Association with the couple’s relationship and parent-baby bond. Journal of Reproductive and Infant Psychology, 25(1):40–50.

67.  Longworth H. 2006. Should fathers be in the labour room? Yes, for support not intervention. British Journal of Midwifery, 14(5): 288.

68.  Parfitt YM, Ayers S. 2009. The effect of post-natal symptoms of post-traumatic stress and depression on the couple’s relationship and parent-baby bond. Journal of Reproductive and Infant Psychology, 27(2):127–142.

69.  Skari H, Skreden M, Malt UF, Dalholt M, Ostensen AB, Egeland T, Emblem R. 2002. Comparative levels of psychological distress, stress symptoms, depression and anxiety after childbirth – A prospective population-based study of mothers and fathers. BJOG: An International Journal of Obstetrics and Gynaecology, 109:1154–1163.

70.  Breslau N, Davis G, Andreski P, Peterson E, Schultz LR. 1997. Sex differences in posttraumatic stress disorder. Archives of Women’s Mental Health, 9:1044–1048.

71.  Ballard CG, Stanly AK, Brockington IF. 1995. Posttraumatic stress disorder after childbirth. British Journal of Psychiatry, 166:525–528.

72.  Czarnocka J, Slade P. 2000. Prevalence and predictors of post-traumatic stress symptoms following childbirth. British Journal of Clinical Psychology, 39:25–51.

73.  Joseph S, Bailham D. 2004. Traumatic childbirth: What we know and what we can do. Midwives, 7(6):258–261.

74.  Trowell J. 1982. Possible effects of emergency caesarean section: A research study of the mother/child relationship. Early Human Development, 7:41–51.

75.  Boorman RJ, Devilly GJ, Gamble J, Creedy DK, Fenwick J. 2014. Childbirth and criteria for traumatic events. Midwifery, 30:255–261.

76.  Ford E, Ayres S. 2011. Support during birth interacts with prior trauma and birth intervention to predict postnatal post-traumatic stress symptoms. Psychology and Health, 26(12):1553–1570.

77.  Calam RM, Lambrenos K, Cox AD, Weindling AM. 1999. Maternal appraisal of information given around the time of preterm delivery. Journal of Reproductive and Infant Psychology, 17(3):267–280.

78.  Ayers S. 2007. Thoughts and emotions during traumatic birth: A qualitative study. Birth, 34(3):253–263.

79.  National Institute for Clinical Excellence (NICE). Postnatal care up to 8 weeks after birth NICE guideline 37. London; 2006 (Updated 2014, modified 2015). Available at https://www.nice.org.uk/guidance/cg37 (accessed September 7, 2015).

80.  Redshaw M, Heikkilä K. 2011. Ethnic differences in women’s worries about labour and birth. Ethnicity and Health, 16(3):213–223.

81.  Ternström E, Hildingsson I, Haines H, Rubertsson C. 2015. Higher prevalence of childbirth related fear in foreign born pregnant women – Findings from a community sample in Sweden. Midwifery, 31:445–450.

82.  National Institute for Health and Care Excellence (NICE). 2014. Intrapartum Care for Healthy Women and Babies. Available at http://www.nice.org.uk/guidance/cg190 (accessed Feb 24, 2016).

83.  Zauderer C, Galea E. 2010. Breastfeeding and depression: Empowering the new mother. British Journal of Midwifery, 18(2):88–91.

84.  Beck CT, Watson S. 2008. Impact of birth trauma on breast-feeding: A tale of two pathways. Nursing Research, 57:228–236.

85.  Erlandsson K, Dsilna A, Fagerberg I, Christensson K. 2007. Skin-to-skin care with the father after cesarean birth and its effect on newborn crying and prefeeding behavior. Birth, 34(2):105–113.

86.  Johnson K. 2013. Maternal-infant bonding: A review of literature. International Journal of Childbirth Education, 28(3):17–22.

87.  Obeidat HM, Bond EA. Callister LC. 2009. The parental experience of having an infant in the newborn intensive care unit. Journal of Perinatal Education, 18(3):23–29.

88.  Sargent AN. 2009. Predictors of needs in mothers with infants in the neonatal intensive care unit. Journal of Reproductive and Infant Psychology, 27(2):195–205.

89.  Crathern L. 2009. Dads matter too: A review of the literature focusing on the experiences of fathers of preterm infants. MIDIRS Midwifery Digest, 19(2):159–167.

90.  Brockington IF. 2004. Diagnosis and management of post-partum disorders: A review. World Psychiatry, 3:89–95.

91.  Mapp T. 2005. Feelings and fears post obstetric emergencies – 2. British Journal of Midwifery, 13(1):36–40.

92.  Ayers S, Claypool J, Eagle A. 2006. What happens after a difficult birth? Postnatal debriefing services. British Journal of Midwifery, 14(3):157–161.

93.  Symon A. 1997. Improving communication: Apologies and explanations. British Journal of Midwifery, 5(10):594–596.

94.  Baxter J, McCourt C, Jarrett P. 2014. What is current practice in offering debriefing services to post partum women and what are the perceptions of women in accessing these services: A critical review of the literature. Midwifery, 30:194–219.

95.  Alexander J. 1998. Confusing debriefing and defusing postnatally: The need for clarity of terms, purpose and value. Midwifery, 14:122–124.

96.  Rowan C, Bick D, Bastos MH. 2007. Postnatal debriefing interventions to prevent maternal mental health problems after birth: Exploring the gap between UK policy and practice. World Views on Evidence-based Nursing, 4(2):97–105.

97.  Gamble J, Creedy D, Webster J, Moyle W. 2002. A review of the literature on debriefing or non-directive counselling to prevent postpartum emotional distress. Midwifery, 18:72–79.

98.  Kershaw K, Jolly J, Bhabra K, Ford J. 2005. Randomised controlled trial of community debriefing following operative delivery. British Journal of Obstetrics and Gynaecology, 112:1504–1509.

99.  Priest SR, Henderson J, Evans SF, Hagan R. 2003. Stress debriefing after childbirth: A randomised controlled trial. Medical Journal of Australia, 178:542–545.

100.  Rose S, Bisson J, Churchill R, Wessely S. 2002. Psychological debriefing for preventing post-traumatic stress disorder. Cochrane Database of Systematic Reviews, 2: Art. No. CD000560. doi:10.1002/14651858.CD000560.

101.  Small R, Lumley J, Donohue L, Potter A, Waldenstrom U. 2000. Randomised controlled trial of midwife led debriefing to reduce maternal depression after operative birth. BMJ, 321:1043–1047.

102.  Gamble J, Creedy D, Moyle W, Webster J, McAllister M, Dickson P. 2005. Effectiveness of a counselling intervention after a traumatic childbirth: A randomised controlled trial. Birth, 32:11–19.

103.  Gamble J, Creedy D. 2004. Content and process of postpartum counselling after a distressing birth experience: A review. Birth, 31(3): 213–218.

104.  Gamble J, Creedy D. 2009. A counselling model for postpartum women after distressing birth experiences. Midwifery, 25: e21–e30.

105.  Kitzinger C, Kitzinger S. 2007. Birth trauma: Talking with women and the value of conversation analysis. British Journal of Midwifery, 15(5):256–264.

106.  Ayres S, Wright D, Wells N. 2007. Symptoms of post-traumatic stress disorder in couples after birth: Association with the couple’s relationship and parent-baby bond. Journal of Reproductive and Infant Psychology, 25(1):40–50.

107.  Wenzel A, Haugen EN, Jackson LC, Brendle JR. 2005. Anxiety symptoms and disorders at eight weeks postpartum. Journal of Anxiety Disorders, 19:295–311.

Glossary

Antenatal: Before birth; during or related to pregnancy

Bandl’s ring: An abnormal junction between upper and lower uterine segments, associated with obstructed labour; also known as a pathological retraction ring

Cell salvage: A procedure involving recovering blood lost during surgery and re-infusing it into the patient; also called ‘intraoperative blood salvage’ or ‘autologous blood transfusion’

Cleidotomy: Division (either surgically or digitally) of the clavicle of the fetus, usually during shoulder dystocia, to facilitate delivery

Clonus: Involuntary, rhythmic muscular contractions and relaxations denoting neurological response

Cotyledon: Small section, or lobe, of the placenta

Dehiscence: Rupture of a previously sutured (and/or healed) wound along the suture line

Diplopia: Double vision

Doppler: Evaluation of blood flow through a blood vessel; commonly used in pregnancy to look at the blood flow through the umbilical cord of the fetus

Entonox: A medical analgesic gas consisting of a mixture of nitrous oxide (50%) and oxygen (50%); also known as ‘gas and air’

Fulminating: Sudden, severe; worsening quickly

HELLP (haemolysis, elevated liver enzymes and low platelets) syndrome: A serious complication usually associated with pre-eclampsia

Ischaemia: A restriction in blood supply to the tissues

Orthopnea: Shortness of breath while lying down

Papilloedema: A swelling of the optic disc, usually caused by increased intracranial pressure

Paresis: A condition involving weak or impaired voluntary movement

Syntocinon: Synthetic oxytocin

Syntometrine: An obstetric combination drug used to contract the uterus, consisting of 5 units oxytocin and 0.5 mg ergometrine

Thrombocytopenia: Deficiency of thrombocytes (platelets) in the blood causing bleeding into the tissues, bruising, and slow blood clotting after injury

Thrombophilia: An abnormality of blood coagulation which increases the risk of thrombosis; also known as ‘hypercoagulability’ or a ‘prothrombotic state’

Tocolytic: A medication given to suppress labour (usually premature labour)

Tokophobia: A pathological fear of pregnancy and/or giving birth

Index

A

ABC, see Airway, breathing and circulation

Abdominal palpation, 95

ABG, see Arterial blood gas

ABUO, see Antepartum bleeding of unknown origin

ACE, see Angiotensin-converting enzyme

ACOG, see American Congress of Obstetricians and Gynecologists

Acquired thrombophilia, 62

Action on Pre-eclampsia (APEC), 77

Activated partial thromboplastin time (APTT), 70

Acute fatty liver of pregnancy (AFLP), 90; see also HELLP syndrome; Pre-eclampsia; Severe pre-eclampsia

clinical features, 90

midwifery responsibilities, 91

outcomes and postnatal issues for, 91

predisposing/risk factors, 90

Swansea criteria for diagnosis of, 90

Acute respiratory distress syndrome (ARDS), 170, 214

Adenosine triphosphate (ATP), 21

Advanced life support, 24; see also Maternal resuscitation

drugs, 25

electrode pad placement for defibrillation, 24

fluid replacement, 24–25

AEDs, see Automated external defibrillators

AES, see Anti-embolic stockings

AFE, see Amniotic fluid embolism

AFLP, see Acute fatty liver of pregnancy

AIMS, see Association for Improvement of Maternity Services

Airway, breathing and circulation (ABC), 196

ALSO, see Advanced Life Support in Obstetrics

American Congress of Obstetricians and Gynecologists (ACOG), 145

Amniotic fluid embolism (AFE), 181, 188

clinical features, 183–185

complications and long-term effects, 188

drugs, 187

epidemiology, 182

management, 186–188

midwifery responsibilities, 188–189

pathophysiology, 182–183

predisposing/risk factors, 185–186

treatment aims, 187

Tumultuous labour, 185

UKOSS case definition for, 184

Anaphylaxis, 214–215

Angiotensin-converting enzyme (ACE), 80

Angiotensin II receptor blockers (ARBs), 80

Antepartum bleeding of unknown origin (ABUO), 37

Antepartum haemorrhage (APH), 37, 163, 165; see also Placental abruption; Placenta praevia; Primary postpartum haemorrhage

causes of, 37–38

early pregnancy bleeding, 38

high parity and older age, 38

immediate management of major/massive, 46

midwifery responsibilities, 49

multiple pregnancy, 39

outcomes of, 48–49

previous caesarean section, 38

RCOG definitions used for assessing the severity of, 45

risk and predisposing factors for, 38–39

team members for managing major/massive, 46

treatment of, 45–48

unclassified bleeding, 37

vasa praevia, 37

vitamin deficiency, 38

Anticoagulation treatment, 68; see also Thromboembolism

checklist for midwives, 71

education, advice for women taking, 71–72

heparin, 68–69

laboratory tests for heparin, 70

during labour and delivery, 69

low molecular weight heparin, 69

Anti-embolic stockings (AES), 63

Anti phospholipid syndrome (APS), 62

Anxiety disorders, 227

APEC, see Action on Pre-eclampsia

APH, see Antepartum haemorrhage

Appendicitis, 215

APS, see Anti phospholipid syndrome

APTT, see Activated partial thromboplastin time

ARBs, see Angiotensin II receptor blockers

ARDS, see Acute respiratory distress syndrome

Artificial rupture of membranes (ARM), 185, 231

Association for Improvement of Maternity Services (AIMS), 231

Asthma, 215–216

Atonic uterus, 164

ATP, see Adenosine triphosphate

Automated external defibrillators (AEDs), 24

B

Bandl ring, 148, 249; see also Uterine rupture

Basic life support, 19, 21–24; see also Maternal resuscitation

advanced life support, 24

hand position for maternal chest compression, 23

head position for performing mouth-to-mask ventilation, 24

in-hospital resuscitation, 22

Being Open Framework, 9

Bladder 67, 100

Blood pH levels, 21

BMI, see Body mass index

Body mass index (BMI), 57, 128

Bohr effect, 29

Breech, 95; see also Malpresentation

abdominal palpation, 98

alternative and complementary therapies, 100–101

antenatal diagnosis, 98

birth, 104

Breech Trial, 96

to cephalic presentation, 98

classifications of, 96–97

delivery, 102–104

ECV, 98–100

emergency extraction, 104

features, diagnosis and reduction of, 97–98

historical context, 96

Lovset’s manoeuvre, 103

mechanism of labour in LSA position, 101–102

risks/predisposing factors, 97

undiagnosed breech, 101

vaginal breech delivery checklist, 105

vaginal examination, 101

Breech Trial, 96

Brow presentation, 110; see also Malposition

C

Carboprost, 170

Cardiopulmonary resuscitation (CPR), 23

Cardiotocography (CTG), 28, 42, 83, 99, 121

Care

bundles, 9

pathways, 8

CAS, see Central Alerting System

CBT, see Cognitive behavior therapy

CCT, see Controlled cord traction

Cell salvage, 171, 249

Central Alerting System (CAS), 5

Cerebrovascular accident, 216

Childbed fever, see Puerperal sepsis

Chorioamnionitis, 40

Cleidotomy, 249

Clonus, 249

Clot formation, 56

CMACE, see Centre for Maternal and Child Enquiries

Cognitive behavior therapy (CBT), 241

Compound presentation, 107; see also Malposition

Compulsive status epilepticus, 218

Computed tomography (CT), 215

Computed tomography pulmonary angiogram (CTPA), 67

Controlled cord traction (CCT), 551

Cord prolapse, 119, 120

bladder filling following, 122

clinical issues, 120

diagnosis and outcomes, 121

exaggerated Sims position, 123

knee-chest position, 123

management, 121, 122–124

midwifery responsibilities, 125

mode of delivery, 124

professional considerations, 124–125

risk factors, 119–120

Cotyledon, 249

Couvelaire uterus, 39

CPR, see Cardiopulmonary resuscitation

CS, see Caesarean section

CT, see Computed tomography

CTPA, see Computed tomography pulmonary angiogram

CVP, see Central venous pressure

D

D&C, see Dilatation and curettage

Data Protection Act, 10

DC, see Dichorionic

Debriefing, 239

Deep vein thrombosis (DVT), 55; see also Thromboembolism

anticoagulation treatment and prevention, 68

diagnostic tests for, 65–66

management of, 66

symptoms of, 65

Dehiscence, 249

Department of Health (DH), 5

DH, see Department of Health

Diabetic ketoacidosis (DKA), 216–217

DIC, see Disseminated intravascular coagulation

Dichorionic (DC), 78

Dilatation and curettage (D&C), 145

Diplopia, 249

Disseminated intravascular coagulation (DIC), 20, 48, 90, 166

DKA, see Diabetic ketoacidosis

Doppler, 249

DVT, see Deep vein thrombosis

E

Eclampsia, 88; see also Acute fatty liver of pregnancy; HELLP syndrome; Pre-eclampsia; Severe pre-eclampsia

care of woman, 88

immediate care of woman with, 89

magnesium sulphate toxicity, 89

midwifery responsibilities, 91

outcomes and postnatal issues for, 91

phases, 88

treatment regime, 89

Ectopic pregnancy, 217

ECV, see External cephalic version

EmCS, see Emergency caesarean section

EMDR, see Eye movement desensitization and reprocessing

E-P-A, see European Pathway Association

Epilepsy, 217–218

Ergometrine, 170

ERPC, see Evacuation of the uterus

European Pathway Association (E-P-A), 8

Evacuation of the uterus (ERPC), 171

External cephalic version (ECV), 40, 41, 95, 98; see also Moxibustion

contraindications to, 99

follow up, 100

potential risks associated with, 99

Eye movement desensitization and reprocessing (EMDR), 241

F

Face presentation, 110; see also Malposition

features and diagnosis, 110

immediate care/treatment, 111–112

mechanism, 111

referral, 112

FBC, see Full blood count

FDPs, see Fibrin degradation products

Fetal surveillance, 88

FFP, see Fresh frozen plasma

Fibrin degradation products (FDPs), 166

Fibroids, 218

Flu, see Influenza

Fresh frozen plasma (FFP), 175

Fulminating, 249

pre-eclampsia, see Severe pre-eclampsia

G

GAD-2, see Generalised Anxiety Disorder scale

GAS, see Group A betahaemolytic streptococcus

GCS, see Graduated compression stockings

Generalised Anxiety Disorder scale (GAD-2), 230; see also Psychological health and childbirth

Graduated compression stockings (GCS), 64

Group A betahaemolytic streptococcus (GAS), 194, 198, 200

H

Haematoma, 164

Hands and knees technique, 133

Hannah Trial, see Breech Trial

HCPC, see Health and Care Professions Council

Health and Care Professions Council (HCPC), 5

Healthcare organisations

accountability and duty of care, 3

Being Open Framework, 9

care bundles, 9

care pathways, 8

communication, 8–10

Compassion in Practice, 9–10

Data Protection Act, 10

elements for positive working culture, 6

human factors contributing to risk, 4

leadership, 6–7

local interprofessional training, 7

multiprofessional communication, 9

NRLS, 5

Nursing and Midwifery Order 2001, 5

positive culture creation, 6–7

professional issues and safe practice, 1, 12

professional standards of practice, 2

record-keeping, 10–12

risk assessment and management, 3–6

social media, 12

teamwork and multiprofessional training, 7–8

working together, 6

HELLP syndrome, 70, 84, 249; see also Acute fatty liver of pregnancy; Eclampsia; Pre-eclampsia; Severe pre-eclampsia

management of, 84

midwifery responsibilities, 91

optimal management of, 85

outcomes and postnatal issues for, 91

HELPERR mnemonic, 131

HemoCue, 174

Heparin, 68–69; see also Anticoagulation treatment

laboratory tests for monitoring, 70

HIE, see Hypoxic ischaemic encephalopathy

High regional blocks, 217

4Hs, 20

Hydralazine, 83–84

Hypertension, 78, 80

Hypoglycaemia, 219

Hypoxic ischaemic encephalopathy (HIE), 129

I

ICM, see International Confederation of Midwives

Infanticide Acts, 227

Infections, 193; see also Influenza; Pneumonia; Sepsis

clinical response to severe, 194

risk categories for respiratory, 201

risk factors, 195, 196

Influenza (Flu), 200; see also Infections

babies of mothers with, 203

clinical features and complications of, 201

deterioration symptoms, 200

emergency medical help, 204

features of serious breathlessness in pregnancy, 202

midwifery responsibilities, 205

pregnant women and, 202–203

to prevent spread of, 203

recommendations for management, 203–205

respiratory function assessment, 200

symptoms of, 202

vaccination, 205

Inherited thrombophilia, 62

INR, see International normalised ratio

International Confederation of Midwives (ICM), 3

International normalised ratio (INR), 70

Intrapartum haemorrhage (IPH), 161, 175; see also Primary postpartum haemorrhage

atony management, 170–171

causes, 163

diagnosis and management of, 167–172

management after delivery of placenta, 172–175

manual removal of placenta, 169, 172

midwifery responsibilities, 176–178

physiological/medical predisposing factors, 164

preparation for immediate delivery by caesarean section, 168

Intrauterine growth restriction (IUGR), 28, 77, 99

IPH, see Intrapartum haemorrhage

IUGR, see Intrauterine growth restriction

J

Johnson manoeuvre, 152

L

Labetalol, 83

LCHAD, see Long-chain acyl-CoA dehydrogenase

Leadership, 6

situational, 7

Left sacroanterior (LSA), 101

LMWH, see Low molecular weight heparin

Local interprofessional training, 7

Local Supervising Authority (LSA), 6

Long-chain acyl-CoA dehydrogenase (LCHAD), 90

Lovset’s manoeuvre, 103; see also Breech

Low molecular weight heparin (LMWH), 57, 61, 69

LSA, see Left sacroanterior; Local Supervising Authority

LSCS, see Lower segment caesarean section

LUS, see Lower uterine segment

M

Magnesium sulphate, 84, 89

Magnetic resonance imaging (MRI), 44, 215

Major Obstetric Haemorrhage (MOH), 46, 174

Malposition, 95, 112

brow presentation, 110

compound presentation, 107

definitions, 95

face presentation, 110–112

midwifery responsibilities, 112

oblique lie, 106–107

ongoing care, 112

OP position, 108–109

transverse lie, 106–107

Malpresentation, 95

Managing Obstetric Emergencies and Trauma (MOET), 131, 197

MAP, see Mean arterial pressure

Maternal cardiac arrest, 19

Maternal collapse, 211

abdominal pain, 213

anaphylaxis, 214–215

ARDS, 214

asthma, 215–216

cerebrovascular accident, 216

chest pain, 212

confusion, 212

convulsion, 213

DKA, 216–217

ectopic pregnancy, 217

emergency care, 213

epilepsy, 217–218

fibroids, 218

haematoma, 218

high regional blocks, 217

hypoglycaemia, 219

loss of consciousness, 211–212

myocardial infarction, 219

PPCM, 219

presenting symptoms, 211–214

pulmonary oedema, 219–220

rate of maternal collapse, 19

recognition of maternal collapse, 21

shock, 212–213

sickle cell crisis, 220

specific conditions, 214–220

thyroid storm, 220

trauma, 213

Maternal resuscitation, 19; see also Advanced life support; Basic life support

aortal and inferior vena caval compression, 26

4Hs and 4Ts, 20

maternal cardiac arrest, 19

midwifery responsibilities, 35

modifications to resuscitation for pregnant women, 25–27

normal blood pH levels, 21

physiological changes in pregnancy, 20, 21

uterine displacement, 26

Mauriceau-Smellie-Veit (MSV), 103; see also Breech

MBRRACE–UK, 5

McRoberts manoeuvre, 132, 133

Mean arterial pressure (MAP), 81

Methyldopa, 83

MI, see Myocardial infarction

Midwifery care, 12–13; see also Healthcare organisations

in AFE, 188–189

in APH, 49

assessment of respiratory function, 200

in cord prolapse, 125

emergency procedures, 171

in flu, 205

in haemorrhage, 176–178

in malpositions, 112

in pneumonia, 206–207

in pre-eclampsia, 91

in psychological health and childbirth, 242

in pulmonary embolism emergency, 69

in resuscitation, 35

in sepsis, 200

in shoulder dystocia, 137

in thromboembolism, 72

in uterine inversion, 154

in uterine rupture, 149–150

Midwives, 1; see also Healthcare organisations; Midwifery care; Nurses

Compassion in Practice, 9–10

effective supervision of, 6

Misoprostol, 170

MOH, see Major Obstetric Haemorrhage

Moxibustion, 100; see also External cephalic version

MRI, see Magnetic resonance imaging

MSV, see Mauriceau-Smellie-Veit

Multiprofessional communication, 9

Myocardial infarction (MI), 219

N

National Health Service Litigation Authority (NHSLA), 5

National Patient Safety Association (NPSA), 4

National Reporting and Learning System (NRLS), 4

Newborn life support, 32

Newborn resuscitation, 27

bag and valve, 30

Bohr effect, 29

care following resuscitation, 34–35

‘C’ grip for holding the mask, 30

clamping and cutting cord, 31

drugs, 34

equipment, 29–30

fetal adaptations in utero, 28

fetal physiology, 28

finger positions for neonate chest compressions, 33

head position for optimum airway opening, 33

in utero to ex utero transition support, 31–34

meconium, 34

midwifery responsibilities, 35

newborn life support, 32

outcome, 34

oxygen, 30

preparation for birth, 30–31

Resuscitation Council Guidelines, 27

risk factors for neonatal resuscitation, 28

two-person jaw thrust, 33

NHSLA, see National Health Service Litigation Authority

Nifedipine, 83

NMC, see Nursing and Midwifery Council

NPSA, see National Patient Safety Association

NRLS, see National Reporting and Learning System

Nurses, 1; see also Healthcare organisations; Midwives

Compassion in Practice, 9–10

Nursing and Midwifery Council (NMC), 1, 19, 136

Nursing and Midwifery Order 2001, 5

O

OA, see Occiput anterior

Oblique lie, 106–107

Obstetric haemorrhage, 163; see also Primary postpartum haemorrhage, Antepartum haemorrhage

Occipito posterior position (OP position), 108; see also Malposition

clinical features and diagnosis, 108

immediate care/treatment, 109

mechanism, 108–109

Occiput anterior (OA), 95

position, 108

OP position, see Occipito posterior position

P

Paresis, 249

PCR, see Protein:creatinine ratio

PE, see Pulmonary embolism

PEA, see Pulseless electrical activity

Peak expiratory flow rate (PEFR), 16

peep, see Positive end-expiratory pressure

PEFR, see Peak expiratory flow rate

Peripartum cardiomyopathy (PPCM), 219

Persistent occipitoposterior (POP), 109

Placenta accreta, 166

Placenta increta, 166

Placental abruption, 39; see also Antepartum haemorrhage

aetiology and risk factors, 40

chorioamnionitis, 40

direct trauma to abdomen, 40

factors, 40

hypertensive disorders, 40

migraines, 40

pathophysiology of, 39

placental implantation, 42

recurrence, 42

respiratory diseases, 42

risk factors for, 41

smoking, 41–42

sudden decompression of uterine cavity, 40

symptoms, 42

thrombophilias, 42

treatment of, 47

vascular changes in pregnancy, 40

Placenta percreta, 166

Placenta praevia, 42; see also Antepartum haemorrhage

classification, 43

diagnosis and antenatal management of, 43–44

pathophysiology of, 43

risk factors for, 41

symptoms, 44

treatment of, 48

PND, see Postnatal depression

Pneumonia, 205; see also Infections

clinical features of, 206

management in pregnancy, 206

midwifery responsibilities, 206–207

POP, see Persistent occipitoposterior

Positive end-expiratory pressure (peep), 29

Postnatal depression (PND), 225, 226, 227, 241; see also Psychological health and childbirth

postnatal interventions to reduce, 240

Postnatal psychosis, 227

Post thrombotic syndrome (PTS), 56, 64

Post-traumatic stress (PTS), 225

Post-traumatic stress disorder (PTSD), 225, 241; see also Psychological health and childbirth

childbirth risk factors for, 233–237

DSM-V diagnostic criteria for, 228

postnatal interventions to reduce, 240

PPCM, see Peripartum cardiomyopathy

Pre-eclampsia, 62–63, 77, 78; see also Acute fatty liver of pregnancy; Eclampsia; HELLP syndrome; Severe pre-eclampsia

antenatal screening and specific care, 80

blood pressure, 80

clinical features, 78

diagnosis, 80

drugs, 83–84

full blood count, 82

liver function tests, 82

management, 82

MAP, 81

midwifery responsibilities, 91

outcomes and postnatal issues for, 91

pathophysiology, 79

PET screening, 81

prediction, 78

predisposing/risk factors, 78–79

proteinuria, 81

renal function tests, 82

serology, 81–82

symptoms of, 80

tissue hypoxia, 79

women at risk of developing, 79

Primary postpartum haemorrhage (Primary PPH), 161, 175; see also Intrapartum haemorrhage

causes, 163

disseminated intravascular coagulopathy, 175

four Ts, 163–164

incidence of, 162–163

internal bimanual compression, 174

management after delivery of placenta, 172–175

maternal symptoms of primary, 162

midwifery responsibilities, 176–178

physiological/medical predisposing factors, 164–167

rubbing up contraction, 173

Primary PPH, see Primary postpartum haemorrhage

Pro-coagulant factors, 56

Professionalism, 1

principles to be upheld, 2

Protamine titration (PT), 70

Protein:creatinine ratio (PCR), 81

Proteinuria, 81

Psychological health and childbirth, 225, 226, 241

antenatal care and pre-existing psychological factors, 229–231

antenatal mental health screening questions, 230

anxiety disorders, 227

birth traumas, 231–233, 234

CEMACE, 229

childbirth risk factors for PTSD, 233–237

debriefing, 239

DSM-V diagnostic criteria for PTSD, 228

GAD-2 scale, 230

Infanticide Acts, 227

midwifery responsibilities, 242

PND, 227

postnatal care following birth emergency, 238–241

postnatal interventions to reduce PTSD and PND, 240

postnatal psychosis, 227

psychological disturbances, 226

PTSD, 228–229

six ‘Cs’, 231

strategies to minimise emotional trauma, 237

PT, see Protamine titration

PTS, see Post thrombotic syndrome; Post-traumatic stress

PTSD, see Post-traumatic stress disorder

Puerperal sepsis, 193

Pulmonary embolism (PE), 55; see also Thromboembolism

anticoagulation treatment and prevention, 68

clinical manifestations of, 66

diagnostic tools for, 66–67

midwife’s responsibilities in, 69

treatment of, 67–68

Pulmonary oedema, 219–220

Pulseless electrical activity (PEA), 24

R

RCM, see Royal College of Midwives

Recombinant factor VIIa (rFVIIa), 171

Record-keeping, 10; see also Healthcare organisations

during childbirth emergencies, 12

critical points to include in, 11

functions of, 11

local training, 10

Rectus, 218

Refusal of blood and blood components, 44–45

Renal function test (RFT), 88

Resuscitation, 19; see also Maternal resuscitation; Newborn resuscitation

RFT, see Renal function test

rFVIIa, see Recombinant factor VIIa

Right OP (ROP), 108

ROM, see Rupture of membranes

ROP, see Right OP

Royal College of Midwives (RCM), 5

S

SaFE, see Simulation and Fire drill Evaluation

SBAR (situation, background, assessment, recommendation), 8

Sepsis, 193, 194; see also Infections

assessment and diagnosis, 195

clinical features, 197–198

GAS, 194, 198, 200

investigations for, 197

management, 198–199

midwifery responsibilities, 200

risk factors, 195, 196

septic shock, 194–195

sites of infection, 195

symptoms, 197

Severe pre-eclampsia, 85; see also Acute fatty liver of pregnancy; Eclampsia; HELLP syndrome; Pre-eclampsia

blood pressure measurement, 85–86

care of woman with, 85, 86–88

midwifery responsibilities, 87, 91

postnatal issues for, 91

renal function, 86

serology, 86

symptoms of, 86

Shoulder dystocia, 127

cleidotomy, 135

critical points to include within record-keeping during, 136

degrees of, 127–128

episiotomy, 132

fetal/neonate complications, 129

first-line manoeuvres, 132–134

hands and knees technique, 133

HELPERR, 131

incidence, 128

internal rotational manoeuvre, 136

issues around management of, 130

maternal complications, 130

McRoberts manoeuvre, 132, 133

midwifery responsibilities, 137

professional considerations, 136–137

release of posterior arm, 135

risk factors, 128, 129

second-line manoeuvres, 134–135

suprapubic pressure, 132–133

symphysiotomy, 135

third-line manoeuvres, 135

Zavanelli manoeuvre, 135–136

Sialyl Tn antigen (STN), 183

Sickle cell crisis, 220

Simulation and Fire drill Evaluation (SaFE), 8

SIRS, see Systemic inflammatory response syndrome

Six ‘Cs’, 231; see also Psychological health and childbirth

SOAPS, 131

Statutory supervision, 5

STN, see Sialyl Tn antigen

Stroke, 216

Suprapubic pressure, 132

Syntocinon, 165, 249

Syntometrine, 170, 249

Systemic inflammatory response syndrome (SIRS), 194

T

T1DM, see Type I diabetes mellitus

TCM, see Traditional Chinese medicine

TEDS, see Thromboembolic deterrent stockings

Thrombocytopenia, 249

Thromboembolic deterrent stockings (TEDS), 57, 63

Thromboembolism, 55, 72; see also Anticoagulation treatment; Deep vein thrombosis; Pulmonary embolism; Venous thromboembolism

antenatal prophylaxis with LMWH, 61

caesarean section, 62

compression stockings, 63

epidemiology, 55–56

guidance on compression stockings, 64

immobility, 63

inherited or acquired thrombophilia, 62

intermittent pneumatic compression devices, 65

medical and midwifery measures, 63–65

midwifery responsibilities, 72

obstetric thromboprophylaxis risk assessment and management, 58, 59

pathophysiology, 56–57

post-thrombotic syndrome, 56

pre-eclampsia, 62–63

prophylactic measures, 64

raised BMI, 62

risk assessment, 57

risk factors, 61–63

thrombophilia conditions, 62

triad of factors, 56

vascular damage, 57

venous stasis, 56

women with mechanical heart valves, 63

Thrombophilia, 249

Thyroid storm, 220

Tocolytic, 249

Tokophobia, 249

Traditional Chinese medicine (TCM), 100

Tranexamic acid, 171

Transverse lie, 106–107; see also Malpresentation

Tumultuous labour, 185

Type I diabetes mellitus (T1DM), 216

U

U&E, see Urea and electrolyte

UAD, see Umbilical artery Doppler

UH, see Unfractionated heparin

Umbilical artery Doppler (UAD), 78

Umbilical cord prolapse, see Cord prolapse

Umbilical venous catheter (UVC), 34

Unfractionated heparin (UH), 67

Urea and electrolyte (U&E), 88

Uterine complications, 143; see also Uterine inversion; Uterine rupture

Uterine dehiscence, 148; see also Uterine rupture

Uterine inversion, 150

aetiology, 150

diagnosis, 152

factors associated with, 151

management, 152–154

midwifery responsibilities, 154

professional issues, 154

risk factors for, 150

severity of, 150

symptoms, 151–152

timing, 150

Uterine rupture, 143

incomplete, 148

management, 148

midwifery responsibilities, 149–150

outcome, 148–149

risk factors for, 144–147

symptoms, 147–148

Uteroplacental apoplexy, see Couvelaire uterus

UVC, see Umbilical venous catheter

V

Vaginal birth after Caesarean (VBAC), 143

Vasa praevia, 37, 167; see also Antepartum haemorrhage

VBAC, see Vaginal birth after Caesarean

Venous thromboembolism (VTE), 55; see also Thromboembolism

previous history of, 61–62

risk assessment for, 60

risk factors for, 57

Ventilation/perfusion (V/Q), 67

Ventricular fibrillation (VF), 24

Ventricular tachycardia (VT), 24

VF, see Ventricular fibrillation

V/Q, see Ventilation/perfusion

VT, see Ventricular tachycardia

VTE, see Venous thromboembolism

Z

Zavanelli manoeuvre, 135–136